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Causes of Cancer
Epidermal Growth Factor Receptor (EGFR), transcription factors such as c-Myc, or cell
signaling proteins such as Kirsten ras (KRAS), act as “on switches” for cellular growth
(when amplified -can lead to uncontrolled cell proliferation)
Note: genetic alterations in the gene for KRAS have been associated with pancreatic,
lung, and colorectal cancers
Cancer Suppressor Genes -“turn off” or regulate, unneeded cellular proliferation; when
mutated, resulting in loss of function or expression, the cells begin to produce mutant cells
Initiation Stage - carcinogens can cause mutations in cellular DNA; mutations are
reversed by DNA repair mechanisms, apoptosis, or cell senescence
Promotion Stage - damaged or mutated cell begins to divide and multiply, forming a
small cluster of abnormal cells; repeated exposure to promoting agents or co-carcinogens
can cause the expansion and proliferation of initiated cells, leading to increased
expression or manifestation of abnormal genetic information
Progression Stage – altered cells exhibit increasingly malignant behavior cells
acquire the ability to stimulate angiogenesis to invade adjacent tissues, and to
metastasize
Proliferative Patterns -how cells multiply and spread
atrophy
hypertrophy,
hyperplasia,
metaplasia
dysplasia
Etiology
Factors that induce carcinogenesis:
I. Viruses/Bacteria – DNA viruses insert a part of their own DNA near the infected
cell genes causing cell division
human papillomavirus (HPV) -cervical and head and neck cancers
hepatitis B virus (HBV) -liver cancer
Epstein–Barr virus (EBV) -Burkitt lymphoma; nasopharyngeal
cancer
II. Physical Agents –
sunlight
radiation - ionizing radiation from repeated diagnostic x-ray
procedures; radiation therapy; radioactive materials at nuclear
weapon manufacturing sites or nuclear power plants; radon
chronic irritation inflammation
tobacco carcinogens
industrial chemicals
asbestos
III. Chemical Agents -chemicals produce their toxic effects by altering DNA
structure
Tobacco -can cause cancer of:
o oral cavity and pharynx
o larynx
o lung
o esophagus
o pancreas
o uterine cervix
o kidney
o bladder
o stomach
o colorectal
o liver
o myeloid leukemia.
Environmental Tobacco Smoke (ETS) – linked with cancers of the:
o Larynx
o Pharynx
o nasal sinuses
o brain
o bladder
o rectum
o stomach
o breast
Electronic Nicotine Delivery Systems (ENDS) - e-cigarettes, e-pens,
e-pipes, e-hookah and e-cigars (contain highly addictive nicotine and
other potentially harmful substances, such as volatile organic
compounds, formaldehyde, and flavoring chemicals)
Note: the long-term health effects of these products
remain unknown
Smokeless tobacco products -chewing tobacco, snuff and snus;
associated with an increased risk of oral, pancreatic, and esophageal
cancer
aromatic amines and aniline dyes
pesticides
formaldehydes
arsenic
soot
tars
asbestos
benzene
cadmium
chromium
compounds
nickel and zinc ores
wood dust
beryllium compounds
polyvinyl chloride
IV. Genetics and Familial Factors - extra chromosomes, too few chromosomes, or
translocated chromosomes; the associated genetic mutation is found in all cells in
the body (germline mutation) and represents an inherited susceptibility to cancer
for all family members who carry the mutation.
Predisposition Hallmarks:
o cancer in two or more first-degree relatives (the parent, sibling,
or child of an individual)
o onset of cancer in family members younger than 50 years
o the same type of cancer in several family members
o individual family members with more than one type of cancer
o rare cancer in one or more family members
Familial Inheritance Syndromes:
o hereditary breast and ovarian cancer syndrome (BRCA1 and
BRCA2)
o multiple endocrine neoplasia syndrome (MEN1 and MEN2)
o nephroblastomas
o pheochromocytomas
o colorectal
o stomach
o thyroid
o renal
o prostate
o lung cancers
V. Lifestyle Factors
Obesity - cancers of the breast (in postmenopausal women), colon
and rectum, endometrium, esophagus, kidney, and pancreas,
gallbladder, liver, ovary, and cervix, and for multiple myeloma,
Hodgkin lymphoma, and aggressive forms of prostate cancer
Note: excess fat may cause:
a. chronic inflammation resulting in DNA damage
b. increased levels of certain hormones (e.g.,
estrogen, insulin, adipokines)
c. disruptions in levels of cell growth regulators
(e.g., mammalian target of rapamycin and AMP-
activated protein kinase
Alcohol intake -risk of cancers of the mouth, pharynx, larynx,
esophagus, liver, colon, rectum, and breast
Poor diet -fats, alcohol, salt-cured
or smoked meats, nitrate- and nitrite-containing foods, and red and
processed meats
Physical inactivity
VI. Hormonal Agents - Tumor growth may be promoted by disturbances in
hormonal balance, either by the body’s own (endogenous) hormone production or
by administration of exogenous hormones
Cancers of the breast, prostate, ovaries, and
endometrium are thought to depend on endogenous hormonal levels
for growth.
