Scientific American Biology For A Changing World With Core Physiology 3Rd Edition Shuster Test Bank Full Chapter PDF

Scientific American Biology for a
Changing World with Core Physiology

3rd Edition Shuster Test Bank
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Name: __________________________ Date: _____________
1. In an otherwise normal cell, what happens if one mistake is made during DNA
replication?
A) Nothing; mistakes just happen.
B) A cell cycle checkpoint detects the error and pauses the cell cycle so the error can
be corrected.
C) The cell will begin to divide out of control, forming a malignant tumor.
D) Mistakes are never made during DNA replication.
E) The mutation will be inherited by the individual's offspring.
2. Why does wearing sunscreen reduce cancer risk?

A) Sunscreen can repair damaged DNA.
B) Sunscreen can activate checkpoints in skin cells.
C) Sunscreen can reduce the chance of mutations caused by exposure to UV radiation
present in sunlight.
D) It does not reduce cancer risk; sunscreen causes mutation and actually increases
cancer risk.
E) Sunscreen can prevent cells with mutations from being destroyed.
3. A mutation can cause a change _____.

A) in the amino acid sequence of a protein
B) in the shape of a protein
C) in the way the cell cycle is regulated
D) that is beneficial to the cell
E) all of these
4. At which point does a mutation exert its potentially dysfunctional effects in a cell?
A) during DNA replication
B) during protein translation
C) after a protein is produced
D) during DNA transcription
E) only during cell division
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5. DNA mutations can arise from uncorrected errors in DNA replication, inheritance, and
_____.
A) a poor diet lacking in vitamins and minerals
B) chronic sleep deprivation
C) environmental insults
D) catching an influenza virus from a person with mutated genes
E) abnormal cell division
6. Look at the mutagens illustrated in Infographic 10.3. Of these, which are most easily
avoidable, and which are not avoidable?
7. Are all mutations bad? Explain your answer.
8. What are some differences and some similarities between tumor suppressor genes and
oncogenes?
9. What would you say to a niece if she asked you how she could reduce her risk of breast
cancer? (Assume there is no family history of breast cancer.) How might each of your
suggestions reduce her risk?
10. Why is age a risk factor for cancer?
11. What is the role of BRCA1 in normal cells?
12. A 28-year-old male graduate student was born with an inherited predisposition to colon
cancer due to a mutation in a DNA repair gene called MLH1. He has recently been
diagnosed with colon cancer. At the cellular and genetic level, was he born with colon
cancer? Was he born with a predisposition to colon cancer? At birth, were cells in his
colon genetically identical to cells in his liver? Now that he has colon cancer, are his
cancer cells genetically identical to his normal colon cells? Explain your answers.
13. People like Lorene Ahern have inherited a mutated version of BRCA1. Why does this
mutation pose a problem? Why are these people at high risk of developing breast cancer
when they still have a functional BRCA1 allele? Describe how the protein encoded by
normal BRCA1 compares to that encoded by mutant alleles of BRCA1.
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14. Nellie has a family history similar to Lorene Ahern's. Nellie's mother died at an early
age from breast cancer, as did her maternal aunt (her mother's sister). Nellie is not yet
35 but has started having annual mammograms. She has also been tested for BRCA1 and
BRCA2 mutations. She has a BRCA2 mutation and is considering prophylactic surgery.
Her younger sister, Anne, doesn't want to know the results of Nellie's genetic testing
because if Nellie has a BRCA2 mutation, then there is a chance that Anne could have
inherited the same mutation from their mother. Does Nellie or Nellie's doctor have an
obligation to tell Anne about the test results? What about Nellie's older brother? Should
he be told? There are personal and medical benefits and risks to consider here.
15. José is a 32-year-old landscaper living in Phoenix, Arizona. He and his 64-year-old
father, Ray, were both diagnosed with metastatic melanoma within 2 months of one
another. Both had their tumors biopsied to look for potential targets for targeted therapy.
The BRAF proto-oncogene from each of their tumors was sequenced. Their cancer cells
were analyzed for expression of PD-L1 (see Infographic 10.7). The data are shown in
the table below.
a. Transcribe and translate the BRAF gene sequences from José's and Ray's tumors.
What amino acid is at position 600 in each?
b. Zelboraf is a drug that stops division of metastatic melanomas by blocking the
activity of a mutant (oncogenic) BRAF protein that has a glutamic acid at position 600
(the proto-oncogene has a valine at position 600). Keytruda is an antibody drug that
blocks the interaction between PD-L1 on cancer cells and its binding partner (PD-1) on
immune cells (see IG 10.7). Given their individual tumors, what treatment(s) are
available for José and for Ray? Consider both targeted and traditional therapies and
justify your answer.
c. From the information presented, do you think this is more likely to be a case of
inherited cancer, or two cancers that just happened to occur in these two family
members? Explain your answer, and consider other risk factors that may be involved for
José and Ray.
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16. If you wanted to change your lifestyle to reduce your risk of developing cancer, what
specific steps could you take with respect to each of the following? Be as specific as you
can. Take your age and gender into consideration as you consider each factor.
a. alcohol consumption
b. sun exposure
c. tobacco use
d. exposure to pesticides
e. meat preparation (cooking method)
17. A mutation causes a substitution of one amino acid for another in the encoded protein.
What type of mutation is this?
A) silent
B) nonsense
C) missense
D) insertional frameshift
E) deletional frameshift
18. Which of the following is a known mutagen?

A) cigarette smoke
B) sunlight
C) charred meat cooked at high temperatures
D) X-rays
E) All of the answers are known mutatgens.
19. Why does wearing sunscreen reduce cancer risk?

A) Sunscreen can repair damaged DNA.
B) Sunscreen can activate checkpoints in skin cells.
C) Sunscreen can reduce the chance of mutations caused by exposure to UV radiation
present in sunlight.
D) It doesn't; sunscreen causes mutation and actually increases cancer risk.
E) Sunscreen can prevent cells with mutations from being destroyed.
20. In an otherwise normal cell, what happens if one mistake is made during DNA
replication?
A) Nothing; mistakes just happen.
B) A cell cycle checkpoint detects the error and pauses the cell cycle so the error can
be corrected.
C) The cell will begin to divide out of control, forming a malignant tumor.
D) A checkpoint will force the cell to carry out apoptosis, a form of cellular suicide.
E) The mutation will be inherited by the individual's offspring.
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21. Which of the following can cause cancer to develop and progress?
A) a proto-oncogene
B) an oncogene
C) a tumor suppressor gene
D) a mutated tumor suppressor gene
E) both an oncogene and a mutated tumor suppressor gene
F) both an oncogene and a tumor suppressor gene
22. Which form of breast cancer treatment is the least specific for the cancer cells?
A) chemotherapy
B) targeted therapy
C) immunotherapy
D) lumpectomy
23. A woman with a BRCA1 mutation

A) will definitely develop breast cancer.
B) is at increased risk of developing breast cancer.
C) must have inherited it from her mother because of the link to breast cancer.
D) will also have a mutation in BRCA2.
E) None of the answers are correct.
24. Which of the following family histories most strongly suggests a risk of inherited breast
cancer due to BRCA1 mutations?
A) many female relatives who were diagnosed with breast cancer in their 70s
B) many relatives with skin cancer
C) many relatives diagnosed with skin cancer at an early age
D) many female relatives diagnosed with breast cancer at an early age
E) many female relatives with both early breast cancer and ovarian cancer
25. Which of the following women would be most likely to benefit from genetic testing for
breast cancer?
A) a 25-year-old woman whose mother, aunt, and grandmother had breast cancer
B) a healthy 75-year-old woman with no family history of breast cancer
C) a 40-year-old woman who has a cousin with breast cancer
D) a 55-year-old woman whose older sister was just diagnosed with breast cancer
E) All women can benefit from genetic testing for breast cancer.
26. Define apoptosis. Why is apoptosis important?
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27. What is the purpose of the cell cycle checkpoints? What happens when a cell no longer
responds to these checkpoints?
28. Define metastasis. Do all cancers enter this stage?
29. Where do cancer cells differ in their cell cycle from normal cells?
30. Dermatologists looking for skin cancer usually don't worry about circular moles with
smooth edges, but they are concerned about moles with irregular shapes. What does the
shape of the mole tell the dermatologist about what is likely going on at a cellular level?
31. Doctors always hope to detect cancer in the early stages of tumor formation. What are
the problems associated with detecting cancer in the late stages?
32. Why do cancer patients undergoing chemotherapy and radiation therapy lose their hair?
33. Explain how radiation leads to apoptosis.
34. Explain why radiation therapy is NOT appropriate treatment for a metastasized cancer.
35. Most adults survive chemotherapy, but unborn children frequently do not. Why do you
think that is? Specifically, what is the difference between an adult and an unborn child
that would account for this difference?
36. You are trying to discover a new way to treat breast cancer that would specifically target
cancerous cells and not normal cells. You notice that cancerous breast cells express a
specific protein on their membranes, which normal cells do not express. Can you think
of a way to use this fact to your advantage?
37. List three types of genetic mutations that may occur.
38. Doctors will screen individuals with a strong family history of breast cancer for
mutations in the BRCA1 gene. Explain why someone who does not test positive for a
mutation can still be at risk for a BRCA1 mutation and breast cancer.
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39. How often do mistakes occur when copying DNA? Do all these mistakes appear in the
final, copied DNA?
40. Why should pregnant women never be given X-rays?
41. How can changing the DNA sequence change a protein's function?
42. Which type of mutation do you think is most harmful to a cell, a base substitution (e.g.,
an A is replaced by a G) or a base insertion (e.g., ACG becomes ACTG)? Why?
43. What is a mutagen?
44. What are the three main ways a person can acquire a mutation in their DNA?
45. For a mutation to become an allele it must occur in one of three possible locations. What
are those three?
46. Even though DNA repair enzymes correct most errors, approximately 1 in every one
billion nucleotides still contains an error. The human genome, however, is 3 billion
bases long. In an average adult, there are 50 trillion to 100 trillion cells, all of which
contain these 3 billion bases, and these trillions of cells divide all the time. Given all
this, why do you think people don't have cancer more often?
47. Explain how alterations of the BRCA proteins could lead to cancer.
48. If one has an inherited allele known to be linked to an increased risk of cancer, what are
some suggestions to lower the risk?
49. What is a carcinogen?
50. List at least five carcinogens.
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51. You have just had a BRCA analysis, in which your doctor ran tests to check for
abnormal BRCA alleles. You learn that you have a BRCA allele that has been associated
with cancer. Neither of your parents has this allele. How could this occur?
52. You've just received the results of your BRCA analysis (a check for abnormal BRCA
alleles). The results say that you carry one normal BRCA1 allele and one BRCA1 allele
associated with cancer, and two BRCA2 alleles that are associated with cancer. Does this
mean you will get cancer? Explain.
53. DNA insertions can have significant effects on an organism. How can adding DNA
cause an impact?
54. A woman who desires children but is about to undergo chemotherapy is told by her
doctor that she should consider having several of her eggs removed and stored for future
use. Why might a doctor encourage her to do this?
55. Under normal conditions, when a cell has too much DNA damage to be repaired, what
happens?
56. Explain the difference between an oncogene and a proto-oncogene. How is this related
to cancer?
57. There are two classes of genes that, when mutated, frequently lead to cancer. Which
class of these two types of genes promotes cell division and differentiation, and which
class of genes inhibits the cell cycle in order to make repairs?
58. What role does an oncogene play in generating a tumor?
59. Why do people become more likely to develop cancer as they age?
60. You are accidentally exposed to high levels of radiation in the upper part of your body
that damaged your DNA and caused you to develop throat cancer. You are concerned
that you will pass these mutations on to your children. Should you be concerned? Why
or why not?
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61. “A person who inherits a mutation in a cell cycle regulatory gene will develop cancer.”
Is this a true statement? Explain.
62. You have a family history of breast cancer and your doctor has just confirmed that you
have several alleles that have been linked to cancer. Is there anything you can do to
avoid cancer? Explain.
63. How can mutations in BRCA1 lead to an accumulation of mutations in the cell?
64. What is the role of estrogen in a woman's risk of developing breast cancer, especially if
she has a mutation in one of her BRCA genes?
65. Explain the effect of environmental mutagens in determining whether a woman with a
mutation in one of her BRCA genes will actually get cancer.
66. Women with mutations in their BRCA genes who have developed cancer may choose to
have their breasts, ovaries, or both removed. Does this eliminate or just reduce the risk
of cancer coming back? Explain your answer.
67. If a man inherits a mutation in one of his BRCA genes, is he at increased risk for cancer
compared with men who inherit normal copies of BRCA genes? Is he at a lower or
higher risk for cancer than a woman with the same mutation? Explain your answers.
68. If a cell sustains irreparable DNA damage during the S phase of the cell cycle the cell
will undergo _________.
69. Chemotherapy and radiation target both __________ and ___________ cells.
70. Mutations in a gene can lead to the development of new ______ for the gene.
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71. A specific gene, called GRAB, prevents a cell from entering mitosis if there are any
signs of DNA damage. This means that GRAB would be a type of
A) cell cycle checkpoint.
B) tumor-causing gene.
C) non-hereditary gene.
D) growth signal.
E) mutation.
72. Apoptosis
A) occurs in normal cell division.
B) contains several checkpoints.
C) is programmed cell death.
D) is a mechanism of cell repair.
E) ensures equal DNA in cytokinesis.
73. Cell cycle checkpoints detect and control

