Cancer Biology: Tumor Suppressor Genes
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Questions and Answers

What type of tumor is associated with the risk of medulloblastoma?

  • Cerebellar tumor (correct)
  • Renal cell tumor
  • Pheochromocytoma
  • Retinal angioma
  • What syndrome is caused by a loss-of-function mutation in the STK11 (LKB1) gene?

  • Von Hippel-Lindau Syndrome
  • Marfan Syndrome
  • Peutz-Jeghers Syndrome (correct)
  • Gardner Syndrome
  • Which apoptotic factor is most commonly inhibited in cancers?

  • APAF
  • Caspase 3
  • Fas/CD95 (correct)
  • BCL-2
  • What is a critical factor for the immortality of cancer cells?

    <p>Evasion of senescence</p> Signup and view all the answers

    What biological process is indicated by telomere shortening during cell division?

    <p>Apoptosis activation</p> Signup and view all the answers

    How do tumors with increased glucose metabolism relate to imaging techniques?

    <p>They can be visualized via PET scans</p> Signup and view all the answers

    What is suggested by the presence of telomerase activity in cancer cells?

    <p>Capacity for self-renewal exists</p> Signup and view all the answers

    What is the minimum tumor size that typically requires blood supply for its growth?

    <p>2mm</p> Signup and view all the answers

    What effect does a mutation in APC have on tumor cells?

    <p>It allows β-catenin to enter the nucleus without WNT binding.</p> Signup and view all the answers

    Which tumor suppressor gene is associated with benign bilateral schwannomas?

    <p>NF2</p> Signup and view all the answers

    Which of the following is a characteristic feature of carcinomas related to E-cadherin mutation?

    <p>Loss of contact inhibition.</p> Signup and view all the answers

    What is the role of PTCH1 in tumor suppression?

    <p>It negatively regulates the Hedgehog signaling pathway.</p> Signup and view all the answers

    What results from reduced expression of E-cadherin in cancer cells?

    <p>Easier disaggregation and invasion of cells.</p> Signup and view all the answers

    What is a consequence of a loss-of-function mutation in E-cadherin?

    <p>Formation of malignant phenotypes.</p> Signup and view all the answers

    Which tumor is associated with a mutation on chromosome 11p13?

    <p>Wilms tumor</p> Signup and view all the answers

    What syndrome is caused by germline loss-of-function mutations in PTCH1?

    <p>Gorlin's Syndrome</p> Signup and view all the answers

    What type of mutation in tumor suppressor genes is sufficient to allow tumor proliferation?

    <p>Single allele mutation causing haploinsufficiency</p> Signup and view all the answers

    How do loss-of-function mutations in DNA repair genes contribute to cancer development?

    <p>By impairing the cell's ability to repair DNA damage</p> Signup and view all the answers

    Which process allows tumor cells to proliferate without external growth signals?

    <p>Self-sufficiency in growth signals</p> Signup and view all the answers

    What is characterized by the switch to aerobic glycolysis in cancer cells?

    <p>Warburg effect</p> Signup and view all the answers

    What type of mutations in the PIK3 gene are commonly associated with breast carcinomas?

    <p>Gain-of-function mutations</p> Signup and view all the answers

    Which of the following oncogenes is tightly regulated and involved in immediate early response genes?

    <p>MYC</p> Signup and view all the answers

    What is the primary consequence of apoptosis-regulating gene mutations in cancer cells?

    <p>Decreased cell death</p> Signup and view all the answers

    What characteristic of cancer is associated with the ability to invade and metastasize?

    <p>Ability to undergo limitless replication</p> Signup and view all the answers

    What is the consequence of MYC translocation in the context of cancer?

    <p>It leads to the overexpression of telomerase.</p> Signup and view all the answers

    Which of the following is NOT a hallmark of cancer?

    <p>Increased sensitivity to environmental stimuli</p> Signup and view all the answers

    What type of genetic alteration is responsible for creating a constitutively active BCR-ABL tyrosine kinase?

    <p>Chromosomal translocation</p> Signup and view all the answers

    In which type of cancer is loss-of-function of the PTEN suppressor gene commonly observed?

    <p>Endometrial carcinoma</p> Signup and view all the answers

    What phenomenon is described as mutations accumulating in a stepwise fashion over time leading to cancer?

    <p>Mutator phenotype</p> Signup and view all the answers

    What is a primary function of the MYC oncogene?

    <p>Activates expression of growth-related genes</p> Signup and view all the answers

    What type of genetic abnormality is linked to NMYC amplification in cancer?

