Exam III: Lecture 10 Flashcards
Over __% of human cancers are caused by viruses
20
What are 5 common viruses that cause cancer?
- EBV
- HBV
- HCV
- HTLV I
- HPV
1 in 3 people will suffer from cancer
true
Cancer can be caused by a huge number of factors damaging the cell and when a critical number or hits have damaged the cell it can get ____
Transformed = cancer
How did scientist figure out that viruses can induce cancer?
1908 = discovered leukemia in chickens was infectious
1911 = a tumor in chicken caused by a virus. Can induce tumor formation in another chicken by injecting the sercoma of a cancerous chicken
Names Rous Sarcoma Virus
HBV; family, cancer type, cases/year
Hepatitis B Virus
Hepadnavirus
Hepatocellular (Liver) Cancer
340,000
HCV; family, cancer type, cases/year
Hepatitis C Virus
Flavivirus
Hepatocellular (Liver) Cancer
195,000
EBV: family, cancer type, cases/year
Epstien-Barr Virus
Herpesvirus
Burkitt’s, Hodgkin’s, Post transplantation lymphoma Nasopharyngeal carcinoma
113,400
HPV: family, cancer type, cases/year
Human papilloma virus
Papillomavavirus
Cervical cancer, anal cancer, penis cancer, head and neck carcinoma
561,180
HTLV I: family, cancer type, cases/year
Human T Lymphotrophic Virus
Retrovirus
Adult T cell leukemia
3,300
KSHV: family, cancer type, cases/year
Kaposi’s Sarcoma-associated herpes virus
Herpesvirus
Kaposi’s sarcoma, pleural effusion lymphoma
102,000
HBV: mechanism, oncogene, onc. function
Hepatitus B Virus
Chronic Inflammation
X protein
Molecular-signaling dysregulation inhibition of p53
HCV: mechanism, oncogene, onc. function
Hep C
Chronic inflammation
unknown
EBV: mechanism, oncogene, onc. function
Epstein-bar
Oncogenic
LMP-I
Molecular signaling dysregulation of NFkB activation lymphoproliferation
HPV: mechanism, oncogene, onc. function
Human Papaloma Virus
Oncogenic
E6, E7
Inhibition of p53 and Rb Cell adhesion dysregulation
HTLV I: mechanism, oncogene, onc. function
Human T Lymphotrophic Virus
Oncogenic
Tax
Molecular signaling dysregulation NFkB activation immortalization
KSHV: mechanism, oncogene, onc function
Kaposi’s Sarcoma-associated herpes virus
Oncogenic
8 differnent ones (vCyclin)
Cell cycle dysregulation, inhibition of apoptosis, immune evasion, autocrine and paracrine fucntions
Talk me through the regulation of the cell cycle from G1/S-cyclin to DNA synthesis
G1/S-cyclin > activates G1-Cdk (cyclin dependent kinase) > G1-Cdk phosphylated Rb protien = inactivating it > Active E2F ? S-phase gene trascnription > S-cyclin > Activates S-Cdk > DNA synthesis
Talk me through the regulation of the cell cycle from mitogen to the production of G1/S cyclin
Mitogen = growth factor binds to TKR (tyrosine kinase receptor) > activated Ras > MAP kinase cascade > activation of gene reculatory protein > immediate early gene expression > Myc = gene regulatory protein»_space;> G1/S cyclin
Is Ras an oncogene or a tumor supressor?
Oncogene
Is p53 an oncogene or a tumor suppressor?
Tumor Suppressor
What are 4 causes for p53 to be in stabilized and active?
- Hyperproliferative signals
- DNA damage
- Telomere shortening
- Hypoxia
What are 3 effects of p53 being stable and active?
- Cell cycle arrest
- Senescence
- Apoptosis
Talk me through the protection of the cell cycle from DNA damage to Inactivated G1/S /S-Cdk
DNA damage > ATM/ATR activation > Chk1/Chk2 kinase activation > phosphorylation of p53 > p53 is stable and active > p53 acts as a TF > produces p21 > p21 binds to Cdk and inhibits it
Viruses have devised a variety of ways to activate the cell cycle
true
Why is activating the cell cycle advantageous to the virus?
- Lead to cell death
2. Latent and persistant viruses often trigger transformation