A) DNA content.
B) signals that promote cell division.
C) DNA damage.
D) proper chromosome alignment.
E) All of the above.
74. Cell division is usually kept under control by

A) apoptosis.
B) a single checkpoint in cytokinesis.
C) several checkpoints in the cell cycle and by apoptosis.
D) suicide checkpoints.
E) cell cycle repair mechanisms.
75. At the G2 checkpoint, cells pause to

A) wait until there is a need for them to divide.
B) make sure that all chromosomes have been copied and are undamaged.
C) make sure that the spindle is fully formed.
D) wait until all chromosomes are lined up properly.
E) make sure that the homologous chromosomes are wrapped around each other.
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76. At the G1 checkpoint, cells pause to
A) wait until there is a need for them to divide.
B) make sure that all chromosomes have been copied and are undamaged.
C) make sure that the nuclear envelope is intact.
D) make sure that all chromosomes are lined up properly.
E) make sure that the homologous chromosomes are wrapped around each other.
77. Programmed cell death is called

A) apoptosis.
B) endocytosis.
C) cytokinesis.
D) cytolysis.
E) mitosis.
78. Proteins scan chromosomes for damage during the

A) G1 checkpoint.
B) beginning of the synthesis phase.
C) apoptosis phase.
D) G2 checkpoint.
E) metaphase checkpoint.
79. There are several points during the cell cycle when the cell will check to be sure
everything is progressing normally, without mistakes, and confirm that the cell should
continue to the next phase of the cycle. When do these “cell cycle checkpoints” occur?
A) between G1 and S, and between G2 and mitosis
B) between G1 and G2, between G2 and mitosis, and during mitosis
C) between G1 and S, between G2 and mitosis, and during mitosis
D) between S and G2, between G2 and mitosis, and during cytokinesis
E) during S and cytokinesis
80. The cell cycle checkpoints are responsible for checking that the cell is prepared to move
on to the next stage in cell division. For example, the G1-to-S checkpoint ensures that
the cell has all the components and signals necessary to go on to S phase and that the
appropriate signals are present. The G2 checkpoint checks whether the
A) chromosomes have been separated properly.
B) DNA has been replicated properly.
C) chromosomes have aligned properly.
D) DNA has decondensed.
E) cell organelles have duplicated properly.
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81. What might be the result of a mutation in one of the proteins responsible for the G1
checkpoint?
A) The cell would continue to S phase without signals to divide being present.
B) The cell would divide uncontrollably.
C) The cell would move through the cell cycle more rapidly than normal.
D) Nothing; one of the other checkpoints would make up for its absence.
82. If a cell is irreparably damaged, it undergoes programmed cell death, called

A) apoptosis.
B) cell division.
C) metastasis.
D) cytokinesis.
E) mitosis.
83. Cancer consists of too much

A) cell division.
B) translation.
C) apoptosis.
D) toxin production.
E) DNA replication.
84. Which of the following help(s) to prevent cancer?

A) cell cycle checkpoints
B) apoptosis
C) DNA repair enzymes
D) regulation of the cell cycle
85. Cancer is
A) an organ that becomes malignant.
B) a metastatic cell.
C) unregulated apoptosis.
D) unregulated cell division.
E) regulated cell division.
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86. Cancer may be caused by
A) a cell cycle checkpoint problem.
B) failure in apoptosis.
C) unregulated cell division.
D) failure in DNA repair mechanisms.
87. Cell division in cancerous tumors

A) proceeds until apoptosis.
B) is regulated by the cell cycle.
C) progresses at a predicted rate.
D) is regulated by checkpoints.
E) accumulates DNA damage.
88. The medical condition of cells growing out of control is called

A) cytokinesis.
B) cancer.
C) metastasis.
D) apoptosis.
E) tumorization.
89. Cells that have accumulated too much chromosomal damage can
A) lead to the formation of a tumor.
B) lead to cancer.
C) cause the cell to destroy itself (apoptosis).
D) lead to uncontrolled cell division.
90. How could a cancerous cell evade apoptosis?

A) The cell responds to environmental signals.
B) The cell goes through the cell cycle too quickly for apoptosis to occur.
C) The cell has a mutation in a checkpoint protein.
D) The cell is stuck in one phase of the cell cycle.
E) Cancerous cells can't evade apoptosis.
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91. What causes cancer to kill people?
A) Cancer cells accumulate DNA mutations.
B) Tumors can spread to other parts of the body.
C) Cancer cells crowd out normal cells and disrupt organ functions.
D) Cancer cells have uncontrolled cell division.
E) Tumors cells contain abnormal DNA
92. True or False: Chemotherapy treatments only kill the cancer cells and don't affect
normal, healthy cells.
A) True
B) False
93. Chemotherapy is used in the battle against

A) breast cancer.
B) colon cancer.
C) skin cancer.
D) prostate cancer.
94. Chemotherapeutics act on

A) all dividing cells.
B) cancer cells.
C) all cells.
D) apoptotic cells.
E) dividing cancer cells.
95. Radiation therapy for cancer works by

A) burning the cells, thereby killing them.
B) damaging the cell's DNA, resulting in cell death.
C) interfering with the cell's mitotic spindle.
D) dissolving the tumor through heating.
E) freezing the cells, thereby killing them.
96. Physical side-effects from chemotherapy and radiotherapy could be maximally reduced
by
A) targeting specific tumor cells.
B) reducing amounts of drug or radiation.
C) reducing exposure time.
D) better detection methods.
E) using multiple drugs with radiation.
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97. Side-effects of chemotherapy, such as vomiting, hair loss, and bruising occur because
A) cancerous cells release toxins that poison the rest of the body.
B) cancerous cells have overtaken normal cells, causing malfunctions.
C) chemotherapeutic drugs specifically target cancerous cells.
D) chemotherapeutic drugs kill both normal and cancerous cells.
E) the body has an immune reaction to chemotherapeutic drugs.
98. Radiation and chemotherapy typically have all of the following side-effects EXCEPT
A) blurry vision.
B) nausea.
C) diarrhea.
D) vomiting.
E) hair loss.
99. Metastasis is
A) an effective form of treatment for cancer.
B) part of cell division, when chromosomes line up.
C) a state of rest for the cell, between divisions.
D) a state of active cell division.
E) the spread of cancer from one location in the body to another.
100. When cancer has spread to many areas of the body, the most common form of treatment
is
A) surgery to remove the tumors.
B) radiation directed at the tumors.
C) chemotherapy drugs injected into the bloodstream.
D) heat therapy directed at the tumors.
E) cold therapy directed at the tumors.
101. What is the name of the organization that oversees the quality control of pharmaceutical
drugs produced in the United States?
A) National Institutes of Health (NIH)
B) Environmental Protection Agency (EPA)
C) Federal Drug Administration (FDA)
D) Centers for Disease Control (CDC)
E) U.S. Department of Agriculture (USDA)
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102. Why would a drug that specifically kills rapidly dividing cells make a good
chemotherapeutic agent?
A) The drug would only target cancer cells.
B) The drug would not affect normal cells.
C) Cancer cells divide more rapidly than most normal cells.
D) Unlike radiation therapy, the drug would target a specific population of cells.
E) Cancer cells are the only cells dividing in a mature human.
103. Most chemotherapy drugs are effective because they

A) increase protein production.
B) increase the immune system response needed to fight cancer.
C) kill cancer cells only without affecting healthy cells.
D) interrupt cell division.
E) destroy the plasma membrane, thus causing cell death.
104. All of the following could be effective cancer treatments EXCEPT

A) a drug that enhances apoptosis.
B) a drug that increases DNA replication.
C) a drug that prevents formation of the mitotic spindle.
D) a drug that increases the immune system response.
E) a drug that makes cells more permeable to drugs.
105. Chemotherapy drugs interfere with

A) cell division.
B) chromosome duplication.
C) spindle formation.
D) chromosome separation during mitosis.
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106. One promising new treatment for cancer uses “angiogenesis inhibitors” such as
Avastin®. This treatment works because a growing tumor requires additional nutrients,
and thus excretes substances to encourage growth of new blood vessels to “feed” the
tumor. Angiogenesis inhibitors prevent that blood vessel growth. What might be one
benefit of this treatment over traditional chemotherapy?
A) It would not affect most dividing cells, and so it would be more specific than
traditional chemotherapy.
B) It would be able to target all tumors, and so it would be less selective than
C) It would starve cells in a tumor, which would kill them more gradually than
D) It targets only rapidly dividing cells because those are the ones that form tumors.
107. If you ran a pharmaceutical company, what would be the most effective series of steps
for your company to discover new drugs from plants and bring them to market?
A) Identify likely drug sources, test chemicals on cultured cells, select the most
effective chemical, convert chemical into a form for delivery into humans, do
clinical trials, get FDA approval for drug sales, scale up drug supply.
B) Identify likely drug sources, select the most effective chemical, convert chemical
into a form for delivery into humans, test chemicals on cultured cells, do clinical
trials, get FDA approval for drug sales, scale up drug supply.
C) Identify likely drug sources, select the most effective chemical, test chemicals on
cultured cells, convert chemical into a form for delivery into humans, do clinical
trials, scale up drug supply, get FDA approval for drug sales.
D) Get FDA approval for drug sales, identify likely drug sources, test chemicals on
cultured cells, select the most effective chemical, convert chemical into a form for
delivery into humans, do clinical trials, scale up drug supply.
E) Get FDA approval for drug sales, identify likely drug sources, test chemicals on
cultured cells, do clinical trials, select the most effective chemical, convert
chemical into a form for delivery into humans, scale up drug supply.
108. If you were going to set up a clinical trial of a new chemotherapy drug that would be
used in addition to traditional treatment for prostate cancer, who would you use as the
control group for your experiment?
A) patients with prostate cancer who received no treatment
B) patients with prostate cancer who received traditional treatment alone
C) patients with prostate cancer who were given the trial drug but no traditional
treatment
D) patients with prostate cancer who received traditional treatment plus the trial drug
E) healthy patients with no prostate cancer
Page 17
109. How many alleles for a single trait are present in each human cell?
A) 1
B) 2
C) 23
D) 46
E) 4
110. Alleles are located

A) on chromosome 17 only.
B) in random locations on chromosomes.
C) at a specific position on each of a pair of chromosomes.
D) on one chromosome of each pair.
E) on chromosomes 13 and 17.
111. What is an example of a mutation in an allele?

