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Figure 3.2 The Biology of Cancer (© Garland Science 2007)
RNA Tumor Viruses - The Rous Sarcoma Virus Story
Retroviruses – The Very Short Course
Reteroviruses – Basic Structure
Fields Virology by Knipe et al 2007
Figure 3.17 The Biology of Cancer (© Garland Science 2007)
Retroviruses & Their Replication
(+ Integrase & Protease)
Polyprotein
All Employ Reverse Transcriptase
Figure 3.17 The Biology of Cancer (© Garland Science 2007)
Retroviruses & Their Replication
(+ Integrase & Protease)
Polyprotein
Figure 3.7a The Biology of Cancer (© Garland Science 2007)
PC
EM
Normal Infected
Focus formation by an RNA Tumor Virus
Figure 3.8 The Biology of Cancer (© Garland Science 2007)
Figure 3.19 The Biology of Cancer (© Garland Science 2007)
Figure 3.20 The Biology of Cancer (© Garland Science 2007)
Figure 3.21 The Biology of Cancer (© Garland Science 2007)
Figure 3.22 The Biology of Cancer (© Garland Science 2007)
Table 3.3 The Biology of Cancer (© Garland Science 2007)
Figure 3.23b The Biology of Cancer (© Garland Science 2007)
Retroviral Insertion Has the Potential to Transform by Activation of Oncogenes
Table 3.4 The Biology of Cancer (© Garland Science 2007)
DNA TUMOR VIRUSES
Figure 3.3 The Biology of Cancer (© Garland Science 2007)
General scheme for Replication of ds DNA Viruses
Replication & Variety of DNA Viruses
SV40 Virion Epstein-Barr VirusA Herpes Virus
HPV 16 Virion
SV40 – A Small DNA Tumor Virus in Permissive & nonPermissive Hosts
Hman Papilloma Virus (HPV) (More than 75 types)
HPV 16 & 18 are most tumorigenic
Progression from cervical SIL to invasive cervical carcinoma typically takes many years.
Outline of mechanism of HPV tumorigenisis
The Promise of Global Cervical-Cancer PreventionMark Schiffman, M.D., M.P.H., and Philip E. Castle, Ph.D., M.P.H. Cytologic screening has significantly reduced the rates of cervical cancer in many developed countries. However, cervical cancer remains a leading form of cancer among women living in low-resource regions of the world (see map) and often kills women at young ages The current standard of cervical-cancer prevention requires three clinical visits: one for screening, one for a colposcopically guided (i.e., magnified) biopsy for women with abnormal screening results, and one for treatment of precancerous conditions. Single cytologic screenings are insensitive and do not provide sustained reassurance with regard to the risk of cancer. Program effectiveness is achieved by repeated iterations of the three-visit cycle, but such repeated testing is usually unachievable in resource-limited regions. Fortunately, as discussed by Goldie et al. in this issue of the Journal (pages 2158–2168), new practical options for cervical-cancer prevention are becoming available.
Some Herpes viruses can cause cancer
EBV (Epstein Barr virus) : Burkitt’s Lymphoma; Nasopharangyel Cancer; some B cell lymphomas (LMP 1, 2 and others). Crucial interaction of environment and infection required for lymphoma induction.
HHV8/KSHV (human herpes virus 8) Kaposi’s Sarcoma (LANA -latency associated nuclear antigen )
HBV’s Extraordinary genome and mode of replication
Knipe et al 2007
Hepatitis B Virus Induced Liver Cancer