| MOST DISRUPTED CHECKPOINT IN CANCER | G1/S CHECKPOINT |
| WHAT ARE THE 3 GROUPS OF CDK | G1 : CDK 2, 4, 5, 6
S : CDK 2
G2 / M : CDK 3 (CDC 2) |
| WHAT ARE THE 3 GROUPS OF CYCLIN | G1 : CYCLIN D, E
S: CYCLIN A
G2 / M : CYCLIN B/A |
| NORMAL GENES THAT ARE ACTIVATED WHEN THERE IS A NEED FOR PROLIFERATION AND GROWTH | PROTO-ONCOGENES |
| PROTO-ONCOGENES IS REGULATED BY __________ | TUMOR SUPPRESSOR GENE |
| CELL UNDERGOES DNA MUTATIONS AND TARGET PROTO-ONCOGENE TO BE MUTATED | ONCOGENES |
| A TYPE OF MUTATION WHEREIN PROTO-ONCOGENE BECOMES ONCOGENES | DOMINANT MUTATION |
| A TYPE OF MUTATION WHEREIN TUMOR SUPPRESSOR GENE OR DNA REPAIR GENE BECOME DANGED AND LOSE FUNCTION | RECESSIVE MUTATION |
| CHARACTERISTIC OF CANCER | 1. COLONALITY
2. AUTONOMY
3. ANAPLASIA
4. INVASION AND METASTASIS |
| TUMORS ARISES AS CLONES FROM A SINGLE CELL | CANCER IS A GENETIC DISEASE |
| REGULATES CELL CYCLE | PROTEIN KINASE |
| REGULATES CELL CYCLE | CYCLIN (CDK) |
| DETERMINES WHETHER THE CELL PROCEEDS TO THE NEXT PHASE OF CYCLE | CHECKPOINT |
| IMPORTANT CHECKPOINTS | G1/ S CHECKPOINT |
| IMPORTANT CHECKPOINTS | G2/ M CHECKPOINT |
| ACTIVITY OF G2/M CHECKPOINT | CHROMOSOME CONDENSATION |
| ACTIVITY OF G2/M CHECKPOINT | NUCLEAR MEMBRANE BREAKDOWN |
| ACTIVITY OF G2/M CHECKPOINT | SPINDLE FORMATION |
| ACTIVITY OF G1/S CHECKPOINT | ACTIVATES SEVERAL GENES THAT NEEDS S PHASE PROGRESSION |
| ACTIVITY OF G1/S CHECKPOINT | PROMOTES DIFFERENTIATION OF CELL VIA TRANSCRIPTION FACTOR |
| WHAT WILL HAPPEN IF PRB IS INHIBITED (HYPOPHOSPHORYLATED STATE) | THERE IS NO REPLICATION OF CELL |
| WHAT WILL HAPPEN IF PRB IS INHIBITED (HYPOPHOSPHORYLATED STATE) | PRB WILL BIND TO E2F NO TRANSCRIPTION WILL OCCUR |
| WHAT WILL HAPPEN IF PRB IS INHIBITED (HYPOPHOSPHORYLATED STATE) | CELL ARREST |
| WHAT WILL HAPPEN IF PRB IS STIMULATED (HYPERPHOSPHORYLATED STATE) | THERE WILL BE CELL PROGRESSION |
| WHAT WILL HAPPEN IF PRB IS STIMULATED (HYPERPHOSPHORYLATED STATE) | PRB CANNOT BIND TO E2F CAUSING IT TO ACTIVATE TRANSCRIPTION |
| REGULATES THE CHECKPOINT OF G1/S CHECKPOINT | RB GENE (TUMOR SUPRESSOR GENE) |
| CYCLINS AND CDK ARE REGULATED BY ____ | CDKI OR CDK INHIBITOR |
| A CDKI THAT INHIBITS CELL CYCLE PROGRESSION AND PERMITS DNA REPAIR` | P21 |
| A CDKI THAT REGULATES SEVERE DAMAGE CELL TO UNDERGO APOPTOSIS BY INCREASING BAX
ALSO KNOWN AS GUARDIAN GENOME | P53 |
| TRUE OR FALSE
P43 HALTS THE DAMAGED CELL IN PROCESSING BY ACTIVATING P21 | TRUE |
| FORMATION OF NEW BLOOD VESSEL | ANGIOGENESIS |
| PROVIDE NUTRIENTS TO TUMOR CELL | ANGIOGENESIS TO TUMOR CELL |
| NEEDS NUTRIENTS AND THROUGH THE FORMATION OF NEW BLOOD VESSEL. | TUMOR CELL |
