Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026764 (multiple myeloma)
 36,148 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We assessed the risk of occurrence of cancer associated with exposure to metronidazole in the 771 female residents of Rochester, Minnesota, who were treated with metronidazole for vaginal trichomoniasis during the period 1960 through 1969 and were followed up for a total of 12,628 person-years. Standardized morbidity and mortality ratios were determined by using an expected number calculated by applying age-specific incidence rates from Rochester studies and Cancer Surveillance, Epidemiology, and End-Results Reporting (SEER) data to the person-years of follow-up. The overall standardized morbidity ratios for cancer at all sites were 1.4 (Rochester, 1978 through 1983), 1.5 (SEER data for Iowa, 1978 through 1981), and 1.2 (SEER data for Connecticut, 1978 through 1981). By site of the cancers, the standardized morbidity ratios greater than unity were those for malignant lesions of the lung, breast, thyroid, bladder, brain, kidney, nasopharynx, and oral cavity, as well as for multiple myeloma and malignant melanoma; however, the only significantly elevated standardized morbidity ratio was that for bronchogenic carcinoma. After adjustment for smoking status, the standardized morbidity ratio for bronchogenic cancer was 2.5 (95% confidence interval of 1.3 to 4.4). The standardized mortality ratio for cancer at all sites was 1.4 (95% confidence interval of 0.9 to 2.2). The analysis of these data suggests no significant increase in cancer-related morbidity or mortality for women exposed to metronidazole for treatment of vaginal trichomoniasis.
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PMID:Cancer after exposure to metronidazole. 333 6

We calculated 5-year crude and relative survival rates, by age and sex, for patients in Alberta in whom cancer was diagnosed between 1974 and 1978. Cancers with low overall 5-year relative survival rates (less than 35%) included stomach cancer, cancer of the pancreas, lung cancer, brain cancer, multiple myeloma and myeloid leukemia. Cancers with high overall 5-year relative survival rates (more than 70%) included melanoma, breast cancer, cancer of the uterus, cancer of the bladder and Hodgkin's disease. Five-year relative survival rates were generally lower in the highest age group (75 years or more). A strong inverse relation between age and survival was noted for brain cancer, non-Hodgkin's lymphoma, Hodgkin's disease and myeloid leukemia.
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PMID:Survival rates among patients with cancer in Alberta in 1974-78. 337 May 94

Five-year relative case-survival rates for all cancers collectively are similar in South Australia (49%) and the United States (50%). This suggests that outcomes of cancer treatment do not vary appreciably between the two populations. There is an indication of higher survival rates in South Australia for melanoma, Hodgkin's disease, multiple myeloma and gastric cancer, but lower survival rates for cancers of the thyroid, corpus uteri, prostate, colon, kidney and lung. The differences in point estimates of the rates were most conspicuous for Hodgkin's disease, multiple myeloma and prostatic cancer. The reasons for a cautious interpretation of these findings are discussed and some possible explanations are suggested. South Australian data point to an upward trend in survival rates between the diagnostic periods 1977-1980 and 1981-1985 for patients with Hodgkin's disease, diffuse large-cell lymphomas, melanomas and cancers of the prostate and rectum.
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PMID:Cancer case-survival rates for South Australia: a comparison with US rates and a preliminary investigation of time trends. 337 24

Mouse Sp2/10 myeloma cells were fused with spleen cells from mice that had been immunized with freshly obtained primary human uveal melanoma cells. Hybrids that produced antibodies binding to the uveal melanoma cells, but not to fibroblasts, uveal or retinal cells of healthy donors, were cloned. Extensive specificity tests showed that the antibodies produced by the ten clones bound strongly to fresh or short-time cultures of primary human uveal melanoma tumor cells (UMEL-H, UMEL-K). Weaker binding occurred with a human uveal melanoma cell line (VUP-1), and with human skin melanoma cell lines (HMB-2, B-HM8), respectively. Binding assays with carcinoma cells, fibroblasts, uveal and retinal cells were negative. An intensive screening of this type is now under way.
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PMID:A preliminary report on monoclonal antibodies against human uveal melanoma. 343 9

