Genetics Unit 21: Genetics Of Cancer

Front 1

Number of mutational events necessary for cancer in oncogene vs.tumor suppressor gene.

Back 1

Oncogene - 1 (dominant)
TSG - 2 (recessive)

Front 2

Function of mutant allele in oncogene vs.tumor suppressor gene.

Back 2

Onco = gain of function, TSG = loss of function

Front 3

Origin of mutation in oncogene vs.tumor suppressor gene.

Back 3

Onco = somatic
TSG = Inherited or somatic

Front 4

Mechanism of action in oncogene vs.tumor suppressor gene.

Back 4

Onco = to stimulate cell division
TSG = to restrain cell division

Front 5

Gene Amplification leading to oncogenes and examples

Back 5

Cells which contain multiple copies of structurally normal oncogenes via:
1) Double minutes (small separate chromosomes). Ex = Leukemia
2) Insertions within the normal chromosome (homogeneously staining regions). Ex. = retinoblastoma

Front 6

Point mutations leading to oncogenes and example

Back 6

A single amino acid substitution can change how a regulatory protein works making it turn off other genes more slowly for example. Ex = RAS gene in many cancers has a mutation making it deactivate more slowly causing increased activity.

Front 7

Transposition to an active chromatin domain leading to oncogenes.

Back 7

When an oncogene is translocated next to an Ig locus; a part of chromatin which is actively transcribed in antibody producing B cells.

Front 8

Translocation leading to oncogenes and example

Back 8

Translocation at a break point creating a new chimeric protein which causes constant replication. Ex = Burkitts lymphoma

Front 9

Clinically how do u tell apart inherited v.s. sporadic mutations in retinoblastoma?

Back 9

Inherited = Early onset, bilateral
Sporadic = Late onset, unilateral

Front 10

Mismatch repair genes

Back 10

Tumor suppressor genes which are supposed to repair any issues in DNA replication. Mutation causes multiple structural and numerical chromosomal problems.

Front 11

6 capabilities necessary for a tumor to be successful

Back 11

1) Becomes independent of external growth signals
2) Becomes insensitive to external anti-growth signals.
3) Becomes able to avoid apoptosis
4) Becomes capable of indefinite replication
5) Becomes capable of sustained angiogenesis
6) Becomes capable of tissue invasion and metastasis.