A) a base change in the gene coding sequence
B) a base change in the gene's regulatory regions
C) a deletion of a base within the gene
D) an insertion of a base within the gene
112. How many copies of any particular gene does an individual human have?
A) 4
B) 1
C) 2
D) 46
E) 23
113. True or False: Different versions of a gene are called alleles; a mutation in a gene can
create an allele.
A) True
B) False
114. Gene mutations can arise when nucleotides are

A) added to the gene.
B) taken away from the gene.
C) changed within the gene.
D) mismatched within the gene.
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115. An allele is
A) any section of DNA.
B) a gene.
C) a specific section of a chromosome.
D) an alternate version of a gene.
E) a pair of genes.
116. Different alleles are the result of

A) mutations in RNA sequences.
B) any change in DNA sequences.
C) changes in DNA sequence within a gene.
D) changes in the size of a chromosome.
E) any kind of radiation damage.
117. How many different alleles of a gene like BRCA1 can an individual have?
A) Several hundred, since there are hundreds of known BRCA1 alleles
B) Four: two from their father and two from their mother
C) Only two: one from their father and one from their mother
D) One for males and hundreds for females
E) One for males and two for females
118. A mutation is best described as an error in

A) DNA.
B) mRNA.
C) protein.
D) enzymes.
E) cell division.
119. Most new alleles arise via

A) large rearrangements of genes.
B) exchanges of genes during crossing over.
C) mutations in existing genes.
D) changes in DNA polymerase that alter how polymerase copies DNA.
E) changes in the beginning and ending of a gene.
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120. Bob and Linda are a newly married couple. They hope to have a child but are having
trouble getting pregnant. They visit a fertility clinic, where they receive a variety of
tests. One test shows that Bob is healthy but carries a single disease-causing allele for
CFTR (the gene that can cause cystic fibrosis), but Linda does not. This means that
A) Bob's DNA sequence for CFTR is different from Linda's.
B) Bob has two different versions of the CFTR gene.
C) Linda does not have any copies of the CFTR gene.
D) Bob is unable to ever have children.
E) Both A and B
121. There are several different alleles for flower color in carnations. One of them causes
white flowers; a different allele of the same gene causes red flowers. This means that all
of the following are true, EXCEPT
A) white carnations have different DNA sequences than red carnations.
B) white carnations and red carnations have somewhat different proteins.
C) a carnation plant could have one copy of the white allele and one copy of the red
allele.
D) a carnation plant could have two copies of the white allele and two copies of the
red allele.
122. A newly identified mutation in mice, called “darkened dorsal,” causes a dark stripe
along the mouse's back. This mutation is located at a specific location on chromosome
2. A different sequence at this same chromosomal position results in a fur color pattern
called “nonagouti.” Based on this information, darkened dorsal and nonagouti are
different
A) genes for fur color.
B) alleles for the same gene.
C) mutations of the same chromosome.
D) chromatids.
123. Which of the following is TRUE?

A) Alleles are usually harmful because they result from mutations.
B) Alleles are just different versions of the same gene.
C) Normal, healthy individuals don't usually carry alleles.
D) An individual may have one, two, or three alleles for a particular trait.
E) None of the above.
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124. What would be the best way to distinguish between two alleles and two genes?
A) Examine the proteins they produce; most genes would produce very similar
versions of the same protein, but two alleles would produce very different proteins.
B) Examine the proteins they produce; a gene produces one protein, and an allele
produces two different proteins.
C) Examine their DNA; the DNA sequences of two different alleles would be more
similar to each other than the sequences of two different genes.
D) You can't distinguish between them; there's no actual difference between alleles
and genes.
E) Determine their chromosomal location; alleles will always be on different
chromosomes, but genes will always be on different copies of the same
chromosome.
125. A mutation would most likely be inherited if it is located in a ____ cell.

A) skin
B) body
C) sperm
D) liver
126. Which sequence is the complementary DNA sequence of ATG GGC CTG?
A) ATG GGC CTG
B) TAC CCG GAG
C) TUC CCG GUC
D) TAC CCG GAC
E) TAC CCC GAC
127. Which sequence is a result of a single mismatch in DNA replication of the sequence
ATG GGC CTG?
A) ATG GGC CTC
B) AAG GGC CTC
C) TAC CCG GTC
D) TGC CCG GAG
E) TUC CCG GUC
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128. The number of errors made by DNA polymerase during DNA replication that pass
through the cell's repair checkpoints is estimated at
A) 1 in 100 bases mismatched.
B) 1 in 1000 bases mismatched.
C) 1 in 1,000,000 bases mismatched.
D) 1 in 10,000,000,000 bases mismatched.
E) 1 in 10 bases mismatched.
129. The enzyme that copies DNA makes a mistake approximately every 10,000 to 100,000
bases. Surprisingly, however, if we examine newly copied DNA, we see that the actual
error rate is lower than this. How is that possible?
A) The bases are self-correcting; the DNA will fix any errors as it is copied.
B) The cell is immediately killed if it contains a mistake in its DNA.
C) There are other enzymes that find errors in DNA and repair them.
D) All of the above.
130. DNA mutations can

A) be detrimental.
B) be beneficial.
C) have no effect.
D) All of the above.
E) A or B only
131. Why aren't all mutations that occur in DNA inherited by our offspring?
A) Only mutations in the DNA contained in the sperm and eggs will be inherited.
B) Each cell has different DNA in it, with only the genes that cell needs.
C) DNA that is mutated can't be inherited; the cell corrects it before passing it on.
D) DNA that is inherited can't have more than one mutation in it.
E) Some mutations occur in noncoding regions of genes, so they are not inherited.
132. What would happen if the enzyme that makes DNA added a nucleotide to the middle of
a coding region of a gene?
A) It would change the reading frame of the DNA and possibly lead to a change in the
amino acid sequence of the protein made from that gene.
B) It wouldn't matter because it is in a coding region.
C) It is only one nucleotide so it wouldn't matter; more than one nucleotide would
need to be added to change a protein.
D) It would make longer mRNA and protein from that gene.
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133. Do all mutations that occur within the DNA sequence result in abnormal protein
expression, and therefore affect the function of the protein?
A) Yes, regardless of the location of the mutation, protein expression and function will
be adversely affected.
B) No, mutations occurring within the noncoding regions of the DNA sequence will
not affect overall protein structure.
C) No, DNA repair enzymes are designed specifically to “proofread” the DNA and
they catch most mistakes.
D) Yes, any mutations located within the DNA sequence will affect the structure of
the protein.
E) B and C
134. Which of the following cannot lead to a mutation?

A) replacing thymine with uracil when making RNA
B) deleting a portion of a gene
C) replacing thymine with guanine when copying DNA
D) inserting three base pairs into a gene
E) inserting one base pair into a gene
135. DNA damage is usually repaired

A) in the egg or sperm cells before fertilization.
B) at or before checkpoints in the cell cycle.
C) in the ribosome during translation.
D) by the mitotic spindle.
E) by the complementary strand of DNA.
136. Mutations are

A) always harmful.
B) never neutral.
C) always helpful.
D) never helpful.
E) sometimes harmful, sometimes helpful, and sometimes neutral.
137. Radioactive Man, a comic-book superhero, gained his abilities by falling into a vat of
industrial toxic waste. Is this a likely outcome?
A) Yes, because mutations can be helpful, harmful, or neutral.
B) No, because most mutations are either harmful or neutral.
C) No, because toxic waste is not mutagenic.
D) No, because so many mutations would probably cause cancer or other disease.
E) Both B and D
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138. Amino acid sequences result from the process of
A) transcription.
B) translation.
C) replication.
D) regulation.
E) complementary base pairing.
139. Mutations in DNA sequences may occur during the process of

A) transcription.
B) translation.
C) replication.
D) tumor suppression.
E) apoptosis.
140. Substitution of a nucleotide base in the coding sequence of a gene may alter the protein's
A) amino acid sequence.
B) 3D shape.
C) folding.
D) function.
141. Why might a change in its amino acid sequence lead to a change in the way a protein
functions?
A) Amino acids determine a protein's shape. The wrong shape may not function
normally.
B) A change in the amino acid sequence would not change the final protein.
C) A change in the amino acid sequence would cause a change in the DNA, which
alters the protein.
D) A change in the amino acid sequence causes the DNA to pair incorrectly.
142. How does a mutation in a noncoding region of DNA affect the final shape of the
protein?
A) A mutation in a noncoding region would not affect the final protein shape, but it
could affect gene regulation.
B) A change in the noncoding region leads to a change in amino acid sequence, which
changes the way the protein folds.
C) A change in the amino acid sequence causes the DNA to pair incorrectly.
D) A change in the noncoding region causes the protein to fold “inside out.”
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143. Is the way a protein folds important for its function?
A) Yes, protein function depends on the protein's 3-D structure.
B) Yes, because DNA mutations are caused by protein folding incorrectly.
C) No, as long as the sequence is correct.
D) No, as long as the protein is still soluble.
144. Mutations in DNA occur during

A) transcription.
B) translation.
C) protein modification.
D) RNA duplication.
E) DNA duplication.
145. Which of the following statements is always TRUE?

A) A mutation is harmful.
B) Mutations lead to changes in protein function.
C) Changes in DNA lead to changes in protein function.
D) A change in the DNA may change a protein's shape and function.
E) A change in DNA will lead to cancer.
146. The Ashkenazi Jews have a higher rate of mutated alleles than the general public. All of
the following are possible reasons for this, EXCEPT
A) in their Middle Eastern homeland, intense sunlight led to increased mutations.
B) they are descendants of a small number of individuals.
C) their population expanded and contracted.
D) members usually marry others within the same group.
E) new alleles were not introduced through intermarriage with other groups.
147. Mutations usually affect a protein's

A) size.
B) shape.
C) length.
D) electrical charge.
E) longevity.
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148. If a mutation alters a protein, which of the following is NOT a likely outcome of the
mutation?
A) The shape of the protein may be different.
B) The protein may function differently.
C) The protein may cause a disease or illness.
D) The protein may not function at all.
E) The protein may be repaired by enzymes.
149. Not all mutations are dangerous. Why?

