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Questions and Answers
What is one function of BCL-2 family proteins in relation to apoptosis?
What is one function of BCL-2 family proteins in relation to apoptosis?
Which mechanism distinguishes apoptosis from necrosis?
Which mechanism distinguishes apoptosis from necrosis?
What is the primary consequence of necrosis?
What is the primary consequence of necrosis?
What role do Inhibitors of Apoptosis Proteins (IAPs) play regarding caspases?
What role do Inhibitors of Apoptosis Proteins (IAPs) play regarding caspases?
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Which of the following accurately describes apoptosis?
Which of the following accurately describes apoptosis?
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What is a characteristic of cancer cells in relation to cellular transformation?
What is a characteristic of cancer cells in relation to cellular transformation?
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Which of the following processes requires ATP for execution?
Which of the following processes requires ATP for execution?
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Which of the following is NOT a feature of necrosis?
Which of the following is NOT a feature of necrosis?
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What role do RB proteins play in cell cycle progression?
What role do RB proteins play in cell cycle progression?
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Which protein is responsible for phosphorylating the ATP binding site of CDKs to inhibit their activity?
Which protein is responsible for phosphorylating the ATP binding site of CDKs to inhibit their activity?
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How does p53 contribute to cell cycle regulation under stress conditions?
How does p53 contribute to cell cycle regulation under stress conditions?
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What is the significance of the restriction point in the cell cycle?
What is the significance of the restriction point in the cell cycle?
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What is one consequence of loss-of-function mutations in WEE1?
What is one consequence of loss-of-function mutations in WEE1?
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Which CDK inhibitors specifically target CDK4 and CDK6 without affecting other CDKs?
Which CDK inhibitors specifically target CDK4 and CDK6 without affecting other CDKs?
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In cancer biology, what is a common result of R-point deregulation?
In cancer biology, what is a common result of R-point deregulation?
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What additional role does mitogenic signaling play in normal physiological cell proliferation?
What additional role does mitogenic signaling play in normal physiological cell proliferation?
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What is the primary role of the CDK1-cyclin B complex during the cell cycle?
What is the primary role of the CDK1-cyclin B complex during the cell cycle?
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Which of the following accurately describes the relationship between mitogens and D-type cyclins?
Which of the following accurately describes the relationship between mitogens and D-type cyclins?
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What happens at the R-point in the cell cycle?
What happens at the R-point in the cell cycle?
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Which protein family acts as transcriptional repressors by sequestering E2F transcription factors?
Which protein family acts as transcriptional repressors by sequestering E2F transcription factors?
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How do cyclins contribute to the regulation of the cell cycle?
How do cyclins contribute to the regulation of the cell cycle?
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What is the effect of mitogens on the cell cycle?
What is the effect of mitogens on the cell cycle?
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What initiates the signaling pathway associated with mitogens?
What initiates the signaling pathway associated with mitogens?
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Which cellular phase do most adult cells reside in when not actively dividing?
Which cellular phase do most adult cells reside in when not actively dividing?
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What is a key feature of cancer related to the cell cycle?
What is a key feature of cancer related to the cell cycle?
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What typically allows cancer cells to bypass the dependency on mitogens?
What typically allows cancer cells to bypass the dependency on mitogens?
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What is one of the mechanisms by which cancer cells achieve independence from mitogens?
What is one of the mechanisms by which cancer cells achieve independence from mitogens?
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Why do normal cells exhibit limited proliferative capacity?
Why do normal cells exhibit limited proliferative capacity?
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What role does telomerase play in cancer cells?
What role does telomerase play in cancer cells?
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What happens to telomeres in normal cells with each division?
What happens to telomeres in normal cells with each division?
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What is a consequence of dysfunction in telomere maintenance due to absence of telomerase?
What is a consequence of dysfunction in telomere maintenance due to absence of telomerase?
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What cellular mechanism attempts to repair critically short telomeres without telomerase?
What cellular mechanism attempts to repair critically short telomeres without telomerase?
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What is the primary effect of telomerase reactivation in cancer cells?
What is the primary effect of telomerase reactivation in cancer cells?
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How does metaplasia differ from dysplasia?
How does metaplasia differ from dysplasia?
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What cellular process is characterized by a cell transforming into a more specialized type?
What cellular process is characterized by a cell transforming into a more specialized type?
