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29 Cards in this Set

  • Front
  • Back
Cancer viruses
-15% human cancers
-large percentages of liver and cervical cancers
Mutagens
-in cancer and act with viruses to help cancer proliferation
-act with other non viral factors
Cell transformation
-accompanied by persistence of all or part of viral genome
-continual expression of a limited number of vrial genes
Viral oncogenes
-used to be normal cells, modified, no longer have normal cellular gene expressioin and signal transduction pathways
Retroviruses
-activate oncogenes
Pap viruses
-suppress tumour suppressing genes
RNA viruses
-activate oncogenes
-replication not cytocodial nor required for tumourigenesis
DNA viruses
-negate tumour suppressors
Mechanisms cell transformation by retroviruses
1. Retroviral transduction of oncogene
2. Oncogene activation by retroviral insertion
3. Oncogenesis mediated by essential retrovirus proteins
Retroviral transduction of oncogene
-transducing retrovirus
-viral acquisition of proto-oncogene with capacity to transform if deregulated, replacing viral coding sequences (except RSV = src oncogene)
-overexpression and structural change can occur in v-onc
-can result in tumorgeneic cell
Oncogene activation by retroviral insertion
-cis-acting/non-transducing retrovirus
-long latency
-viruses replication competent, carry all their genes
-insert by promoter or insertional mutagenesis
-sometimes insertion occurs inside a gene deactivating it, so virus inserting next to exon 1 and only have activity from exon 2 and 3 mediate by right LTR
-this way virus doesn't need to integrate sequence like myc, can just insert near myc sequence and promote transcription by acting as an artificial promoter
-left LTR needs to be modified before right LTR can act as promoter
-small amount cancers stem from this because insertion viral promoters near potential oncogenes is rare
-result infection is monoclonal tumours
Oncogenesis mediated by essential retrovirus proteins
-trans-activating/non-transducing long-latency retrovirus
Tumourgeneic cell
-when viral oncogene (v-onc) inserts itslef into critical cellular oncogene (c-onc)
Acute transforming virus
-acquisition of an oncogene by transforming retrovirus
-formed by retroviral transduction of a cellular proto-oncogene (cONC)
-provirus integrated upstream of cONC, may increase level transcription of oncogene
-viral oncogene readthrough transcript made or provirus and cONC gene fused by deletion, giving rise to hybrid RNA transcript initiating in 5' LTR of provirus and extending into oncogene
-proviruses integrated elsehwere in genome provide helper function, forming virion particles that contain helper and hybrid RNAs
-recombination between two RNAs during reverse transcription joins ends of viral genome to hybrid RNA
-one or two corssover required depending on structure starting RNA
-during insertion genes (gal, pol, env) damaged, so to have replication competent cell need virus that is functional, then two viral genes recombine
-recombination quite frequently
Reverse Transcription
-gives rise to fully transmissible retroviral genome carrying oncogene
-transmission to new genome from doubly infected cells can occur at high efficiency without rearrangements
Dominant acting transforming retroviruses
-Rous sarcoma virus
-Avian erythroblastosis virus
-Avian myelocytomatosis virus
-can take over signaling networks, actin less important (no tumours)
-cells now have new genes and cell growth will be completely different
Rous sarcoma virus
-replicate in many kinds of cells and rapidly transform them
-has extra src domain (Vsrc)
-can take over actin network (non-tumourgenic)
src domain
-homologous to tyrosine kinase domains
-switched on in cell infected with Rous sarcoma virus
-tyrosine modified by phosphorylation, src domain can change cellular processes
-actually a recombination of exons that would normally formed src in cell
-associated with cellular membrane, closely regulated by cellular phosphatase to phosphorylate components cytoskeleton
Avian EV
-causes hematopoetic tumor
-has an erb B domain that will encode an epidermal growth factor receptor
AMV
-myc produced as a fusion protein of gag-myc
-over-expresses Myc, so increased protein production used in transcription (loss control cell cycle)
Myc
-cell cycle regulator
-normally carefully regulated
Vsrc
-colinear to a Csrc found near LTR
-always active
-not located on OM, free to roam in cytoplasm (activate many proteins)
Sis
-protein taken by viruses that encode for growth factors
Cell receptors
-erb B
-FMS
-kit
-can be virally hijacked
Cascade intermediates
-kinases: src, abl, fgr, raf, mos
-can be virally hijacked
Transcription factors
-jun
-fos
-myc
-rel
-can be virally hijacked
v-oncs
-when present in cell leads to rapid transformation cell into a cancer
-all that is needed to induce carcinogenesis (single-hit)
-kinase-activity from cell taken into virus, fusion protein with gag produced
-permanently active, kinase activates all sorts of proteins
Polyclonal tumour growth
-initiated in every infected cell when kinase not turned off
-tumours form rapidly
-many animal viruses
Monoclonal tumours
-result when proviral sequences are integrated at same chromosomal site (location is important)
-grow more slowly (months( since tumour derived from singel cell