A) Many mutations occur in noncoding regions.
B) Some mutations can have no effect on proteins.
C) Many DNA mutations are corrected by enzymes
D) Some cells don't use all their genes.
150. If you consider most of the mutations that occur in your DNA, the majority have ______
effects.
A) few or no
B) helpful
C) harmful
D) reversible
E) lethal
151. True or False: If you avoid dangerous chemicals and radiation for your entire life, you
prevent all mutations in your DNA.
A) True
B) False
152. What is the difference between a somatic cell mutation and a germ-line mutation?
A) Only mutations in germ-line cells can be passed on to offspring.
B) Only mutations in somatic cells can be passed on to offspring.
C) Somatic cell mutations cannot lead to cancer, but germ-line mutations can.
D) Germ-line mutations do not involve DNA, but somatic cell mutations do.
E) Somatic cell mutations do not involve DNA, but germ-line mutations do.
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153. Which of the following is a mutagen?
A) UV light
B) smoking
C) blackened meats
D) excessive drinking
154. If a person is a carrier for a disease; he or she has

A) one normal and one defective disease allele and is affected by the disease.
B) two defective disease alleles and is unaffected by the disease.
C) one normal and one defective disease allele and is unaffected by the disease.
D) two defective disease alleles and is affected by the disease.
E) two normal disease alleles and is affected by the disease.
155. Why are Ashkenazi Jews more susceptible to certain hereditary diseases?
A) They have inherited predispositions and carcinogen exposure.
B) They have increased occupational exposure and environmental insults.
C) They are predisposed by exposure to occupational risks.
D) They have an increased carrier rate for these diseases from their ancestors.
E) They all have increased errors in DNA proofreading.
156. How can a person acquire mutations in their DNA?

A) inheritance
B) carcinogens
C) replication errors
D) mutagens
157. Which of the following is NOT a known source of mutations?

A) DNA repair or replication errors
B) chemical or environmental exposure
C) heredity
D) insufficient sleep and poor diet
E) None of the above; all are known sources of mutations.
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158. Inherited mutations
A) predispose individuals to cancer.
B) come from DNA sequence mistakes contained in germ cells.
C) can come from one's mother or father.
D) are errors in DNA that go uncorrected.
159. Which of the following is NOT a known carcinogen?

A) ultraviolet light
B) alcohol
C) charred food
D) smoking
E) None of the above; all are known carcinogens
160. Which of the following are mutagens?

A) sunlight
B) cigarette smoke
C) alcohol
D) blackened meat
161. Which of the following will lead to a new, inheritable allele?

A) a mutation in a sperm cell
B) a mutation in an egg cell
C) a mutation in an embryo
D) a mutation in the brain
E) All of the above except D.
162. A woman with normal BRCA alleles has a child with a man who has one mutated
BRCA1 allele. What is the probability that the child will have a mutated BRCA1 allele?
A) 0%
B) 25%
C) 50%
D) 75%
E) 100%
163. True or False: To get cancer, all you need is a mutation in one essential gene.
A) True
B) False
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164. In a cell with the following mutations, which would you expect to be MOST likely to
cause tumors?
A) BRCA1 and BRCA2
B) BRCA1 and p53 mutation
C) BRCA1, BRCA2, Her2, and p53 mutations
D) BRCA1, BRCA2, and p53 mutations
E) BRCA1, Her2, and p53 mutations
165. Which combination(s) of mutated genes would be most likely to make a cell cancerous?
A) one oncogene
B) one tumor suppressor gene
C) two oncogenes
D) two oncogenes and two tumor-suppressor genes
166. In a cell with the following mutations, which would you expect to be LEAST likely?
A) BRCA1 and BRCA2
B) BRCA1
E) BRCA1, Her2, and p53 mutation
167. What is the number-one preventable cause of cancer?

A) smoking
B) UV light exposure
C) grilled meats and vegetables
D) pollution exposure
E) alcohol
168. The most common cancer among women is

A) prostate cancer.
B) breast cancer.
C) ovarian cancer.
D) nonmelanoma skin cancer.
E) lung cancer.
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169. A normal BRCA1 allele produces normal protein that
A) inhibits transcription.
B) inhibits translation.
C) ensures correct, error-free DNA transcription.
D) allows cells to repair DNA damage.
E) recognizes and destroys incorrectly translated proteins.
170. All of the following are TRUE of breast cancer, EXCEPT

A) it is the second-most common form of cancer in women.
B) mutations in the BRCA genes affect only the breasts and ovaries.
C) BRCA mutations cause only about 50% of all hereditary breast cancers.
D) it affects about 200,000 women in the United States per year.
E) a woman may pass the predisposition for breast cancer to her children.
171. All of the following are TRUE of BRCA genes, EXCEPT

A) there are two genes, and a mutation in either can lead to cancer.
B) when mutated, they produce proteins that are unable to regulate the cell cycle.
C) just one mutated BRCA gene increases a woman's lifetime cancer risk to greater
than 90%.
D) mutations in BRCA genes can lead to either breast or ovarian cancer in women.
E) mutations in BRCA genes can lead to prostate cancer in men.
172. Which of the following would most likely increase an individual's risk of cancer?
A) a mutation in the noncoding region of DNA
B) a mutation in their mother's somatic cells
C) a mutation in a gene for a DNA repairing enzyme
D) an error in transcribing DNA into RNA
173. Which of the following types of mutations is LEAST likely to lead to cancer?
A) a mutation of proto-oncogenes
B) a mutation of tumor suppressor genes
C) a mutation of a gene that codes for DNA polymerase
D) a mutation of a gene that codes for DNA repair enzymes
E) a mutation in a noncoding sequence of a gene
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174. A gene found in a somatic cell is mutated. The resulting protein regulates mitosis but
now has a different 3D shape. What is a likely result?
A) germ-line mutations
B) hereditary mutations
C) cancer
D) down syndrome
E) cystic fibrosis
175. Which of these does NOT directly cause cancer?

A) inherited predispositions
B) solar radiation (UV)
C) tobacco smoking or chewing
D) DNA damage from viruses
E) mutagens in drinking water
176. Which occupation is high risk for a predisposition to cancer?

A) chimney sweeping
B) coal mining
C) cabinet making
D) shoe repair and manufacture
177. Somatic cells are

A) cancer cells.
B) cells that become tumors.
C) cells that become eggs.
D) cells that become sperm.
E) cells that do not become reproductive cells.
178. Which of the following statements is FALSE?

A) All carcinogens are mutagens.
B) Some cancers are hereditary.
C) All mutations can cause cancer.
D) Ultraviolet light can lead to skin cancers, so it is a mutagen.
E) Ultraviolet light can lead to skin cancers, so it is a carcinogen.
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179. Which of the following is most likely to be an INHERITED cancer?
A) skin cancer
B) liver cancer
C) lung cancer
D) prostate cancer
E) stomach cancer
180. A new gene is discovered, called GRAB. It prevents a cell from entering mitosis if there
are any signs of DNA damage. This means that GRAB would be a type of
A) oncogene.
B) tumor-suppressor gene.
C) nonhereditary gene.
D) somatic gene.
E) proto-oncogene.
181. What kind of mutation causes most types of cancer?

A) mutations in skin cells
B) mutations in transcription factors
C) mutations in blood cells
D) mutations in cell cycle genes
182. Many cells in your body stop at the G1 checkpoint and never divide again. Some cells,
like skin cells, will continue past the G1 checkpoint. What types of genes tell a skin cell
to move on past the G1 checkpoint?
A) proto-oncogenes
B) tumor-suppressor genes
C) cell-enhancing genes
D) oncogenes
E) tumor-deflecting genes
183. In healthy cells, if a mutation occurs in a proto-oncogene, what is the gene now termed?
A) tumor regulator
B) Her2
C) cell-cycle regulator
D) tumor suppressor
E) oncogene
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184. Proto-oncogenes are
A) tumor regulators.
B) required for normal cell division.
C) tumor suppressors.
D) cancer causing in normal cells.
E) mutations in oncogenes.
185. In normal cells, tumor suppressors are

A) oncogenes.
B) not required.
C) carcinogens.
D) required for DNA repair or programmed cell death.
E) underexpressed.
186. Permanent activation or overexpression of proto-oncogenes

A) turns tumor suppressors off.
B) is required for normal cell division.
C) has been linked to breast cancer.
D) keeps a cell from dividing.
E) turns tumor suppressors on.
187. In normal cells, lack of functional tumor suppressors would cause

A) an accumulation of mutations in the DNA.
B) division of damaged cells.
C) cancer, possibly.
D) uncontrolled cell division.
188. Apoptosis can be described as

A) division of damaged cells.
B) abnormal cell behavior.
C) uncontrollable cell division.
D) programmed cell death.
E) immortalization of cells.
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189. A proto-oncogene is a gene that
A) tells the cell when to stop the cell cycle.
B) is responsible for DNA repair.
C) is responsible for detecting mutations.
D) tells the cell to go through the cell cycle.
E) causes apoptosis.
190. A tumor suppressor gene is a gene that

A) tells the cell when to stop the cell cycle.
B) is responsible for DNA repair.
C) is responsible for detecting mutations.
D) tells the cell to go through the cell cycle.
E) prevents apoptosis from occurring.
191. When would you need a gene that can stop the cell cycle?
A) when a mutation occurred and the cell needed time to repair it before continuing
B) when there was no immediate need for more cells
C) when a cell had completed DNA replication
D) A and C only
E) A and B only
192. What would happen if a tumor suppressor, such as BRCA1, was mutated?
A) DNA may not be able to be repaired.
B) The cell cycle could continue without stopping when needed.
C) Cells would stop dividing and be unable to get through the cell cycle.
D) A and B only
193. What would happen if a proto-oncogene, such as Her2, were mutated?

A) DNA may not be able to be repaired.
B) The cell cycle would continue without stopping when needed.
C) Cells would stop dividing and be unable to get through the cell cycle.
D) A and B only
Page 34
194. Which of the following would NOT lead to cancer?
A) an active oncogene
B) a misshapen tumor-suppressor protein
C) a mutated proto-oncogene
D) a tumor-suppressor allele missing 20% of its bases
E) an active proto-oncogene
195. Mutations that cause the cell to divide rapidly, even in the absence of a signal to divide,
are usually mutations of
A) proto-oncogenes.
B) tumor-suppressor genes.
C) DNA polymerase.
D) cell-surface proteins.
E) DNA-repair enzymes.
196. Tumor-suppressor genes can act by making proteins that

