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Questions and Answers
What is the main distinction between invasiveness and metastasis in cancer?
What is the main distinction between invasiveness and metastasis in cancer?
Which type of cancer is typically classified as benign due to its naming convention?
Which type of cancer is typically classified as benign due to its naming convention?
What characterizes dysplasia in tissue architecture?
What characterizes dysplasia in tissue architecture?
Stage 3 cancer is associated with what level of survival prognosis?
Stage 3 cancer is associated with what level of survival prognosis?
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Among the following, which cancer type does NOT typically metastasize?
Among the following, which cancer type does NOT typically metastasize?
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What does neoplasia refer to in the context of cancer?
What does neoplasia refer to in the context of cancer?
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What is the primary cause of death due to cancer?
What is the primary cause of death due to cancer?
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Which statement accurately defines hyperplasia?
Which statement accurately defines hyperplasia?
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What is a defining feature of oncogenes that differentiates them from tumor suppressors?
What is a defining feature of oncogenes that differentiates them from tumor suppressors?
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Which pathway is primarily modulated by Ras and is involved in cancer signaling?
Which pathway is primarily modulated by Ras and is involved in cancer signaling?
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How does Myc contribute to the progression of cancer?
How does Myc contribute to the progression of cancer?
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Which of the following factors is NOT considered a potential cause of cancer?
Which of the following factors is NOT considered a potential cause of cancer?
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The Ames Test is known for its ability to detect what type of mutations?
The Ames Test is known for its ability to detect what type of mutations?
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What is a major limitation of the Ames Test?
What is a major limitation of the Ames Test?
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The concept of monoclonal tumors indicates that these tumors arise from:
The concept of monoclonal tumors indicates that these tumors arise from:
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Which cancer type has been associated with the mutation of the N-Ras oncogene?
Which cancer type has been associated with the mutation of the N-Ras oncogene?
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What is the primary mechanism through which oncogenic Myc is activated in cancer?
What is the primary mechanism through which oncogenic Myc is activated in cancer?
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What does the Two-Hit Hypothesis propose regarding tumor suppression?
What does the Two-Hit Hypothesis propose regarding tumor suppression?
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What is the role of BH3-only proteins in the apoptotic process?
What is the role of BH3-only proteins in the apoptotic process?
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How does Akt influence cellular processes in relation to apoptosis?
How does Akt influence cellular processes in relation to apoptosis?
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What is a primary consequence of overexpression of pro-survival Bcl proteins?
What is a primary consequence of overexpression of pro-survival Bcl proteins?
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Which model describes how p53 differentiates between activating cell cycle arrest and apoptosis?
Which model describes how p53 differentiates between activating cell cycle arrest and apoptosis?
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What role does Smac/Diablo play in the apoptotic signaling pathway?
What role does Smac/Diablo play in the apoptotic signaling pathway?
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What is the main consequence of Rb loss-of-function mutations in relation to tumor suppressor activity?
What is the main consequence of Rb loss-of-function mutations in relation to tumor suppressor activity?
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How does the Two-Hit Hypothesis explain the development of hereditary retinoblastoma?
How does the Two-Hit Hypothesis explain the development of hereditary retinoblastoma?
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What role does p53 play in cellular response to DNA damage?
What role does p53 play in cellular response to DNA damage?
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What can result from a missense mutation in the p53 gene?
What can result from a missense mutation in the p53 gene?
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What is a primary function of the retinoblastoma protein (Rb) in the cell cycle?
What is a primary function of the retinoblastoma protein (Rb) in the cell cycle?
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What mechanism primarily regulates p53 activity in response to stress conditions?
What mechanism primarily regulates p53 activity in response to stress conditions?
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What is the consequence of the inactivation of the Rb protein in cells?
What is the consequence of the inactivation of the Rb protein in cells?
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Which of the following is NOT a target gene regulated by p53?
Which of the following is NOT a target gene regulated by p53?
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How does cyclin-CDK activity affect Rb?
How does cyclin-CDK activity affect Rb?