| TUMORS SECRETE AND IT HELPS GROW BLOOD VESSELS AND THEREFORE HELPS GROW AND SPREAD THE TUMOR. | VEGF |
| ENCODES P21 IN CELL CYCLE AND PROMOTES CELL ARREST | RAS GENE |
| RAS PROTO-ONCOGENE BECOME RAS ONCOGENE BY A MUTATION REPLACEMENT OF ___ TO ___ AT CODON ___ | GLYCINE : VALINE : CODON 12 |
| CLASSIFICATION OF TUMOR SUPPRESSOR GENE; CELL ADHESION | APC AND DCC |
| REGULATORS OF CELL CYCLE | TP53 AND RB1 |
| SUBTYPE OF KNUDSON'S TWO HIT HYPOTHESIS | TS MUTATION |
| SUBTYPE OF KNUDSON'S TWO HIT HYPOTHESIS | GROSS CHROMOSOMAL LOSS |
| SMALL ISOLATED CHANGES IN THE GENE | TS MUTATION OF KNUDSON'S TWO HIT HYPOTHESIS |
| COMPLETE LOSS OF THE CHROMOSOME | GROSS CHROMOSOMAL LOSS OF KNUDSON'S TWO HIT HYPOTHESIS |
| TRANSLOCATION OF CHRONO MYELONGENIC LEUKEMIA | BCR-ABL FUSION OF CHROMOSOME 9 TO 22 |
| c- myc IS TRANSLOCATED FROM CHROMOSOME 8 TO CHROMOSE 14 | BURKITTS LYMPHOMA |
| KEEPS CELL FROM DIVIDING TO FAST AND PROVIDE INSTRUCTION IN MAKING PRB GENE | RB1 GENE |
| PRODUCT OF P53, IT WILL STOP DAMAGED CELL AND ACTIVATE P21 TO REPAIR IT | TP 53 |
| IT WILL STOP DAMAGED CELL AND ACTIVATE P21 TO REPAIR IT | TP 53 |
| STIMULATE INCREASE PRODUCTION OF BAX THAT WILL TRIGGER CELL APOPTOSIS OR CELL DEATH | TP 53 |
| THERE WILL BE NO DETECTION OF DAMAGED CELL WHICH MAY LEAD TO INAPPROPRIATE CELL SURVIVAL AND FORMATION OF CANCER | MUTATION OF TP 53 |
| activates the cyclin/cdk complex | VEGF |
| It is regulated mainly by intracellular signals | G1/S cell cycle checkpoint |
| The second hit involves a gross chromosomal loss | Knudson's Two-Hit Hypothesis |
| cell cycle arrest | Phosphorylation of pRB |
| It is a mutation resulting from conversion of proto-oncogene to oncogene | dominant mutation in oncogenes |
| pRB is inhibited | pRB is in the phosphorylated state |
| Provides the pivotal decisional checkpoint in the fate of the cell after a death stimulus | BCL-2 |
| Apoptotic pathway important after chemotherapy and radiation: | p53-mediated |
| The activity of this cyclin complex results to some condensation: | cyclin B/cdk1 |
| They are mutated forms of protooncogenes | oncogenes |
| They are overexpressed in oncogenesis | oncogenes |
| Mutation involving oncogenes are usually dominant | oncogenes |
| The mutation results to fusion of BCR-ABL gene | chronic myelogenous leukemia |
| contains a TAX gene which activates transcription of genes encoding for lL-2 | Human T-Cell Leukemia Virus HTLV-1 |
| Viral oncoprotein which facilitates degradation of p53 | E6 |
| The single most common genetic change in human neoplasia involves. | p53 |
| Viral oncoprotein which inhibits pRB | E7 |
| stimulates viral mRNA transcription | Tax protein |