A) repair damaged DNA.
B) stop the cell from dividing when there are problems.
C) induce apoptosis.
D) cause cell death.
197. BRCA1 and BRCA2 are ___________, p53 is a ___________, and Her2 is a
__________.
A) tumor-suppressor genes, tumor-suppressor gene, proto-oncogene
B) tumor-suppressor genes; proto-oncogene; tumor-suppressor gene
C) proto-oncogenes; tumor-suppressor gene; proto-oncogene
D) proto-oncogenes; tumor-suppressor gene; tumor-suppressor gene
E) proto-oncogenes; proto-oncogene; tumor-suppressor gene
198. You isolate cells from a tumor and study them. You observe that the cells continue
dividing, even when DNA is damaged, when the cells become crowded, or even when
nutrients run low. These observations lead you to suspect that the cells
A) contain a proto-oncogene.
B) contain an oncogene.
C) contain a mutated tumor-suppressor gene.
D) are infected by a virus.
E) are breast-cancer cells.
Page 35
199. True or False: To get cancer, all you need is a mutation in one essential gene.
A) True
B) False
200. Which set of mutations in a cell would you expect to be LEAST tumorigenic?
A) BRCA1 and BRCA2
B) BRCA1
E) BRCA1, Her2, and p53 mutation
201. A mutation in one cancer-related gene is not enough to cause a cell to become
cancerous. Why?
A) We have more than two copies of every gene.
B) Cell division is controlled by many proteins, not just one.
C) We have two copies of every gene.
D) Nearby cells will repair the mutation.
E) The cell has to divide more times to become cancerous.
202. Which of the following steps (in order) would most likely lead to tumor formation?
A) A mutation in a single cell-cycle gene occurs, then the cell rapidly divides and
spreads.
B) A mutated tumor-suppressor gene is inherited, several proto-oncogenes become
mutated, and the cell dies.
C) A mutation in a cell-cycle gene occurs, then shortly afterwards the cell dies.
D) A mutated tumor-suppressor gene is inherited, other mutations in proto-oncogenes
occur, and the cell rapidly divides and spreads.
E) A proto-oncogene is inherited, mutation converts it into an oncogene, and the cell
rapidly divides and spreads.
203. Why does cancer affect older individuals more frequently than younger people?
A) Older people have more genes than younger people, so the tendency for the genes
to be mutated increases.
B) Cells become more fragile and die more rapidly as people age.
C) Older people tend to smoke, which is a carcinogen and causes cancer.
D) Older people have had more time to accumulate mutations from various sources.
E) Older DNA is more susceptible to mutation than younger DNA.
Page 36
204. What is the difference between mutagens and carcinogens?
A) All mutagens are carcinogens.
B) All carcinogens are mutagens.
C) Carcinogens are any substance that damages DNA and can lead to cancer.
D) B and C
E) None of the above; they are the same thing with different names.
205. Predict what would most likely happen in a cell if BRCA1 were mutated.
A) DNA errors would occur more frequently.
B) The cell would divide much faster.
C) Tumors would form immediately.
D) The cell would pause forever and wait for damage to be repaired.
E) The cell would copy DNA faster and more accurately.
206. You learn from DNA testing that for BRCA1 you have one normal allele and one allele
associated with cancer. For BRCA2, you have two alleles associated with cancer. How
does this affect your risk for cancer?
A) Your risk is the same as any other average human being.
B) You will almost certainly get cancer at a very young age.
C) Your risk is definitely higher than for someone with all mutant alleles for BRCA1
and BRCA2.
D) Your risk is the same as that for someone with a single mutant BRCA1 allele.
E) Your risk is higher than average but depends on other genes you carry and your
lifestyle.
207. The mutant BRCA2 gene predisposes people to cancer. If mutant BRCA2 runs in
Isadora's family, will she automatically get cancer?
A) Yes, because genes like BRCA2 are always inherited if one of your parents has a
mutation.
B) No. Although inherited genes may carry an increased predisposition toward cancer,
it is often nonhereditary mutations that lead to cancer.
C) Yes, because inherited genes that are mutated will cause cancer.
D) No, because more than one mutation is needed to develop cancer.
E) B and D
Page 37
208. Why do people with inheritable high-risk mutations develop cancer at an earlier age?
A) People who have inherited high-risk mutations start life with at least one
predisposing mutation, so they require fewer additional mutations.
B) People who have inherited high-risk mutations always have other environmental
risk factors putting them at higher risk for developing cancer at a younger age.
C) People with inheritable high-risk mutations start expressing the mutated genes at a
younger age.
D) The inherited mutations cause new mutations to occur more easily.
E) All the above.
209. What factors have made the Ashkenazi Jewish population more susceptible to genetic
diseases?
A) They descended from a small group of people.
B) The population has expanded and contracted over time.
C) They tend to marry other Ashkenazis.
D) B and C
E) All the above.
210. If you mother has a single copy of a harmful BRCA gene, what are the chances you
inherited the harmful BRCA allele from her?
A) 0%
B) 25%
C) 50%
D) 75%
E) 100%
Page 38
211. What is the increased risk of breast cancer by age 70 if you have one copy of a
deleterious BRCA1 allele when compared with the general population?
A) 12%
B) 25%–42%
C) 43%–53%
D) 55%–65%
E) 65%
212. What is the increased risk of ovarian cancer by age 70 if you have one copy of a
deleterious BRCA2 allele when compared to the general population?
A) 1.3%
B) 9.7%
C) 11%
D) 39%
E) 55%-65%
Page 39
213. For those women with a mutation in their BRCA1 genes, the risk of developing breast
cancer by age 70 is as high as _________, while in the general population the risk is
_________.
A) 45%; <5%
B) 45%; 12%
C) 45%; 15%
D) 65%; 12%
E) 65%; 15%
214. Why is a person who has inherited one copy of a harmful BRCA allele much more likely
to have early-onset breast cancer or ovarian cancer than a person with two functioning
alleles?
A) Apoptosis is increased, as the tumor suppressors are not functioning.
B) Cell growth is accelerated, as oncogenes are switched on.
C) With the increase of BRCA protein, apoptosis is induced and cell death occurs.
D) Mutations accumulate as DNA repair is slowed and cell growth may accelerate.
E) Cells fail to enter apoptosis and eventually become a tumor.
215. Why does inheriting a mutation in a gene increase one's risk of developing cancer?
A) It takes more than one mutation to develop cancer. People who inherit a mutation
need fewer additional mutations to develop cancer.
B) It takes one mutation to develop cancer. People who inherit a mutation are already
developing cancer as soon as they are born.
C) It takes one mutation in the right gene to develop cancer, so if they inherit a
mutation in a key gene, then they will develop cancer.
D) Inheriting a mutation means we don't need mutations from outside sources to
develop cancer.
Page 40
216. What kinds of preventative measures are available for individuals who have a strong
genetic predisposition to breast cancer?
A) genetic counseling, so they know the risks
B) regular medical screening for cancer
C) a healthy lifestyle, a good diet, and an exercise regimen
D) prophylactic surgery
217. Which of the following is MOST accurate?

A) Women with just one abnormal BRCA allele are less likely to develop skin cancer
than women with no abnormal alleles.
B) Women with two abnormal BRCA alleles are less likely to develop skin cancer than
women with no abnormal alleles.
C) Women with just one abnormal BRCA allele are more likely to develop cancer than
women with no abnormal alleles.
D) Women with just one abnormal BRCA allele are more likely to develop ovarian
cancer than women with two abnormal alleles.
E) Women with two abnormal BRCA alleles are less likely to develop breast cancer
than women with no abnormal alleles.
218. For those women with a mutation in their BRCA genes, the risk of developing breast
cancer by age 50 is as high as _________, while in the general population the risk is
_________.
A) 10%; <5%
B) 20%; <5%
C) 20%; 10%
D) 50%; <5%
E) 50%; 20%
219. In addition to breast cancer, women with a mutation in one of their BRCA genes have an
increased likelihood of developing which of the following other types of cancer?
A) liver
B) lung
C) ovarian
D) skin
E) bone
Page 41
220. If an individual has a germ cell mutation, which of these is a possible source of that
mutation?
A) excessive sun exposure
B) a maternal or paternal allele
C) a paternal allele only
D) a maternal allele only
E) overuse of alcohol
221. How does an acquired mutation in a gene alter the function of a cell?
A) Base pair changes in the gene are passed directly into altered amino acids by a
ribosome.
B) Base pair mutations in a gene are passed directly into mRNA via translation.
C) Base pair mutations in mRNA are passed directly into a protein via transcription.
D) Base pair mutations in a gene are passed directly into mRNA via transcription.
E) Base pair mutations in a gene are passed from mRNA into a protein via
transcription.
222. A potential cancer-causing gene coding for a protein with cell cycle control
responsibilities is a _____, and a gene coding for a protein that stimulates cell division is
a _____.
A) oncogene; mutagen
B) oncogene; proto-oncogene
C) carcinogen; proto-oncogene
D) tumor suppressor; oncogene
E) oncogene; tumor suppressor
223. What is the role of BRCA1 in normal cells?

A) BRCA1 is a proto-oncogene.
B) BRCA1 is an oncogene.
C) BRCA1 is a tumor suppressor.
D) BRCA1 is a mutagen.
E) BRCA1 is a carcinogen.
224. Which of these does not cause cancer to develop and progress?
A) a proto-oncogene acting alone
B) an oncogene acting alone
C) a tumor suppressor gene acting alone
D) a proto-oncogene and a tumor suppressor gene acting together
E) an oncogene and a BRCA1 acting together
Page 42
225. A chemical that causes alterations in DNA is a _____, and if this chemical causes cancer
it is called a(n) _____.
A) mutagen; carcinogen
B) carcinogen; mutagen
C) tumor suppressor; oncogene
D) tumor suppressor; proto-oncogene
E) tumor suppressor; mutagen
226. Tumors that will not spread throughout the body are _____, and those that do spread are
termed _____.
A) malignant; benign
B) benign; malignant
C) mutagen; carcinogen
D) tumor suppressor; proto-oncogene
E) benign; mutagen
227. Which statement accurately describes cancer development?

A) It is a one-step process by which a mutation drives cancer development.
B) It is inherited and is independent of environmental factors.
C) It is a caused by carcinogens that act on inherited alleles that cause cancer.
D) It is a multistep process by which multiple mutations cause a series of events that
lead to cancer.
E) It is a multistep process by which multiple mutagens cause a series of
cancer-causing alleles.
228. What would you say to a niece if she asked you how she could reduce her risk of breast
cancer? (Assume there is no family history of breast cancer.)
A) Reduce sun exposure.
B) Reduce alcohol consumption.
C) Avoid tobacco.
D) Utilize early screening.
E) all of these
229. Why is age a risk factor for cancer?

A) Age provides more time for the cancer cells to accumulate.
B) Age extends the amount of exposures to environmental factors, which can lead to
the progression of cancer.
C) Age causes additional mutations to be acquired that can predispose one to cancer.
D) none of these
E) all of these
Page 43
230. We would all have many more mutations in our genes if not for the _____.
A) activity of repair enzymes
B) death of all mutant cells, removing them from our bodies
C) fact that everybody carries a "good" allele to counter every "bad" allele
D) fact that dividing cells remove all their mutations when they replicate their DNA
E) fact that mutations tend to cancel each other out, leaving mostly functional genes
231. Which is the correct order of events in which breast cancer might develop?
A) inheritance of a mutant BRCA gene > mutation of p53 > additional mutations
permit spreading > replication errors create an oncogene
B) mutation of p53 > inheritance of a mutant BRCA gene > additional mutations
permit spreading > replication errors create an oncogene
C) replication errors create an oncogene > mutation of p53 > inheritance of a mutant
BRCA gene > additional mutations permit spreading
D) inheritance of a mutant BRCA gene > replication errors create an oncogene >
mutation of p53 > additional mutations permit spreading
E) inheritance of a mutant BRCA gene > additional mutations permit spreading >
replication errors create an oncogene > mutation of p53
232. Which statement about decreasing a woman's breast cancer risk if she inherits one of the
mutant BRCA genes is true?
A) Diet and lifestyle changes will effectively decrease her risk to near zero.
B) She can take several medications that make it almost impossible to get breast
cancer, even if she inherits the BRCA gene.
C) Surgical removal of the breasts will decrease a woman's cancer risk to near zero.
D) A woman cannot decrease her cancer risk, so she might as well live life to its
fullest.
E) none of these
233. A woman with a BRCA1 mutation _____.

