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Questions and Answers
Which types of cancer are associated with Erbb2 (Her2)?
Which types of cancer are associated with Erbb2 (Her2)?
What cancer is primarily linked with a reciprocal translocation involving c-Myc?
What cancer is primarily linked with a reciprocal translocation involving c-Myc?
What is the primary function of FTIs in cancer therapy?
What is the primary function of FTIs in cancer therapy?
Which genes are activated by Myc to push the cell cycle forward?
Which genes are activated by Myc to push the cell cycle forward?
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Which form of retinoblastoma is characterized by a higher incidence of spontaneous cases?
Which form of retinoblastoma is characterized by a higher incidence of spontaneous cases?
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What does loss of heterozygosity (LOH) indicate in the context of tumor suppressor genes?
What does loss of heterozygosity (LOH) indicate in the context of tumor suppressor genes?
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Which of the following cancers is NOT linked to Myc amplification?
Which of the following cancers is NOT linked to Myc amplification?
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According to the Two-Hit Hypothesis, how many hits are required for tumorigenesis in tumor suppressor genes?
According to the Two-Hit Hypothesis, how many hits are required for tumorigenesis in tumor suppressor genes?
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What is the primary consequence of missense mutations in p53?
What is the primary consequence of missense mutations in p53?
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What is the primary role of Fas in the extrinsic death receptor pathway?
What is the primary role of Fas in the extrinsic death receptor pathway?
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Which of the following roles does p21 serve when activated by p53?
Which of the following roles does p21 serve when activated by p53?
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What effect does MDM2 have on p53 protein levels under normal conditions?
What effect does MDM2 have on p53 protein levels under normal conditions?
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What effect can environmental asymmetry have on stem cells?
What effect can environmental asymmetry have on stem cells?
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How does FLIP function in the context of death receptor signaling?
How does FLIP function in the context of death receptor signaling?
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How does p53 become activated in response to cellular stress?
How does p53 become activated in response to cellular stress?
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How do cancer stem cells differ from normal stem cells?
How do cancer stem cells differ from normal stem cells?
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What triggers the autoactivation of procaspase 8 in the extrinsic death pathway?
What triggers the autoactivation of procaspase 8 in the extrinsic death pathway?
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What is a key advantage of death receptor pathways in lymphocyte regulation?
What is a key advantage of death receptor pathways in lymphocyte regulation?
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What role does Numb play in nerve differentiation?
What role does Numb play in nerve differentiation?
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What is a characteristic feature of null mutations in p53?
What is a characteristic feature of null mutations in p53?
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What is the role of cytotoxic T cells and natural killer cells in apoptosis?
What is the role of cytotoxic T cells and natural killer cells in apoptosis?
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What method is used to isolate stem cells based on cell-surface proteins?
What method is used to isolate stem cells based on cell-surface proteins?
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Which mechanism is involved in regulating p53's localization within the cell?
Which mechanism is involved in regulating p53's localization within the cell?
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What is the role of Bax in relation to p53?
What is the role of Bax in relation to p53?
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What proportion of total tumor cells identified had high CD44 expression and low CD24 in breast cancer patients?
What proportion of total tumor cells identified had high CD44 expression and low CD24 in breast cancer patients?
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What is the first step in the ubiquitination process of regulatory proteins?
What is the first step in the ubiquitination process of regulatory proteins?
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How is apoptosis primarily characterized?
How is apoptosis primarily characterized?
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What triggers necrosis?
What triggers necrosis?
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Which proteins are associated with the intrinsic pathway of apoptosis?
Which proteins are associated with the intrinsic pathway of apoptosis?
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What is the role of p53 in regulating apoptotic versus arrest genes?
What is the role of p53 in regulating apoptotic versus arrest genes?
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Which protein interaction is crucial for enhancing p53 binding to apoptotic targets?
Which protein interaction is crucial for enhancing p53 binding to apoptotic targets?
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What is the function of cytochrome c in the apoptosis cascade?
What is the function of cytochrome c in the apoptosis cascade?
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What effect do mutations in Bcl-2 proteins have based on the provided information?
What effect do mutations in Bcl-2 proteins have based on the provided information?
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What role do BH3-only proteins play in apoptosis?
What role do BH3-only proteins play in apoptosis?
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What is the role of pro-survival Bcl proteins in the intrinsic pathway of apoptosis?
What is the role of pro-survival Bcl proteins in the intrinsic pathway of apoptosis?
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What effect does loss of growth factor signaling have on glucose metabolism?
What effect does loss of growth factor signaling have on glucose metabolism?
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How does the Warburg effect influence cancer cells?
How does the Warburg effect influence cancer cells?
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What role does Akt play in cell survival and metabolism?
What role does Akt play in cell survival and metabolism?
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What can be a potential treatment strategy targeting pro-survival Bcl proteins?
