Neoplasia III: Tumour Occurrence
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Questions and Answers

Which of the following conditions is primarily associated with inherited susceptibility to tumors?

  • Xeroderma pigmentosum (correct)
  • Cirrhosis
  • Ulcerative colitis
  • Chronic atrophic gastritis

    • Which of the following oncogenes is associated with breast cancer?

  • p53
  • ras
  • retinoblastoma
  • c-erbB-2 (HER-2) (correct)

    • What stage of carcinogenesis involves the promotion of tumor growth after initiation?

  • Promotion (correct)
  • Initiation
  • Progression
  • Metastasis

    • Which of the following factors is classified as an extrinsic factor contributing to tumor development?

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

    Which of the following medical conditions is associated with an increased risk of malignancy?

    <p>Hashimoto’s thyroiditis (C), Cirrhosis (D)</p> Signup and view all the answers

    Which of the following represents an intrinsic factor associated with cancer development?

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

    What type of tumor is familial adenomatous polyposis predominantly associated with?

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

    Which agent is known to induce mutations leading to cancer development?

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

    What is the most important polycyclic aromatic hydrocarbon that is converted to its active form by hydroxylation?

    <p>3,4-Benzpyrene (C)</p> Signup and view all the answers

    Which chemical compound is converted in the liver to a compound that contributes to bladder cancer?

    <p>B-naphthalamines (C)</p> Signup and view all the answers

    Which virus is associated with Burkitt's lymphoma?

    <p>Epstein-Barr virus (A)</p> Signup and view all the answers

    What type of cancer is associated with the hormonal factors mentioned in the content?

    <p>Breast cancer (B)</p> Signup and view all the answers

    Which of the following is a known environmental carcinogen linked to mesothelioma?

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

    What is the role of oncogenes in cancer development?

    <p>Stimulation of cell growth and division (D)</p> Signup and view all the answers

    Which genetic change can lead to the activation of oncogenes?

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

    Which condition is characterized by a defect in DNA repair mechanisms leading to photosensitivity?

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

    What factor is NOT typically associated with an increased incidence of cancer?

    <p>Adolescent lifestyle choices (B)</p> Signup and view all the answers

    What type of genetic alteration is associated with Li Fraumeni syndrome?

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

    Which type of damage to DNA is commonly caused by high doses of radiation?

    <p>Double stranded breaks (C)</p> Signup and view all the answers

    What role do promoters play in chemical carcinogenesis?

    <p>They can induce tumors in initiated cells. (C)</p> Signup and view all the answers

    What is a defining characteristic of direct-acting chemical carcinogens?

    <p>Do not require metabolic conversion. (B)</p> Signup and view all the answers

    Which type of cancer has been linked to unprotected miners exposed to ionizing radiation?

    <p>Lung cancer (B)</p> Signup and view all the answers

    Which of the following is NOT an extrinsic factor that can lead to DNA damage?

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

    What is the consequence of the initiation step in chemical carcinogenesis?

    <p>It results in sufficient changes to cells to make them capable of tumorigenesis. (D)</p> Signup and view all the answers

    What role does p53 play in cellular function?

    <p>It encodes a protein for DNA repair and apoptosis. (A)</p> Signup and view all the answers

    Which of the following statements about oncogenes is true?

    <p>Mutations in oncogenes can lead to uncontrolled cell growth. (C)</p> Signup and view all the answers

    How do mutations in DNA repair genes influence cancer development?

    <p>They lead to increased mutation rates in other genes. (D)</p> Signup and view all the answers

    What percentage of retinoblastoma cases are familial?

    <p>40% (C)</p> Signup and view all the answers

    What chromosomal location is associated with the p53 gene?

    <p>Chromosome 17q (A)</p> Signup and view all the answers

    The progression phase in carcinogenesis is primarily characterized by what factor?

    <p>Accumulation of genetic alterations. (D)</p> Signup and view all the answers

    What is a common outcome of familial retinoblastoma patients as they reach their teenage years?

    <p>Development of osteosarcoma. (A)</p> Signup and view all the answers

    Which DNA repair system defect is specifically linked to cancer development?

    <p>Mismatch repair dysfunction. (B)</p> Signup and view all the answers

    Flashcards

    What causes cancer?

    Changes to the genetic code that lead to the development of cancer. Can be caused by external factors like radiation or chemicals, or internal factors like genetics.

