JNCI: Journal of the National Cancer Institute

doi: 10.1093/jnci/56.4.CO3pmid: N/A

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doi: 10.1093/jnci/56.4.695pmid: N/A

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doi: 10.1093/jnci/56.4.697pmid: 176406

Article PDF first page preview Close This content is only available as a PDF. Author notes Editor's note: Periodically, the Journal publishes solicited guest editorials as a means of transmitting to investigators in cancer research the essence of current work in a special field of study. The Board of Editors welcomes suggestions for future editorials that succinctly summarize current work toward a clearly defined hypothesis regarding the causes or cure of cancer.

Gravell,, M.;Levine, P., H.;McIntyre, R., F.;Land, V., J.;Pagano, J., S.

doi: 10.1093/jnci/56.4.701pmid: 176407

Summary Epstein-Barr virus (EBV) DNA (17.7 genome equivalents/cell) was found in tumor tissue from an American patient with Burkitt's lymphoma who had never traveled outside the United States. A lymphoid cell line (NAB) containing the EBV genome was established from tumor tissue from this patient; characteristics of this cell line were described. Previous Burkitt's tumors found in Americans and examined by molecular hybridization were negative for EBV DNA. Our results suggested that EBV is associated with at least some American Burkitt's tumors. 2 Supported by Public Health Service contracts N01 CP43252 and N01 CP33336 within the Virus-Cancer Program, Division of Cancer Cause and Prevention, National Cancer Institute (NCI). This content is only available as a PDF. Author notes 3 Litton Bionetics, Inc., Kensington, Md. 20795. 4 NCI, National Institutes of Health (NIH), Public Health Service, U.S. Department of Health, Education, and Welfare, Bethesda, Md. 20014. 5 Present address: National Institute of Neurological and Communicative Disorders and Stroke, NIH. 6 St. Louis Children's Hospital, St. Louis, Mo. 63110. 7 University of North Carolina, Chapel Hill, N.C. 27514. 8 We thank Dr. Lauren Ackerman, St. Louis Children's Hospital, for pathologic diagnosis of Burkitt's lymphoma in patient 72-12096; Dr. Costan Berard, NCI, for confirming this diagnosis; Dr. Mitsuo Takasugi, University of California School of Medicine, Los Angeles, for HL-A typing; Dr. Dale Matheson, Litton Bionetics, Inc., for karotyping; Dr. Chien Hui Huang, University of North Carolina, Chapel Hill, for DNA renaturation kinetics; and Dr. Gary Pearson, NCI, for reviewing the manuscript and offering many helpful suggestions.

Canevari,, Silvana;Fossati,, Giuseppe;Porta, Giuseppe, Della

doi: 10.1093/jnci/56.4.705pmid: 1255793

Summary An in vitro microassay was used to study cytotoxic reactivity of lymphocytes of 19 patients with malignant melanoma, 8 patients with breast carcinoma, and 18 normal subjects on celt cultures of malignant melanoma and breast carcinoma. In each of the twelve experiments, peripheral blood lymphocytes from individuals with and without cancer were tested simultaneously on two or three different target cells. Cytotoxic reactivity, evaluated by a comparison of the number of target cells remaining after incubation with lymphocytes with those incubated with medium only, was found in 20 cancer patients (74%) and 13 individuals without cancer (72%). The strength of lymphocyte reactivity of the cancer and of the non-cancer group did not differ significantly. Of the 27 cancer patients, 8 were positive only on the homologous target cells, 7 only on the opposite cells, and 5 on both types; 7 were negative. Short-term melanoma cell cultures were more lysable than were established cell lines; however, no direct correlation between the growth rate during the test period and susceptibility to lysis was seen. The blood group of the lymphocyte donors had no influence on cytotoxic reactivity. 2 Supported in part by a grant from the Consiglio Nazionale delle Richerche, Rome, Italy. This content is only available as a PDF. Author notes 3 Division of Experimental Oncology A, Istituto Nazionale per lo Studio e la Cura dei Tumori, Via G. Venezian 1, 20133 Milan, Italy. 4 We thank Mrs. Iris Storchi for her skilled technical assistance, and the surgical staff and the blood transfusion service of the Institute for their help in the collection and study of human material.

