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Query: UMLS:C0025202 (melanoma)
 69,561 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Occupational and social class differences in cancer mortality among New Zealand males aged 15-64 are examined for the period 1974-78. Age-standardized cancer mortality rates are presented for the Registrar General's social classes as well as for each of six occupational orders and 79 occupational groups. The rates for specific cancer sites are also presented for each social class and for those occupational groups with significantly elevated relative risks. The findings of the social class analyses were generally consistent with those of recent British studies with mortality from cancer of the liver, larynx, lung, buccal cavity and stomach being particularly high in the lower social classes and mortality from multiple myeloma, malignant melanoma and lymphatic leukaemia being particularly high in the upper social classes. The findings of the occupational group analyses were also generally in line with those of recent British studies and those associations which have been found in British studies and were also present in the New Zealand data are discussed. It is concluded that there are a number of associations which warrant further investigation including: large bowel cancer in woodworkers and printers; bladder cancer in hairdressers and beauticians; and malignant lymphoma in farmers.
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PMID:Occupation, social class and male cancer mortality in New Zealand, 1974-78. 381 52

Until now, measurement of human antitumor immunity to organ-specific cancer neoantigen (OSN) by the leukocyte adherence inhibition (LAI) assay depended on using crude extracts of cancer. In this study, a new method is presented to generate and to isolate a highly enriched OSN from spent medium of a lung cancer cell line, NCI-H69, grown in chemically defined medium. Production of large quantities of OSN with minimal contamination by extraneous proteins was possible. Four physicochemical steps were used to give a 1000-fold enrichment of OSN activity: anion-exchange and molecular-sieve chromatography; Blue Sepharose affinity chromatography; and finally anion-exchange high-pressure liquid chromatography. The enriched OSN isolates showed dose-response antigenicity when tested in LAI assay with leukocytes from lung cancer patients but had no antigenicity with leukocytes from control subjects or patients having malignant melanoma, colon cancer, or pancreatic cancer. Cross-reactive antigenicity was observed with leukocytes from patients with breast cancer and slight reactivity with leukocytes from bladder cancer patients. The final isolate from the four-step separation procedure as well as the isolates produced using additional separation techniques consistently had antigenicity at less than 10 ng in blocking LAI and 500 ng in the direct assay and showed components with molecular weights of about 62,000 +/- 3,000 (SD) (p62), 40,000 +/- 3,000 (p40), and 25,000 +/- 1,000 (p25) by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. The OSN isolates on two-dimensional gels showed p40 to have microheterogeneity (seven spots), with a pl from 6.2 to 7.6, and p62 and p25 as even more basic streaks. The polypeptide bearing the antigenic determinant was not purified, although we tried to separate p62, p40, and p25 to determine whether they carried the OSN determinant. The results of this study are important in showing that an isolate of an organ-specific tumor antigen containing 5 to 13 components, as determined by highly sensitive silver stains and radiolabeled patterns on single and two-dimensional gels, can be used successfully in LAI to measure tumor immune responses.
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PMID:An isolated enriched organ-specific cancer neoantigen of human lung cancer for leukocyte adherence inhibition assays. 388 36

