References

Aisenberg, A. C. 1993. Utility of gene rearrangements in lymphoid malignancies. Annu. Rev.. Med. 44:75.

Allison, J. P., A. A. Hurwitz, and D. R. Leach. 1995. Manipulation of costimulatory signals to enhance antitumor T-cell responses. Curr. Opin. Immunol. 7:682.

Baselga J., et al. 1996. Phase II study of weekly intravenous recombinant humanized anti-p185HER2 monoclonal antibody in patients with her2/neu-overexpressing metastatic breast cancer. Journal of Clinical Oncology 14:737.

Boon, T., P, G. Coulie, and B. Van den Eynde. 1997.Tumor antigens recognized by T cells. Immunol Today. 18:267.

Coulie, P. G., et al. 1994. A new gene coding for a differentiation antigen recognized by autologous cytolytic T lymphocytes on HLA-A2 melanomas. J. Exp. Med. 180:35.

Cournoyer, D., and C. T. Caskey. 1993. Gene therapy of the immune system. Annu. Rev. Immunol. 11:297.

DeVita, V. T., S. Hellman, and S. A. Rosenberg. 1997. Cancer Principles & Practice of Oncology, 5th ed., Lippincott Williams & Wilkins.

Houghton, A. N., J. S. Gold, and N. E. Blachere. 2001. Immunity against cancer: lessons learned from melanoma. Curr. Opin. Immunol. 13:134.

Hsu, F. J., et al. 1997. Tumor-specific idiotype vaccines in the treatment of patients with B-cell lymphoma. Blood. 89:3129.

Kufe, D. W. 2000. Smallpox, polio and now a cancer vaccine? Nature Med. 6:252

Pardoll, D. M. 1996. Cancer vaccines: a road map for the next decade. Curr. Opin. Immunol. 8:619.

Paterson, Y., and G. Ikonomidis. 1996. Recombinant Listeria monocytogenes cancer vaccines Curr. Opin. Immunol. 8:651.

Rosenberg, S. A. 2001. Progress in human tumour immunology and immunotherapy. Nature 411:380.

Rosenberg, S. A, et al. 1994. Treatment of patients with metastatic melanoma with autologous tumor-infiltrating lymphocytes and interleukin 2. Journal of the National Cancer Institute 86:1159.

Sahin, U., O. Tureci, and M. Pfreundschuh. 1997. Serological identification of human tumor antigens. Curr. Opin. Immunol. 9:709.

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Srivastava, S. 2002. Roles of heat-shock proteins in innate and adaptive immunity. Nature Rev.. Immunol. 2:185.

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http://www.oncolink.upenn.edu/

Oncolink is a site that offers comprehensive information about many types of cancer. It is a good source of information about cancer research and advances in cancer therapy. The site is regularly updated and it includes many useful links to other resources.

http://www.cancer.org/index_4up.html

This is the Web site of the American Cancer Society. It contains a great deal of information on the incidence, treatment, prevention of cancer. The site also highlights significant achievements in cancer research.

http://www.cytopathnet.org/

A good resource for information on the cytological examination of tumors and on matters related to staining patterns that are typical of the cell populations found in a number of cancers.

Study Questions

Clinical Focus Question You are an oncologist and wish to treat a patient with one of the newly available cancer vaccines, but the only tumor from this patient is preserved in formaldehyde. Can you still use a vaccine? If so, what type of vaccine is available for your use? If you have a tumor sample containing living cells, are there other types of vaccines available?

1. Indicate whether each of the following statements is true or false. If you think a statement is false, explain why.

a. Hereditary retinoblastoma results from overexpression of a cellular oncogene.

b. Translocation of c-myc gene is found in many patients with Burkitt's lymphoma.

c. Multiple copies of cellular oncogenes are sometimes observed in cancer cells.

d. Viral integration into the cellular genome may convert a proto-oncogene into a transforming oncogene.

e. All oncogenic retroviruses carry viral oncogenes.

f. The immune response against a virus-induced tumor protects against another tumor induced by the same virus.

g. LAK cells are tumor specific.

2. You are a clinical immunologist studying acute lymphoblas-tic leukemia (ALL). Leukemic cells from most patients with ALL have the morphology of lymphocytes but do not express cell-surface markers characteristic of mature B or T cells. You have isolated cells from ALL patients that do not express membrane Ig but do react with monoclonal antibody against a normal pre-B-cell marker (B-200). You therefore suspect that these leukemic cells are pre-B cells. How would you use genetic analysis to confirm that the leukemic cells are committed to the B-cell lineage?

3. In a recent experiment, melanoma cells were isolated from patients with early or advanced stages of malignant melanoma. At the same time, T cells specific for tetanus-toxoid antigen were isolated and cloned from each patient.

a. When early-stage melanoma cells were cultured together with tetanus-toxoid antigen and the tetanus toxoid-specific T-cell clones, the T-cell clones were observed to proliferate. This proliferation was blocked by addition of chloroquine or by addition of monoclonal antibody to HLA-DR. Proliferation was not blocked by addition of monoclonal antibody to HLA-A, -B, -DQ, or -DP. What might these findings indicate about the early-stage melanoma cells in this experimental system?

b. When the same experiment was repeated with advanced-stage melanoma cells, the tetanus-toxoid T-cell clones failed to proliferate in response to the tetanus-toxoid antigen. What might this indicate about advanced-stage melanoma cells?

c. When early and advanced malignant melanoma cells were fixed with paraformaldehyde and incubated with processed tetanus toxoid, only the early-stage melanoma cells could induce proliferation of the tetanus-toxoid-T-cell clones. What might this indicate about early-stage melanoma cells?

d. How might you confirm your hypothesis experimentally?

4. What are three likely sources of tumor antigens?

5. Various cytokines have been evaluated for use in tumor im-munotherapy. Describe four mechanisms by which cytokines mediate antitumor effects and the cytokines that induce each type of effect.

6. Infusion of transfected melanoma cells into cancer patients is a promising immunotherapy.

a. Which two genes have been transfected into melanoma cells for this purpose? What is the rationale behind use of each of these genes?

b. Why might use of such transfected melanoma cells also be effective in treating other types of cancers?

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Responses

  • tesmi
    When early stage melonoma cells were cultured together with tetanustoxoid antigen and the?
    28 days ago

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