    <p>Neuroblastoma</p> Signup and view all the answers

    Which treatment is commonly used for Chronic Myelogenous Leukemia (CML) due to its efficacy in inhibiting the BCR-ABL kinase?

    <p>Imatinib mesylate</p> Signup and view all the answers

    What is the primary factor stabilizing HIF1α under conditions of low oxygen?

    <p>Relative lack of oxygen or hypoxia</p> Signup and view all the answers

    Which factor is NOT typically associated with the promotion of angiogenesis in tumors?

    <p>Angiostatin</p> Signup and view all the answers

    What mechanism directly contributes to the abnormal vasculature seen in tumors?

    <p>Neovascularization or vasculogenesis</p> Signup and view all the answers

    Which growth factor is typically associated with the increase of ligands that activate the Notch signaling pathway in angiogenesis?

    <p>VEGF</p> Signup and view all the answers

    What role do matrix metalloproteinases (MMPs) play in cancer progression?

    <p>They degrade the basement membrane and connective tissue</p> Signup and view all the answers

    What is the primary consequence of the increased growth factor secretion in angiogenic tumors?

    <p>Formation of new blood vessels</p> Signup and view all the answers

    In the context of cancer metabolism, what characterizes the Warburg effect?

    <p>A shift towards aerobic glycolysis irrespective of oxygen levels</p> Signup and view all the answers

    What cellular change is indicated by the downregulation of E-cadherins in the metastatic cascade?

    <p>Enhanced detachment of tumor cells from one another</p> Signup and view all the answers

    Study Notes

    Tumor Suppressor Genes

    • Tumor suppressor genes (TSGs) prevent uncontrolled cell growth and division.
    • Loss-of-function mutations in TSGs allow cells to proliferate without any control.
    • In most cases, both alleles of the tumor suppressor gene need to be mutated before cancer occurs.
    • Haploinsufficiency refers to a condition where a single allele mutation in the TSG is sufficient to allow tumor proliferation.
    • Apoptosis-regulating genes can acquire mutations that either increase or decrease cell death, ultimately impacting cancer progression.
    • Loss-of-function mutations in DNA repair genes contribute to cancer by impairing the cell's ability to fix DNA damage, resulting in increased mutations and genomic instability.

    Hallmarks of Cancer

    • Cancer cells exhibit various hallmarks, characteristics that distinguish them from normal cells.
    • Self-sufficiency in growth signals: Tumor cells possess the ability to proliferate without any external stimuli due to oncogene activation.
    • Insensitivity to growth inhibitory signals: Cancer cells can bypass normal cell cycle checkpoints and continue dividing even in the presence of inhibitory signals.
    • Altered cellular metabolism: Cancer cells often switch to aerobic glycolysis, known as the Warburg effect, to generate energy and macromolecules.
    • Evasion of apoptosis: Cancer cells acquire mutations that allow them to evade programmed cell death, ensuring their survival and further proliferation.
    • Limitless replicative potential: Cancer cells become immortal due to their ability to bypass replicative senescence and overcome the Hayflick limit.
    • Sustained angiogenesis: Cancer cells induce the formation of new blood vessels (angiogenesis) to provide oxygen and nutrients, and facilitate tumor growth.
    • Ability to invade and metastasize: Cancer cells can invade surrounding tissues and spread to distant locations through metastasis.

    MYC Oncogene

    • MYC proto-oncogene is a key regulator of cell growth and proliferation.
    • It is tightly regulated under normal conditions.
    • MYC is involved in various types of cancer, including Burkitt's lymphoma, neuroblastoma, and other B and T cell tumors.
    • MYC mutations, such as translocations and amplifications, can lead to uncontrolled cell growth and cancer development.

    RAS

    • RAS is a proto-oncogene involved in intracellular signaling pathways.
    • Loss-of-function mutations in RAS can cause it to be trapped in an active, signaling state, leading to continuous cell proliferation.

    PI3K and PTEN

    • PI3K is a key signaling pathway involved in cell growth, survival, and metabolism.
    • Mutations in PI3K, particularly gain-of-function mutations, are found in a significant percentage of cancers.
    • PTEN is a tumor suppressor gene that counteracts the activity of PI3K.
    • Loss-of-function mutations in PTEN contribute to cancer development.

    E-Cadherin

    • E-cadherin is a cell adhesion protein that helps maintain cell-cell junctions.
    • Mutations in E-cadherin can lead to loss of contact inhibition, allowing cells to detach from each other.
    • This detachment facilitates tumor cell invasion and metastasis.
    • Reduced E-cadherin expression is observed in various types of carcinomas.
    • Germline loss-of-function mutations in the E-cadherin gene can cause familial gastric carcinoma.

