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Cancer
| Question | Answer |
|---|---|
| In the beginning of metastases, cells enter the _________ and adhere to _____ _________ | bloodstream, blood vessel |
| How is micro metastasis initiated? | Cancer cells escape from the blood vessel into surrounding tissue |
| How are oncogenes activated? | An activating mutation promotes cell transformation |
| How are tumor suppressors inhibited? | They are inactivated on both chromosomes, thus promoting cell transformation |
| Activation of proto-oncogenes: 1. ________ or ________________ in coding sequence disables ________ | deletion, point mutation, kinase regulatory region |
| Activation of proto-oncogenes: 2. repressor is ________ so that it doesnt work | mutated |
| Activation of proto-oncogenes: 3. errors in _________ lead to multiple gene ________, which leads to ___________ | replication, copies, amplification |
| Activation of proto-oncogenes: 4. Chromosomal __________ into new promoter | rearrangement |
| What does TFGR stand for? | Tumor growth factor receptor |
| Name three signaling molecules that inhibit cell growth | 1. PTEN 2. PP2A 3. PP1 4. ATM 5. CHK2 |
| Name one transcription factor that inhibits cell growth | 1. p53 2. FOXO |
| Name 2 cell cycle proteins that inhibit cell growth | 1. p21 2. p16 3. Rb 4. ARF |
| A class of tumor suppressors are inducers of ________ repair | DNA |
| Name one inducer of apoptosis | 1. Bid 2. Bad 3. Bak |
| What is the easy analogy to remember classes of tumor suppressors? | Transcription activator U def need signals like PTEN PP26 Atm May there be DNA repair and cell death Bid Bak Bad Of course you need cell cycle signals Receptors TGFR |
| How does p16 relate to oncogenes and tumor repressors? | The growth factor is usually turned off with p16. If there is No p16, the cell keeps growing |
| How does Rb relate to oncogenes and tumor repressors? | RB normally blocks E2F, the activator of transcription of genes to enter S phase |
| Growth Signals: __________ regulates cell cycle progression | Mitogen |
| Growth Signals: Growth Factors regulate _____________ | glucose uptake |
| Glucose creation due to growth factors, why is too much PIP3 made? | PTEN is an oncogene and is supposed to tell PI3 kinase when to stop creating PIP3 |
| What is the downside to PIP3 being overproduced? | PIP3 creates more Akt creates more mTOR creates more glucose intake which causes the cell to grow uncontrollably |
| How is Bcr/Abl created? | A DNA fusion of Bcr/Abl genes which are translated into a fusion protein |
| How is leukemia inhibited by Bcr-Abl? | BCr-Abl is inactivated by the phosophorylation of a substrate protein that it is attached to, as well as the loss of ADP. This substrate signals cell proliferation |
| How does Gleevec stop leukemia? | It occupies the ATP binding site on Bcr-Abl, which does not trigger the substrate to produce a signal |
| p53 in response to DNA damage: 1. DNA damage triggers ___ kinase to be activated | ATM |
| p53 in response to DNA damage: 2. ATM stimulates ____ or ____ to phosphorylate ____-- | Chk1, CHk2, p53 |
| p53 in response to DNA damage: 3. active p53 detaches from ____ and initiates transcription of ____ | Mdm, p21 |
| p53 in response to DNA damage: 4: p21 protein binds to ____ at checkpoint to inhibit _____ binding | CDK, cyclin |
| In cancerous cells, ______ blocks ______ and cycle does not stop | T-antigen, p53 |
| Colon cancer damages end with the loss of ______ | p53 |
| What is an indicator that one has colon cancer? | There is no p53 detected in the system |
Created by:
neeck
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