Term
Describe Cancer and the Cell cycle
1. Checkpoints
2. Contact inhibition |
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Definition
1. Bypass checkpoints (energy, environmental readiness, DNA is damaged)
*CDK4 relies on Cyclin D to pass through G1
2. Lack contact inhibition (uncontrolled growth) |
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Term
| Describe Cancer and Apoptosis |
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Definition
1. Cell death is normal biology
2. Caspases play a role in inactivating cell proteins
3. Die too little and grow too fast |
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Term
| What are evidences that cancer is genetic? |
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Definition
1. cancerous state is clonally inherited
2. viruses can induce cancer- insert and damage DNA
3. cancer can be induced by DNA mutagens
4. certain types run in families
5. certain WBC cancers are related to translocations |
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Term
| Describe Oncogenes and Tumor suppressors |
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Definition
Oncogenes- mutant genes that promote cancer
1. promoter changes 2. gene mutations/deletions
Tumor suppressors- fail to control growth |
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Term
| Describe the role of Ras in cancer |
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Definition
*oncogene
1. Ras acts as signal transduction in cytoplasm and must be activated by GTP
-signal regulates gene that controls cell division
2. Guanine exchange factor brings GTP to replace GDP
3. Mutation in GTPase leaves too much GTP
-If too much GTP is available, Ras will be overactivated which can lead to uncontrolled growth-> cancer
Dominant activator- one mutant gene will cause mutant Ras |
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Term
| Describe the Two Hit Hypothesis |
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Definition
*Knudson
-having one dominant activator (mutant oncogene) is not enough for cancer
-other mutations in tumor suppressors are needed
1. mutant oncogene
2. mutation tumor suppressor |
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Term
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Definition
Retinoblastoma- cancer of the eye in children
pRB- tumor suppressor
E2F- major TF; inhibits cell from entering G1
1. pRB binds to TF E2F and inhibits it from binding to enhancers in early G1
2. when pRB is phosphorylated by CDK, it releases E2F
-mitosis can start
3. pRB is dephos and binds to E2F-> mitosis inhibited
*in cancer, both pRB genes are mutant which leads to uncontrolled growth |
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Term
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Definition
-tumor suppressor in most cancers
-most mutations in DBD (some in OD)
-phosphorylated in response to DNA damage
-dimerizes and becomes activated and binds to DNA, stopping synthesis
-can halt cell cycle or induce apoptosis if damage is present |
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Term
| Describe the role of p53 in Cell Cycle Arrest |
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Definition
1. acts as TF and induces synthesis of p21
2. p21 inhibits phos of CDK
3. pRB is not phos
4. hypophos pRB inhibits E2F from starting mitosis
5. proteins induced by E2F are not made
-cell cycle is arrested |
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Term
| Describe the role of p53 in Apoptosis |
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Definition
1. acts as TF and induced BAX
2. BAX antagonizes BCL-2, a repressor of apoptosis
3. apoptosis can occur because BCL-2 is released |
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Term
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Definition
Tumor suppressor in colorectal cancer
-polyps form from epithelium that overdivide
-high probability to become malignant (second hit)
1. beta catenin is synthesized in signal transduction to induce mitosis
2. pAPC binds to beta catenin and degrades it
*should only received the signal if close to progenitor cell
*without pAPC cell will divide uncontrollably and cause tumor near lumen of intestine |
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Term
| Describe the Hallmarks of Cancer |
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Definition
1. Self sufficient in regards to growth factors- make their own
2. Loss of growth inhibition
-no contact inhibition and tumor sup mutate
3. Evade apoptosis
4. Immortal- limitless replicative potential
5. Angiogenesis
6. Metastasis |
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