Libyan International Medical University

Faculty of Pharmacy

[Cancer]
Student Name : Nouralhodah Almukasaby
Student no: 3103
Tutor Name : Khadeja Najeb
Block No.6
Week No.4
Date of Submission : 2021/12/22
Academic Year

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 2020-2021
Table of content

 Introduction………………………………………………………….3
(1)-Discuss The effect Heredity and age on incidence cancer………….4
(2)-Discuss The Types of Transplants…………………………………..6
(3)-Discuss Immunological Surveillance……………………………….7
(4)-State Cancer incidence environmental and geographic factors…….8
(5)-Discuss Type and action of phopholipase………………………….11
(6)-Define drug information resources…………………………………11
 Summary…………………………………………………………….12
 References…………………………………………………………...13

Table of Figures
(1)-Figure1: incidence cancer statistics in woman and men………………6
(2)-Figure2: The degradation of phosphoglycerides……………………..11

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 Introduction
This problem to talk about Discuss The effect Heredity and age on incidence cancer
and Discuss The Types of TransplantsDiscuss and Immunological Surveillance and
State Cancer incidence environmental and geographic factors and Discuss Type and
action of phopholipase and Define drug information resources and finally summary.

3
(1)-Discuss The effect Heredity and age on incidence cancer:
*Heredity*
The evidence now indicates that for many types of cancer, including the most common
forms, there exist not only environmental influences but also hereditary predisposi_tions.
Hereditary forms of cancer can be divided into three categories based on their pattern of
inheritance.(DeLong, 2013)
Autosomal Dominant Cancer Syndromes
Autosomal dominant cancer syndromes include several well-defined cancers in which
inheritance of a single mutant gene greatly increases the risk of developing a tumor. The
predisposition to these tumors shows an auto_somal dominant pattern of inheritance.
Childhood retino_blastoma is the most striking example of this category. Approximately
40% of retinoblastomas are familial. As is discussed later, inherited disabling mutations
in a tumor suppressor gene are responsible for the development of this tumor in families.
Carriers of this gene have a 10,000-fold increased risk of developing retinoblastoma.
Unlike those with sporadic retinoblastoma, patients with familial retino_blastoma
develop bilateral tumors, and they also have a greatly increased risk of developing a
second cancer, par_ticularly osteosarcoma Tumors within this group often are associated
with a specific marker phenotype. There may be multiple benign tumors in the affected
tissue, as occurs in familial polyposis of the colon and in multiple endocrine neoplasia
(see Table 5–3). Sometimes, there are abnormalities in tissue that are not the target of
transformation (e.g., Lisch nodules and café-au-lait spots in neurofibromatosis type 1)
(DeLong, 2013)
Autosomal Recessive Syndromes of Defective DNA Repair
A group of rare autosomal recessive disorders is collec_tively characterized by
chromosomal or DNA instability and high rates of certain cancers. One of the best-
studied is xeroderma pigmentosum, in which DNA repair is defec_tive. This and other
familial disorders of DNA instability are described later.(DeLong, 2013)
Age

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In general, the frequency of cancer increases with age. Most cancer deaths occur between
ages 55 and 75; the rate declines, along with the population base, after age 75. The rising
incidence with age may be explained by the accumu_lation of somatic mutations
associated with the emergence of malignant neoplasms (discussed later). The decline in
immune competence that accompanies aging also may be a factor. Cancer causes slightly
more than 10% of all deaths among children younger than 15 years (Chapter 5). The
major lethal cancers in children are leukemias, tumors of the central nervous system,
lymphomas, and soft tissue and bone sarcomas. As discussed later, study of several
childhood tumors, such as retinoblastoma, has provided fundamental insights into the
pathogenesis of malignant transformation.(DeLong, 2013)

EPIDEMIOLOGY
A. The most common causes of death in adults and children:
 In adults
1) Cardiovascular disease
2) Cancer
 Cerebrovascular disease in children
1) Accidents
2) Cancer
3) Congenital defects.
B. The most common cancers by incidence in adults are:
1) breast/prostate
2) Lung
3) Colorectal
The most common causes of cancer mortality (destined to die)
C. in adults are:
1) Lung Breast
2) Prostate
3) Colorectal(1).(WHO, 2018)

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0 to 1 year:

 Developmental and genetic conditions that were present at birth

 Conditions due to premature birth (short gestation)

 Health problems of the mother during pregnancy

1 to 4 years:

 Accidents (unintentional injuries)

 Developmental and genetic conditions that were present at birth

 Homicide

5 to 14 years:

 Accidents (unintentional injuries)

 Cancer

 Suicide(001915 @ Medlineplus.Gov, n.d.)

