Genetics of Cancer

Posted by e-Medical PPT Sunday, March 6, 2011
Cancers result from mutations in the genes that regulate cell growth.DNA damage increases the risk of developing cancer.Familial cancer syndromes are due to mutations in genes affecting DNA repair or genes that regulate cell growth.
Chronic myelogenous leukemia (CML) is a malignant disorder of blood cells that ultimately evolves into acute leukemia, which is rapidly fatal.In 1960, Nowell demonstrated that the leukemic cells from CML patients had a characteristic chromosomal abnormality, t(9:22).This was not present in the patient’s normal cells. Thus, the Ph1 chromosome is an acquired genetic abnormality.This was the first example of a genetic abnormality consistently associated with cancer.

DNA is responsible for transforming normal cells into cancer cells
The demonstration that certain transduced cellular genes (“oncogenes”) cause cancer earned Varmus and Bishop the Nobel Prize in Medicine. This provided direct evidence that DNA was the element of cancerous “transformation.”Similarly, Weinberg demonstrated that DNA extracted from human bladder cancer could transform cultured cells, independently confirmed the that DNA was the element responsible for cancerous transformation.

Cancers are associated with mutations that “inactivate” proteins that inhibit cell growth
SV40 T-Ag binds to a normal cellular protein, p53.
Oncogenic strains of human papillomavirus bind p53 and RB.
Binding of viral proteins to p53 & RB lead to their inactivation.

p53
Activated in cells with damaged DNA
Activates transcription of the CDK inhibitor, p21 and the pro-apoptotic protein, Bax.
p21 arrests cells in the G1 phase of the cell cycle (inhibits cdk4/cyclin D complexes) (checkpoint control).
Bax causes apoptosis of cells with extensive DNA damage
p53 is mutated in over 50% of human cancers.


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