This is a summary of Molecular Biology of Cancer chapter 1-6. This is the perfect summary to prepare yourself for the first exam in the Oncology course. It contains figures and detailed explanations. My exam grade was an 8!
SUMMARY OF
PECORINO’S MOLECULAR BIOLOGY OF
CANCER
Chapter 1: Introduction
1.1 What is cancer?
Cancer:
- Group of disease characterized by unregulated cell growth and invasion and spread
of cells from site of origin or primary site to other sites in body.
o Carcinomas: occurring in epithelial cells
o Sarcomas: occurring from mesoderm cells (bone or muscle)
o Adenocarcinomas: occurring from glandular cells (breast)
Hallmarks of cancer:
- Growth signal autonomy:
o Can happen through acquired mutations
- Evasion of growth inhibitory signals:
o Acquired mutations or gene silencing influences this
- Reprogramming energy metabolism:
o Uncontrolled cell division needs more energy and therefore increases of fuel
and biosynthetic precursors by adjusting energy metabolism. Cancer cells
carry out glycolysis, even when oxygen is around.
- Avoiding immune destruction:
o Successful cancer cells may not stimulate immune responses or are able to
interfere with the response to avoid it.
- Evasion of cell death:
o Cancer cells evade apoptotic signals
- Unlimited replicative potential:
o Cancer cells have active telomerase
- Genome instability and mutation:
o By faulty DNA repair
- Tumor-promoting inflammation:
o All tumors contain inflammatory immune cells
o The inflammation can provide growth factors and enzymes to promote
angiogenesis and invasion. It can also produce ROS.
- Angiogenesis:
o Growth of new blood cells
o Usually by altering the balance between inhibitors and inducers.
- Invasion and metastasis:
o Alterations of genome may affect activity or level of involved enzymes to
promote invasion.
, Benign tumors can still be dangerous, because of their location, but are not cancer.
1.2 Evidence suggests that cancer is a disease of the genome at the
cellular level
Carcinogens:
- Can cause cancer by causing alterations to DNA sequence (mutations).
- Inheritable modifications of genome and chromatin structure can play a role in
carcinogenesis
Development of cancer is clonal: all cells in a primary tumor arise from a single cell. Only
one in 1014 cells needs to accumulate enough mutations and then a tumor can arise. This
also explains heterogeneity of tumors, as selection of the fittest plays a role in selecting
mutations. Mutations that do not get repaired continue to the daughter cell.
Processes affecting number of cells:
- Proliferation
- Apoptosis
- Differentiation
Carcinogenesis relies on:
- Oncogenes: a gene that’s mutated to form more or more active proteins and can
ensure tumor formation. A mutation in only one allele is enough. An oncogene can
also be a gene that produces a higher quantity of a certain receptor, so it’ll always be
on and does not require signals.
- Tumor suppressor genes: genes that make proteins who inhibit formation and
growth of tumors. Loss of growth inhibition happens when mutations result in loss of
function. Both of the alleles need to be nonfunctional.
Haploinsufficiency:
- Only one mutated allele can lead to cancer, because one allele only produces half of
what it normally does.
1.3 Influential factors in human carcinogenesis
Chimney sweeps resulted in chronic exposure to soot, which resulted in scrotal and nasal
cancer.
UVB radiation can alter DNA by forming pyrimidine dimers and then cause mutations.
Having children reduces the breast cancer risk for women. Also, age of woman at time of
giving birth and start of menstrual cycle affect cancer risk and so do hormonal contraception
and fertility treatments. Breast cancer risk can be reduced if women were more physically
active.
Kaposi’s sarcoma arises from HPV type 8 infection, usually only in people who have a bad
immune system because of HIV infection.
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