Cancer

Question 1

V-onc

Answer 1

Viral oncogene

Question 2

c-onc

Answer 2

cellular oncogene

a group of genes that cause normal cells to become cancerous when they are upregulated

Question 3

v-myc

Answer 3

virus capture oncogene of myc
viral homologue

Question 4

myc

Answer 4

family of regulator/protooncogenes

Question 5

acutely transforming retrovirus

Answer 5

directly cause cell transformation
generated by viral capture during viral replication in genome

Question 6

proviral insertion

Answer 6

virus itself doesn’t contain oncogene
inserts upstream of protooncogene
messes with regulation of gene = oncogene

Question 7

oncogene capture

Answer 7

1. Integrates closeby to oncogene usually upstream
   a. Needs to have deletion in 3’LTR = polyadenylation signal which shuts off polymerase
   b. Many defective upon integration - loses chunks of genome
2. RNA replicated w no poly a signal to stop - transcribe all the way through oncogene
   a. Now contains retroviral genome + oncogene
3. Gets spliced oncogene attached to viral RNA
4. Packaged into virion - dimeric genome
   a. Packaging signal in 5’ end
   b. Packaged w wild type RNA molecule as well
5. Template switching event can happen to put oncogene in RNA genome
   Additional point mutations = incapable of being regulated by host cell

Question 8

RSV

Answer 8

Rous Sarcoma Virus
Involved in causes sarcomas in chickens

Question 9

RSV genes

Answer 9

gag – encodes capsid proteins
pol – encodes reverse transcriptase
env – encodes the envelope gene
src – encodes a tyrosine kinase that attaches phosphate groups to the amino acid tyrosine in host cell proteins.

Question 10

src gene

Answer 10

RSV oncogene
Src is a tyrosine kinase involved in regulation of cell growth and differentiation

Question 11

ALV

Answer 11

avian leukosis virus
closely related to RSV but doesn’t contain src gene

Question 12

Why do most oncoviruses require a helper virus?

Answer 12

Defective most of the time after oncogene capture
Need to coinfect with WT virus to use their replication and polymerase machinery

Question 13

proto-oncogene

Answer 13

can become an oncogene if mutated

Question 14

chronically transforming viruses

Answer 14

retrovirus integrates near host proto-oncogene and alters their expression

Question 15

types of chronically transforming viruses

Answer 15

promoter insertion
enhancer insertion

Question 16

MMTV

Answer 16

Mouse mammary tumour virus
chronically transforming virus

Question 17

Adenovirus

Answer 17

Silences p53 and retinoblastoma, thus preventing apoptosis
E genes expressed at high levels
E1B binds to p53
E1A binds to rb

Question 18

Podosomes

Answer 18

Conical and actin rich structures on outer membrane surface
formed by v-src in cancer

Question 19

p53

Answer 19

Homotetrameric transcription factor activated by stress

P53 induces apoptosis in nontransformed cells mostly by direct transcriptional activation of the pro-apoptotic BH3-only proteins PUMA

Question 20

Retinoblastoma gene

Answer 20

proto-oncogenic tumor suppressor protein that is dysfunctional in several major cancers.[5] One function of pRb is to prevent excessive cell growth by inhibiting cell cycle progression until a cell is ready to divide. When the cell is ready to divide, pRb is phosphorylated, inactivating it, and the cell cycle is allowed to progress. It is also a recruiter of several chromatin remodeling enzymes such as methylases and acetylases.

Question 21

SV40

Answer 21

Polyoma virus - dsDNA, nonenveloped
Early and late genes which encodes large and small T antigens (early)

Question 22

What kind of cells does SV40 cause cancer in?

Answer 22

Non-permissive cells e.g. rodents

Question 23

Non-permissive cells

Answer 23

Cells in which infection is not productive are called nonpermissive cells.

Question 24

How does SV40 cause cancer?

Answer 24

Large T antigen binds to and inactivates p53 and Rb