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Questions and Answers
What are the three major categories of 'cancer genes'?
What is the central importance of the p53 gene product in cancer genetics?
How do the following cancer genes deregulate cell growth and differentiation: APC, p53, & NF1?
What is the function of telomerase in cancer?
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What is the main function of the p53 protein?
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Which type of genes enhance cell proliferation when activated?
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What is the role of cyclins in cell cycle regulation?
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Which proteins can inactivate the complex formed by cyclin-dependent kinases and cyclins?
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What is the mechanism through which Ras becomes an oncogenic protein?
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Which gene product is centrally important in cancer genetics?
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What is the function of telomerase in cancer?
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Which proteins are modified or expressed inappropriately in the context of cancer genetics?
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What is the main role of DNA repair genes in cancer?
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Which molecule can bind to a growth factor receptor and signal without the ligand being bound?
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What is the function of the CKI protein p21 in cancer genetics?
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Which gene is responsible for maintaining the integrity of the genome?
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Which proteins are involved in integrating both apoptotic and anti-apoptotic signals in cells?
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What is the function of telomerase in cells?
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Which pathway is induced by growth factor withdrawal, cell injury, or high intracellular calcium?
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Which protein is responsible for inhibiting its co-receptor smoothened?
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What is the main function of p53 in relation to apoptosis?
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Which protein family are cysteine proteases that are activated from zymogens by proteolysis?
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What is the consequence of loss of NF-1 (Neurofibromin, a GAP)?
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Which pathway involves Fas/CD95, TNF1, and Death Receptor 3?
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What may make cancer cells resistant to apoptosis?
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What is the main function of telomerase in relation to cell proliferation?
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Which proteins are involved in hormone and growth factor signaling pathways?
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What is the main consequence of dysregulation of normal functions in cancer progression?
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Study Notes
Cancer Genetics and Apoptosis Overview
- p53 induces transcription of p21 Tumor Suppressors and Ras family, involved in hormone and growth factor signaling pathways
- Loss of NF-1 (Neurofibromin, a GAP) leads to neurofibromatosis
- Tumor suppressors and oncogenes can work together normally, e.g., Patched inhibits its co-receptor smoothened
- Telomerase maintains telomere length to prevent senescence and limit cell divisions
- Apoptosis is programmed cell death, removing damaged cells through two pathways: death receptor and mitochondrial integrity
- Caspases are cysteine proteases that are activated from zymogens by proteolysis
- Bcl-2 family of proteins integrate both apoptotic and anti-apoptotic signals in cells
- Death receptor pathway involves Fas/CD95, TNF1, and Death Receptor 3, leading to caspase activation
- Mitochondrial integrity pathway is induced by growth factor withdrawal, cell injury, or high intracellular calcium
- Mutations in oncogenes may make cancer cells resistant to apoptosis, such as the PDGF/Akt/BAD pathway
- Dysregulation of normal functions is key to cancer progression, with genes mutated in cancer being categorized as oncogenes, tumor suppressors, or DNA repair
- Cell cycle control requires normal function of tumor suppressors and oncogenes, while telomerase can enhance cell proliferation by maintaining chromosome ends
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Description
Test your knowledge of cancer genetics and apoptosis with this comprehensive overview. Explore key concepts such as p53, NF-1, telomerase, apoptosis pathways, caspases, Bcl-2 family, death receptor pathway, mitochondrial integrity pathway, and the role of oncogenes and tumor suppressors in cancer progression.