Monoclonal antibodies (McAbs) to human bladder carcinoma were generated by fusion of NS-1 mouse myeloma cells with spleen cells from BALB/c mice immunized with either cultured human bladder cancer cells or cells obtained from a fresh surgically removed bladder tumor. Four hybridomas which reacted strongly with bladder tumor cells and not to normal skin fibroblasts or urothelial cells were identified and cloned by limiting dilution to obtain monoclonality. One McAb, 3G2-C6, raised with cultured tumor bladder cells MGH-U1 (EJ) as the immunogen reacted more strongly to the bladder tumor lines tested than any of the other McAbs resulting from various fusion experiments. Hybridoma 3G2-C6 was found to secrete murine immunoglobulin G1 and to produce high titer ascites fluid when grown in BALB/c mice. Results from quantitative enzyme-linked immunosorbent assays on a panel of more than 35 cell lines demonstrated that McAb 3G2-C6 reacted with several bladder tumor cell lines 50 to 90 times more than with normal transitional urothelium. Two kidney and two testicular tumor lines also bound 10 times more 3G2-C6 than with normal cells. The 3G2-C6 antigen was only marginally detected on a number of other cancer and noncancerous cells tested such as breast and lung tumor cells, melanoma, fetal cells, and peripheral blood lymphocytes. To identify the antigen 125I-labeled membrane components from MGH-U1 cells were extracted with detergent, immunoprecipitated with Protein-A bound 3G2-C6, and analyzed by sodium dodecyl sulfate-gel electrophoresis. This revealed that McAb 3G2-C6 binds to a Mr 90,000 cell surface component. Indirect immunofluorescence microscopy with fluorescein isothiocyanate-anti-mouse immunoglobulin G also identified the antigen on the surface of cultured and fresh tumor cells and detected the antigen on 16 of 17 Grade 3 bladder tumor specimens as well as on some kidney and testicular tumor cells. This study confirms the potential of the hybridoma technique for producing McAbs capable of identifying tumor associated antigens which may be useful in the diagnosis and treatment of bladder cancer.
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PMID:Production and characterization of mouse monoclonal antibodies to human bladder tumor-associated antigens. 389 80

A Phase I study of interferon alfa-2a was conducted in 20 patients with disseminated cancer to establish the relationship between dose and interferon-related side effects. Fever was the most common side effect, and was not dose-related. Other side effects not related to dose included flu-like symptoms, gastrointestinal symptoms, and numbness of fingers and toes. A dose-response relationship was seen for leukopenia, thrombocytopenia, and the elevation of serum glutamic oxaloacetic transaminase (SGOT) and serum glutamic pyruvic transaminase (SGPT). A Phase II study was then conducted in 641 patients to evaluate the efficacy of interferon alfa-2a in a number of disseminated malignant neoplasms. The 415 male and 226 female patients, almost all of whom had malignancies refractory to standard therapy, were treated with interferon alfa-2a at an initial daily dose of 3 X 10(6) U for 3 days. Doses were increased gradually at 3- to 7-day intervals until the therapeutic dosage was established. The daily dose could not exceed 50 X 10(6) U, and treatment was continued for at least one month. Efficacy rates, for 65 patients who achieved partial or complete responses, based on the total number of evaluable patients by cancer type were: 11/49 (22.4%), multiple myeloma; 4/21 (19%), lymphomas; 15/108 (13.8%), renal cell carcinoma; 2/30 (6.6%), bladder cancer; 4/39 (10.2%), brain tumors; 5/26 (19.2%), melanoma; 12/12 (100%), cutaneous lymphoma; 10/19 (52.6%), other skin cancers; 2/30 (6.6%), bone and soft tissue sarcomas. Overall, 65/371 (17.5%) of evaluable subjects responded.
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PMID:Clinical studies of recombinant interferon alfa-2a (Roferon-A) in cancer patients. 394 42

The risk of developing a second primary cancer was evaluated in approximately 19,000 persons with initial cancers of the lymphatic and hematopoietic system in Connecticut between 1935 and 1982. Significant excesses for all second cancers were observed among patients with leukemia (34%), Hodgkin's disease (70%), non-Hodgkin's lymphoma (25%), and multiple myeloma (24%). In general, the risk of second cancers was greater in males than in females, even for cohorts not showing an excess of surveillance-related prostate cancer. Among patients with leukemia, significant excesses of cancers of the lung, kidney/ureter, and prostate were noted; cutaneous melanoma was elevated only in males. These excesses did not persist in the small number of long-term survivors. Possible etiologic factors included tobacco smoking for lung and kidney cancers, medical surveillance artifact for prostate cancer, and immunosuppression for malignant melanoma and lung cancer. The large number and good prognoses of patients with chronic lymphocytic leukemia strongly influenced the pattern of second cancers when all leukemias were analyzed together; no evidence was found for an increased risk of second cancer in patients with acute lymphocytic leukemia. A disproportionate number of subsequent cancers, particularly those of the kidney and ureter, were diagnosed incidentally at autopsy. Patients with Hodgkin's disease displayed significant excesses of cancers of the buccal cavity and pharynx, lung, female breast, and thyroid. The latter 3 sites remained significantly elevated in long-term survivors (10 yr or more postdiagnosis), so that radiation therapy may have contributed to their development. Among persons with non-Hodgkin's lymphoma, cancers of the stomach, lung, brain, and connective tissue occurred excessively. The first 3 sites, plus cancers of the urinary bladder, remained elevated among long-term survivors. The brain cancer excess, not previously reported, may represent misclassification of central nervous system lymphoma. The risk of gastric cancer is reminiscent of similar findings in patients with both acquired and genetically determined immunodeficiency disorders. The alkylating agent, cyclophosphamide, used extensively in the treatment of non-Hodgkin's lymphoma, is known to cause bladder cancer in man.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Second cancer following lymphatic and hematopoietic cancers in Connecticut, 1935-82. 408 98

