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28 Cards in this Set
- Front
- Back
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Cancer can only be reproduced __________.
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In vivo
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What are the characteristics of normal, transformed, and immortalized cells?
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Normal: cells that require growth factors for growth, attachment to a substrate, are contact inhibited, and will only undergo a certain # of cell divisions before scenesing.
Immortalized cells:retain many of the normal characteristics but will undergo unlimited cell divisions in culture. Transformed: cells are immortal and have lost most if not all their restrictions. |
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Explain the typical retroviral provirus?
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LTR's at each end (5' and 3')
5' end serves as a promoter and the 3' end is the polyadenylation site. |
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What changes occur once the virus is integrated into host DNA, as far as viral replication?
What are protoncogenes?1 |
Once integrated into host DNA, viral products are no longer needed in order for the virus to replicate.
Protoncogenes are normal host genes that when mutated or altered in expression can lead to tumor formation. |
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What are acutely transforming retroviruses?
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retroviruses that contain a copy of an oncogene that was originally derived from a protoncogene
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What are viral oncogenes? Why are they considered defective viruses?
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Viral oncogenes contains mutations relative to their related cellular proto-oncogenes, and these changes are important for oncogenesis.
They are defective because they have lost essential viral genes in order to make room for oncogenes |
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What is required before a defective virus can replicate?
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Before it can replicate, the virus must receive the help from a "helper" virus to supply the missing viral products.
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Acutely transforming viruses are highly efficient at ____________.
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transforming cells and causing the induction of tumors --> causing changes in signal tranduction pathways that overide + constituitely activate normal cellular growth pathways.
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What is the difference between chronic and acute transforming retroviruses?
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Acute: REQUIRES a helper virus to help with its replication because it has inserted an oncogene that has deleted some of its natural viral genome.
Chronic transforming doesn't required helper viruses and can replicate on their own --> THEY ARE AUTONOMOUS and they take longer to develop |
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Where do chronic transforming viruses insert in their host genome? Why is this significant?
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Close to protooncogenes and they alter the expression of these genes
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Why is the probability of a chronic transforming virus causing transformation a low likelihood?
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Because they can insert anywhere within the host genome and the probability of them inserting near a protooncogene is NOT a high probability.
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What are the 2 ways that protocogenes can be activated by viruses?
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The virus can act as a promotor or it can act as an enhancer
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What are examples of human retroviruses? What is important to keep in mind when considering these viruses and the formation of cancer?
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HIV-1/HIV-2/HTLV-1/HTLV-2
The cancers are a frequent and important aspect of AIDS, but HIV is NOT shown to directly cause these cancers and are probably a result of HIV-induced immunosupression. |
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What is a major way that DNA and RNA viruses differ? How can this pose a problem to the virus?
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DNA viruses replicate in the nucleus and utilize host DNA synthesis machinery
Most hosts are not actively replicating so the virus must DRIVE the cell into the S phase by encoding genes that remove the blocks on cell cycle progression. --> DRIVE host into the S phase |
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What is E2F, how is it regulated and why is it a target for viruses?
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E2F is a transcription that binds to and activates cellular promoters...pRB binds to E2F and prevents it from activating genes and preventing cell cycle progression. When pRB is phosphorylated it releases E2F and it can bind promoters...the viruses will produce proteins that will bind pRB and NOT allow it to bind E2F, so that E2F will continuously allow cell cycle progression.
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What are the consequences of p53 expression?
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p53 increases p21 which blocks cell cycle production to stall synthesis until DNA damage is repaired
p53 upregulates BAX which blocks the antiapoptotic activity of BCL-2 p53 is mutated in MANY cancers which is a key that shows the importance of it in the generation of cancer. |
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What does a mutation in p53 imply?
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It implies that the cell is no longer able to put the breaks on the cell cycle when there is damage and to evade apoptosis.
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How does the HPV virus work to cause cancer?
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The E7 binds to pRB so that it allows for continued cell replication and prevents the breaks on the cell cycle
E6 binds to p53 and induces its degradation so that you continue the cell cycle. |
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What is the difference between direct and indirect oncogenic mechanisms?
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Direct: involves either the insertion of a viral oncogene or the enhancement of an existing proto-oncogene
Indirect: Involves chronic infectivity |
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What cells are infected in EBV? Infection of these cells causes which cancer?
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B cells
Burkitt's lymphoma |
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What is the pathology of African Burkitt's Lymphoma?
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EBNA-1 is the only protein produced, by the EBV virus and it isn't enough to immortalize the cell , so there is also a translocation that dysregulates the c-myc gene by moving it near the immunoglobulin enhancer.
EBNA-1 is also very resistant to antigen processing and presentation to MHC class 1 So the EBV virus can evade host immunity and the translocation will allow continued proliferation via its position to the enhancer. |
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What cells does Kaposi's sarcoma affect? What population does this disease affect?
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Lymphatic endothelium
Immunocompromised |
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What proteins are involved in helping Kaposi's going?
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LANA functions like EBNA-1 in African BL and keeps the KS from being noticed by the immune system and also binds to pRB to stop cell cycle regulation and p53 to prevent apoptosis
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What is the HTLV & what is its pathogenesis?
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HTLV: associated with T-cell leukemia + Myelopathy
The Tax protein is believed to activate infected T-cells to secrete IL-2 and bind to the receptor (in an autocrine fashion) and cause T-cell proliferation. Tax also degrades p53 |
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What is remarkable about the fact that the actual tumor cells don't express the Tax protein?
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There are 2 mechanisms that happen: the first involves the replication of the T-cells and the then then VIRAL mechanism can then be shut off & now a cellular mechanism is used to create a continuously replicating cell population that will cause mutations.
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What is the only retrovirus to cause a lymphoma in humans?
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HTLV-1
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How do the Hepatitis B & C virus cause pathology?
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The virus will cause liver damage (virus induced) and because the liver is a regenerative organ the damage will drive cell proliferation and the probability of accumulating cellular mutations is greater -->hepatocellular carcinoma
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Which of the DNA viruses are associated with human cancers?
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EBV, HTLV-1, HPV, KSHV, HCV, and HBV
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