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Questions and Answers
What leads to the accumulation of the key characteristics of cancer?
What leads to the accumulation of the key characteristics of cancer?
What role do oncogenes play in cancer cell behavior?
What role do oncogenes play in cancer cell behavior?
Which of the following is a physiologic regulator of cell proliferation?
Which of the following is a physiologic regulator of cell proliferation?
How do cancer cells achieve uncontrolled growth regarding growth factors?
How do cancer cells achieve uncontrolled growth regarding growth factors?
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What is the function of GAPs in cancer signaling pathways?
What is the function of GAPs in cancer signaling pathways?
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When is cancer typically detectable?
When is cancer typically detectable?
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Which of the following statements about oncoproteins is true?
Which of the following statements about oncoproteins is true?
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What is one of the roles of nuclear regulatory proteins in cancer?
What is one of the roles of nuclear regulatory proteins in cancer?
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What characteristic allows cancer cells to proliferate without the influence of external growth signals?
What characteristic allows cancer cells to proliferate without the influence of external growth signals?
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Which hallmark of cancer enables cancer cells to avoid programmed cell death?
Which hallmark of cancer enables cancer cells to avoid programmed cell death?
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What is primarily responsible for the genetic alterations leading to cancer?
What is primarily responsible for the genetic alterations leading to cancer?
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Which of the following best describes the process by which normal cells can transform into cancerous cells?
Which of the following best describes the process by which normal cells can transform into cancerous cells?
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Which mutation target is most closely associated with inhibiting cellular growth?
Which mutation target is most closely associated with inhibiting cellular growth?
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How do cancer cells typically ensure a sufficient blood supply for their growth?
How do cancer cells typically ensure a sufficient blood supply for their growth?
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The ability of cancer cells to evade the immune response is crucial for their survival. Which process describes this characteristic?
The ability of cancer cells to evade the immune response is crucial for their survival. Which process describes this characteristic?
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What mechanism do cancer cells employ to satisfy their increased energy demands?
What mechanism do cancer cells employ to satisfy their increased energy demands?
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What is the primary function of tumor suppressor genes?
What is the primary function of tumor suppressor genes?
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Which of the following is a key tumor suppressor protein responsible for regulating the G1-S checkpoint of the cell cycle?
Which of the following is a key tumor suppressor protein responsible for regulating the G1-S checkpoint of the cell cycle?
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What is the significance of TP53 mutations in cancer development?
What is the significance of TP53 mutations in cancer development?
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What is the role of MDM2 in the regulation of p53?
What is the role of MDM2 in the regulation of p53?
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What are the primary mechanisms through which p53 opposes neoplastic transformation?
What are the primary mechanisms through which p53 opposes neoplastic transformation?
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Which genetic disorder is associated with germline loss-of-function mutations in the APC gene?
Which genetic disorder is associated with germline loss-of-function mutations in the APC gene?
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Which of the following is NOT a characteristic of tumor suppressor genes?
Which of the following is NOT a characteristic of tumor suppressor genes?
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What is the primary function of APC?
What is the primary function of APC?
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What is the primary function of GAPs in the context of RAS signaling?
What is the primary function of GAPs in the context of RAS signaling?
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Which of the following correctly describes the mechanism by which BRAF contributes to cancer development?
Which of the following correctly describes the mechanism by which BRAF contributes to cancer development?
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In chronic myelogenous leukemia (CML), the ABL gene undergoes a translocation event. What is the consequence of this translocation?
In chronic myelogenous leukemia (CML), the ABL gene undergoes a translocation event. What is the consequence of this translocation?
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Which of the following correctly describes the relationship between PDGF and glioblastomas?
Which of the following correctly describes the relationship between PDGF and glioblastomas?
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Which of the following is NOT a characteristic of oncogenic versions of receptor tyrosine kinases?
Which of the following is NOT a characteristic of oncogenic versions of receptor tyrosine kinases?
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Which of the following transcription factors is described as a master regulator of cell growth and is frequently implicated in human tumors?
Which of the following transcription factors is described as a master regulator of cell growth and is frequently implicated in human tumors?
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What is the role of cyclin-dependent kinases (CDKs) in the cell cycle?
What is the role of cyclin-dependent kinases (CDKs) in the cell cycle?
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Which of the following is NOT a recognized example of a gene that encodes a receptor tyrosine kinase associated with cancer development?
Which of the following is NOT a recognized example of a gene that encodes a receptor tyrosine kinase associated with cancer development?