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What cellular event occurs when p53 accumulates in response to DNA damage?
What cellular event occurs when p53 accumulates in response to DNA damage?
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Which kinase is NOT involved in the phosphorylation of p53 that impairs its binding to MDM2?
Which kinase is NOT involved in the phosphorylation of p53 that impairs its binding to MDM2?
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What role does p19ARF play in relation to p53 and MDM2?
What role does p19ARF play in relation to p53 and MDM2?
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Which is a characteristic feature that distinguishes embryonic stem cells from adult stem cells?
Which is a characteristic feature that distinguishes embryonic stem cells from adult stem cells?
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Which of the following statements about death receptors is true?
Which of the following statements about death receptors is true?
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What differentiates cancer stem cells from normal stem cells?
What differentiates cancer stem cells from normal stem cells?
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Which of the following best describes the function of FLIP in death receptor signaling?
Which of the following best describes the function of FLIP in death receptor signaling?
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Which of the following factors is involved in maintaining the 'stemness' of stem cells?
Which of the following factors is involved in maintaining the 'stemness' of stem cells?
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What may lead to the transformation of normal stem cells into cancer stem cells?
What may lead to the transformation of normal stem cells into cancer stem cells?
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Which pathway is characterized by the ligand FasL binding to its receptor to induce apoptosis?
Which pathway is characterized by the ligand FasL binding to its receptor to induce apoptosis?
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Study Notes
Introduction to Cancer
- Cancer is a group of diseases affecting multicellular species.
- Cancer causes death through organ destruction, infections (due to immune system impairment), cachexia, and hemorrhage.
- Cancer cells grow through tissue, forming tumors.
Invasiveness vs. Metastasis
- Invasiveness: Cancer cells grow beyond normal tissue boundaries, often within connective tissue capsules.
- Metastasis: Cancer cells spread and grow in new locations. A hallmark of malignancy, although some cancers are highly invasive but don't metastasize (e.g., gliomas, basal cell carcinomas).
Cancer Types and Terminology
- Hyperplasia: Excessive cell growth; cells are typically normal.
- Metaplasia: Replacement of one cell type with another.
- Dysplasia: Abnormal cells characterized by altered size/shape (nucleus), increased mitosis, and cytoplasmic changes; a transitional state between benign and premalignant.
- Neoplasia: Abnormal/disorganized growth forming a mass (both malignant and nonmalignant).
- Anaplasia: Dedifferentiated tumor cells; tissue origin is indistinguishable.
- "-oma" suffix usually associated with benign tumors.
Cancer Staging and Prognosis
- Cancer staging reflects prognosis.
- Stage 1: High survival (75-90%)
- Stage 2: Moderate survival (45-55%)
- Stage 3: Low survival (15-25%)
- Stage 4: Very low survival (<5%)
Major Cancer Classifications
- Carcinoma: Most common; epithelial origin.
- Sarcoma: Connective/mesenchymal tissue origin.
- Leukemias/Lymphomas: Blood (hematopoietic) cell origin.
- Neuroectodermal: Glioblastomas, neuroblastomas, Schwannomas.
Cancer as a Genetic Disease and Aging
- Cancer development requires multiple genetic changes.
- Inherited mutations influence risk, but additional factors are necessary for cancer development.
- Cancer incidence is strongly correlated with age (e.g., colon cancer).
Cancer as a Monoclonal Disease
- Cancer arises from a single mutated cell.
- Examples: Leiomyomas (uterine wall) and myelomas (B cell precursors).
Cancer Epidemiology/Causative Factors
- Viral infections
- Carcinogens (physical and chemical)
- Lifestyle factors influence cancer prevalence globally.
Ames Test
- The Ames test measures the frequency of back mutations in Salmonella strains requiring histidine.
- Strengths include simplicity, sensitivity to mutagens, and use of metabolic activation.
- Limitations include prokaryotic system, inherent false positives/negatives, and limited scope, missing non-mutagenic carcinogens.