Krueger, Robert, G.;Staneck, Linda, D.;Boehlecke, Jeanne, M.

doi: 10.1093/jnci/56.4.711pmid: 56451

Summary Antiserum was generated in rabbits to the RPMI 8226 tissue culture line of human myeloma cells, and its reaction with fixed smears of bone marrow aspirates from patients with multiple myeloma, macroglobulinemia, benign monoclonal gammopathy (BMG), leukemia, and nonneoplastic plasmacytosis was assessed by indirect immunofluorescence. After absorption with preparations of bone marrow from normal individuals, the antiserum reacted to a significantly higher titer with a specific subpopulation of plasma cells in smears from 81% of patients having multiple myeloma and 50% of patients having BMG than with cells in smears of bone marrow aspirates from normal individuals or patients having leukemia or nonneoplastic plasmacytosis, or than with cells in smears of peripheral blood from patients having Hodgkin's and non-Hodgkin's lymphoma. Absorption of the antiserum with RPMI 8226 cells or with a bone marrow preparation from a patient with multiple myeloma but not the Jijoye line of Burkitt's lymphoma reduced reactivity for cells in myeloma bone marrow. The antiserum reacted at a lower titer with the Jijoye and EB-3 lines of Burkitt's lymphoma, the RPMI 4098 cell line of normal human lymphocytes, and culture lines of human melanoma and osteogenic sarcoma than with the RPMI 8226 cells or bone marrow from certain patients having multiple myeloma. Approximately 50% of the cells reactive with antiserum to RPMI 8226 cells in the bone marrow of patients with multiple myeloma were not producing immunoglobulin, as assessed by double immunofluorescence assay. The data suggested that a subpopulation of plasma cells in the bone marrow of patients with multiple myeloma possesses a tumor-associated antigen. 2 Supported by Public Health Service grant CA11911 from the National Cancer Institute. This content is only available as a PDF. Author notes 3 Department of Microbiology, Mayo Medical School, Mayo Foundation, Rochester, Minn. 55901. 4 Present address: The Christ Hospital Institute for Medical Research, 2141 Auburn Ave., Cincinnati, Ohio 45219.

Mustacchi,, Piero;Millmore,, Don

doi: 10.1093/jnci/56.4.717pmid: 1255794

Summary During 1956–65, white and nonwhite San Francisco male residents did not have equal risks of developing testicular cancer. The lower risk observed for nonwhites could not be attributed entirely to genetic factors, since among whites a risk gradient seemed to correlate directly with broad socioeconomic indices such as occupation and census tract of residence. Although incidence rates for testicular cancer have progressively increased in the United States and now parallel rates in Danish towns and rural areas, they are still lower than rates observed in Copenhagen, where a “technology” effect has been postulated. In this perspective, the San Francisco findings are compatible with a hypothesis that certain occupational groups may have become epidemiologic indicators of testicular carcinogens in a changing environment. This content is only available as a PDF. Author notes 2 Department of International Health, University of California, San Francisco, and Children's Hospital, San Francisco, Calif. 3 Address reprint requests to the Department of International Health, 1699 HSW, University of California, San Francisco, Calif. 94143. 4 1974 Summer Research Fellow from the University of California, San Francisco, at Children's Hospital, San Francisco.

Gotlieb-Stematsky,, T.;Ramot,, B.;Vonsover,, A.;Aghai,, E.;Kende,, G.;Ninio,, M.;Modan,, M.