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What is the consequence of mutations in the TERT promoter?
What is the consequence of mutations in the TERT promoter?
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Which of the following is NOT a characteristic of metaplasia?
Which of the following is NOT a characteristic of metaplasia?
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What does dysplasia indicate with respect to cell growth?
What does dysplasia indicate with respect to cell growth?
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In which condition is squamous metaplasia most commonly observed?
In which condition is squamous metaplasia most commonly observed?
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Which statement accurately describes telomerase in relation to cancer?
Which statement accurately describes telomerase in relation to cancer?
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What defines metaplasia?
What defines metaplasia?
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Which condition is an example of metaplasia?
Which condition is an example of metaplasia?
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What is the main difference between metaplasia and dysplasia?
What is the main difference between metaplasia and dysplasia?
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Which of the following factors is considered a common cause of metaplasia?
Which of the following factors is considered a common cause of metaplasia?
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Which aspect of dysplasia makes it a pre-cancerous condition?
Which aspect of dysplasia makes it a pre-cancerous condition?
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What percentage of people with Barrett's oesophagus are likely to develop oesophageal adenocarcinoma?
What percentage of people with Barrett's oesophagus are likely to develop oesophageal adenocarcinoma?
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What cellular feature is characteristic of metaplasia?
What cellular feature is characteristic of metaplasia?
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Which statement best explains the reversibility of metaplasia?
Which statement best explains the reversibility of metaplasia?
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Study Notes
The Cell Cycle
- The cell cycle describes the phases of cell division
- G1 phase (Gap 1): Interval between mitosis and DNA synthesis; cells commit to division at a restriction point, influenced by growth signals; cells may arrest due to insufficient conditions or inhibitory signals.
- S phase (Synthesis): DNA replication occurs, doubling the genetic material from 2n to 4n (diploid to tetraploid).
- G2 phase (Gap 2): The interval between DNA synthesis and mitosis; error correction occurs to prevent replication errors; spindle assembly begins.
- M phase (Mitosis): Cell division into two identical daughter cells; includes nuclear envelope breakdown, chromosome condensation and alignment, mitotic spindle assembly, Golgi and nucleolus disassembly, and cell rounding.
- Mitogens trigger cell cycle progression through signalling pathways involving receptors, Ras proteins, and D-type cyclins.
- Cyclins and Cyclin-dependent kinases (CDKs) regulate cell cycle progression.
- Inhibitory factors control the cell cycle, prevent uncontrolled progression, and ensure precise timing of events (e.g., p21, p27).
- R-point (restriction point): A critical point in G1 where cells commit to the cell cycle, independent of mitogens.
- Telomere shortening limits cell division in normal cells.
Cellular Transformation
- Cellular transformation involves the transition of normal cells to a tumorigenic state, including changes in morphology and function.
- Cancer cells often bypass the need for mitogens to divide.
- They may exhibit uncontrolled proliferation due to defects in checkpoints.
- Telomerase activation in cancer cells prevents the shortening of telomeres, allowing unlimited cell division.
Apoptosis
- Apoptosis (programmed cell death) is a regulated process removing damaged or unnecessary cells.
- It involves cellular components being recycled through phagocytosis, and does not trigger inflammation.
- Factors promoting apoptosis include proteolytic caspases, TNF receptor superfamily members (e.g., TNF-a, FasL), and p53.
- Inhibitors of apoptosis include BCL-2 family proteins and IAPs.
- Necrosis is an uncontrolled cell death, characterized by cell swelling, membrane damage, and inflammation.
Cellular Differentiation and Metaplasia
- Cellular differentiation is the process where cells change into a specialized type during development.
- Metaplasia is the replacement of one fully differentiated cell type by another.
- Dysplasia describes abnormal cellular growth and maturity, often linked to pre-cancerous conditions.
Barrett's Oesophagus
- Barrett's esophagus involves the replacement of normal squamous epithelial cells in the esophagus with abnormal columnar epithelial cells.
- It's a pre-cancerous condition and linked to chronic acid reflux and an increased risk of esophageal adenocarcinoma.
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Description
Test your knowledge on the mechanisms of apoptosis and cell cycle regulation. This quiz covers key concepts such as the role of BCL-2 proteins, apoptosis vs. necrosis, and the function of CDKs and their inhibitors. Perfect for students studying cell biology or cancer biology.