The results of complement fixation tests on 202 sera from people without cancer and from patients with cancer in 29 different areas of the body indicated that only those with nine varieties of advanced cancer (lip, mouth, oropharynx, nasopharynx, kidney, urinary bladder, prostate, cervix uteri, and vulva-all of 56 tested) gave positive specific reactions with nonvirion antigens induced by the DNA herpes simplex (HSV 1) and herpes genitalis (HSV 2) viruses. None of 57 people without cancer (including 10 with current and 18 with recurrent HSV 1 or HSV 2 infections), none of 81 patients with 20 other varieties of advanced cancer (gum, tongue, tonsil, salivary gland, accessory sinus, epiglottis, lung-bronchus, stomach, colon, breast, corpus uteri, ovary, testis, liver, thyroid, Wilms' embryonal kidney, melanoma, Hodgkin's disease, acute lymphocytic leukemia, and acute myelocytic leukemia), and none of four women with early malignant changes in the cervix uteri gave positive results. The seven patients with advanced cancer of the lip or oropharynx gave positive reactions with HSV 1 but not with HSV 2 nonvirion antigens (compatible with involvement of only HSV 1), all of the 13 women with advanced cancer of the cervix uteri and the one woman with advanced cancer of the vulva gave positive reactions with both HSV 1 and HSV 2 nonvirion antigens (compatible with involvement of only HSV 2), while among the 35 other positive patients only two (one with cancer of the kidney and one with cancer of the bladder) reacted with HSV 1 and not at all with HSV 2 nonvirion antigens. Positive sera failed to react with cells harvested at different times after high-multiplicity infection with the DNA vaccinia virus. Massive absorption of positive sera with trypsinized, uninfected human embryonic kidney cells failed to remove, or lower the titer of, the HSV 1 and HSV 2 nonvirion antibodies. All of these data taken together are interpreted as indicating that HSV 1 and HSV 2 play an etiologic role in certain human cancers, because they provide the kind of evidence by which virus-free experimental cancers can be proved to have been originally induced by such DNA viruses as polyoma, Simian Virus 40, or certain types of adenovirus.
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PMID:Herpes simplex and herpes genitalis viruses in etiology of some human cancers. 436 85

A new modification of our detergent technique for the preparation of nuclei for flow cytometric DNA analysis is described. The attainment of low coefficients of variation of the peaks and of quantitative staining of nuclei from different tissues was a problem with the original method. This was solved in the new modification by trypsinization of the unfixed nuclei. The nuclei were stabilized by spermine. A simple procedure for long-term storage of samples at -80 degrees C was integrated into the method. The fluorescence of the nuclei was stable for at least 3 hours after staining. Light exposure protection of the samples was essential. No cell loss was caused by storage or staining. The method was successfully applied on samples including: (a) Normal tissues--human lymphocytes, granulocytes and spleen. Mouse lymphocytes, bone marrow, spleen, liver, kidney and thymus. (b) Human neoplasms--lung cancer, breast cancer, lymphoma, leukemia, bladder cancer and cancer of the oral cavity. (c) Human tumors in nude mice--breast cancer, lung cancer, melanoma and colon cancer. (d) Mouse ascites tumors--JB-1, L 1210, Ehrlich and P 383. It therefore seems well suited as a routine clinical procedure.
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PMID:A detergent-trypsin method for the preparation of nuclei for flow cytometric DNA analysis. 618 86

