Neoplasia II pg. 1-6 Templeton
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| Are the majority of cases of cancer familial or sporadic | sporadic
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| what cells are affected in familial and sporadic cancers | sporadic (somatic cells) familial (germline)
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| How do Oncogenes contribute to cancer | new or increased biochemical acivity leads to altered cell phenotype
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| How can a tumor suppressor gene contribute to cancer | loss of activity leads directly to altered cell phenotype
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| How many genes have to be altered to form a cancer | 4-10 (estimate)
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| what are proto-oncogenes | normal genomic constituents with required normal functions in develpment and/or homeostasis
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| how are proto-oncogenes activated | change in genetic coding sequence will lead to new or altered biochemical activity
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| what happens when bcl-2 is translocated to chromosome 18 where there is a transcriptional enhancer of immunoglobulin | the bcl-2 gene product inhibits the activation of the apoptosis protease cascade in the mitochondria protecting from the action of regulatory T cells during tumorigenesis
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| what are two mechanisms of chromosomal translocation in activation of a proto-oncogene | place proto-oncogene under new regulatory elements producing wild-type gene or Splices two coding sequences together resulting in disregulation of biochemical activity of one of the subunits
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| If Ig enhancers are translocated to the myc gene (chrom 8) you will get inappropriate levels of the myc gene as seen in Burkitt's lymphoma. What is the most common chain to be translocated | t(8;14) Ig heavy chain
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| bcr-able translocation is seen in? | leukemia
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| what is the philadelphia chromosome | t(9;22) seen in CML and ALL
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| How can the same translocation t(9;22) be seen with two different cancers | the breakpoint between bcr and abl differ in CML and ALL
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| what does Gleevec do? | inhibits bcr-able kinase activity
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| what is gene amplification | copying of normal genes and their promoters many times
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