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Questions and Answers
What type of tumor is associated with the risk of medulloblastoma?
What syndrome is caused by a loss-of-function mutation in the STK11 (LKB1) gene?
Which apoptotic factor is most commonly inhibited in cancers?
What is a critical factor for the immortality of cancer cells?
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What biological process is indicated by telomere shortening during cell division?
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How do tumors with increased glucose metabolism relate to imaging techniques?
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What is suggested by the presence of telomerase activity in cancer cells?
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What is the minimum tumor size that typically requires blood supply for its growth?
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What effect does a mutation in APC have on tumor cells?
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Which tumor suppressor gene is associated with benign bilateral schwannomas?
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Which of the following is a characteristic feature of carcinomas related to E-cadherin mutation?
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What is the role of PTCH1 in tumor suppression?
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What results from reduced expression of E-cadherin in cancer cells?
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What is a consequence of a loss-of-function mutation in E-cadherin?
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Which tumor is associated with a mutation on chromosome 11p13?
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What syndrome is caused by germline loss-of-function mutations in PTCH1?
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What type of mutation in tumor suppressor genes is sufficient to allow tumor proliferation?
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How do loss-of-function mutations in DNA repair genes contribute to cancer development?
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Which process allows tumor cells to proliferate without external growth signals?
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What is characterized by the switch to aerobic glycolysis in cancer cells?
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What type of mutations in the PIK3 gene are commonly associated with breast carcinomas?
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Which of the following oncogenes is tightly regulated and involved in immediate early response genes?
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What is the primary consequence of apoptosis-regulating gene mutations in cancer cells?
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What characteristic of cancer is associated with the ability to invade and metastasize?
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What is the consequence of MYC translocation in the context of cancer?
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Which of the following is NOT a hallmark of cancer?
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What type of genetic alteration is responsible for creating a constitutively active BCR-ABL tyrosine kinase?
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In which type of cancer is loss-of-function of the PTEN suppressor gene commonly observed?
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What phenomenon is described as mutations accumulating in a stepwise fashion over time leading to cancer?
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What is a primary function of the MYC oncogene?
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What type of genetic abnormality is linked to NMYC amplification in cancer?
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Which treatment is commonly used for Chronic Myelogenous Leukemia (CML) due to its efficacy in inhibiting the BCR-ABL kinase?
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What is the primary factor stabilizing HIF1α under conditions of low oxygen?
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Which factor is NOT typically associated with the promotion of angiogenesis in tumors?
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What mechanism directly contributes to the abnormal vasculature seen in tumors?
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Which growth factor is typically associated with the increase of ligands that activate the Notch signaling pathway in angiogenesis?
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What role do matrix metalloproteinases (MMPs) play in cancer progression?
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What is the primary consequence of the increased growth factor secretion in angiogenic tumors?
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In the context of cancer metabolism, what characterizes the Warburg effect?
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What cellular change is indicated by the downregulation of E-cadherins in the metastatic cascade?
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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.