doi: 10.1093/jnci/56.4.721pmid: 233958

Summary Before and/or after chemotherapy was administered to patients with Burkitt's lymphoma (BL) or lymphoblastic lymphosarcoma (LLS), their sera and those of matched controls were tested for antibodies to Epstein-Barr virus (EBV) capsid antigen (VCA) and early antigen by the indirect immunofluorescence method. Ten of the 16 BL patients were Arab children and 8 of the 11 LLS patients were Jews of Asian-African origin. Although half the BL patients did not have elevated antibody titers when their disease was diagnosed, significantly higher ones were detected in the BL group as compared with the LLS patients and their matched controls; Arab patients had the highest titers. IgM antibodies specific for VCA were found in 2 patients concurrently with elevated titers. We found no correlation between the clinical course of BL and the patients' antibody titers to EBV. 2 Supported by a grant to Dr. Gotlieb-Stematsky from the Chief Scientist, Ministry of Health, Israel. This content is only available as a PDF. Author notes 3 Central Viral Laboratory, Ministry of Health, Tel-Aviv-Jaffa, and Department of Human Microbiology, Sackler School of Medicine, Tel-Aviv University, Tel-Aviv, Israel. 4 Institute of Hematology, the Chaim Sheba Medical Center, and the Sackler School of Medicine, Tel-Aviv University. 5 Department of Clinical Epidemiology, the Chaim Sheba Medical Center, and the Sackler School of Medicine. 6 We gratefully acknowledge the technical assistance of Mrs. Y. Shlomo-David, Central Viral Laboratory.

Zimmerman,, B.;Chapman, M., L.

doi: 10.1093/jnci/56.4.725pmid: 1255795

Summary Surface antigens from lymphocytes of patients with chronic lymphocytic leukemia (CLL) and from normal peripheral blood lymphocytes (PBL) were examined by radioimmunoassay; antisera to lymphocytes (ALS) were used to bind the labeled antigens. Cells from patients with CLL, normal PBL, thymus cells (THY), and cultured human lymphoblasts (CHL) were labeled by lactoperoxidase-catalyzed iodination. ALS (prepared against THY and CHL) were used to bind the labeled antigens solubilized in nonionic detergent. PBL resembled THY, but the CLL resembled CHL. Thus ALS(CHL) had greater potency for CLL antigens than for PBL antigens when compared to ALS(THY). Furthermore, the electrophoretic profiles of the immunoprecipitates from CLL cells revealed a peak of approximately 30,000–35,000 mol wt, which was not found for PBL or THY, but was associated with CHL. 2 Supported by the Medical Research Council of Canada. This content is only available as a PDF. Author notes 3 Department of Immunology, Research Institute, The Hospital for Sick Children, Toronto, Ontario, Canada M5G 1X8. 4 Scholar of the Medical Research Council of Canada. 5 We thank Dr. N. Sniffman for his cooperation.

Morrison, Alan, S.

doi: 10.1093/jnci/56.4.731pmid: 3662

Summary Risk of cancer of the testis was related to non-descent and hernia in a comparison of 596 testicular cancer patients and 602 unaffected men who had been in active service in the U.S. Army between 1950 and 1970. Medical histories were obtained from routine service records. Undescended testis was associated with a testicular cancer risk 8.8 times that of normal. Among cancer patients with a history of undescended testis, seminomas were nearly twice as frequent as in the remaining patients. Of 14 patients with unilateral undescended testis, 12 had the tumor on the side of the defect. Testicular cancer risk was estimated to be 2.9 times higher in men who had reported having had an inguinal hernia than in those who had not. Side of hernia and side of tumor were not associated; histologic type was not related to history of hernia. 2 Supported in part by Public Health Service grant 5 P01 CA06373 from the National Cancer Institute. 3 This material has been reviewed by the Walter Reed Army Institute of Research, and there is no objection to its presentation and/or publication. The opinions or assertions contained herein are the private views of the author and are not to be construed as official or as reflecting the views of the Department of the Army or the Department of Defense. This content is only available as a PDF. Author notes 4 Division of Preventive Medicine, Walter Reed Army Institute of Research, Washington, D.C., and the Department of Epidemiology, Harvard School of Public Health, 677 Huntington Ave., Boston, Mass. 02115. Address reprint requests to Dr. Morrison at the Department of Epidemiology, Harvard School of Public Health. 5 I thank Dr. F.K. Mostofi, the tumor registrars of the Army teaching hospitals, and Mr. Seymour Jablon for help in assembling lists of patients and control subjects. I am grateful to Dr. Thomas Mack, who suggested that hernias be studied. Ms. Charlene Evans and Mrs. Hazel Coven assisted with record abstracting and coding.