Q.63 Identify the correct statements: Tumor cells differ from normal cells by changes in the regulation of growth. Proto-oncogenes encode defective proteins. Tumor cells can display tumor-specific antigens/novel antigens. Several cytokines including IFN and TNF help to mediate tumor-cell killing. Choose the correct answer from the options given below: A, C and D only B, C and D only A, B and C only A, B and D only

Q.63 Identify the correct statements:

  1. Tumor cells differ from normal cells by changes in the regulation of growth.
  2. Proto-oncogenes encode defective proteins.
  3. Tumor cells can display tumor-specific antigens/novel antigens.
  4. Several cytokines including IFN and TNF help to mediate tumor-cell killing.

Choose the correct answer from the options given below:

  1. A, C and D only
  2. B, C and D only
  3. A, B and C only
  4. A, B and D only

    The correct answer is A, C and D only.

    Tumor cells exhibit dysregulated growth due to oncogene activation and tumor suppressor inactivation, express neoantigens recognizable by immune cells, and succumb to cytokine-mediated cytotoxicity, while proto-oncogenes encode normal regulatory proteins.

    Option Analysis

    A, C and D only
    A: Correct—tumor hallmark is growth deregulation via oncogene activation/tumor suppressor loss. C: Correct—tumor-specific antigens (neoantigens from mutations) or novel antigens trigger immune recognition. D: Correct—IFN-α/β, TNF-α induce apoptosis/Fas upregulation in tumor cells. B false. Correct.

    B, C and D only
    B incorrect: Proto-oncogenes encode normal functional proteins (growth factors, receptors, cyclins); oncogenes are mutated hyperactive versions. A true. Incorrect.

    A, B and C only
    B false (as above); D true—cytokines central to tumor immunosurveillance. Incorrect.

    A, B and D only
    B false; C true—tumor immunogenicity from mutated proteins displayed on MHC. Incorrect.

    Tumor cells differ from normal cells primarily through six acquired capabilities (Hanahan-Weinberg hallmarks), with growth dysregulation universal across malignancies.

    Growth Regulation Defects

    Normal cells require mitogenic signals, exhibit contact inhibition, and undergo apoptosis; tumor cells ignore these via RAS/MAPK pathway constitutive activation, p53/RB loss, enabling limitless replication.

    Immunogenicity and Cytokine Response

    Tumor cells display tumor-specific antigens (neoantigens from nonsynonymous mutations) or cancer-testis antigens on MHC-I, targeted by CD8+ T cells/NK cells. Type I IFNs (IFN-α/β) upregulate MHC-I, activate JAK-STAT apoptosis; TNF-α triggers caspase-8 extrinsic pathway in sensitive tumors.

    Proto-Oncogene Clarification

    Proto-oncogenes (c-MYC, c-FOS, c-SRC) encode physiologic growth promoters requiring one hit for dominant oncogene activation; tumor suppressors need biallelic inactivation. Mutated proto-oncogenes become oncogenes encoding defective gain-of-function proteins.

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