    Extrinsic factors

    Factors that influence the development of cancer from outside the body, such as exposure to radiation or carcinogenic chemicals.

    Intrinsic factors

    Factors that influence the development of cancer from within the body, such as genetic predisposition or immune system deficiencies.

    Inherited susceptibility to tumors

    Inherited conditions that increase the risk of developing tumors, often due to defects in DNA repair mechanisms.

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    Oncogenes

    Genes that promote cell growth and division. When mutated, they can contribute to uncontrolled cell growth, leading to cancer.

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    Tumor suppressor genes (TSG)

    Genes that suppress cell growth and division. When mutated or inactive, they can fail to control cell growth, leading to cancer.

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    Carcinogenesis

    A multi-step process in which normal cells are transformed into cancer cells through a series of genetic and epigenetic alterations.

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    Initiation (in carcinogenesis)

    The initial event in carcinogenesis, where a DNA mutation occurs, potentially causing the first step in tumor development.

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    Carcinogens

    Chemicals that can cause cancer. Examples include polycyclic aromatic hydrocarbons (found in coal tar and cigarette smoke), aromatic amines (found in rubber and aniline dyes), and nitrosamines (formed by gut bacteria from dietary nitrates/nitrites).

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    Polycyclic Aromatic Hydrocarbons

    A type of carcinogen found in coal tar, cigarette smoke, and other sources. It's converted to an active form in the body through a process called hydroxylation.

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    Aromatic Amines

    A group of chemicals, some of which are carcinogens, found in rubber and aniline dyes.

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    Nitrosamines

    A type of carcinogen produced by gut bacteria when they convert dietary nitrates/nitrites. They can lead to gastrointestinal cancers.

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    Tumor Suppressor Genes

    Genes that normally suppress tumor development. When these genes are inactivated or mutated, they can contribute to cancer development.

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    DNA Repair Genes

    Genes that normally repair damaged DNA. Inactivation or mutations in these genes can increase the risk of cancer, as damaged DNA is not repaired effectively.

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    Cancer

    A collection of genetically altered cells that grow and divide uncontrollably, often forming a tumor.

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    Ras

    A type of oncogene involved in intracellular signaling, often mutated in cancers like colon and lung cancer.

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    c-erbB-2 (HER-2)

    A growth factor receptor that, when amplified, can lead to increased cell growth and contribute to breast cancer development.

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    p53

    A tumor suppressor gene that plays a crucial role in DNA repair, cell cycle control, and apoptosis.

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    BRACA1

    A type of DNA repair gene, mutations in which can increase the risk of developing various cancers, including breast cancer.

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    Accumulation of alterations

    A hallmark of cancer, meaning that many mutations accumulate over time in various genes, contributing to the development of a tumor.

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    Xeroderma Pigmentosum (XP)

    A rare genetic disorder characterized by increased sensitivity to sunlight, leading to skin pigmentation abnormalities and a high risk of skin cancer. It results from defects in DNA repair mechanisms, specifically nucleotide excision repair (NER), which is crucial for removing damaged DNA caused by ultraviolet radiation.

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    Ataxia Telangiectasia (AT)

    A genetic disorder characterized by an increased risk of developing cancer, particularly leukemia. It occurs due to defects in DNA repair pathways, specifically non-homologous end joining (NHEJ), which is crucial for repairing double-strand breaks in DNA. This defect leaves cells vulnerable to damage from radiation and other DNA-damaging agents.

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    Fanconi Anemia (FA)

    A rare genetic disorder characterized by an increased risk of leukemia and other cancers. It results from defects in the Fanconi anemia pathway, which is involved in repairing DNA damage caused by cross-linking agents, which link strands of DNA together. This defect leads to impaired DNA repair and increased genomic instability.

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    Familial Adenomatous Polyposis (FAP)

    A genetic predisposition to colon cancer characterized by multiple polyps in the colon. It arises due to mutations in the APC (adenomatous polyposis coli) gene, a tumor suppressor gene involved in regulating cell growth and division.

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    Hereditary Nonpolyposis Colon Cancer (HNPCC)

    A genetic predisposition to colorectal cancer characterized by an increased risk of developing colon, endometrial, and other cancers. It occurs due to mutations in mismatch repair genes (MMR), which are involved in correcting errors during DNA replication, leading to increased genomic instability.

