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cancer genetics I

Stack #176333

QuestionAnswer
Malignancies are clonal (derived from a single abnormal cell)
Malignicies are Initiated by change in cell’s DNA sequence (somatic mutation)
Changes in DNA/gene expression result in selective growth advantage for some cells
A single genetic alteration is usually not enough
genes involved in cancer process Proteins in signaling pathways for cell proliferation
genes involved in cancer process Cytoskeletal components involved in contact inhibition
genes involved in cancer process Regulators of the mitotic cycle
genes involved in cancer process Components of programmed cell death machinery
genes involved in cancer process Proteins involved in detecting and repairing mutations
Different mutations cause cancer Activating gain-of-function mutations in one allele of proto-oncogene, Loss of function of both alleles of tumor suppressor gene, Chromosomal translocations that cause misexpression of genes or create chimeric, genes with altered or new function
Different types of mutations cause cancer Activating gain-of-function mutations in one allele of proto-oncogene
Different types of mutations cause cancer Loss of function of both alleles of tumor-suppressor gene
Different types of mutations cause cancer Chromosomal translocations that cause misexpression of genes or create chimeric genes with altered or new function
Cytogenetic abnormalities are common in cancer Random rearrangements/aneuploidy/loss; Specific translocations are associated with specific cancers; loss of specific chromosomes
Chromosomal translocations and proto-oncogenes Translocations lead to disruption and rearrangement of genes and their regulating elements; Chimeric (fusion) genes to chimeric proteins; New “gain of function” for proto-oncogene corresponds to activation/deregulation
Burkitt lymphoma B-cell tumor, Translocation; positioning of MYC proto-oncogene near actively transcribed immunoglobulin heavy chain gene; MYC activation/deregulation; Lymphomatous transformation
Chronic myelogenous leukemia and the Philadelphia chromosome Involves translocation and Fusion of (ABL) proto-oncogene to BCR gene; Chimeric BCR-ABL; altered protein kinase expression and function of (ABL) oncogene
Tumor supressor genes prevent tumor development, loss of function leass to cancer
gatekeepers regulate cell growth
caretakers genes involved in repairing DNA damage and maintaining genomic integrity (mismatch repair genes)
Mechanisms which lead to loss of function point mutation in TS gene; deletion of TS gene and surrounding chromosomal material; other structural rearrangements epigenetic events
epigenetic events transcriptional silencing, alterations in DNA methylation and chromatin configuration
In Tumor suppressor genes recessive in the cell (both copies of tumor suppressor gene must be mutated to see initiation of malignancy)
Tumor suppressor genes loss of function may occur in germline or somatic tissue
germline mutation confers autosomal dominant predisposition to malignancy (familial cancer syndrome)
Tumor suppressor genes Examples Breast/ovarian – BRCA1/2 and Familial adenomatous polyposis (FAP)
Two-Hit Origin of Cancer Basis for both hereditary & sporadic cancers; Involves loss of tumor suppressor function; Retinoblastoma (RB) as the model; Loss of both copies of RB1 gene leads to tumor
Retinoblastoma (RB) as the model for two hit origin of cancer Sporadic cases - 2 somatic mutations same cell; Hereditary cases - inherited (germline) mutation (first hit); second somatic mutation in same cell (second hit)
Loss of heterozygosity (LOH) Molecular evidence for the existence of a tumor suppressor gene; Involves analysis of DNA polymorphisms near tumor suppressor gene; Testing is done on tumor tissue
Loss of RB1 gene function without loss of heterozygosity seen with point mutations, gene conversion, transcriptional silencing
Created by: knpearso on 2008-11-13



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