Podcast
Questions and Answers
What is the Warburg effect in cancer cell metabolism?
What is the function of p16 in the cell cycle?
Which gene is commonly mutated in colorectal cancers?
What is the role of telomerase in cancer cells?
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What is the main difference between oncogenes and tumor suppressor genes?
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What is the significance of hypermethylation in cancer?
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What type of mutation is found in all progeny and begins the process towards malignant transformation?
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Which type of gene mutation generally involves gain-of-function mutations?
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Which type of mutation generally involves loss-of-function mutations and contributes to the formation of oncogenes?
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Which gene family is commonly associated with gain-of-function mutations in certain cancers?
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Which gene, induced by Ras/MAPK signaling, contributes to cancer by increasing cell proliferation and growth?
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Which gene functions as a key negative regulator of the G1/S checkpoint and is directly or indirectly inactivated in most human cancers?
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Which gene is known as the 'Guardian of the Genome' and regulates cell cycle progression, DNA repair, cellular senescence, and apoptosis?
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Which type of mutations in cyclin D and Cdk4 affect progression through the G1/S checkpoint and are implicated in various cancers?
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Which gene is a tumor suppressor that applies brakes to cell proliferation and recognizes genotoxic stress?
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Which downstream component of receptor tyrosine kinases signaling pathways is the most common abnormality in human tumors?
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Which gene family is frequently mutated or silenced in many human malignancies, with inherited mutations implicated in familial forms of melanoma?
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Which gene contributes to carcinogenesis by failing to arrest the cell cycle?
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Which gene family is also common in certain cancers, with 30% of breast carcinomas having gain-of-function mutations?
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Passenger mutations have a low malignant effect
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Myc is an early response gene that increases telomerase activity
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Match the following cancer hallmark with its description:
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Most tumor suppressor genes affect the cell cycle at.....
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p16, cyclin D, CDK4, and RB are all oncogenes
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Both RB and P53 can recognize genotoxic stress
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p53 is the most frequently mutated oncogene in cancer
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A mutation to Mdm2 could lead to carcinogenesis
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A cancer cell evading senescence is an example of......
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Study Notes
Oncogenes and Tumor Suppressor Genes in Cancer Progression
- Tumors evolve genetically based on survival of the fittest subclones, becoming more aggressive over time
- Oncogenes promote excessive cell growth, driven by mutations in proto-oncogenes
- Ras, a downstream component of receptor tyrosine kinases signaling pathways, is the most common abnormality in human tumors
- The PI3K family is also common in certain cancers, with 30% of breast carcinomas having gain-of-function mutations
- MYC, induced by Ras/MAPK signaling, increases cell proliferation and growth, contributing to cancer
- Gain-of-function mutations in cyclin D and Cdk4 affect progression through the G1/S checkpoint, implicated in various cancers
- Tumor suppressor genes, such as RB and p53, apply brakes to cell proliferation and recognize genotoxic stress
- RB functions as a key negative regulator of the G1/S checkpoint and is directly or indirectly inactivated in most human cancers
- TP53, "Guardian of the Genome," regulates cell cycle progression, DNA repair, cellular senescence, and apoptosis
- Mutated p53 contributes to carcinogenesis by failing to arrest the cell cycle until DNA repair is successful
- Loss of p53 leads to unrepaired DNA damage and accumulation of driver mutations in oncogenes, driving malignant transformation
- CDKIs, such as p16, are frequently mutated or silenced in many human malignancies, with inherited mutations implicated in familial forms of melanoma
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Description
Test your knowledge of oncogenes and tumor suppressor genes in cancer progression with this quiz. Explore the role of key genes like Ras, MYC, RB, p53, and more in the development and progression of various cancers.