    NF2 (Neurofibromatosis Type 2)

    • NF2 is a tumor suppressor gene involved in the regulation of cell growth and adhesion.
    • Germline mutations in NF2 predispose individuals to neurofibromatosis type 2.
    • Somatic mutations in NF2 are observed in sporadic meningiomas and ependymomas.
    • Neurofibromin 2 (Merlin), the protein product of NF2, is responsible for maintaining cell-cell junctions and regulating cell growth.

    APC

    • APC is a tumor suppressor gene involved in the Wnt signaling pathway, regulating cell proliferation and differentiation.
    • Mutations in APC can lead to the uncontrolled accumulation of β-catenin in the nucleus, promoting cell division.
    • Somatic mutations in APC are found in familial adenomatous polyposis (FAP) and sporadic colorectal cancer.

    PATCHED

    • PTCH1 is a tumor suppressor gene that encodes a protein called PATCHED1, which regulates the Hedgehog signaling pathway.
    • Mutations in PTCH1 can lead to the overactivation of Hedgehog signaling, promoting cell proliferation and tumor growth.
    • Germline mutations in PTCH1 cause Gorlin's Syndrome, also known as nevoid basal cell carcinoma syndrome.

    VHL (Von Hippel-Lindau)

    • VHL is a tumor suppressor gene involved in the regulation of oxygen sensing and angiogenesis.
    • Mutations in VHL can lead to the uncontrolled growth of blood vessels, promoting tumor development.
    • Germline mutations in VHL are associated with Von Hippel-Lindau syndrome, a multi-organ disorder characterized by various tumors.

    STK11 (LKB1)

    • STK11 is a tumor suppressor gene that encodes a serine/threonine kinase, playing a role in cellular metabolism and growth regulation.
    • Mutations in STK11 can lead to the development of Peutz-Jeghers syndrome, characterized by benign polyps in the gastrointestinal tract.

    WARBURG EFFECT

    • The Warburg effect is a metabolic hallmark of cancer cells, characterized by increased glucose uptake and aerobic glycolysis.
    • Cancer cells rely on glucose fermentation to produce ATP and generate biomass.
    • Elevated glucose uptake in cancer cells allows them to be visualized using positron emission tomography (PET) scans.

    EVASION OF APOPTOSIS

    • Cancer cells often evade apoptosis, or programmed cell death, to survive and proliferate.
    • This evasion can occur through various mechanisms, including reduced levels of Fas/CD95, inactivation of caspase 8, upregulation of anti-apoptotic factors (BCL-2, BCL-XL, MCL-1), loss of P53, and upregulation of inhibitors of apoptosis (IAPs).

    LIMITLESS REPLICATIVE POTENTIAL

    • Cancer cells exhibit limitless replicative potential, due to their ability to bypass the Hayflick limit and overcome senescence.
    • Cancer cells often express telomerase, an enzyme that maintains telomere length, preventing the shortening of telomeres associated with cell division and senescence.

    SUSTAINED ANGIOGENESIS

    • As tumors grow, they require a constant supply of oxygen and nutrients, which necessitates angiogenesis, the formation of new blood vessels.
    • The angiogenic switch refers to the transition from a dormant state to an angiogenic state, often driven by hypoxia.
    • This switch results in the activation of pro-angiogenic factors, such as VEGF and FGF, and the repression of angiogenesis inhibitors.

    INVASION

    • Invasion is a crucial step in the metastasis of cancer cells.
    • To invade, tumor cells must detach from their surrounding cells, degrade the extracellular matrix, and migrate through tissues.
    • The loss of cell-cell adhesion, driven by factors such as decreased E-cadherin expression and secretion of proteolytic enzymes, facilitates invasion.
    • Matrix metalloproteinases (MMPs) are a family of proteolytic enzymes that break down the extracellular matrix, allowing cancer cells to penetrate surrounding tissues.

    METASTASIS

    • Metastasis is the spread of cancer cells from the primary tumor site to distant locations.
    • The metastatic cascade encompasses a series of steps, including invasion, intravasation, circulation, extravasation, and colonization.
    • Metastasis is a complex process involving various cellular and molecular events, and the specific steps and mechanisms can vary among cancer types.

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    Description

    This quiz covers the role of tumor suppressor genes in cancer biology, detailing how their mutations contribute to uncontrolled cell proliferation. Explore the differences between haploinsufficiency and loss-of-function mutations, along with their implications for cancer progression and genomic stability.

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