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16 Cards in this Set

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  • Back
what cancer causing viruses did she want us to know about?
HPV, EBV, HBV, HHV8. She really only went over the DNA cancer causing viruses.
what happens to the host and viral geomes once integration happens? what genes must be made for tumorgnesis?
the early genes are necessary for making tumors.

also, both the host and viral DNAs are messed up by the process of integration.
HPV - what are the strains to know and the resultant diseases?
the low numbers (6 and 11) are low risk for cancer, causing genital warts.

16 and 18, the higher numbers, are a higher risk for cancer. these cause squamous cell carcinoma of the cervix, anogenital region, and upper respiratory tract.
what's the genetic/biochemical reason that some HPV's cause cancer and others don't?
the non-cancer causers (6 and 11) DON'T INTEGRATE - they exist as EPISOMES.

Cancerous lesions have viral genomes integrated into the DNA.

This is known because clonal cancer cells show the same viral integration point - because it's random, we know a tumor represents a single cell's infection = clonality.

KNOW - this is on the test - that HPV's genome is interrupted at the E1/E2 reading frame, which leads to an OVEREXPRESSION of E6 and E7, which go after the tumor suppressors p53 and RB, respectively.

NOTE - infection is an INITIATIATING event - not everybody infected gets cancer, so further somatic mutations are required.
EBV - what tumors are associated?
Burkitt's lymphoma, B-cell lymphoma in immunosuppressed, Hodgkins' lymphoma, Nasopharyngeal carcinoma, NK/T-cell lymphomas.
Where does EBV DNA take up residence in the cell? How is cancer caused, generally? We know they infect B cells - how?
EBV, unlike some of the cancer causing HPV's, remains extrachromosomal - lives in EPISOMES. Know - LMP-1 and EBNA-2

Cancer is caused through super-proliferation of B cells. Use CD-21 as a receptor (we know that this is the C3d receptor).

KNOW = the protein LMP-1 - this is what dysregulates B cell replication and causes them to go out of control. EBNA-2 as well.
How does LMP-1 work to make B cells grow like crazy?
Normal B cell proliferation requires that the B-cell come in contact with a T-helper cell, which signals the B cell to divide.

This interaction happens through the CD40 receptor.

The EBV protein LMP-1 has the ability to mimic T-cells - it binds to CD40 and tells the B cells to divide.

Might want to know that this signaling is through a jak/stat/NFkB pathway.
what does EBNA-2 do?
it activates CYCLIN D, so you get more cell proliferation. again, happening in B cells. Gets out of G0 into G1.
what causes Burkitt's lymphoma?
this requires a translocation: 8:14, resulting in C-myc being put after the IgH promoter on 14. This makes TONS of C-myc.

Likely because EBV causes B cells to divide so much, eventually you get this translocation and don't repair it.

Seen in AFrica more, maybe requires previous infection with malaria or something. Probably p53 mutations required as well.
How does HBV cause HCC?
likely due to chronic inflammation.

also, the HBx protein!

this has 2 functions needed to know:
1. Activate growth factors (Iinsulin like growth factor)

2. Bind and inactivate P53.
what's HTLV associated with?
T cell leukemia, TSP (tropical spastic paralysis).

note that this isn't due to integration events, but more to the TAX gene, which enhances cyclin D and stops DNA repair.
what can H.pylori cause?
MALToma - lymphoma in the gut. Also, of course, stomach cancer.
side note - this is likely "marginal" small B cell lymphoma, generally associated with a 11:18 translocation.
what is tumor immunity?
Two ways that tumors survive - lack of immune surveillance, and IMMUNOediting.

immunoediting: you're inadvertantly selecting for immune-evading cancer cells (the immunogenic ones are killed off).
What do Ca-125, Ca19-9, and Muc-1 represent?
Ca-125 is ovarian, ca19-9 is pancreas, and Muc-1 is adenocarcinomas (think of mucous producing.
what immune cells fight off tumors, and what do we need to know about them?
CD8's, NK's, macs, and antibodies. Need to know that CD8 (killer T cells) use MHC I, that NK cells go around chomping up everything, and THIS IS GOING TO BE ON THE TEST:
Macrophages work through INTERFERON GAMMA. Phagocytosis, kil with reactive oxygen species.

I'd remember that NK cells are capable of killing cells WITHOUT MHC requirement - so even cancer cells that downregulate their MHC can still be kil ed by NK's.
so with all these anti cancer mechanisms, why do we still get sick?
we can fail to recognize tumor cell antigens, tumors can hide their antigens in glycocaylacies, tumors produce proteins that innactivate the immune response, tumors can turn off MHC,

also, tumors can activate the FAS ligand on T cells - remember that the fas ligand is for activating the extracellular apoptosis pathway.