Prenatal exposure to diethylstilbestrol (a synthetic form of the female
hormone estrogen) -risk factor for clear cell adenocarcinoma of the
lower genital tract
Increased risk of breast cancer:
o Hormonal changes related to the female reproductive cycle
o Early onset of menses before age 12
o Delayed onset of menopause after age 55
o null parity (never giving birth)
o Delayed childbirth after age 30
Note: increased numbers of pregnancies are associated
with a decreased incidence of breast, endometrial, and
ovarian cancers
Mnemonic for CANCER
C -arcinogens
A -ging
N -utrition
C -ommon virus and bacteria
E -xcessive alcohol intake and smoking
R -ace and sex
THEORIES OF CANCER
a) Cellular Transformation Theory –
exposure to carcinogenic chemicals can damage the DNA of normal
cells, leading to genetic mutations that can cause the cells to become
cancerous
carcinogenic chemicals can cause damage to the DNA of cells by
directly interacting with the DNA or by generating reactive oxygen
species that can cause oxidative stress and DNA damage
this damage can lead to alterations in the expression of genes
involved in cell growth, division, and death, leading to uncontrolled
cell proliferation and the formation of tumors
the effects of chemical exposure on cell transformation can depend
on various factors, such as the type and dose of chemical, the
duration of exposure, and the individual's genetic susceptibility
b) The Failure of the Immune Response Theory
the immune system can sometimes fail to recognize and destroy
cancer cells, allowing them to grow and proliferate
cancer cells can use various mechanisms to evade the immune
system, such as producing proteins that suppress the immune
response or altering their surface proteins to avoid detection
cancer cells can create an environment that is hostile to immune cells,
making it difficult for them to function properly
can also be related to a weakened immune system, which can occur
due to various factors such as aging, chronic infections, or certain
medical treatments
a weakened immune system may not be able to mount an effective
response against cancer cells, allowing them to grow and proliferate.
Note: Immunotherapy is a type of cancer
treatment that works by boosting the immune
system's ability to recognize and destroy cancer
cells. This treatment involves:
o use of drugs that target specific proteins
on cancer cells or that stimulate the
immune system's response
o adopting healthy behaviors, managing
chronic infections, and reducing
exposure to environmental toxins.
BODY DEFENSES AGAINST TUMOR
T cell (T lymphocyte)
A type of leukocyte (white blood cell) that is an essential part of the immune system
one of two primary types of lymphocytes
originate in the bone marrow
The T cell system
a. recognize specific proteins, called antigens, on the
surface of cancer cells and become activated to attack
the cancer cells directly
b. cancer cells may evade detection by the immune system
by producing proteins that suppress the immune
response or by altering their surface proteins to avoid
detection
Note: Immunotherapy is a type of cancer
treatment that works by boosting the immune
system's ability to recognize and destroy cancer
cells. This treatment can involve the use of drugs
that target specific proteins on cancer cells or
that stimulate the immune system's response.
The B Cell System
a. B-cells sometimes inhibit tumor development
by producing antibodies that may attack cancer cells or
oncogenic viruses, such as human papillomavirus
(HPV), which is responsible for most cervical, anal,
penile and other reproductive cancers
b. B cells create antibodies. These antibodies bind to
pathogens or to foreign substances, such as toxins, to
neutralize them
c. B cells can also recruit other cells to help destroy an
infected cell.
