General Cancer Information and Molecular Basis
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Which of the following statements accurately describes the mechanism by which the BCR-ABL fusion protein contributes to the development of leukemia?

  • BCR-ABL directly inhibits the activity of DNA repair enzymes, causing genetic instability and tumor formation.
  • BCR-ABL is a constitutively active tyrosine kinase, promoting uncontrolled cell growth and survival. (correct)
  • BCR-ABL activates growth suppressor genes, leading to uncontrolled cell proliferation.
  • BCR-ABL acts as a transcription factor, directly altering the expression of genes involved in cell cycle control.

    • Which of the following is NOT a characteristic of the MYC proto-oncogene?

  • It is a growth suppressor gene that inhibits cell proliferation. (correct)
  • It is a transcription factor that is commonly involved in human tumors.
  • It is an immediate early response gene, rapidly induced by growth factor stimulation.
  • It is expressed in virtually all eukaryotic cells.

    • Which of the following scenarios represents a mechanism by which the MYC gene can contribute to the development of cancer?

  • The MYC gene undergoes a translocation to another chromosome, leading to its increased expression. (correct)
  • A mutation in the MYC gene leads to the production of a non-functional protein, inhibiting cell growth.
  • MYC is downregulated in response to DNA damage, preventing uncontrolled cell division.
  • MYC is silenced by methylation, preventing the expression of its protein.

    • Which of the following is a correct statement regarding the relationship between cyclin-dependent kinases (CDKs) and cyclins?

    <p>CDKs bind to cyclins, leading to the activation of CDKs and subsequent progression of cells through the cell cycle. (A)</p> Signup and view all the answers

    Which of the following statements accurately describes the role of the G1/S checkpoint in the cell cycle?

    <p>The G1/S checkpoint determines whether the cell has accumulated sufficient nutrients and growth factors for cell division. (A)</p> Signup and view all the answers

    Which of the following is NOT a common target of phosphorylation by CDK-cyclin complexes?

    <p>Proteins involved in cell cycle arrest. (B)</p> Signup and view all the answers

    Which of the following scenarios represents a potential mechanism by which dysregulation of CDK activity could contribute to cancer development?

    <p>CDK activity becomes independent of cyclin regulation, leading to uncontrolled cell proliferation. (D)</p> Signup and view all the answers

    Which of the following is a correct statement regarding the relationship between transcription factors and oncogenes?

    <p>Transcription factors can act as oncogenes, promoting uncontrolled cell growth and proliferation when mutated or dysregulated. (B)</p> Signup and view all the answers

    Which of the following oncogene-related proteins are implicated in the development of chronic myelogenous leukemia (CML)?

    <p>ABL nonreceptor tyrosine kinase (C)</p> Signup and view all the answers

    Which of the following proteins, when mutated, is directly involved in regulating cell cycle progression by promoting the transition from the G1 to the S phase?

    <p>CDK4 (C)</p> Signup and view all the answers

    Which of the following statements accurately describes the relationship between proto-oncogenes and oncogenes?

    <p>Oncogenes arise from mutations or overexpression of proto-oncogenes. (C)</p> Signup and view all the answers

    Which of the following scenarios is NOT a mechanism by which oncogenes contribute to cancer development?

    <p>Increased expression of genes involved in DNA repair (B)</p> Signup and view all the answers

    Which of the following is a characteristic of tumor suppressor genes, in contrast to proto-oncogenes, in the context of cancer development?

    <p>Loss of function mutations in tumor suppressor genes contribute to cancer development, while gain of function mutations in proto-oncogenes contribute to cancer development. (A)</p> Signup and view all the answers

    Which of the following oncogenes is directly involved in the development of Burkitt lymphoma?

    <p>MYC (D)</p> Signup and view all the answers

    Which of the following statements accurately describes the role of CDK4/D cyclin complexes in the cell cycle?

    <p>They promote the transition from the G1 to the S phase by phosphorylating RB. (A)</p> Signup and view all the answers

    Which of the following is NOT a mechanism by which oncoproteins can contribute to cancer development?