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    Li-Fraumeni Syndrome (LFS)

    A genetic syndrome associated with an increased risk of various cancers, including leukemia, sarcoma, and breast cancer. It arises due to mutations in the p53 tumor suppressor gene, a critical regulator of cell growth and DNA repair.

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    Familial Breast/Ovarian Cancer (BRCA1/BRCA2)

    A genetic predisposition to breast and ovarian cancer characterized by an increased risk of developing these cancers. It occurs due to mutations in the BRCA1 or BRCA2 genes, which are involved in DNA repair and cell cycle regulation.

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    Retinoblastoma

    A genetic disorder leading to an increased risk of developing retinoblastoma, a rare but aggressive eye cancer. It arises from mutations in the RB1 gene, a tumor suppressor gene that controls cell cycle progression and prevents uncontrolled cell division.

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    Study Notes

    Neoplasia III: Tumour Occurrence

    • Tumour development is attributed to alterations or mutations in the genetic code.
    • Tumours can be induced in somatic cells by extrinsic factors (carcinogens, chemicals, radiation, viruses) and intrinsic factors (heredity, 5%).
    • Intrinsic factors include inheritance, host factors (age, immune system, hormones), and conditions predisposing to tumours (related to DNA repair).
    • Inherited conditions increase susceptibility to specific or groups of tumours due to altered genes.
    • DNA repair mechanisms play a vital role in preventing tumour development
    • Defects in DNA repair mechanisms are associated with inherited predispositions to tumours. (Xeroderma pigmentosa, Ataxia telangiectasia, Fanconi's anaemia).

    Objectives of Neoplasia

    • Understand inherited susceptibility to tumour development (Xeroderma pigmentosa, Ataxia telangiectasia).
    • Understand the inheritance of certain tumours (Familial adenomatous polyposis, Breast cancer, Retinoblastoma).
    • Understand the functions of oncogenes and tumour suppressor genes (TSG) and their changes in neoplasia, particularly the role of oncogenes (ras, c-myc, c-erbB-2 (HER-2)) and TSG (retinoblastoma, p53).
    • Recognize the stages in carcinogenesis (initiation, promotion).
    • Identify agents that cause tumour development and their mechanisms of action (radiation, chemicals, viruses, hormonal, asbestos, aflatoxins, parasites).
    • Identify occupations (asbestos exposure, dye industry) and medical conditions (ulcerative colitis, cirrhosis, Hashimoto's thyroiditis, chronic atrophic gastritis) associated with an increased risk of malignancy.
    • Recognize geographical variations in the incidence of malignant tumours (gastric cancer, breast cancer, Burkitt's lymphoma).

    Causes of Cancer

    • Changes in genetic code (alterations/mutations) cause cancer.
    • Extrinsic factors: Carcinogens, chemicals, radiation, some viruses.
    • Intrinsic factors: Hereditary (5%).

    Intrinsic Factors

    • Inheritance: Inherited conditions predisposing to tumour development related to DNA repair.
    • Host factors: Age, immune system, hormones.

    Extrinsic Factors

    • Radiation: (UV, ionizing)
    • Chemicals: Polycyclic hydrocarbons, aromatic amines, nitrosamines
    • Viruses: (Epstein Barr, Hepatitis)
    • Other Factors: Hormones, Aflatoxins, Parasites

    Radiation

    • Evidence linking radiation to cancer includes skin cancer in radiologists, increased lung cancer risk in unprotected miners exposed to ionizing radiation, and increased risk of thyroid carcinoma in children from H&N radiotherapy.
    • Hiroshima bombing: initial cancers included leukaemia and lymphoma; later-occurring cancers included breast and thyroid cancer.
    • Radiation causes various DNA damage (single/double-strand breaks, base damage), the impact varies with exposure type and dose.

    Chemical Carcinogenesis

    • Carcinogens interact with DNA in various ways, causing specific base damage and single-strand breaks.
    • Damage is often repaired, but potentially imperfectly.
    • Carcinogens can be directly acting (with no metabolic conversion, like alkylating agents) or indirectly acting (requiring metabolic conversion, like polycyclic hydrocarbons).
    • Polycyclic aromatic hydrocarbons (PAH) are found in coal tar and cigarette smoke; 3,4-Benzpyrene is an example.
    • Aromatic amines (e.g., B-naphthalamines) are implicated in bladder cancer in certain industries.
    • Nitrosamines form from dietary nitrates/nitrites in the gut, leading to gastrointestinal cancer.