Phagocytic Cells (macrophages and neutrophils)
a. cells are able to engulf and digest foreign particles,
including cancer cells.
b. recognize and respond to cancer cells by recognizing
specific proteins on the surface of the cancer cells. Once
activated, these cells can engulf and digest the cancer
cells, helping to prevent their growth and spread.
CELL SIGNALING PROCESS THAT CONTROL CELL GROWTH - prevent cell mutations and
maintain normal cellular growth. When these processes become disrupted, it can lead to abnormal cell
growth and the development of cancer.
1. DNA repair mechanisms -detect and repair mutations before they become permanent
and lead to abnormal cell growth
2. Apoptosis -a programmed cell death process that occurs when a cell is damaged or no
longer needed; this process helps eliminate cells with damaged DNA or other abnormalities
that could lead to cancer
3. Cell cycle checkpoints -help ensure proper DNA replication and division; at these
checkpoints, the cell checks for DNA damage and other abnormalities before proceeding to
the next phase of the cell cycle
4. Tumor suppressor genes -help prevent the development of cancer by regulating cell
growth and division; mutations in these genes can lead to uncontrolled cell growth and
contribute to the development of cancer
5. Immune system surveillance -the immune system plays a role in detecting and
eliminating abnormal cells, including those with mutations that could lead to cancer
DIAGNOSIS
Warning Signs of Cancer
C – change in bowel or bladder habits
A – sore throat that does not heal
U – unusual bleeding or discharge
U – unexplained sudden weight loss
T - thickening or lump in the breast or elsewhere
I – indigestion or difficulty in swallowing
O – obvious change in warts or moles
N – nagging cough or hoarseness of voice
CANCER DETECTION EXAMINATION
1. Pap Smear -cells are scraped from the cervix and examined under a microscope to check
for cancer or other problems
2. Biopsy – removal of cells or tissue for analysis
3. Ultrasound - a noninvasive imaging test that shows structures inside the body using high-
intensity sound waves.
4. MRI (Magnetic Resonance Imaging) - a type of scan that uses strong magnetic fields and
radio waves to produce detailed images of the inside of the body
5. Fluoroscopy -a medical procedure that makes a real-time video of the movements inside
a part of the body by passing x-rays through the body over a period of time
DIAGNOSTIC EXAMINATIONS
1. TUMOR MARKER IDENTIFICATION -used for breast, colon, lung, ovarian, testicular
analysis of the substance found in the body
2. MAMMOGRAPHY -for breast examination
3. MRI -neuro, pelvic, thoracic, breast
4. FLUOROSCOPY -skeletal, lung
CANCER CLASSIFICATION
I. Grading -identifies what type of tissue arises from the original
a) G1 -well-differentiated
b) G2 -moderately well-differentiated
c) G3 – poorly differentiated
d) G4 – very poorly differentiated with high degree of malignancy
II. Staging - determines the size of the tumor and extent metastasis; determines extent of the disease
a) Stage 0 – in situ
b) Stage I – limited to tissue of origin; localized
c) Stage II – limited local spread
d) Stage III –regional spread
e) Stage IV – metastasis
III. TNM Staging –provides categorization of primary lesion and extent of involvement in the clinical
assessment of cancer
a) T – primary tumor extent
b) N – lymph node involvement
c) M – metastasis
MANAGEMENT
I. Dietary Management
a) Avoid obesity
b) Cut down on Fats
c) High fiber diet
d) Food rich in Vit A & C
e) Vegetable Diet
f) Moderation in alcoholic beverage
g) Moderation in salty food, preservatives
II. Therapeutic Modalities -surgery, chemotherapy, radiation therapy,
immunotherapy, bone marrow transplantation
1. Surgery
1) Diagnostic – biopsy
2) Radical surgery (wide resection) – remove all tumors
2. Chemotherapy - admin. of cytotoxic meds and chem to promote death of tumor cells; iv
is the best route; oral is the most convenient
a. Side Effects
o malnutrition
o infection related to immunosuppression
o bleeding
b. Management
o monitor for graft versus host disease
o provide a private room for 6 to 8 weeks
o encourage other means of
communication
5. Immunotherapy -immunotherapy is treatment that uses the body's own immune system
to fight cancer; the immune system is stimulated by an outside source, such as an
antibody, or synthetic immune system proteins; also known as “Biological Response
Modifiers”