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Questions and Answers
Which type of mutation causes cancer in somatic cells?
Which type of mutation causes cancer in somatic cells?
What is the two-hit hypothesis for tumor suppressor genes?
What is the two-hit hypothesis for tumor suppressor genes?
What is the primary function of oncogenes?
What is the primary function of oncogenes?
How does genetic instability relate to cancer evolution?
How does genetic instability relate to cancer evolution?
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What does CAR stand for in CAR-T therapy?
What does CAR stand for in CAR-T therapy?
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How are the engineered receptors used in CAR-T therapy expressed?
How are the engineered receptors used in CAR-T therapy expressed?
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What is the process of incorporating receptor gene into the genome in CAR-T therapy?
What is the process of incorporating receptor gene into the genome in CAR-T therapy?
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Why are CAR-T therapies not as effective for solid tumors?
Why are CAR-T therapies not as effective for solid tumors?
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What is one of the challenges associated with preventing genetic instability in cancer diagnostics?
What is one of the challenges associated with preventing genetic instability in cancer diagnostics?
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What is the purpose of suppressing the immune system in cancer treatment?
What is the purpose of suppressing the immune system in cancer treatment?
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What was the antitumor effect observed in the study involving SF1126 and sorafenib?
What was the antitumor effect observed in the study involving SF1126 and sorafenib?
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What is the potential reason for the increase in tumor area after 30-35 days of drug treatment?
What is the potential reason for the increase in tumor area after 30-35 days of drug treatment?
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Which gene is associated with colorectal cancer and regulates the canonical Wnt pathway growth?
Which gene is associated with colorectal cancer and regulates the canonical Wnt pathway growth?
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Which gene causes Li-Fraumeni syndrome and inhibits cell cycle progression and stimulates apoptosis?
Which gene causes Li-Fraumeni syndrome and inhibits cell cycle progression and stimulates apoptosis?
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Which gene is involved in TGF-beta signaling and its variants result in loss of growth inhibitory signals?
Which gene is involved in TGF-beta signaling and its variants result in loss of growth inhibitory signals?
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Which gene codes for two proteins involved in cell cycle regulation, and inactivation mutations lead to over activation of Rb and lack of activation of p53?
Which gene codes for two proteins involved in cell cycle regulation, and inactivation mutations lead to over activation of Rb and lack of activation of p53?
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What is the consequence of loss of PTEN?
What is the consequence of loss of PTEN?
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Which genes are associated with breast and ovarian cancer and are involved in DNA repair and genetic instability?
Which genes are associated with breast and ovarian cancer and are involved in DNA repair and genetic instability?
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What can result from loss of cell cycle control and DNA repair pathways?
What can result from loss of cell cycle control and DNA repair pathways?
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What can genetic instability in cancer lead to within a cancer cell line over months to years of culture?
What can genetic instability in cancer lead to within a cancer cell line over months to years of culture?
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What is used for pathological/molecular analysis to identify cancer in current diagnostics?
What is used for pathological/molecular analysis to identify cancer in current diagnostics?
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What is genomic analysis for cancer moving towards for early diagnostics and specific treatment options?
What is genomic analysis for cancer moving towards for early diagnostics and specific treatment options?
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What is the average number of somatic cells in the human body?
What is the average number of somatic cells in the human body?
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How are tumors classified based on invasiveness and likelihood of lethality?
How are tumors classified based on invasiveness and likelihood of lethality?
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What increases the likelihood of mistakes (mutations) in the cell cycle?
What increases the likelihood of mistakes (mutations) in the cell cycle?
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What percentage of cancers are germ-line linked?
What percentage of cancers are germ-line linked?
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What induces most somatic mutations in cancers?
What induces most somatic mutations in cancers?
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What provides a selective advantage for proliferation and/or inhibition of senescence/apoptosis in cancer stem cells?
What provides a selective advantage for proliferation and/or inhibition of senescence/apoptosis in cancer stem cells?
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What does cancer evolution involve?
What does cancer evolution involve?
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What makes it more difficult to treat cancer with anticancer drugs as it grows and evolves?
What makes it more difficult to treat cancer with anticancer drugs as it grows and evolves?
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What did Bert Vogelstein and colleagues develop to describe the histological and genetic changes involved in tumorigenesis?
What did Bert Vogelstein and colleagues develop to describe the histological and genetic changes involved in tumorigenesis?
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What aspects does the text emphasize related to cancer basics?
What aspects does the text emphasize related to cancer basics?
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What are the two main types of mutant cancer genes?
What are the two main types of mutant cancer genes?
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What can lead to the activation of oncogenes?
What can lead to the activation of oncogenes?
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What are examples of oncogenes mentioned in the text?
What are examples of oncogenes mentioned in the text?
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What is the function of tumor suppressor genes like TP53 and RB?
What is the function of tumor suppressor genes like TP53 and RB?
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What is the result of mutations in oncogenes?
What is the result of mutations in oncogenes?
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What is a characteristic of mutations in tumor suppressor genes?
What is a characteristic of mutations in tumor suppressor genes?
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What is the role of cancer genes in cellular pathways?
What is the role of cancer genes in cellular pathways?
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What does genetic instability in cancers lead to?
What does genetic instability in cancers lead to?
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What can cancer genes be used for?
What can cancer genes be used for?
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What are mutant forms of proto-oncogenes that code for proteins involved in cell growth and differentiation?
What are mutant forms of proto-oncogenes that code for proteins involved in cell growth and differentiation?
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What are the roles of RAS, MYC, and ERBB2?
What are the roles of RAS, MYC, and ERBB2?
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What can mutations in tumor suppressor genes result in?
What can mutations in tumor suppressor genes result in?
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Study Notes
Understanding Cancer Genetics
- Cancer genetics theory includes two main types of mutant cancer genes: oncogenes and tumor suppressor genes
- Cancers demonstrate genetic instability, leading to chromosomal aberrations and increasing mutagenesis
- Cancer genes are involved in cellular pathways that promote survival in harsh environments and drug resistance
- Different types of cancers harbor a variety of cancer genes, with some mutations being cancer-type specific
- Cancer genes can be used for early disease detection and treatment development
- Oncogenes are mutant forms of proto-oncogenes that code for proteins involved in cell growth and differentiation
- Mutations in oncogenes typically result in a gain of function and are often caused by somatic mutations
- Examples of oncogenes include RAS, MYC, and ERBB2, which play roles in cell growth signaling and increased signaling for growth
- Chromosomal translocations and gene duplications/amplifications can lead to the activation of oncogenes
- Tumor suppressor genes like TP53 and RB are involved in DNA damage repair, cell cycle regulation, and growth inhibition
- Tumor suppressor genes can be "driver genes" that initiate cancer progression and "follower genes" that facilitate cancer cell survival
- Mutations in tumor suppressor genes can result in loss of function through various mechanisms, with most mutations being somatic
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Description
Test your knowledge of cancer genetics with this quiz! Explore the role of oncogenes and tumor suppressor genes, genetic instability, cellular pathways, and the potential for early disease detection and treatment development.