Tumor Viruses - Ornelles Flashcards Preview

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Flashcards in Tumor Viruses - Ornelles Deck (8)
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1
Q

• Kaposi HV (HHV__)–> Kaposi’s sarcoma (endothelial cells), primary effusion ___ & ____’s dx (B cells), bypass cell growth control (____) and promote growth (IL-6, GCR, cyclin D) through a diverse array of molecular ____, ____ cells w/ high ____ & ____ filtrate seen on H&E stain (Kaposi’s triad)

A

• Kaposi HV (HHV8) –> Kaposi’s sarcoma (endothelial cells), primary effusion lymphoma & Castleman’s dx (B cells), bypass cell growth control (Bcl-2) and promote growth (IL-6, GCR, cyclin D) through a diverse array of molecular mimics, spindle cells w/ high vascularity & inflammatory filtrate seen on H&E stain (Kaposi triad)

2
Q

• EBV –> _____ lymphoma (African Burkitt’s via ___ translocation, LMP-1 rescuing of cells destined for death), ____ lymphoma (>50%), ____ carcinoma in Asians, and post-transplant lymphoproliferative disease, __ ___leukoplakia

A

• EBV–>Non-Hodgkin lymphoma (African Burkitt’s via c-myc translocation, LMP-1 rescuing of cells destined for death), Hodgkin lymphoma (>50%), nasopharyngeal carcinoma in Asians, and post-transplant lymphoproliferative disease, oral hairy leukoplakia

3
Q

• Hep B (aflatoxin, algal toxin in water, curious X oncogene) more so than hep C (no oncogene) –> hepatocellular carcinoma d/t chronic ____ (chronic growth of regenerating live cells, damage)—incidence is rising (more common in men—if males are born with it then they have a ____% chance of developing cancer, ½ million/year worldwide)

A

• Hep B (aflatoxin, algal toxin in water, X oncogene) more so than hep C (no oncogene)–> hepatocellular carcinoma d/t chronic inflammation (chronic growth of regenerating live cells, damage)—incidence is rising (more common in men—if males are born with it then they have a 50% chance of developing cancer, ½ million/year worldwide)

4
Q

• ____ –> Adult T cell leukemia (__ and __ genes promote growth stability), other diseases include smoldering leukemia and tropical spastic paraparesis

A

• HTLV–>Adult T cell leukemia (tax and rex genes promote growth stability), other diseases include smoldering leukemia and tropical spastic paraparesis

5
Q

• Merkel cell virus –> Merkel cell carcinoma (rare ____l tumor arising from ____ cells), mutations inactivate the ___ activity of the viral large T Ag and is present in tumors b/c if it was intact and promoting repeated rounds of DNA replication, ___ ___ would have occured

A

• Merkel cell virus–>Merkel cell carcinoma (rare neuroectodermal tumor arising from mechanoreceptor cells), mutations inactivate the helicase activity of the viral large T Ag and is present in tumors b/c if it was intact and promoting repeated rounds of DNA replication, cell death would have occured

6
Q

• HPV __ and __ –> 99% of cervical cancer and 60% of oropharyngeal cancer d/t activity from __ (p53 degradation) and ___ (Rb inactivation), normal infection enters through lesions in cornified epithelial layer to infect ___ cells & break down ___ filament system

A

• HPV 16 and 18–> 99% of cervical cancer and 60% of oropharyngeal cancer d/t activity from E6 (p53 degradation) and E7 (Rb inactivation), normal infection enters through lesions in cornified epithelial layer to infect basal cells & break down keratin filament system

7
Q

• Common targets of cancer-causing viruses are cell growth control proteins ___ (inactivation keeps cell in cell cycle by binding E2F1 transcription factor no longer repressed by Rb) and p53 (degradation/inhibition prevents apoptosis)

A

• Common targets of cancer-causing viruses are cell growth control proteins Rb (inactivation keeps cell in cell cycle by binding E2F1 transcription factor no longer repressed by Rb) and p53 (degradation/inhibition prevents apoptosis)

8
Q

• Viruses cause cancer: promote/stabilize growth of a cell line that becomes vulnerable to oncogenic changes (such as __ and ___) or viral gene products bypass more mutations needed during carcinogenesis (HPV, Merkel cell), __% of cancer burden worldwide

A

• Viruses cause cancer: promote/stabilize growth of a cell line that becomes vulnerable to oncogenic changes (Hep B, HTLV) or viral gene products bypass more mutations needed during carcinogenesis (HPV, Merkel cell), 20% of cancer burden worldwide