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Study Notes
Molecular Basis of Cancer
- Cancer development is a multi-step process involving multiple genetic alterations
- Nonlethal genetic damages (mutations) initiate carcinogenesis
- Mutations may be environmental, inherited, or spontaneous
- A tumor arises from the clonal expansion of a single precursor cell with genetic damage
- Key targets of cancer-causing mutations include growth-promoting proto-oncogenes, growth-inhibiting tumor suppressor genes, apoptosis regulators, and DNA repair genes
- Cancer progression involves stepwise acquisition of complementary mutations
- Eight fundamental changes in cell physiology define cancer hallmarks
Cellular and Molecular Hallmarks of Cancer
- Self-sufficiency in growth signals
- Insensitivity to growth-inhibitory signals
- Altered cellular metabolism
- Evasion of apoptosis
- Limitless replicative potential (immortality)
- Sustained angiogenesis
- Ability to invade and metastasize
- Ability to evade the host immune response
Acquired DNA Damage Agents
- Chemicals
- Radiation
- Viruses
Normal Cell Cycle
- The cell cycle progression is tightly regulated by cyclins and cyclin-dependent kinases (CDKs), and their inhibitors
- Checkpoints at G1/S and G2/M transitions monitor DNA damage and ensure proper progression
- The G1/S checkpoint prevents replication of cells with DNA damage, ensuring accurate copying is performed
- The G2/M checkpoint prevents cell division if DNA is damaged or incompletely replicated
Cell Cycle Checkpoints
- The cell cycle has internal controls called checkpoints at G1/S and G2/M transitions
- DNA damage sensors, signal transducers and effector molecules are required for proper checkpoint function
G1/S Checkpoint
- The S phase is the point of no return in the cell cycle, where cells commit to DNA replication
- A G1/S checkpoint checks for DNA damage before proceeding
- If DNA damage is detected, DNA repair mechanisms are activated. If repair fails, apoptosis is triggered
- DNA damage that arises after replication can also be repaired as long as chromatids haven't separated
Oncogenes and Proto-oncogenes
- Oncogenes promote autonomous cell growth in cancer
- Proto-oncogenes are their normal counterparts that encode proteins for normal cell function
- Mutations or overexpression of proto-oncogenes leads to oncogenic forms which are constitutively active, driving cell growth independently of external cues
Functional Category of Oncogenes
- Growth factors
- Growth factor receptors
- proteins involved in signal transduction
- Nuclear regulatory proteins
- Cell cycle regulators
Downstream Components of Receptor Tyrosine Kinase Pathway
- RAS mutations are common events in human cancers
- RAS proteins are involved in signal transduction pathways
- Mutant RAS proteins lose their ability to hydrolyze GTP, causing constitutive activation and downstream signaling
Oncogenic BRAF and PI3K Mutations
- BRAF and PI3K are serine/threonine protein kinases involved in signal pathways
- Mutations in these genes either increase an enzyme's activity leading to uncontrolled signal activation, or inactivate inhibitory proteins
Alterations in Nonreceptor Tyrosine Kinases
- ABL (nonreceptor tyrosine kinase) translocations frequently occur in leukemias
- The resultant chimeric BCR-ABL gene encodes for constitutively active oncogenic tyrosine kinase
Transcription Factors
- Signal transduction pathways converge on the nucleus, where expression of target genes take place
- Transcription factors, such as MYC, MYB, JUN, FOS, and REL proto-oncogenes, play essential roles in regulating gene expression
- MYC is frequently involved in human tumors
Oncogenes, Oncoproteins
- MYC is one of the handful of transcription factors that can reprogram somatic cells into pluripotent stem cells
- MYC is commonly mutated in various cancers, resulting in constitutive expression and uncontrolled cell proliferation
Cyclins and CDKs
- Progression of cells through cell cycle is orchestrated by cyclin-dependent kinases(CDKs) activated through binding to cyclins
- Cyclins drive cells forward through the cell cycle by phosphorylating crucial target proteins
- Two major checkpoints exist at G1/S and G2/M transitions, regulated by growth-promoting and suppressing factors
Tumor Suppressor Genes
- Tumor suppressor genes apply brakes to cell proliferation
- Abnormalities in these genes lead to uncontrolled growth
- Tumor suppressor proteins function as check points, preventing uncontrolled growth
TP53: Guardian of the Genome
- TP53 is a tumor suppressor gene that regulates cell cycle progression, DNA repair, senescence, and apoptosis
- Loss-of-function mutations in TP53 are found in more than 50% of cancers
- TP53 encodes for the protein p53 that is tightly regulated on several levels
- MDM2 and related proteins are frequently overexpressed in malignancies with normal TP53 alleles
- p53 activation is stimulated by DNA damage and hypoxia, prompting either cell-cycle arrest, senescence or apoptosis
APC: Gatekeeper of Colonic Neoplasia
- APC is a tumor suppressor gene that downregulates growth-promoting signaling pathways
- Mutations in APC are associated with familial adenomatous polyposis, leading to an increased risk of colorectal cancer
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Description
Explore the intricate mechanisms underlying cancer development through this quiz. Learn about genetic mutations, tumor formation, and the hallmarks of cancer physiology. Test your knowledge on how these processes contribute to the complexities of cancer biology.