(D
eLong, 2013)
Figure1: incidence cancer statistics in woman and men

(2)-Discuss The Types of Transplants:

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 i. Autograft: Itis self-tissue transferred from one body site to another in the same
individual.
ii. Isograft: It is tissue transferred between genetically identical individuals. In
humans, an isograft performed between genetically identical (monozygomatic)
twins and in inbred strains of mice, an isograft performed from one mouse to
another syngeneic mouse are examples of isografts.
iii. Allograft: It is tissue transferred between genetically different members of the
same species.
iv. Xenograft: It is tissue transferred between different species (e.g. the graft of a
baboon heart into a human) (2).(S. Kumar, 2016)

(3)-Discuss Immunological Surveillance:

The immune surveillance theory was first conceptualized in the early 1900s (1906) by
Paul Ehrlich. He suggested that cancer cells frequently arise in the body but are
recognized as foreign and eliminated by the immune system. Some 50 years later, Lewis
Thomas revived it in 1950s and was developed by Burnet. It postulates that the primary
function of cell mediated immunity is to ‘seek and destroy’ malignant cells that arise by
somatic mutation. Such malignant mutations are believed to occur frequently and would
develop into tumors but for the constant vigilance of the immune system. Inefficiency of
the surveillance mechanism, either as a result of ageing or in congenital or acquired
immunodeficiencies, leads to an increased incidence of cancer.
The development of tumors represents a lapse in surveillance. It is evident that tumor
cells must develop mechanisms to escape or evade the immune system in
immunocompetent hosts.Several such mechanisms may be operative:
1. Weak immunogenicity: Some tumors are weakly immunogenic, so in small
numbers they do not elicit an immune response. But when their numbers increase
enough to provoke immune response the tumor load may be too great for the host’s
immune system to mount an effective response.

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 2. Modulation of surface antigens: Certain tumor-specific antigens disappear from
the surface of tumor cells in the presence of serum antibody and then to appear after
the antibody is no longer present.
3. Masking tumor antigens: Certain cancers produce copious amounts of a
mucoprotein called sialomucin. It binds to the surface of the tumor cells. Immune
system does not recognize these tumor cells as foreign since sialomucin is a normal
component
4. Induction of immune tolerance: Some tumor cells can synthesize various
immunosup_pressants.
5. Production of blocking antibodies: Antitumor antibody itself acts as a blocking
factor.
6. Low levels of HLA class I molecules: This impairs presentation of antigenic
peptides to cytotoxic T-cells(3).(S. Kumar, 2016)

(4)-State Cancer incidence environmental and geographic factors:

For the year 2012, the World Health Organization (WHO) estimated that there were
about 14.1 million new cancer cases worldwide, leading to 8.2 million deaths
(approxi_mately 22,500 deaths per day). Moreover, due to increasing population size, by
the year 2035 the WHO projects that the numbers of cancer cases and deaths worldwide
will increase to 24 million and 14.6 million, respectively (based on current mortality
rates). Additional perspective on the likelihood of developing a specific form of cancer
can be gained from national incidence and mortality data. In the United States, it is
estimated that the year 2016 will be marked by approximately 1.69 million new cases of
cancer and 595,000 cancer deaths. Incidence data for the most common forms of cancer,
with the major killers identified, Over several decades, the death rates for many forms of
cancer have changed. Since 1995, the incidence of cancer in men and women in the
United States has been roughly stable, but the cancer death rate has decreased by roughly
20% in men and 10% in women. Among men, 80% of the decrease is accounted for by
lower death rates for cancers of the lung, prostate, and colon; among women, nearly 60%
of the decrease is due to reductions in death rates from breast and colorectal cancers.

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Decreased use of tobacco products is responsible for the reduction in lung cancer deaths,
while improved detection and treatment are responsible for the decrease in death rates for
colorectal, female breast, and prostate cancers.
The last half-century has also seen a sharp decline in death rates from cervical cancer and
gastric cancer in the United States. The decrease in cervical cancer is directly attributable
to widespread use of the Papanicolaou (PAP) smear test for early detection of this tumor
and its precur_sor lesions. The deployment of the human papillomavirus (HPV) vaccine
may nearly eliminate this cancer in coming years. The cause of the decline in death rates
for cancers of the stomach is obscure; it may be related to decreasing exposure to
unknown dietary carcinogens.
Environmental exposures appear to be the dominant risk factors for many common
cancers, suggesting that a high fraction of cancers are potentially preventable. This notion
is supported by the geographic variation in death rates from specific forms of cancer,
which is thought to stem mainly from differences in environmental exposures. For
instance, death rates from breast cancer are about four to five times higher in the United
States and Europe than in Japan. Con_versely, the death rate for stomach carcinoma in
men and women is about seven times higher in Japan than in the United States. Liver cell
carcinoma is relatively infrequent in the United States but is the most lethal cancer among
many African populations. Nearly all the evidence indicates that these geographic
differences have environmental rather than genetic origins. For example, Nisei
(second_generation Japanese living in the United States) have mor_tality rates for certain
forms of cancer that are intermediate between those in natives of Japan and in Americans
who have lived in the United States for many generations. The two rates come closer with
each passing generation.
There is no paucity of environmental factors that con_tribute to cancer. They lurk in the
ambient environment, in the workplace, in food, and in personal practices. They can be as
universal as sunlight or be largely restricted to urban settings (e.g., asbestos) or particular
occupations (Table 6.2). The most important environmental exposures linked to cancer
include the following:

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 • Diet. Certain features of diet have been implicated as predisposing influences. More
broadly, obesity, cur_rently epidemic in the United States, is associate with a
modestly increased risk for developing many different cancers.
• Smoking. Smoking, particularly of cigarettes, has been implicated in cancer of the
mouth, pharynx, larynx, esophagus, pancreas, bladder, and, most significantly, the
lung, as 90% of lung cancer deaths are related to smoking.
• Alcohol consumption. Alcohol abuse is an independent risk factor for cancers of
the oropharynx, larynx, esoph_agus, and (due to alcoholic cirrhosis) liver. Moreover,
alcohol and tobacco smoking synergistically increase the risk for developing cancers
of the upper airways and upper digestive tract.
• Reproductive history. There is strong evidence that life_long cumulative exposure
to estrogen stimulation, par_ticularly if unopposed by progesterone, increases the risk
for developing cancers of the endometrium and breast, both of which are estrogen-
responsive tissues.
• Infectious agents. It is estimated that infectious agents cause approximately 15% of
cancers worldwide.
Thus, there is no escape: it seems that everything people do to earn a livelihood, to
subsist, or to enjoy life turns out to be illegal, immoral, or fattening, or—most
disturbing— possibly carcinogenic.(Saunders, 2013)
Geographic factor
An estimated 12,400 American children and adolescents under age 20 were diagnosed
with cancer in 2000. Childhood cancer is rare, and the rate at which new cases develop
among children (incidence) is 15.3 per 100,000 per year, which corresponds roughly to 1
in 6,500 children and adolescents under age 20 (Ries et al., 2002). The risk of any
individual child developing cancer between birth and 20 years of age is about 1 in 300.
There were an estimated 2,300 deaths in 2000 due to cancer in this age group,
representing about 8 percent of all deaths (American Cancer Society, 2000). Cancer is the
third leading cause of death among children age 1 to 4, and the second leading cause of
death among children age 5 to 14 (Minino and Smith, 2001) (4).
(B16514a78d7111a63b72549ea0365259dae8addc @ Pubmed.Ncbi.Nlm.Nih.Gov, n.d.)

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(5)-Discuss Type and action of phopholipase:
The degradation of phosphoglycerides is performed by phospholipases found in all
tissues and pancreatic juice. A number of toxins and venoms have phospholipase activity,
an d several pathogenic bacteria produce phospholipases that dissolve cell membranes
and allow the spread of infection. Sphingomyelin is degraded by the lysosomal
phospholipase, sphingomyelinase.
Phospholipases hydrolyze the phosphodiester bonds of phosphoglycerides, with each
enzyme cleaving the phospholipid at a specific site.
Phospholipases A1, A2, C, and D, Phospholipase A2 is found in pancreatic fluid and
snake venom as well as in many types of cells, phosopholipase C is one of the major
toxins secreted by bacteria; and phospholipase D is known to be involved in mammalian
signal transduction(5).(MORELAND, 1988)

(Mu
rray & Davis, 2003)
Figure2: The degradation of phosphoglycerides

(6)-Define drug information resources:

It is called drug information, medication information, or drug informatics.  It’s really the
discovery, use, and management of information in the use of medications. Drug
information covers the gamut from identification, cost, and pharmacokinetics to dosage
and adverse effects.  You may also need information about the body, health, or diseases
in order to better utilize the drug information(6).(Harvey, 2000)

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 Summary

I understood Discuss The effect Heredity and age on incidence cancer and Discuss
The Types of TransplantsDiscuss and Immunological Surveillance and State Cancer
incidence environmental and geographic factors and Discuss Type and action of
phopholipase and Define drug information resources and finally summary.

12
  References001915 @ medlineplus.gov. (n.d.).
https://medlineplus.gov/ency/article/001915.htm?
fbclid=IwAR1mpdzQp1iHwfXW7CzWyNSUHIaqpdWC4UbmALvll
Cgb37XZSKWcwpSj-Nc
b16514a78d7111a63b72549ea0365259dae8addc @
pubmed.ncbi.nlm.nih.gov. (n.d.).
https://pubmed.ncbi.nlm.nih.gov/25220842/
DeLong, L. (2013). Basic pathology. In General and Oral Pathology for the
Dental Hygienist (pp. 29–44). https://doi.org/10.1136/jcp.47.1.95-d
Harvey, D. (DePauw U. (2000). Modren analytical chemistry. In McGraw-
Hill Higher Education. McGraw-Hill.
Kumar, S. (2016). Essentials of Microbiology. In Essentials of
Microbiology. https://doi.org/10.5005/jp/books/12697
MORELAND, B. H. (1988). Lippincott’s Illustrated Reviews: Biochemistry.
In Biochemical Society Transactions (Vol. 16, Issue 5).
https://doi.org/10.1042/bst0160907
Murray, R. K., & Davis, J. C. (2003). Biochemistry (Lippincotts).
Saunders, E. (2013). No Title (V. Kumar (Ed.); 9th ed). permissions
policies,.
WHO. (2018). cancer @ www.who.Int. In Cancer (p. 1).
http://www.who.int/mediacentre/factsheets/fs297/en/

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