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Path 6

Neoplasia II pg. 1-6 Templeton

Are the majority of cases of cancer familial or sporadic sporadic
what cells are affected in familial and sporadic cancers sporadic (somatic cells) familial (germline)
How do Oncogenes contribute to cancer new or increased biochemical acivity leads to altered cell phenotype
How can a tumor suppressor gene contribute to cancer loss of activity leads directly to altered cell phenotype
How many genes have to be altered to form a cancer 4-10 (estimate)
what are proto-oncogenes normal genomic constituents with required normal functions in develpment and/or homeostasis
how are proto-oncogenes activated change in genetic coding sequence will lead to new or altered biochemical activity
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
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
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
bcr-able translocation is seen in? leukemia
what is the philadelphia chromosome t(9;22) seen in CML and ALL
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
what does Gleevec do? inhibits bcr-able kinase activity
what is gene amplification copying of normal genes and their promoters many times
Created by: UVAPATH1