    <p>Induction of apoptosis (C)</p> Signup and view all the answers

    What is the primary role of MDM2 related proteins in relation to p53?

    <p>Stimulate p53 degradation (A)</p> Signup and view all the answers

    Which event is classified as a key initiator for p53 activation?

    <p>DNA damage (D)</p> Signup and view all the answers

    What consequence results from the accumulation of p53 in stressed cells?

    <p>Induction of apoptosis (A)</p> Signup and view all the answers

    How do ATM and ATR proteins contribute to p53 functionality?

    <p>They stimulate the phosphorylation of p53 and MDM2 (A)</p> Signup and view all the answers

    What is a major consequence of loss of p53 function in cells?

    <p>Accumulation of driver mutations (B)</p> Signup and view all the answers

    Which of the following genes is affected by the activation of p53?

    <p>p21 (D)</p> Signup and view all the answers

    What condition is typically associated with germline loss-of-function mutations in the APC gene?

    <p>Familial adenomatous polyposis (C)</p> Signup and view all the answers

    What role does the APC gene primarily serve in the context of tumor suppression?

    <p>Downregulating growth-promoting signals (C)</p> Signup and view all the answers

    What is the primary role of the G1/S checkpoint in the cell cycle?

    <p>To activate apoptotic pathways if DNA damage is irreparable. (C)</p> Signup and view all the answers

    How do the checkpoint effector molecules differ between the G1/S and G2/M checkpoints?

    <p>They utilize different regulatory mechanisms to arrest the cell cycle. (C)</p> Signup and view all the answers

    What role does p53 play in the G1/S checkpoint?

    <p>It induces the expression of the cell cycle inhibitor p21. (A)</p> Signup and view all the answers

    Which of the following is NOT a characteristic of oncogenes?

    <p>They always cause a complete loss of normal cellular function. (A)</p> Signup and view all the answers

    What is the relationship between protooncogenes and oncogenes?

    <p>Oncogenes are mutated versions of protooncogenes. (B)</p> Signup and view all the answers

    What is the main consequence of a defect in cell-cycle checkpoint components?

    <p>Genetic instability in cancer cells. (D)</p> Signup and view all the answers

    What would happen if a cell were to bypass the G1/S checkpoint with damaged DNA?

    <p>The damaged DNA would be replicated, potentially leading to mutations in daughter cells. (C)</p> Signup and view all the answers

    Which of the following is a characteristic of a cell that has successfully passed the G2/M checkpoint?

    <p>The cell has completed DNA replication without any errors. (D)</p> Signup and view all the answers

    Which of the following proto-oncogenes is associated with the development of multiple endocrine neoplasia 2A and B, and familial medullary thyroid carcinomas, through point mutations?

    <p>RET (A)</p> Signup and view all the answers

    A proto-oncogene that can be activated by translocation, leading to Chronic Myelogenous Leukemia (CML), is:

    <p>ABL (A)</p> Signup and view all the answers

    Which of the following proto-oncogenes is associated with the development of Burkitt lymphoma due to translocation?

    <p>MYC (C)</p> Signup and view all the answers

    Which of the following proto-oncogenes can be activated by both point mutations and translocations, leading to a variety of cancers including melanomas, leukemias, and colon carcinoma?

    <p>BRAF (A)</p> Signup and view all the answers

    Which of the following proto-oncogenes is NOT associated with the development of breast cancer?

    <p>FLT3 (A)</p> Signup and view all the answers

    What is the common characteristic of all the three signal transduction pathways(Growth Factor Receptor, Ras, PI3K) involved in cancer which are mentioned in the content?

    <p>These pathways are involved in cell proliferation and growth. (B)</p> Signup and view all the answers

    Which of the following statements about oncogenes is NOT true?

    <p>Oncogenes are responsible for inducing normal cellular processes, such as growth and differentiation. (C)</p> Signup and view all the answers

    Which of the following proto-oncogenes is directly associated with the development of astrocytomas?

    <p>PDGFB (A), TGFA (D)</p> Signup and view all the answers

    What is the primary mode of activation for the proto-oncogene KRAS that leads to its role in colon, lung, and pancreatic cancers?