Hallmarks of Cancer
- Cancer cells exhibit characteristic features, like uncontrolled growth, resistance to cell death, and ability to metastasize.
- Tumor biology is influenced by surrounding stromal tissues. Understanding stromal influences is important for treatment.
Oncogenes (Lecture 2)
- Oncogenes cause uncontrolled growth through gain-of-function mutations.
- Tumor suppressor genes are inactivated by loss-of-function mutations.
Proto-oncogene Transformation Mechanisms
- Quantitative: Gene amplification (e.g., MYC, HER2).
- Qualitative: Point mutations (e.g., RAS).
RAS Protein
- RAS is a small GTP-binding protein involved in many signaling pathways, like the MAP kinase pathway.
- Mutations in RAS, lock it in an "on" state, leading to cancer.
- It is found in several cancer types, including pancreatic, lung, and colon cancers.
MYC Protein
- MYC is a transcription factor regulating cell growth and proliferation.
- Aberrant expression (amplification or translocation) can drive oncogenesis.
- Myc is implicated in a multitude of cancers.
MAP Kinase Pathway Components and Cancer
- Mutated components of the MAP kinase pathway can contribute to cancer, including ERBB2/HER2, RAF, and NF-1.
Targeted Therapies for Oncogenes
- Therapy targeting the activity of RAS and MYC is a primary focus. Often involves small molecule inhibitors to limit activity.
Tumor Suppressors (Lecture 3)
- LOH (Loss of Heterozygosity): Loss of one copy of a tumor suppressor gene.
- Two-Hit Hypothesis: Usually requires the inactivation of both alleles of a tumor suppressor gene to develop a tumor. This highlights the importance of both genes.
RB Protein and its Function
- RB plays a crucial role in regulating the cell cycle by controlling the restriction point, and is often inactivated in cancer.
- RB normally prevents cells from passing to the next phase and becoming cancerous, blocking E2F gene transcription.
P53 Protein and its Function
- P53 is a key tumor suppressor, acting as a "guardian angel" by inducing cell cycle arrest or apoptosis in response to stress, like DNA damage.
- It's frequently inactivated or mutated in cancer, allowing unchecked cell growth.
P53 Activation and Regulation
- P53 levels are normally kept low through quick degradation.
- Stress leads to accumulation of p53 for proper cellular response.
- MDM2 is an oncoprotein that interacts with and regulates p53 levels.
Cancer Stem Cells (Lecture 4)
- Stem cells are characterized by self-renewal and the ability to differentiate into various cell types.
- Cancer stem cells are a subset of abnormal cells within a tumor that can proliferate and maintain the cancer.
Distinguishing Cancer Stem Cells
- Cancer stem cells often possess distinct surface markers (e.g., CD44, CD24) compared to typical cancer cells using FACS to distinguish.
- Cancer stem cells are more resistant to traditional cancer therapies and often drive tumor recurrence.
Apoptosis and Cancer (Lecture 5)
- Apoptosis: Programmed cell death.
- Necrosis: Uncontrolled cell death.
Pathways of Apoptosis
- Intrinsic (Mitochondrial) Pathway: Activated by cellular stress, involving Bcl-2 family proteins (Bax, Bak, Bcl-2) that regulate mitochondrial membrane integrity.
- Extrinsic (Death Receptor) Pathway: Activated by external signals (ligands binding specific receptors). The receptor pathway relays information to activate the caspase proteins involved in apoptosis.
Warburg Effect
- Cancer cells have increased glucose uptake and metabolic activity, driving glycolysis instead of oxidative phosphorylation in situations of abundant glucose.
p53's Role in Apoptosis vs. Arrest
- p53 can induce apoptosis when stress is severe, or cell cycle arrest in those situations of milder stress. Which pathway p53 activates depends on the level of stress faced by the cell.
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Description
This quiz covers the fundamentals of cancer biology, including its definitions, types, and key terms related to cancer progression. Understand the differences between invasiveness and metastasis, as well as various terminologies such as hyperplasia and dysplasia. Test your knowledge on how cancer affects multicellular organisms.