virology15tumorvir ppt课件共37页文档
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– cell genes (c-onc)
– modified viral versions (vonc) whose expression promotes transformation and tumors
• HepC (no DNA phase) chronic inflammation and repair
– Viral proteins interact with p53 and lead to cell proliferation and prevent apoptosis
oncogenes
• Cell gene is called protooncogene – can induce transformation only after being altered (mutation or coming under the control of a highly active promoter). – usually encodes a protein that affects DNA replication or growth control at some stage of the normal development of the
organism.
Constitutive - agonist independent receptors
V-onc genes - transducing
• Virus LTR is a strong promotor • V-onc is altered form of c-onc • rapid onset, high efficiency
virology15tumorvir ppt课件
Oncogenic Viruses
“There is no single mechanism by which viruses cause tumors”
Transformation and potential tumorigenesis
• Transformation - alteration in a cell’s 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 development of tumors
Cell cycle
• M- mitosis • G1 - cells grow • S - DNA synthesis • G2 - growth and preparation for
• Therefore may depend on host cell
• May – Integrate as part of their cycle (retroviruses) – Viral ORI and genes push cell to S phase (herpes, papilloma)
• If damaged (mutated) cell moves to S phase then it may replicate
Oncogenic viruses may be RNA or DNA
• 20% of human cancers believed to be of viral origin
RNA transforming viruses are retroviruses so
far… (hepC)
• Permissive cells are transformed
• Integration of viral cDNA genome
• Requires expression of oncogenes
mitosis • G1/S decision point for going to
dividing state • Problem for DNA viruses that
need S phase machinery
Cell cycle control proteins
• Activation of cell cycle progression cyclins, cyclin dependent protein kinases (Cห้องสมุดไป่ตู้ks), Cdk inhibitors
• These include: – Cervical cancer – Burkitt’s lymphoma – Hepatocarcinoma – Kaposi’s sarcoma
• Virus is not only factor
Viruses cannot kill cell to be tumorigenic
• Inhibitors of cell cycle progression - tumor suppressors
Tumor suppressor Rb
• Rb binds to transcription factor E2F and prevents gene expression of proteins needed to go to S phase
Tumor suppressor p53
• 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 cytochrome C and activate caspase system
– modified viral versions (vonc) whose expression promotes transformation and tumors
• HepC (no DNA phase) chronic inflammation and repair
– Viral proteins interact with p53 and lead to cell proliferation and prevent apoptosis
oncogenes
• Cell gene is called protooncogene – can induce transformation only after being altered (mutation or coming under the control of a highly active promoter). – usually encodes a protein that affects DNA replication or growth control at some stage of the normal development of the
organism.
Constitutive - agonist independent receptors
V-onc genes - transducing
• Virus LTR is a strong promotor • V-onc is altered form of c-onc • rapid onset, high efficiency
virology15tumorvir ppt课件
Oncogenic Viruses
“There is no single mechanism by which viruses cause tumors”
Transformation and potential tumorigenesis
• Transformation - alteration in a cell’s 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 development of tumors
Cell cycle
• M- mitosis • G1 - cells grow • S - DNA synthesis • G2 - growth and preparation for
• Therefore may depend on host cell
• May – Integrate as part of their cycle (retroviruses) – Viral ORI and genes push cell to S phase (herpes, papilloma)
• If damaged (mutated) cell moves to S phase then it may replicate
Oncogenic viruses may be RNA or DNA
• 20% of human cancers believed to be of viral origin
RNA transforming viruses are retroviruses so
far… (hepC)
• Permissive cells are transformed
• Integration of viral cDNA genome
• Requires expression of oncogenes
mitosis • G1/S decision point for going to
dividing state • Problem for DNA viruses that
need S phase machinery
Cell cycle control proteins
• Activation of cell cycle progression cyclins, cyclin dependent protein kinases (Cห้องสมุดไป่ตู้ks), Cdk inhibitors
• These include: – Cervical cancer – Burkitt’s lymphoma – Hepatocarcinoma – Kaposi’s sarcoma
• Virus is not only factor
Viruses cannot kill cell to be tumorigenic
• Inhibitors of cell cycle progression - tumor suppressors
Tumor suppressor Rb
• Rb binds to transcription factor E2F and prevents gene expression of proteins needed to go to S phase
Tumor suppressor p53
• 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 cytochrome C and activate caspase system