A) will definitely develop breast cancer
B) is at increased risk of developing breast cancer
C) must have inherited it from her mother because of the link to breast cancer
D) will also have a mutation in BRCA2
E) none of these
Page 44
234. Which family history most strongly suggests a risk of inherited breast cancer due to
BRCA1 mutations?
A) many female relatives who were diagnosed with breast cancer in their 70s
B) many relatives with skin cancer
C) many relatives diagnosed with skin cancer at an early age
D) many female relatives diagnosed with breast cancer at an early age
E) many female relatives with both early breast cancer and ovarian cancer
235. Why do people with "inherited cancer" often develop cancer at a relatively young age?
A) Predisposition does not increase the chances that other risk factors will lead to the
progression of cancer.
B) All inherited alleles that are associated with cancer cause childhood cancers.
C) Cancer cannot be truly inherited, but certain alleles weaken the normal control
points that prevent cancer, and this causes cancer to appear earlier in life.
D) Younger people are exposed to more risk factors than older people.
E) all of these
236. Which woman would be most likely to benefit from genetic testing for breast cancer?
A) a 25-year-old woman whose mother, aunt, and grandmother had breast cancer
B) a healthy 75-year-old woman with no family history of breast cancer
C) a 40-year-old woman who has a cousin with breast cancer
D) a 55-year-old woman whose older sister was just diagnosed with breast cancer
E) All women can benefit from genetic testing for breast cancer.
Page 45
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CHAPTER I.
HISTORY AND LITERATURE.
The commencement of the history of Ichthyology

Aristotle. coincides with that of Zoology generally. Aristotle
(384–322 b.c.) had a perfect knowledge of the
general structure of fishes, which he clearly discriminates from the
Aquatic animals with lungs and mammæ, i.e. Cetaceans, and from
the various groups of Aquatic Invertebrates. He says that “the
special characteristics of the true fishes consist in the branchiæ and
fins, the majority having four fins, but those of an elongate form, as
the eels, having two only. Some, as the Muræna, lack the fins
altogether. The Rays swim with their whole body, which is spread
out. The branchiæ are sometimes furnished with an opercle,
sometimes without one, as is the case in the cartilaginous fishes....
No fish has hairs or feathers; most are covered with scales, but
some have a rough or smooth skin. The tongue is hard, often
toothed; and sometimes so much adherent that it seems to be
wanting. The eyes have no lids; nor are any ears or nostrils visible,
for what takes the place of nostrils is a blind cavity. Nevertheless
they have the senses of tasting, smelling, and hearing. All have
blood. All scaly fishes are oviparous, but the cartilaginous fishes
(with the exception of the Sea-devil, which Aristotle places along with
them) are viviparous. All have a heart, liver, and gall-bladder; but
kidneys and urinary bladder are absent. They vary much in the
structure of their intestines: for whilst the mullet has a fleshy stomach
like a bird, others have no stomachic dilatation. Pyloric coeca are
close to the stomach, variable in number; there are even some, like
the majority of the cartilaginous fishes, which have none whatever.
Two bodies are situated along the spine, which have the function of
testicles, and open towards the vent, and which are much enlarged
in the spawning season. The scales become harder with age. Not
being provided with lungs, they have no voice, but several can emit
grunting sounds. They sleep like other animals. In the majority the
females exceed the males in size; and in the Rays and Sharks the
male is distinguished by an appendage on each side of the vent.”
Aristotle’s information on the habits of fishes, their migrations,
mode and time of propagation, utility, is, as far as it has been tested,
surprisingly correct. Unfortunately, only too often we lack the means
of recognising the species of which he gives a description. His ideas
of specific distinction were as vague as those of the fishermen
whose nomenclature he adopted; it never occurred to him that such
popular names are subject to change, or may be entirely lost with
time, and the difficulty of deciphering his species is further increased
by the circumstance that popular names are often applied by him to
the same fish, or that different stages of growth are designated by
distinct names. The number of fishes known to Aristotle seems to
have been about 115, all of which are inhabitants of the Ægean Sea.
That one man should have discovered so many truths, and
formed so sure a base for Zoology, is less surprising than the fact
that for about eighteen centuries a science which seemed to offer
particular attractions to men gifted with power of observation, was no
farther advanced. Yet this is the case. Aristotle’s disciples, as well as
his successors, remained satisfied to be his copiers or
commentators, and to collect fabulous stories or vague notions. With
very few exceptions (such as Ausonius, who wrote a small poem, in
which he describes from his own observations the fishes of the
Mosel) authors entirely abandoned original research. And it was not
until about the middle of the sixteenth century that Ichthyology made
a new step in advance by the appearance of Belon, Rondelet, and
Salviani, who almost simultaneously published their grand works, by
which the idea of species was established definitely and for all times.
P. Belon travelled in the countries bordering on

Belon. the eastern part of the Mediterranean, in the years
1547–50; he collected rich stores of positive
knowledge, which he deposited in several works. The one most
important for the progress of Ichthyology is that entitled “De
aquatilibus libri duo” (Paris 1553; small 4to.) Belon knows about 110
fishes, of which he gives rude, but generally recognisable, figures. In
his descriptions he pays regard to the classical as well as vernacular
nomenclature, and states the outward characteristics, sometimes
even the number of fin-rays, frequently also the most conspicuous
anatomical peculiarities.
Although Belon but rarely gives definitions of the terms used by
him, it is generally not very difficult to ascertain the limits which he
intended to assign to each division of aquatic animals. He very
properly divides them into such as are provided with blood, and into
those without it: two divisions, called in modern language Vertebrate
and Invertebrate aquatic animals. The former are classified by him
according to sizes, the further subdivisions being based on the
structure of the skeleton, mode of propagation, number of limbs,
form of the body, and on the physical character of the localities
inhabited by fishes. This classification is as follows:—
I.The larger fishes or Cetaceans.
A. Viviparous Cetaceans with bony skeletons (= Cetacea).
B. Viviparous Amphibians.
1. “With four limbs: Seals, Hippopotamus, Beaver, Otter, and other
aquatic Mammalia.
2. With two limbs: Mermaids, etc.
C. Oviparous Amphibians (= Reptiles and Frogs).
D. Viviparous Cartilaginous fishes.
1. Of an oblong form (= Sharks).
2. Of a flat form (= Rays and Lophius).
E. Oviparous Cartilaginous fishes (= Sturgeons and Silurus).
F. Oviparous Cetaceans, with spines instead of bones (= large marine
fishes, like the Thunny, Sword-fish, Sciænoids, Bass, Gadoids,
Trachypterus).
II.Spinous Oviparous fishes of a flat form (= Pleuronectidæ).
III.Fishes of a high form, like Zeus.
IV.Fishes of a snake like form (= Eels, Belone, Sphyræna).
V.Small Oviparous, spinous, scaly, marine fishes.
1. Pelagic kinds.
2. Littoral kinds.
3. Kinds inhabiting rocky localities.
VI.Fluviatile and Lacustrine fishes.
The work of the Roman ichthyologist, H. Salviani
Salviani. (1514–72), is characteristic of the high social
position which the author held as the physician of
three popes. Its title is “Aquatilium animalium historia” (Rom. 1554–
57, fol.) It treats exclusively of the fishes of Italy. Ninety-two species
are figured on seventy-six plates which, as regards artistic execution,
are masterpieces of that period, although those specific
characteristics which nowadays constitute the value of a zoological
drawing, were entirely overlooked by the author or artist. No attempt
is made at a natural classification, but the allied forms generally are
placed in close proximity. The descriptions are quite equal to those
given by Belon, entering much into the details of the economy and
usefulness of the several species, and were evidently composed
with the view of collecting in a readable form all that might prove of
interest to the class of society in which the author moved. Salviani’s
work is of a high standard, most remarkable for the age in which he
lived. It could not fail to convey valuable instruction, and to render
Ichthyology popular in the country to the fauna of which it was
devoted, but it would not have advanced Ichthyology as science
generally; and in this respect Salviani is not to be compared with
Rondelet or Belon.
G. Rondelet (1507–1557) had the great advantage

Rondelet. over Belon in having received a medical education at
Paris, and more especially in having gone through a
complete course of instruction in anatomy as a pupil of Guentherus
of Andernach. This is conspicuous throughout his works—“Libri de
Piscibus marinis” (Lugd. 1554, fol.); and “Universæ aquatilium
historiæ pars altera” (Lugd. 1555, fol.) Nevertheless they cannot be
regarded as more than considerably enlarged editions of Belon’s
work. For although he worked independently of the latter, and differs
from him in numerous details, the system adopted by him is
characterised by the same absence of the true principles of
classification. Rondelet had a much more extensive knowledge of
details. His work is almost entirely limited to European, and chiefly
Mediterranean, forms, and comprises not less than 197 marine and
47 freshwater fishes. His descriptions are more complete and his
figures much more accurate than those of Belon; and the specific
account is preceded by introductory chapters in which he treats in a
general manner on the distinctions, the external and internal parts,
and on the economy of fishes. Like Belon, he had no conception of
the various categories of classification—for instance, confounding
throughout his work the terms “genus” and “species;” but he had
intuitively a notion of what his successors called a “species,” and his
principal object was to collect and give as much information as
possible of such species.
For nearly a century the works of Belon and Rondelet remained
the standard works of Ichthyology; but this science did not remain
stationary during this period. The attention of naturalists was now
directed to the products of foreign countries, especially the Spanish
and Dutch possessions in the New World; and in Europe the
establishment of anatomical schools and academies led to the
careful investigation of the internal anatomy of the most remarkable
European forms. Limited as these efforts were as to their scope,
being directed either only to the fauna of some district, or to the
dissection of a single species, they were sufficiently numerous to
enlarge the views of naturalists, and to destroy that fatal dependency
on preceding authorities which had continued to keep in bonds the
minds of even such men as Rondelet and Belon.
The most noteworthy of those who were active in
W. Piso. G. tropical countries are W. Piso and G. Margrav.
Margrav. They accompanied as physicians the Dutch
Governor, Prince Moritz of Nassau, to Brazil (1637–
44). Margrav especially studied the fauna of the country, and
although he died before his return to Europe, his observations were
published by his colleague, and embodied in a work “Historia
naturalis Braziliæ” (Lugd. 1648, fol.), in which the fourth book treats
of the fishes. He describes about 100 species, all of which had been
previously unknown, in a manner far superior to that of his
predecessors. The accompanying figures are not good, but nearly
always recognisable, and giving a fair idea of the form of the fish.
Margrav himself, with the aid of an artist, had made a most valuable
collection of coloured drawings of the objects observed and
described by him, but many years were allowed to pass before it was
scientifically utilised by Bloch and others.
Of the men who left records of their anatomical
Anatomists, researches, we may mention Borelli (1608–79),
1600–1700. who wrote a work “De motu animalium” (Rom. 1680,
4to), in which he explained the mechanism of
swimming, and the function of the air-bladder; M. Malpighi (1628–
94), who examined the optic nerve of the sword-fish; the celebrated
J. Swammerdam (1637–80), who described the intestines of
numerous fishes; and J. Duverney (1648–1730), who entered into
detailed researches of the organs of respiration.
A new era in the history of Ichthyology commences with Ray,

Willughby, and Artedi, who were the first to recognise the true
principles by which the natural affinities of animals should be
determined. Their labours stand in so intimate a connection with
each other that they represent only one stride in the progress of this
science.
J. Ray (born 1628 in Essex, died 1705), was the

Ray and friend and guide of F. Willughby (1635–72). They
Willughby had recognised that a thorough reform of the
treatment of the vegetable and animal kingdoms had
become necessary; that the only way of bringing order into the
existing chaos was that of arranging the various forms with regard to
their structure; that they must cease to be burdened with inapplicable
passages and quotations of the ancient writers, and to perpetuate
the erroneous or vague notions of their predecessors. They
abandoned speculation, and adhered to facts only. One of the first
results, and perhaps the most important, of their method was, that
having recognised the “species” as such, they defined this term, and
fixed it as the base, from which all sound zoological knowledge has
to start.
Although they had divided their work thus that Ray attended to
the plants principally, and Willughby to the animals, the “Historia
piscium” (Oxford, 1686, fol.), which bears Willughby’s name on the
titlepage, and was edited by Ray, is clearly their joint production. A
great part of the observations contained in it were collected during
their common journeys in Great Britain and on the Continent, and it
is no exaggeration to say that at that time these two Englishmen
knew the fishes of the Continent, especially those of Germany, better
than any other Continental zoologist.
By the definition of fishes as animals with blood, breathing by
gills, provided with a single ventricle of the heart, covered with scales
or naked; the Cetaceans are excluded. Yet, at a later period Ray
appears to have been afraid of so great an innovation as the
separation of whales from fishes, and, therefore, he invented a
definition of fish which comprises both. The fishes proper are then
arranged in the first place according to the cartilaginous or osseous
nature of the skeleton; further subdivisions being formed with regard
to the general form of the body, the presence or absence of ventral
fins, the soft or spinous structure of the dorsal rays, the number of
dorsal fins, etc. Not less than 420 species are thus arranged and
described, of which about 180 were known to the authors from
autopsy: a comparatively small proportion, descriptions and figures
still forming at that time in a great measure a substitute for
collections and museums. With the increasing accumulation of forms
the want of a fixed nomenclature is now more and more felt.
Peter Artedi would have been a great ichthyologist

