Cancer Flashcards
V-onc
Viral oncogene
c-onc
cellular oncogene
a group of genes that cause normal cells to become cancerous when they are upregulated
v-myc
virus capture oncogene of myc
viral homologue
myc
family of regulator/protooncogenes
acutely transforming retrovirus
directly cause cell transformation
generated by viral capture during viral replication in genome
proviral insertion
virus itself doesn’t contain oncogene
inserts upstream of protooncogene
messes with regulation of gene = oncogene
oncogene capture
- 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 - RNA replicated w no poly a signal to stop - transcribe all the way through oncogene
a. Now contains retroviral genome + oncogene - Gets spliced oncogene attached to viral RNA
- Packaged into virion - dimeric genome
a. Packaging signal in 5’ end
b. Packaged w wild type RNA molecule as well - Template switching event can happen to put oncogene in RNA genome
Additional point mutations = incapable of being regulated by host cell
RSV
Rous Sarcoma Virus
Involved in causes sarcomas in chickens
RSV genes
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.
src gene
RSV oncogene
Src is a tyrosine kinase involved in regulation of cell growth and differentiation
ALV
avian leukosis virus
closely related to RSV but doesn’t contain src gene
Why do most oncoviruses require a helper virus?
Defective most of the time after oncogene capture
Need to coinfect with WT virus to use their replication and polymerase machinery
proto-oncogene
can become an oncogene if mutated
chronically transforming viruses
retrovirus integrates near host proto-oncogene and alters their expression
types of chronically transforming viruses
promoter insertion
enhancer insertion
MMTV
Mouse mammary tumour virus
chronically transforming virus
Adenovirus
Silences p53 and retinoblastoma, thus preventing apoptosis
E genes expressed at high levels
E1B binds to p53
E1A binds to rb
Podosomes
Conical and actin rich structures on outer membrane surface
formed by v-src in cancer
p53
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
Retinoblastoma gene
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.
SV40
Polyoma virus - dsDNA, nonenveloped
Early and late genes which encodes large and small T antigens (early)
What kind of cells does SV40 cause cancer in?
Non-permissive cells e.g. rodents
Non-permissive cells
Cells in which infection is not productive are called nonpermissive cells.
How does SV40 cause cancer?
Large T antigen binds to and inactivates p53 and Rb