What can be a potential treatment strategy targeting pro-survival Bcl proteins?
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What is a characteristic of cells described by the Warburg effect?
What is a characteristic of cells described by the Warburg effect?
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What is released from the mitochondria as an apoptotic stimulus?
What is released from the mitochondria as an apoptotic stimulus?
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What is one function of BH3-only mimetics in cancer treatment?
What is one function of BH3-only mimetics in cancer treatment?
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Study Notes
Biology 318 - Fall 2024 - Midterm Exam Study Guide
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Cancer Introduction (Lecture 1):
- Cancer is unregulated tissue growth, forming tumors.
- Causes of death include organ damage, infections (from immune suppression), and bleeding.
- Cancer is a group of diseases affecting multicellular organisms.
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Invasiveness vs. Metastasis:
- Invasiveness is the growth of cancer cells past normal tissue boundaries.
- Metastasis is the spread and growth of cancer cells in distant sites; a critical aspect of malignancy.
- Some cancers, like gliomas and basal cell carcinomas of the skin, are highly invasive but don't typically metastasize.
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Key Cancer Terms (Slides 7 & 8):
- Hyperplasia: Increased cell number; cells appear normal, able to form normal tissue despite unregulated proliferation.
- Metaplasia: Replacement of one cell type with another not normally found at that site (e.g., Barrett's esophagus).
- Dysplasia: Cytological abnormalities in cell size/shape and nucleus; increased mitotic activity, and a lack of normal cytoplasmic features relative to differentiated cells; typically a transitional state between benign and precancerous growths.
- Neoplasia: Abnormal and disorganized growth leading to a distinct mass. This includes both malignant (cancerous) and benign growths.
- Anaplasia: The loss of differentiated characteristics of tumor cells, making it hard to identify the original tissue type.
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Cancer Staging & Prognosis:
- Cancer staging classifies cancer based on its extent and progression.
- Stage 1: (75-90% survival)
- Stage 2: (45-55% survival)
- Stage 3: (15-25% survival)
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Cancer as a Genetic Disease & Aging:
- Cancer is a genetic disease, but inherited mutations aren't the only drivers.
- Cancer development is often associated with age. For example, colorectal cancer incidence is significantly higher for older individuals.
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Monoclonal Cancer Examples:
- Leiomyomas: Benign uterine tumors exhibiting X-chromosome inactivation patterns.
- Myelomas: Cancers related to B cell precursors.
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Factors Affecting Cancer Frequencies:
- Viral infections
- Chemical carcinogens
- Lifestyle factors
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Ames Test:
- A test to measure the mutagenic potential of substances.
- Simple and efficient but with limitations. Limited to prokaryotic cells, and can produce false positives or negatives.
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Hallmarks of Cancer:
- Loss of growth factor dependence
- Loss of response to anti-growth signals
- Resistance to apoptosis
- Limitless replicative potential
- Tumor invasion and metastasis
- Genetic instability
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Oncogenes:
- Gain-of-function mutations
- Typically "always on," promoting tumorigenesis.
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Tumor Suppressors:
- Loss-of-function mutations
- Typically inactive, preventing suppression of tumorigenesis.
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Proto-oncogene to Oncogene Transformation Mechanisms:
- Quantitative: Gene amplification (e.g., Myc, HER2)
- Qualitative: Point mutations (e.g., Ras)
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Ras Protein:
- A small G protein that relays signals from cell surface receptors to the nucleus.
- Various forms exist (K-Ras, H-Ras, N-Ras), involved in different cancers.
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Myc Protein:
- A transcription factor that regulates cell growth and proliferation.
- Amplification or translocation of the Myc gene can lead to uncontrolled cell division and contribute to cancers.
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MAP Kinase Pathway:
- A crucial signaling pathway critical in cell growth and differentiation.
- Dysfunction is implicated in different cancers.
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Rb Protein:
- A tumor suppressor inhibiting cell cycle progression and regulating cell proliferation.
- Mutations in Rb can lead to uncontrolled cell division.
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P53 Protein:
- A tumor suppressor monitoring cellular integrity and inducing apoptosis.
- Mutations in p53 commonly observed in many cancers.
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Cancer Stem Cells (Lecture 4):
- Stem cells with unlimited self-renewal and capacity to produce differentiated cells.
- Some cancer cells can exhibit stem cell characteristics which contributes to cancer progression.
-
Apoptosis:
- Programmed cell death.
- Extrinsic and intrinsic pathways are involved.
- Crucial for normal development and tissue homeostasis.
- Defects in the process contribute to cancer uncontrolled growth.
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Prepare for the Biology 318 midterm exam with this study guide, covering essential topics such as cancer introduction, invasiveness versus metastasis, and key cancer terms. Understand the characteristics, causes, and pathology of cancer to perform well on your exam.