P. Artedi. if Ray or Willughby had never preceded him. But he
was fully conscious of the fact that both had
prepared the way for him, and therefore he derived all possible
advantages from their works. Born in 1705 in Sweden, he studied
with Linnæus at Upsala; from an early period he devoted himself
entirely to the study of fishes, and was engaged in the arrangement
and description of the ichthyological collection of Seba, a wealthy
Dutchman who had formed the then perhaps richest museum, when
he was accidentally drowned in one of the canals of Amsterdam in
the year 1734, at an age of twenty-nine years. His manuscripts were
fortunately rescued by an Englishman, Cliffort, and edited by his
early friend Linnæus.
The work is divided into the following parts:—
1. In the “Bibliotheca Ichthyologica” Artedi gives a very complete
list of all preceding authors who have written on fishes, with a critical
analysis of their works.
2. The “Philosophia Ichthyologica” is devoted to a description of
the external and internal parts of fishes; Artedi fixes a precise
terminology of all the various modifications of the organs,
distinguishes between those characters which determine a genus
and such as indicate a species or merely a variety; in fact he
establishes the method and principles which subsequently have
guided every systematic ichthyologist.
3. The “Genera Piscium” contains well-defined diagnoses of forty-
five genera, for which he fixes an unchangeable nomenclature.
4. In the “Species Piscium” descriptions of seventy-two species,
examined by himself, are given; descriptions which even now are
models of exactitude and method.
5. Finally, in the “Synonymia Piscium” references to all previous
authors are arranged for every species, very much in the same
manner which is adopted in the systematic works of the present day.
Artedi has been justly called the Father of
Linnæus. Ichthyology. So perfect was his treatment of the
subject, that even Linnæus could no more improve
it, only modify and add to it; and as far as Ichthyology is concerned,
Linnæus has scarcely done anything beyond applying binominal
terms to the species properly described and classified by Artedi.
Artedi had divided the fishes proper into four orders, viz.
Malacopterygii, Acanthopterygii, Branchiostegi, and Chondropterygii,
of which the third only, according to our present knowledge, appears
to be singularly heterogeneous, as it comprises Balistes, Ostracion,
Cyclopterus, and Lophius. Linnæus, besides separating the
Cetaceans entirely from the class of fishes (at least since the 10th
edition of the “Systema Naturæ”) abandoned Artedi’s order of
Branchiostegi, but substituted a scarcely more natural combination
by joining it with Artedi’s Chondropterygians, under the name of
“Amphibia nantes.”
His classification of the genera appears in the 12th edition of the
“Systema,” thus—
Amphibia Nantes.
Spiraculis compositis.
Petromyzon.
Raia.
Squalus.
Chimæra.
Spiraculis solitariis.
Lophius.
Acipenser.
Cyclopterus.
Balistes.
Ostracion.
Tetrodon.
Diodon.
Centriscus.
Syngnathus.
Pegasus.
Pisces Apodes.
Muræna.
Gymnotus.
Trichiurus.
Anarhichas.
Ammodytes.
Ophidium.
Stromateus.
Xiphias.
Pisces Jugulares.
Callionymus.
Uranoscopus.
Trachinus.
Gadus.
Blennius.
Pisces Thoracici.
Cepola.
Echeneis.
Coryphæna.
Gobius.
Cottus.
Scorpæna.
Zeus.
Pleuronectes.
Chæetodon.
Sparus.
Labrus.
Sciæna.
Perca.
Gasterosteus.
Scomber.
Mullus.
Trigla.
Pisces Abdominales.
Cobitis.
Amia.
Silurus.
Teuthis.
Loricaria.
Salmo.
Fistularia.
Esox.
Elops.
Argentina.
Atherina.
Mugil.
Mormyrus.
Exocœtus.
Polynemus.
Clupea.
Cyprinus.
Two contemporaries of Linnæus attempted a

Gronow and systematic arrangement of fishes; both had
Klein. considerable opportunities for their study, especially
in possessing extensive collections; but neither
exercised any influence on the progress of Ichthyology. The one, L.
T. Gronow, a German who resided in Holland, closely followed the
arrangements proposed by Artedi and Linnæus, and increased the
number of genera and species from the contents of his own
museum. He published two works, “Museum Ichthyologicum” (Lugd.
1754–6, fol.), and “Zoophylacium” (Lugd. 1763–81, fol.); a
posthumous work, containing numerous excellent descriptions of
new forms was published by J. E. Gray in 1854 under the title of
“Systema Ichthyologicum.” To Gronow also is due the invention of
preparing flat skins of fishes in a dry state, and preserving them in
the manner of a herbarium. The specimens thus prepared by him
belong to the oldest which have been preserved down to our time.
Much less important are the ichthyological labours of J. T. Klein
(1685–1759). They are embodied in five parts (Missus) of a work
entitled “Historia naturalis piscium” (Sedæ, 1740–9, 4to.) He
regarded a system merely as the means of recognising the various
forms of animals, not as the expression of their natural affinities; and
that method seemed to him to be the most perfect by which an
animal could be most readily determined. He eschewed all reference
to minute or anatomical characters. Hence his system is a series of
the most unnatural combinations, and we cannot be surprised that
Linnæus passed in silence over Klein’s labours.
The works of Artedi and Linnæus excited fresh

Pupils and activity, more especially in Scandinavia, Holland,
Successors of Germany, and England, such as has not been
Linnæus equalled in the history of biological science either
before or after. Whilst some of the pupils and
followers of Linnæus devoted themselves to an examination and
study of the fauna of their native countries, others proceeded on
voyages of discovery to foreign and distant countries. Of these latter
the following may be specially mentioned:—O. Fabricius worked out
the Fauna of Greenland, Kalm collected in North America,
Hasselquist in Egypt and Palestine, Brünnich in the Mediterranean,
Osbeck in Java and China, Thurnberg in Japan; Forskål examined
and described the fishes of the Red Sea; Steller, Pallas, S. T.
Gmelin, and Güldenstedt traversed nearly the whole of the Russian
Empire in Europe and Asia. Others attached themselves as
naturalists to the celebrated circumnavigators of the last century, like
the two Forsters (father and son), and Solander, who accompanied
Cook; Commerson, who travelled with Bougainville; and Sonnerat.
Numerous new and startling forms were discovered by those men,
and the foundation was laid of the knowledge of the geographical
distribution of animals.
Of those who studied the fishes of their native country the most
celebrated are Pennant (Great Britain), O. F. Müller (Denmark),
Duhamel (France), Meidinger (Austria), Cornide (Spain), Parra
(Cuba).
The materials brought together by those and other zoologists
were so numerous that, not long after the death of Linnæus, the
necessity was felt of collecting them in a compendious form. Several
compilators undertook this task; they embodied the recent
discoveries in new editions of Artedi’s and Linné’s classical works,
but not possessing either a knowledge of the subject or any critical
discernment, they only succeeded in covering those noble
monuments under a mass of confused rubbish. For Ichthyology it
was fortunate that two men at least, Bloch and Lacépède, made it a
subject of long and original research.
Mark Eliezer Bloch, born in the year 1723 at

M. E. Bloch. Anspach in Germany, practised as a physician in
Berlin; he had reached an age of fifty-six years when
he commenced to write on ichthyological subjects. To commence at
his age a work in which he intended not only to give full descriptions
of the species known to him from specimens or drawings, but also to
illustrate every species in a style truly magnificent for his time, was
an undertaking of the execution of which an ordinary man would
have despaired. Yet he accomplished not only this task, but even
more, as we shall see hereafter.
His work consists of two divisions:—
1. “Oeconomische Naturgeschichte der Fische Deutschlands”
(Berl. 1782–4, 4to. Plates in fol.)
2. “Naturgeschichte der auslændischen Fische” (Berl. 1785–95,
4to. Plates in fol.)
Bloch’s work is unique, and probably will for ever remain so.
Although Cuvier fifty years later undertook a similar general work on
fishes, the subject had then become too extensive to allow of an
attempt of giving illustrations of all the species, or illustrations of a
similar size and costliness.
The first division of the work, which is devoted to a description of
the fishes of Germany, is entirely original, and based upon Bloch’s
own observations. His descriptions as well as figures were made
from nature, and are, with but few exceptions, still serviceable; many
continue to be the best existing in literature.
Bloch was less fortunate and is much less reliable in his natural
history of foreign fishes. For many of the species he had to rely on
more or less incorrect drawings and descriptions of travellers;
frequently, also, he was deceived as to the origin of specimens
which he acquired by purchase. Hence his accounts contain
numerous confusing errors which it would have been difficult to
correct, if not nearly the whole of the materials on which his work is
based had been preserved in the collections at Berlin.
After the completion of his Ichthyology Bloch occupied himself
with systematic work. He prepared a general system of fishes, in
which he arranged not only those described in his great work, but
also those with which he had become acquainted afterwards from
the descriptions of others. The work was ably edited and published
after Bloch’s death by a philologist, J. G. Schneider, under the title
“M. E. Blochii Systema ichthyologiæ iconibus ex. illustratum” (Berl.
1801, 8vo.) The number of species enumerated in it amounts to
1519. The system is based upon the number of the fins, the various
orders being termed Hendecapterygii, Decapterygii, etc. We need
not add that an artificial method like this led to the most unnatural
combinations or severances.
Bloch’s Ichthyology remained for many years the
Lacépède. standard work, and, by the great number of excellent
illustrations, proved a most useful guide to the
student. But as regards originality of thought, Bloch was far
surpassed by his contemporary, B. G. E. de Lacépède, born at
Agen, in France, in 1756, a man of great and general erudition, who
died as Professor of the Museum of Natural History of Paris in 1826.
Lacépède had to contend with great difficulties in the preparation
of his “Histoire des Poissons” (Paris, 1798–1803, 4to, in 5 vols.),
which was written during the most disturbed period of the French
Revolution. A great part of it was composed whilst the author was
separated from collections and books, and had to rely on his notes
and manuscripts only. Even the works of Bloch and other
contemporaneous authors remained unknown, or at least
inaccessible, to him for a long time. Therefore we cannot be
surprised that his work abounds in all those errors to which a
compiler is subject. The same species not only appears under two
and more distinct specific names, but it sometimes happens that the
author understands so little the source from which he derives his
information that the description is referred to one genus and the
accompanying figure to another. The names of genera are unduly
multiplied; and the figures with which the work is illustrated are far
inferior to those of Bloch. Thus the influence of Lacépède on the
progress of Ichthyology was infinitely less than that of his fellow-
labourer; and the labour caused to his successors by correcting the
numerous errors into which he has fallen, probably outweighs the
assistance which they derived from his work.
The work of the principal cultivators of Ichthyology in
Anatomists. the period between Ray and Lacépède was chiefly
systematic and descriptive, but also the internal
organisation of fishes received attention from more than one great
anatomist. Haller, Camper, and Hunter, examined the nervous
system and organs of sense; and more especially Alexander Monro
(the son) published a classical work, “The Structure and Physiology
of Fishes explained and compared with those of Man and other
Animals” (Edinb. 1785, fol.) The electric organs of fishes (Torpedo
and Gymnotus) were examined by Réaumur, Allamand, Bancroft,
Walsh, and still more exactly by J. Hunter. The mystery of the
propagation of the Eel called forth a large number of essays, and
even the artificial propagation of Salmonidæ was known and
practised by Gleditsch (1764).
Bloch and Lacépède’s works were almost
Faunists. immediately succeeded by the labours of Cuvier, but
his early publications were of necessity tentative,
preliminary, and fragmentary, so that a short period elapsed before
the spirit infused by this great anatomist into Ichthyology could
exercise its influence on all workers in this field. Several of such
antecuvierian works must be mentioned on account of their
importance to our knowledge of certain Faunas: the “Descriptions
and Figures of Two Hundred Fishes collected at Vizagapatam on the
coast of Coromandel” (Lond. 1803; 2 vols. in fol.), by Patrick Russel;
and “An Account of the Fishes found in the River Ganges and its
branches” (Edinb. 1822; 2 vols. in 4to), by F. Hamilton (formerly
Buchanan)—works distinguished by a greater accuracy of their
drawings (especially in the latter), than was ever attained before. A
“Natural History of British Fishes” was published by E. Donovan
(Lond. 8vo, 1802–8); and the Mediterranean Fauna formed the study
of the lifetime of A. Risso (“Ichthyologie de Nice.” Paris, 1810, 8vo;
and “Histoire naturelle de l’Europe Meridionale.” Paris, 1827, 8vo). A
slight beginning in the description of the fishes of the United States
was made by S. L. Mitchell, who published, besides various papers,
a “Memoir on the Ichthyology of New York,” in 1815.[2]
G. Cuvier did not occupy himself with the study of