    <p>Point mutation (B)</p> Signup and view all the answers

    Which of the following proto-oncogenes is NOT associated with the development of leukemias?

    <p>CCND1 (A)</p> Signup and view all the answers

    What type of mutation leads to constitutive activation of the EGFR tyrosine kinase, contributing to the development of lung adenocarcinomas?

    <p>Point mutations in the ERBB1 gene (C)</p> Signup and view all the answers

    Which of the following statements accurately describes the role of GAPs (GTPase activating proteins) in normal RAS signaling?

    <p>GAPs inactivate RAS by augmenting its intrinsic GTPase activity. (D)</p> Signup and view all the answers

    Which of the following is NOT a characteristic of mutated RAS proteins in cancer cells?

    <p>They are unable to bind to GAPs, preventing their inactivation. (D)</p> Signup and view all the answers

    What is the primary mechanism by which activating mutations in BRAF contribute to tumorigenesis?

    <p>They stimulate a cascade of downstream kinases, ultimately activating transcription factors. (B)</p> Signup and view all the answers

    Which of the following statements accurately describes the role of PI3K in cancer development?

    <p>PI3K mutations are particularly prevalent in breast carcinomas, often targeting the catalytic subunit. (C)</p> Signup and view all the answers

    How do cancer cells differ from normal cells in terms of their response to growth factors?

    <p>Cancer cells can synthesize their own growth factors, establishing an autocrine loop. (D)</p> Signup and view all the answers

    What is the significance of the high prevalence of RAS mutations across various cancer types?

    <p>They indicate a critical role of RAS signaling in regulating normal cell growth. (C)</p> Signup and view all the answers

    Which of the following is NOT a common oncogenic mutation found in the receptor tyrosine kinase signaling pathway?

    <p>Inactivating mutations in the PI3K catalytic subunit. (C)</p> Signup and view all the answers

    Study Notes

    General Cancer Information

    • Cancer develops from nonlethal genetic damage (mutation)
    • Environmental exposures, inherited germline mutations, and spontaneous random mutations can cause cancer
    • A tumor is formed by the clonal expansion of a single precursor cell with genetic damage
    • Tumors are clonal

    Molecular Basis of Cancer

    • Sustaining proliferative signaling
    • Avoiding immune destruction
    • Evading growth suppressors
    • Enabling replicative immortality
    • Deregulating cellular energetics
    • Resisting cell death
    • Inducing angiogenesis
    • Activating invasion and metastasis
    • Tumor-promoting inflammation
    • Genomic instability (mutator phenotype)

    Principal Cancer Targets

    • Growth-promoting proto-oncogenes
    • Growth-inhibiting tumor suppressor genes
    • Genes regulating programmed cell death (apoptosis)
    • Genes involved in DNA repair

    Cancer Development

    • Cancer develops through a stepwise acquisition of complementary mutations
    • Accumulation of driver and passenger mutations
    • Normal cell
    • Carcinogen-induced mutation
    • Mutation affecting genomic integrity
    • Initiated precursor with stem cell-like properties
    • Precursor with mutator phenotype
    • Additional driver mutations
    • Founding cancer cell
    • Additional mutations
    • Emergence of subclones
    • Acquisition of genomic instability
    • Acquisition of cancer hallmarks
    • Further genetic evolution
    • Genetically heterogeneous cancer
    • Diagnosis

    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 Damaging Agents

    • Chemicals
    • Radiation
    • Viruses
    • Normal cell
    • Successful DNA repair
    • DNA Damage
    • Failure of DNA repair
    • Mutations in the genome of somatic cells
    • Inherited mutations
    • Activation of growth-promoting oncogenes
    • Inactivation of tumor suppressor genes
    • Unregulated cell proliferation
    • Alterations in genes regulating apoptosis
    • Decreased apoptosis
    • Clonal expansion
    • Additional mutations
    • Angiogenesis
    • Escape from immunity
    • Tumor progression
    • Malignant neoplasm
    • Invasion and metastasis

