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CANCER BIOLOGY
GENES
| Question | Answer |
|---|---|
| MUTAGENS | BIOLOGICAL, CHEMICAL, & PHYSICAL CHANGE TO THE NUCLEOTIDE SEQUENCE OF DNA TO CAUSE MUTATION |
| MUTATION | CHANGE IN NUCLEOTIDE SEQUENCE |
| ALLELE | AN ALTERNATIVE FORM OF A SINGLE GENE |
| PROTO-ONCOGENES | REGULATE THE CELL CYCLE BY CODING FOR PROTEINS THAT STIMULATE CELL DIVISION IN A REGULATED MANNER. |
| PARTS OF CELL CYCLE THAT CAN BE AFFECTED BY PROTO-ONCOGENES | (GRGCP) GO SIGNALS RECEPTORS G-PROTEINS CYCLINS PROTEIN KINASES/CDKs |
| A GAIN OF FUNCTION MUTATION | -CAN CONVERT A PROTO-ONCOGENE TO AN ONCOGENE THAT STIMULATES CELL DIVISION IN AN UNREGULATED MANNER -IN ONE ALLELE OF A PROTO-ONCOGENE CAN INCREASE THE RISK OF CANCER (1 WILD (NORMAL) ALLELE & 1 ONCOGENE ALLELE) |
| MUTATIONS THAT CONVERT PROTO-ONCOGENES TO ONCOGENES | -TRANSLOCATION/TRANSPOSITION -GENE AMPLIFICATION -POINT MUTATION RESULTS IN: NORMAL-GROWTH STIMULATING PROTEIN IN EXCESS -HYPERACTIVE OR DEGREDATION-RESISTANT PROTEINS BY PROTEASOMES |
| TUMOR SUPPRESSOR GENES (TSG) | REGULATED CELL DIVISION BY CODING FOR PROTEINS THAT INHIBIT CELL DIVISION IN A HIGHLY REGULATED MANNER |
| TUMOR SUPPRESSOR GENE FUNCTIONS | -DNA DAMAGE DETECTION -CELL CYCLE CHECKPOINTS -DNA REPAIR DETECTION -CELL 2 CELL BINDING, CELL BINDING TO ECM GENE REDUCES METASTASIS -APOPTOSIS (DCDCA) |
| LOSS OF FUNCTION MUTATIONS | - IN TSG CAN CAUSE CHECKPOINT FAILURE, PREVENT DNA REPAIR, PREVENT APOPTOSIS, PROMOTE METASTASIS -MUTATIONS IN BOTH ALLELES OF TSG SIGNIFICANTLY INCREASES THE RISK OF CANCER |
| MULTI-STEP MODEL OS COLON CANCER DEVELOPMENT | 1 OR MORE ONCOGENE & 2/3 OR MORE TSG 1. LOSS OF TSG APC = SMALL BENIGN TUMOR FORMS 2. ONCOGENE ACTIVATES 3. LOSS OF TSG (DCC)= LRGER BENIGN TUMOR FORMS 4. LOSS OF TSG (P53) 5. ADDT'L MUTATIONS = MALIGNANT TUMOR FORMS |