G. Cuvier. fishes merely because this class formed part of the
“Règne animal,” but he devoted himself to it with
particular predilection. The investigation of their anatomy, and
especially of their skeleton, was taken up by him at an early period,
and continued until he had succeeded in completing so perfect a
framework of the system of the whole class that his immediate
successors could content themselves with filling up those details for
which their master had no leisure. Indefatigable in examining all the
external and internal characters of the fishes of a rich collection, he
ascertained the natural affinities of the infinite variety of fishes, and
accurately defined the divisions, orders, families, and genera of the
class, as they appear in the various editions of the “Règne animal.”
His industry equalled his genius: he opened connections with almost
every accessible part of the globe; not only French travellers and
naturalists, but also Germans, Englishmen, Americans, rivalled one
another to assist him with collections; and for many years the
Muséum of the Jardin des Plantes was the centre where all
ichthyological treasures were deposited. Thus Cuvier brought
together a collection the like of which had never been seen before,
and which, as it contains all the materials on which his labours were
based, must still be considered to be the most important. Soon after
the year 1820, Cuvier, assisted by one of his pupils, A.
Valenciennes, commenced his great work on fishes, “Histoire
naturelles des Poissons,” of which the first volume appeared in 1828.
The earlier volumes, in which Cuvier himself took his share, bear
evidence of the freshness and love with which both authors devoted
themselves to their task. After Cuvier’s death in 1832 the work was
left entirely in the hands of Valenciennes, whose energy and interest
gradually slackened, to rise to the old standard in some parts only,
as, for instance, in the treatise on the Herring. He left the work
unfinished with the twenty-second volume (1848), which treats of the
Salmonoids. Yet, incomplete as it is, it is indispensable to the
student.
There exist several editions of the work, which, however, have
the same text. One, printed in 8vo, with coloured or plain figures, is
the one in common use among ichthyologists. A more luxurious
edition in 4to has a different pagination, and therefore is most
inconvenient to use.
As mentioned above, the various parts of the work are very
unequally worked out. Many of the species are described in so
masterly a manner that a greater excellency of method can hardly be
conceived. The history of the literature of these species is entered
into with minuteness and critical discernment; but in the later
volumes, numerous species are introduced into the system without
any description, or with a few words only, comparing a species with
one or more of its congeners. Cuvier himself, at a late period of his
life, seems to have grown indifferent as to the exact definition of his
species: a failing commonly observed among Zoologists when
attention to descriptive details becomes to them a tedious task. What
is more surprising is, that a man of his anatomical and physiological
knowledge should have overlooked the fact that secondary sexual
characters are developed in fishes as in any other class of animals,
and that fishes undergo great changes during growth; and,
consequently, that he described almost all such sexual forms and
different stages of growth under distinct specific and even generic
names.
The system finally adopted by Cuvier is the following:—
A. Poissons Osseux.
I.—a branchies en peignes ou en lames.
1. a mâchoire supérieure libre.
a. Acanthoptérygiens.
Percoïdes.
Polynèmes.
Mulles.
Joues cuirassées.
Scienoïdes.
Sparoïdes.
Chétodonoïdes.
Scomberoïdes.
Muges.
Branchies labyrinthiques.
Lophioïdes.
Gobioïdes.
Labroïdes.
b. Malacoptérygiens.
Abdominaux.
Cyprinoïdes.
Siluroïdes.
Salmonoïdes.
Clupeoïdes.
Lucioïdes.
Subbrachiens.
Sparoïdes.
Pleuronectes.
Discoboles.
Apodes.
Murenoïdes.
2. a mâchoire supérieure fixée.

Sclérodermes.
Gymnodontes.
II. a branchies en forme de houppes.

Lophobranches.
B. Cartilagineux ou Chondroptérygiens.
Sturioniens.
Plagiostomes.
Cyclostomes.
We have to compare this system with that of Linnæus if we wish

to measure the gigantic stride Ichthyology has made during the
intervening period of seventy years. The various characters
employed for classification have been examined throughout the
whole class, and their relative importance has been duly weighed
and understood. Though Linnæus had formed a category of
“Amphibia nantes” for fishes with a cartilaginous skeleton, which
should coincide with Cuvier’s “Poissons Cartilagineux,” he had failed
to understand the very nature of cartilage, apparently comprising by
this term any skeletal framework of less firmity than ordinary bone.
Hence he considered Lophius, Cyclopterus, Syngnathus to be
cartilaginous fishes. Adopting the position and development of the
ventral fins as a highly important character, he was obliged to
associate fishes with rudimentary and inconspicuous ventral fins, like
Trichiurus, Xiphias, etc., with the true Eels. The important category of
a “family” appears now in Cuvier’s system fully established as that
intermediate between genus and order. Important changes in
Cuvier’s system have been made and proposed by his successors,
but in the main it is still that of the present day.
Cuvier had extended his researches beyond the living forms, into
the field of palæontology; he was the first to observe the close
resemblance of the scales of the fossil Palæoniscus to those of the
living Polypterus and Lepidosteus, the prolongation and identity of
structure of the upper caudal lobe in Palæoniscus and the
Sturgeons, the presence of peculiar “fulcra” on the anterior margin of
the dorsal fin in Palæoniscus and Lepidosteus: inferring from these
facts that that fossil genus was allied either to the Sturgeons or to
Lepidosteus. But it did not occur to him that there was a close
relationship between those recent fishes. Lepidosteus and, with it,
the fossil genus remained in his system a member of the order of
Malacopterygii abdominales.
It was left to L. Agassiz (born 1807, died 1873) to point out the
importance of the character of the structure of the scales, and to
open a path towards the knowledge of a whole new sub-class of
fishes, the Ganoidei.
Impressed with the fact that the peculiar scales of Polypterus and
Lepidosteus are common to all fossil osseous fishes down to the
chalk, he takes the structure of the scales generally as the base for
an ichthyological system, and distinguishes four orders:—
1. Placoids.—Without scales proper, but with scales of enamel,
sometimes large, sometimes small and reduced to mere points
(Rays, Sharks, and Cyclostomi, with the fossil Hybodontes).
2. Ganoids.—With angular bony scales, covered with a thick
stratum of enamel: to this order belong the fossil Lepidoides,
Sauroides, Pycnodontes, and Coelacanthi; the recent Polypterus,
Lepidosteus, Sclerodermi, Gymnodontes, Lophobranches, and
Siluroides; also the Sturgeons.
3. Ctenoids.—With rough scales, which have their free margins
denticulated: Chætodontidæ, Pleuronectidæ, Percidæ, Polyacanthi,
Sciænidæ, Sparidæ, Scorpænidæ, Aulostomi.
4. Cycloids.—With smooth scales, the hind margin of which lacks
denticulation: Labridæ, Mugilidæ, Scombridæ, Gadoidei, Gobiidæ,
Murænidæ, Lucioidei, Salmonidæ, Clupeidæ, Cyprinidæ.
We have no hesitation in affirming that if Agassiz had had an
opportunity of acquiring a more extensive and intimate knowledge of

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Scientific American Biology for a

Changing World with Core Physiology

2. Why does wearing sunscreen reduce cancer risk?

3. A mutation can cause a change _____.

7. Are all mutations bad? Explain your answer.

10. Why is age a risk factor for cancer?

11. What is the role of BRCA1 in normal cells?

18. Which of the following is a known mutagen?

19. Why does wearing sunscreen reduce cancer risk?

23. A woman with a BRCA1 mutation

26. Define apoptosis. Why is apoptosis important?

28. Define metastasis. Do all cancers enter this stage?

33. Explain how radiation leads to apoptosis.

37. List three types of genetic mutations that may occur.

40. Why should pregnant women never be given X-rays?

43. What is a mutagen?

49. What is a carcinogen?

50. List at least five carcinogens.

58. What role does an oncogene play in generating a tumor?

73. Cell cycle checkpoints detect and control

74. Cell division is usually kept under control by

75. At the G2 checkpoint, cells pause to

77. Programmed cell death is called

78. Proteins scan chromosomes for damage during the

82. If a cell is irreparably damaged, it undergoes programmed cell death, called

83. Cancer consists of too much

84. Which of the following help(s) to prevent cancer?

87. Cell division in cancerous tumors

88. The medical condition of cells growing out of control is called

90. How could a cancerous cell evade apoptosis?

93. Chemotherapy is used in the battle against

94. Chemotherapeutics act on

95. Radiation therapy for cancer works by

103. Most chemotherapy drugs are effective because they

104. All of the following could be effective cancer treatments EXCEPT

105. Chemotherapy drugs interfere with

110. Alleles are located

111. What is an example of a mutation in an allele?

114. Gene mutations can arise when nucleotides are

116. Different alleles are the result of

118. A mutation is best described as an error in

119. Most new alleles arise via

123. Which of the following is TRUE?

125. A mutation would most likely be inherited if it is located in a ____ cell.

130. DNA mutations can

134. Which of the following cannot lead to a mutation?

135. DNA damage is usually repaired

136. Mutations are

139. Mutations in DNA sequences may occur during the process of

144. Mutations in DNA occur during

145. Which of the following statements is always TRUE?

147. Mutations usually affect a protein's

149. Not all mutations are dangerous. Why?

154. If a person is a carrier for a disease; he or she has

156. How can a person acquire mutations in their DNA?

157. Which of the following is NOT a known source of mutations?

159. Which of the following is NOT a known carcinogen?

160. Which of the following are mutagens?

161. Which of the following will lead to a new, inheritable allele?

167. What is the number-one preventable cause of cancer?

168. The most common cancer among women is

170. All of the following are TRUE of breast cancer, EXCEPT

171. All of the following are TRUE of BRCA genes, EXCEPT