Several Louisiana parishes (counties) using the Mississippi River for their source of public drinking water have the highest mortality rates (1950-69) in the United States for several cancers. Therefore, a case-control mortality study on cancer of the liver, brain, pancreas, bladder, kidney, prostate, rectum, colon, esophagus, stomach, non-Hodgkin's lymphoma, multiple myeloma, leukemia, Hodgkin's disease, lung; breast and malignant melanoma, from 1960 to 1975 in South Louisiana parishes grouped for similarities in industrial characteristics, having approximately equal exposure of the population to surface and groundwater, was conducted. Noncancer deaths were randomly selected as controls and matched to the case death on age, race, sex, and year and parish group of death. Water source at death was assigned based on the residence at death and described as surface or ground and chlorinated or nonchlorinated. A significantly increased risk for surface, chlorinated water use was noted for rectal cancer. No risk could be demonstrated for colon cancer. The risk noted for bladder cancer by other investigators is not substantiated. Brain cancer risk appears to be associated with chlorinated groundwater, but this may be industrial confounding. Breast cancer demonstrated a slight, but significant, risk associated with surface chlorinated water. This risk, however, might be due to confounding of rural life style, early childbearing and large families with nonchlorinated water found in these settings. Chlorination risk for kidney cancer was not significant. No risk was observed in association with surface water for other cancers of the gastrointestinal or urinary tract. Multiple myeloma was significantly associated with a risk from ground water.
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PMID:Case-control cancer mortality study and chlorination of drinking water in Louisiana. 715 59

This study was aimed at characterizing the parameters which regulate human monocyte-mediated cytotoxicity to tumor cells as well as characterizing the target cell specificity, kinetics, etc., of the cytotoxic mechanism. Normal human peripheral blood monocytes were cytotoxic to tumor cells in an in vitro assay, measuring release of [3H] thymidine from human target cells. Monocyte cytolysis was observed with several adherent tumor lines including T24, a bladder cancer line; LR, a melanoma line; and an SV40-transformed W138 fibroblast line, with maximal cytolysis observed at 72 h. Lymphokines were not required to induce and only infrequently enhanced monocyte cytotoxicity. Prolonged exposure of monocytes to lymphokines or in vitro culturing of monocytes prior to lymphokine exposure did not alter the monocytes response to lymphokine signals with respect to cytotoxicity. Lymphokines induced monocytes to exhibit enhanced spreading, suggesting that monocytes were susceptible to lymphokine signals but that the development of cytolytic function was independent of lymphokines. In contrast to the cytolysis of adherent tumor cells, monocytes were less effective in killing the non-adherent lymphoid target cells K562, Raji, and CEM. Monocytes were selectively cytotoxic to tumor cells and generally did not kill normal human fibroblast cell lines or PHA-stimulated lymphocytes. Monocytes from cancer patients exhibited normal cytotoxicity to several human tumor lines. Plasmas from some cancer patients were inhibitory to cytotoxicity mediated by both autologous monocytes and normal monocytes.
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PMID:Cytotoxicity to tumor cells of monocytes from normal individuals and cancer patients. 723 18

Interstitial deletions of the short arm of chromosome 9 are associated with glioma, acute lymphoblastic leukemia, melanoma, mesothelioma, lung cancer, and bladder cancer. The distal breakpoints of the deletions (in relation to the centromere) in 14 glioma and leukemia cell lines have been mapped within the 400 kb IFN gene cluster located at band 9p21. To obtain information about the mechanism of these deletions, we have isolated and analyzed the nucleotide sequences at the breakpoint junctions in two glioma-derived cell lines. The A1235 cell line has a complex rearrangement of chromosome 9, including a deletion and an inversion that results in two breakpoint junctions. Both breakpoints of the distal inversion junction occurred within AT-rich regions. In the A172 cell line, a tandem heptamer repeat was found on either side of the deletion breakpoint junction. The distal breakpoint occurred 5' of IFNA2; the 256 bp sequenced from the proximal side of the breakpoint revealed 95% homology to long interspersed nuclear elements. One- and two-base-pair overlaps were observed at these junctions. The possible role of sequence overlaps, and repetitive sequences, in the rearrangement is discussed.
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PMID:Breakpoint junctions of chromosome 9p deletions in two human glioma cell lines. 752 63


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