    Steps in Chemical Carcinogenesis

    • Initiation: Exposure to sufficient dose of initiating agent causes permanent DNA damage (mutation) in a cell, making it capable of tumour development.
    • Promotion: Promoters induce tumours in initiated cells, but they themselves are not tumorigenic. The tumour would not result if the promoter agent is applied before the initiating agent.
    • Progression: Changes in multiple genes promote neoplastic cell growth.

    Viruses

    • Hepatitis B: Associated with hepatocellular carcinoma.
    • Epstein Barr: Linked to Burkitt's lymphoma and nasopharyngeal carcinoma.
    • Human Papillomavirus (HPV): Implicated in cervical carcinoma.

    Other Agents

    • Asbestos: Mesothelioma.
    • Aflatoxins: Liver cancer.
    • Schistosoma: Bladder cancer.
    • Helicobacter: Gastric cancer and lymphoma
    • Hormones (oestrogen and androgen): Breast and liver cancer respectively

    Geographical Variation in Malignant Tumours

    • Genetic factors: Tight family clusters linked to certain types of cancers.
    • Viruses: Hepatitis B and Epstein-Barr viruses.
    • Parasites: Schistosoma.
    • Diet: Gastric cancer in Japan.
    • Other factors: Reproduction and breast/cervical cancer.

    Predisposing Factors

    • Ulcerative colitis: Colorectal carcinoma
    • Liver cirrhosis: Liver cancer
    • Adenoma of the large intestine: Adenocarcinoma

    Host Factors

    • Age: Cancer incidence increases with age.
    • Cumulative exposure to carcinogens.
    • Latency.
    • Accumulating genetic lesions
    • Innate defence
    • Immune factors
    • Hormones

    Molecular Bases of Cancer

    • Cancer is a genetic disease, meaning tumour cells contain genetically altered DNA (point mutation, deletion, translocation).
    • Cancer cells evade natural defence mechanisms like DNA damage repair and apoptosis.

    Genes Involved in Cancer

    • Oncogenes: Proto-oncogenes, altered (amplification, mutation, translocation) to oncogenes, contribute to uncontrolled cell growth and decreased apoptosis, e.g., c-myc, ras, c-erbB-2.
    • Tumour suppressor genes: Normally suppress cell growth; loss/alteration leads to loss of growth suppression, e.g., Retinoblastoma protein (RB) and p53.
    • DNA repair genes: Ensure accurate DNA copying during cell division; mutation increases other gene mutations, e.g., BRCA1, BRCA2, non-polyposis colon cancer (HNPCC) genes.

    p53

    • p53 is a tumour suppressor gene.
    • It's a guardian of the genome.
    • It's a transcription factor on chromosome 17q.
    • Mutated in >50% of cancers
    • It helps in cell repair and prevents cell division if there is heavy damage, therefore halting development of the tumour.
    • p53 regulates cell-cycle arrest, apoptosis, DNA repair, cellular senescence, and angiogenesis, in response to cellular stress,

    DNA Repair Genes

    • These genes ensure accurate DNA copying during cell division.
    • Mutations in DNA repair genes increase the frequency of mutations in other genes (TSG and oncogenes).
    • Defects in DNA repair systems (mismatch repair, nucleotide excision repair, recombination repair) contribute to various cancers.
    • Breast cancer susceptibility genes (BRCA1 and BRCA2) and hereditary non-polyposis colon cancer genes are examples of DNA repair genes.

    Mechanisms in Carcinogenesis

    • A long period of time passes between stimulus exposure and the development of clinical cancer.
    • Different stages: Initiation, Promotion, Progression
    • Factors like genetic factors, DNA repair, local tissue response, immune response impact stimulus-effect during carcinogenesis.
    • Tumour development is an accumulation of alterations, not just a single gene change.

    Hallmarks of Cancer

    • Key characteristics of cancer: Evading apoptosis, self-sufficiency in growth signals, insensitivity to anti-growth signals, tissue invasion & metastasis, sustained angiogenesis, and limitless replicative potential.

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    Neoplasia III Past Paper 2024-2025 PDF

    Description

    Explore the key factors influencing tumour development in this quiz on Neoplasia III. Learn about the roles of intrinsic and extrinsic factors, including genetic mutations and inherited conditions that predispose individuals to various tumours. Understand how DNA repair mechanisms play a critical role in preventing tumour formation.

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