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cancer is fundamentally a

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genetic disorder, arising from genetic alterations in multiple genes that affect cell signaling and cell cycle control.

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Germline mutations:

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Accounts for 5% to 10% of cancer cases, which are called familial cancer. The mutations are present in every cell of the body and are passed from parent to child. e.g. p53, BRCA1, BRCA2, Rb, pTEN

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Somatic mutations:

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Accounts for the majority of cancer cases, which are called sporadic cancer. The mutations are not in every cell of the body and are not passed from parent to child. e.g. mutations in EGFR, RAS, HER2 etc.

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Activation of oncogene: (3)

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1. Mutation (deletion, activation, overexpression; retrovirus) 2. Amplification 3. Translocation

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Inactivation Tumor Suppressor Gene

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1. Mutation 2. Deletion 3. Epigenetic regulation (DNA methylation)

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Mutation of RB gene cause cells to pass through the

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G1/S checkpoint without the normal controls

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P53 tumor suppressor protein is

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the guardian of the genome"

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he p53 protein acts as

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brake pedal to halt cell growth and division at G2/M, allowing DNA repair.

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Clonal Evolution of tumors

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Further genetic changes and micro-environmental influences lead to heterogeneity in the properties of individual cells within the tumors.

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CML leukemic cells

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chromosome translocation BCR-ABL functions as a constantly active tyrosine kinase; - Forced expression of BCR-ABL in the bone marrow cells caused leukemia in mice

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1. Most cancers are assumed to arise through which of the following? a. Errors in transcription b. The production of unbalanced gametes because of nondisjunction during meiosis. c. Genetic or epigenetic changes in somatic cells d. Delayed cell division during early embryogenesis e. None of the above answers is correct.

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c. genetic or epigenetic changes in somatic cells

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2. Which of the following is the major event associated with the retinoblastoma cancer? a. A translocation involving chromosomes 9 and 22 b. Both copies of a tumor-suppressor gene are inactivated c. A translocation results in the enhanced expression of an oncogene d. A mutation results in an activated RAS oncogene e. Inactivation of a major DNA repair system

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b. Both copies of a tumor-suppressor gene are inactivated

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3. The process by which genetic changes occur in tumors and allows them to become increasingly aggressive over time is called? a. Clonal evolution b. Metastasis c. Loss of heterozygosity d. Epigenetic evolution e. Signal transduction

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a. clonal evolution

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4. Which of the following is a process whereby cancer cells travel to other sites in the body and establish secondary tumors? a. Oncogenesis b. Angiogenesis c. Malignancy d. Secondary tumorigenesis e. Metastasis

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e. metastasis

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5. Mutations in proto-oncogenes are generally _________ whereas mutations in tumor-suppressor alleles are generally ______________. a. Deletions; duplications b. Recessive; dominant c. Duplications; deletions d. Dominant; recessive e. Deletions; base-pair substitutions

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d. dominant, recessive

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6. Which of the following groups of proteins is NOT commonly known to include oncogenes? a. Transcription factors b. Growth factors c. Signal-transduction proteins d. Ion channels e. Growth factor receptors

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d. iron channels

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7. Normal cellular genes whose products are involved in facilitating cell division to occur under appropriate conditions are called? a. Proto-oncogenes b. Tumor-suppressor genes c. Passenger genes d. Inhibitor genes e. Driver genes

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a. protogenes

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8. The normal activity of the retinoblastoma (Rb) protein in the cell is to: a. Inhibit p53 activity b. Suppress transcription of tumor suppressor genes c. Regulate the progression of from G1 to S in the cell cycle d. Induce cyclin-CDK complex formation e. Block the initiation of anaphase during the cell cycle

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c.

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9. Which of the following chromosomal abnormalities is associated with chronic myelogenous leukemia? a. A deletion b. An inversion c. A duplication d. A reciprocal translocation e. An aneuploidy involving one of the shorter autosomal chromosomes

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d. reciprocal translocation

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10. In Burkitt lymphoma, there is increased expression of the MYC gene. Which of the following best explains this situation? a. A chromosome deletion has removed a tumor suppressor gene. b. A chromosome deletion has removed an oncogene. c. A chromosome duplication that involves a segment with an oncogene. d. A translocation has brought the MYC gene next to a different regulatory region. e. The MYC gene has been amplified.

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d. A translocation has brought the MYC gene next to a different regulatory region.

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11. What are oncogenes and tumor-suppressor genes? How are they involved in carcinogenesis?

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Answer: The control of the cell division cycle is regulated by stimulatory genes (oncogenes) and inhibitory genes (tumor-suppressor genes), and mutations in either type can lead to cancer by deregulating cellular processes such as cell growth and division, survival, and differentiation. Mutations in an oncogene can lead to an overactive cellular process, resulting in unregulated cellular proliferation, survival and differentiation. A defective tumor-suppressor gene can lead to the same result by blocking the activation of a critical "braking" process necessary for the appropriate control of cell-cycle progression

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12. Describe an example in which environmental factors interact with a genotype to produce cancer.

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is skin cancer in individuals who are genetically defective in DNA repair pathways, which depends on DNA damage from exposure to sunlight. Such individuals likely would be susceptible to a variety of cancers that result from exposure to carcinogens that cause damage to DNA. An example of such a disorder is xeroderma pigmentosum where affected individuals have defective nucleotide-excision repair and are unable to properly repair DNA damage caused by the UV in sunlight.

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13. If you were assigned to study a new form of cancer, you might want to determine whether it has a strong genetic basis or whether it is caused primarily by environmental factors. Propose some ways in which you could attempt to determine which hypothesis is correct. Which methods would be the easiest to use first?

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Initially, it may be helpful to look at family histories to see whether the disease is more common among relatives than in the general population. If there is evidence that the disease runs in families, then more time-consuming molecular genetic analyses can be used to attempt to identify specific genes that may be associated with the disease. Specific molecular techniques can also be discussed. It may also be helpful to look at incidences of the disease in different populations, such as migrant populations, to see whether populations with similar genetic profiles show different disease profiles in different environments. Surveys may be useful to attempt to determine whether any suspected environmental factors differ significantly between groups being studied.

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14. How can defects in DNA-repair mechanisms lead to the development of cancer.

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Defects in DNA-repair mechanisms increase mutation rates, increasing the probability of a mutation that could lead to cancer.

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15. Explain how retroviruses may cause cancers.

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Retroviruses are RNA viruses that use reverse transcriptase to make a DNA copy that can integrate into the host chromosome. Retroviruses can (1) mutate host genes when inserted and (2) alter the expression of host genes (for example, by inserting promoters).

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3. The process by which genetic changes occur in tumors and allows them to become increasingly aggressive over time is called? a. Clonal evolution b. Metastasis c. Loss of heterozygosity d. Epigenetic evolution e. Signal transduction

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a. clonal evolution

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Tumor cells are considered to be malignant if they invade other tissues.

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True

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. Most cancers are assumed to arise through errors in transcription

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False

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Most tumors arise from germ-line mutations that accumulate during out life span

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False

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Cancers is class of diseases sharing several defined cancer hallmarks

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True

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1. Multiple mutations are required for the development of cancer.

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True

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2. Mutations that lead to cancer can occur in proto-oncogenes and tumor-suppressor genes.

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True

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3. Only one copy of tumor-suppressor gene is inactivated in retinoblastoma cancer cells.

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False. two copies

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4. Proto-oncogenes are host genes that normally regulate signal transduction pathways or cell cycle control and has potential to become oncogenes when mutated

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True

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