virology15tumorvirppt课件.ppt
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1、 Transformation-alteration in a cells properties that leads to immortalization and different growth patterns that result from alteration in cell cycle Loss of anchorage dependence Loss of contact inhibition(foci)Decreased requirements for growth factors Tumorigenesis(oncogenicity)-in vivo developmen
2、t of tumors M-mitosisG1-cells growS-DNA synthesisG2-growth and preparation for mitosisG1/S decision point for going to dividing stateProblem for DNA viruses that need S phase machinery Activation of cell cycle progression-cyclins,cyclin dependent protein kinases(Cdks),Cdk inhibitors Inhibitors of ce
3、ll cycle progression-tumor suppressors Rb binds to transcription factor E2F and prevents gene expression of proteins needed to go to S phase P53 halts progression when DNA damaged to give cell time to repair or triggers apoptosis of damaged cell by activating Bcl-2 causing mitochondria to release cy
4、tochrome C and activate caspase system If damaged(mutated)cell moves to S phase then it may replicate20%of human cancers believed to be of viral originThese include:Cervical cancer Burkitts lymphoma Hepatocarcinoma Kaposis sarcomaVirus is not only factorTherefore may depend on host cell May Integrat
5、e as part of their cycle(retroviruses)Viral ORI and genes push cell to S phase(herpes,papilloma)Permissive cells are transformedIntegration of viral cDNA genomeRequires expression of oncogenes cell genes(c-onc)modified viral versions(v-onc)whose expression promotes transformation and tumorsHepC(no D
6、NA phase)-chronic inflammation and repair Viral proteins interact with p53 and lead to cell proliferation and prevent apoptosisCell gene is called proto-oncogene can induce transformation only after being altered(mutation or coming under the control of a highly active promoter).usually encodes a pro
7、tein that affects DNA replication or growth control at some stage of the normal development of the organism.Constitutive-agonist independent receptors Virus LTR is a strong promotorV-onc is altered form of c-oncrapid onset,high efficiency tumorigenesis(acute transforming)time%transformedNondefective
8、 virusesNear c-onc and LTR activationInsertional inactivation of tumor suppressor genesChronic-transforming%transformedTrans-acting transcriptional activationUsually poor efficiencyMust require additional factors C-oncVirus gene productTumor cell DNA(mouse)Restriction fragments used to form circlesP
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