*Cancer

Question 1

Colon cancer series of mutations

Answer 1

1. APC tumor supressor gene lost
2. KRAS oncogene activated
3. DCC tumor supressor gene lost
4. P53 tumor supressor gene lost

Question 2

Cooperativity

Answer 2

The overexpression of multiple oncogenes results in increased tumor formation (myc, rasD)

Question 3

Tumor Suppressor Gene

Answer 3

The brakes. Encode proteins that restrain cell growth. A mutation in BOTH alleles would cause cancer.
The proteins produced by tumor suppressor genes stop cell proliferation.

Question 4

Oncogenes

Answer 4

Encode proteins that promote out-of-control growth and conversion of cell to a malignant state. Dominant: a mutation in one allele is enough to cause out of control growth.

Question 5

Proto-oncogenes

Answer 5

genes that encode proteins for normal cell functioning, but can be converted to oncogenes

Question 6

Proto-oncogenes activated in 3 ways:

Answer 6

1. Gene with proto-oncogene is mutated, making a protein with altered structure or function
2. The gene is duplicated, leading to amplification and making excess protein
3. Chromosome rearrangement that alters expression of gene or nature of product.

Question 7

pRB helps regulate the passage of cells from:

Answer 7

G1 stage to S phase

Question 8

RB

Answer 8

Retinoblastoma tumor suppressor gene. Both copies must be mutated or eliminated to result in a tumor

Question 9

pRB targets ____ family of transcription factors which results in _______.

Answer 9

E2F; repression

Question 10

______ is necessary for pRB to disassociate from E2F so transcription can proceed.

Answer 10

activation of cdk leads to phosphorylation of pRB

Question 11

p53

Answer 11

Tumor suppressor responsible for repair of DNA damage. The p53 protein acts as a TF, activating genes that inhibit transition from G1 to S. If there is damage, p53 concentration rises. If a cell’s DNA is damaged beyond repair, p53 triggers apoptosis.

Question 12

Mutation in p53 leads to:

Answer 12

No more G1 checkpoint control

Question 13

Hereditary nonpolyposis colorectal cancer caused by:

Answer 13

Defect in DNA mismatch repair

Question 14

Xeroderma pigmentosum caused by:

Answer 14

Defect in Nucleotide Excision Repair

Question 15

Defects in repair of double stranded breaks by homologous recombination causes (3)

Answer 15

Bloom’s disease, Fanconi anemia, hereditary breast cancer (BRCA1 and 2 deficiencies)

Question 16

BCL2 gene

Answer 16

overexpression leads to suppression of apoptosis

mRNA that encodes BCL2 gene is inhibited by miRNA.

Question 17

Angiogenesis

Answer 17

Formation of new blood vessels.

Question 18

Avastin (mAB)

Answer 18

Drug that interrupts interaction of VGEF (which the tumor releases) and VGEFR (receptor), thus inhibiting angiogenesis.

Question 19

Passive Immunotherapy

Answer 19

Uses patient’s own antibodies to respond to the tumor.

Question 20

Herceptin

Answer 20

antibody against growth factors that stimulates proliferation of breast cancer cells.

Question 21

Rituxan

Answer 21

antibody that binds to cell surface proteins of non-Hodgkins lymphoma

Question 22

Vestibix

Answer 22

antibody directed against the EGF receptor of colon cancer