    Normal Cell Cycle

    • Molecular regulation of cell cycle is critical in understanding cancer growth
    • Progression of cells through phases is orchestrated by cyclins and cyclin-dependent kinases (CDKs) and their inhibitors
    • Cell cycle checkpoints ensure accurate progression
    • G1/S transition and G2/M checkpoints are essential checkpoints regulating progression

    Main Cell-Cycle Components and Inhibitors

    • Cyclin-Dependent Kinases (CDKs)
    • CDK Inhibitors
    • Checkpoint Components

    Cell-Cycle Inhibitors

    • Activity of cyclin-CDK complexes is tightly regulated by inhibitors
    • Two main classes of CDK inhibitors: the Cip/Kip and INK4/ARF families, frequently altered in tumors
    • Cip/Kip-p21, p27, p57
    • INK4/ARF- p16INK4a, p14ARF

    Cell-Cycle Checkpoints

    • Cell cycle has internal controls called checkpoints
    • Two main checkpoints: One at the G1/S transition and another at the G2/M
    • Checkpoints require DNA damage sensors, signal transducers, and effector molecules

    G1/S Checkpoint

    • S phase is the point of no return in the cell cycle
    • Checkpoint checks for DNA damage before committing to replication
    • DNA repair is initiated
    • Apoptotic pathways are triggered if damage is unrepairable

    Normal Cell Cycle Diagrams

    • Charts illustrating the different stages of the cell cycle, showing checkpoints, and growth regulation pathways

    Functional Category of Oncogenes

    • Growth Factors
    • Growth Factor Receptors
    • Proteins Involved in Signal Transduction
    • Nuclear Regulatory Proteins
    • Cell-Cycle Regulators

    Selected Oncogenes, Their Mode of Activation, and Associated Human Tumors

    • Various oncogenes, their proto-oncogenes, mode of activation, and associated human tumors are provided in charts

    Oncogenic BRAF and PI3K Mutations

    • BRAF is a serine/threonine protein kinase
    • Activating BRAF mutations stimulate downstream kinases
    • Mutations in BRAF have been detected frequently in certain cancers
    • PI3K mutations affect catalytic subunits and increase enzyme activity

    Alterations in Nonreceptor Tyrosine Kinases

    • Chronic myelogenous leukemia (CML)
    • Acute lymphoblastic leukemias(ALL)
    • ABL gene translocation from chromosome 9 to chromosome 22, fusing with BCR gene
    • BCR-ABL tyrosine kinase results in chronically active oncogenic protein

    Transcription Factors

    • Signal transduction pathways converge on the nucleus
    • Include products of various proto-oncogenes like MYC, MYB,JUN, FOS, and REL, with MYC being commonly involved in human tumors

    Oncogenes, Oncoproteins, and Transcription Factors

    • MYC is among the most frequently mutated transcription factors in human tumors

    Cyclins and Cyclin-Dependent Kinases (CDKs)

    • Progression of cells through cell cycle through cyclin-dependent kinases (CDKs)
    • CDKs are activated by binding to cyclins
    • CDKs-cyclin complexes phosphorylate proteins
    • G1/S and G2/M checkpoints are critical
    • Regulation by growth-promoting/suppressing factors and DNA damage sensors

    Oncogenes, Oncoproteins, and Unregulated Cell Proliferation

    • Proto-oncogenes are normal cellular genes that promote cell proliferation
    • Oncogenes are mutated/overexpressed proto-oncogenes that act independently of growth promoters
    • Oncoproteins are encoded by oncogenes and drive cell proliferation
    • Constitutive expression of oncogenes promotes unregulated cell growth (cancer)

    Additional Notes

    • Multiple mechanisms involved in cancer development and progression
    • Mutations, deregulation, alterations in pathways, and gene rearrangements are among the factors
    • Multiple types of cancers, their characteristics, and molecular drivers are listed
    • Tumors are heterogeneous and have complex pathways leading to them
    • Detailed examples of molecular processes behind specific cancers are also provided.
    • Charts and diagrams help illustrate the processes and pathway relationships

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