M/c Cancer Is A Disease Of The Genome

Front 1

Homeostasis balance is disrupted in tumors what are two explanations for this.

Back 1

1. Increase in cell proliferation
2. Decrease in cell death

Front 2

Which is more common hereditary tumors or sporadic tumors?

Back 2

sporadic tumors

Front 3

Tumors develop by the accumulation of multiple mutations. What is the best illustration of this?

Back 3

Tumor incidence and its relationship with age. Cancer is more prevalent in the older population.

Front 4

In oncogenes mutation(s) in _______ allele(s) cause abnormally proliferating cells. This is known as_______?

Back 4

One allele
Over activity mutation ( gain of function)

Front 5

In tumor supressor genes mutation(s) in _______ allele(s) cause abnormally proliferating cells. This is known as_______?

Back 5

Two alleles
Under activity mutation ( loss of function )

Front 6

In order for tumor suppressor genes a mutation in 1 allele will cause partial inactivity. T/F?

Back 6

False, a mutation in both alleles is necessary for loss of function.

Front 7

What are the mechanisms by which proto-oncogenes can be activated in cancer?

Back 7

1. Mutation of single amino acid
2. Gene amplification
3. Gene mutation (Chromosomal Translocation)

Front 8

The RAS gene is most commonly mutated in which type of cancer?>

Back 8

Epithelial Cancer

Front 9

Hereditary Retinoblastoma is caused by...

Back 9

a predisposing mutation followed by a somatic mutation retina

Front 10

Sporadic Retinoblastoma is caused by...

Back 10

two somatic mutations in the retina

Front 11

What is the difference between sporadic and hereditary retinoblastoma?

Back 11

1. Age of onset of disease is younger in hereditary because of germline mutation.
2. Develop tumors in both retina more frequent in hereditary

Front 12

Mutation of _____ is the best at enhancing cell survival in cancer.

Back 12

P53, by preventing apoptosis.

Front 13

List the anti-apoptotic pathways in cancer.

Back 13

1. Most important,genetic inactivation/loss of function of p53.

2. Increased expression/ activity of anti-apoptotic genes(i.e. Bcl-2 in follicular lymphoma;Akt 2 amplification in pancreatic cancer).

3. Decreased expression/activity of pro-apoptotic genes(i.e.BAX truncation in hereditary colon cancer without polyps).

Front 14

Which types of genes have a direct oncogenic property?

Back 14

Oncogenes and tumor supressor genes

Front 15

Which type of genes have an indirect oncogenic property?

Back 15

Genes involved in DNA repair

Front 16

Proteins involved in the maintenance of DNA stability function by...

Back 16

1. repair of mismatches
2. repair of (ds) breaks

Front 17

Which tumor supressor gene must be mutated to initiate the neoplastic process in colon cancer?

Back 17

APC gene

Front 18

Multiple genetic alterations in colorectal tumorigenesis. T/F

Back 18

True, seven or so mutations are necessary. Again this revisits the idea that tumorogenisis requires the accumulation of mutations.

Front 19

APC mutation is inherited in which disease?

Back 19

FAP familial adenomatour polyposis

Front 20

How does Gleevac work?

Back 20

Acts as a competitor with APT for the kinase pocket of oncoprotein BCR/ABL, which prevents phosphorylation. Blocks activity of the oncogenic protein.

Front 21

Why has Gleevac shown more success than other gene-target medications?

Back 21

Epithelial tumors are caused by multiple abnormalities as we have seen, however the BCR/ABL oncogene is the only abnormality in CML, which means it can be easier to target.