The Swedish Cancer-Environment Register was used to study time-related trends in relative risks (RRs) of cancer between 1961 and 1979 in a cohort of 254,417 Swedish men who were employed in agriculture in 1960. The reference cohort consisted of 1,725,845 Swedish men who were gainfully employed in economic activities other than agriculture or forestry in 1960. Altogether 24,763 cancers were observed in the study cohort and 146,900 in the reference cohort, giving an estimated RR for the entire study period of 0.82 (95% confidence interval: 0.81-0.83). The RR for all sites combined increased from 0.80 in 1961-73 to 0.84 in 1974-79 (P less than .01). The RR also increased over time for primary liver cancer (P less than .01), prostate cancer (P less than .01), cancer of other genital organs (P less than .01), cancer of urinary organs (P less than .01), lip cancer (P less than .05), and cancer of the nose and nasal cavities (P less than .05). For most of these sites the RR remained lower than unity. For prostate cancer, however, the RR was unity at the end of the study period. A decrease in the RR over time was observed for skin carcinomas of the trunk and limbs (P less than .05) and malignant tumors of the nervous system (P less than .05). For 27 of the 48 analyzed tumor sites the RR for the entire period 1961-79 was significantly lower than unity. The lowest RRs were seen for cancer of the pleura (0.25), cancer of the larynx (0.35), lung cancer (0.36), cancer of the hypopharynx (0.36), cancer of the floor of mouth (0.40), primary liver cancer (0.44), and cancer of the kidney pelvis (0.49). RRs significantly higher than unity were found for cancer of the lip (1.92), malignant melanoma, and carcinoma of the skin in the head and neck region (1.39 and 1.15, respectively), multiple myeloma (1.20), and cancer of the stomach (1.07).
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PMID:Trends in cancer risks among Swedish agricultural workers. 346 7

Monoclonal antibodies (MoAbs) against human osteosarcoma cells were obtained by the production and cloning of hybrids resulting from the fusion of mouse myeloma cells P3 X 63Ag8.653 with spleen cells from partially purified, osteosarcoma-associated antigen (OSAA)-immunized BALB/c mice. OSAAs were isolated from the spent culture medium of a human osteosarcoma cell line (TE-85). Five hybrid clones were established and designated as OSA1, OSA2, OSA3, OSA4, and OSA5. OSA1 and OSA2 had similar activity. All 5 MoAbs reacted strongly with most osteosarcoma cell lines and with all osteosarcoma tissues tested but not with 10 tumor cell lines and 2 tumor tissues from other cancers. OSA3, OSA4, and OSA5 cross-reacted with a fibrosarcoma cell line, a colon cell line, and fibrosarcoma, respectively, as well as with a melanoma cell line. None of the MoAbs were reactive with activated normal human peripheral blood mononuclear cells (PBMC). Immunoprecipitation of membrane protein isolated from LM cells and TE-85 cells with the MoAbs OSA1 and OSA2 conjugated with Staphylococcus aureus yielded a molecule with molecular weight of approximately 92,000. No detectable membrane protein was precipitated when 125I-labeled membrane protein from pooled activated human PBMC and tumor cells of other histologic types were used in the immunoprecipitation.
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PMID:Monoclonal antibodies to human osteosarcoma-associated antigen(s). 346 10

Some coat-color loci in mice are considered to control melanosome formation. In order to investigate genetic control of melanosome-associated proteins, we prepared monoclonal antibodies against mouse melanosomes. Melanosomes were isolated from B16 mouse melanoma through differential fractionation. BALB/c mice were immunized with an SDS-solubilized melanosome fraction. The spleen cells were subsequently fused with mouse myeloma cells, the resulting hybridomas cloned. Their secreted IgG was screened for reactivity to the SDS-solubilized melanosome fraction. One monoclonal antibody, M10, was shown to react to melanosomes by immunoelectronmicroscopy. It recognized a single protein band of 61,000 dalton on immunoblots of gel-fractionated melanosomes. The reactivities of M10 to skin homogenates from various coat-color mutants were examined by the ELISA method. Five congenic genotypes, non-agouti (a/a), brown (b/b), albino (c/c), dilute (d/d), and pink-eyed dilution (p/p) were examined. Among these, b/b and p/p showed significantly lower reactivities than a/a. Our results seem to suggest that the pigment abnormalities in these mutants result from abnormalities of the melanosomal proteins. In the case of albino mice, the reactivity of M10 to skin homogenate was almost the same as the wild-type mouse. It seems that the albino mice are capable of producing the melanosomal protein.
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PMID:Deficient melanosome formation in some coat-color mutant mice revealed by a monoclonal antibody against melanosome. 350 65

Antimelanosome-associated monoclonal antibody has recognized the common antigenic determinant of melanosomes and cell surface of pigment cells, and it is suggested that melanosomes play a significant role as an antigen in progressive depigmentary disorders, in which melanocytes are selectively altered and disappear presumably by auto-antibodies in vivo. Mouse myeloma cells were fused with spleen cells from BALB/c mice immunized with a melanosomal fraction separated from human melanotic melanoma cells (Mm-1-JCK). The monoclonal antibody (MoAb) A4F11 has been found to react with premelanosomes, melanosomes, and probably with Golgi-associated endoplasmic reticulum lysosomes, but not with mitochondria, nuclei, and cytosol from human melanoma cells, by immunoelectron microscopy using the saponin permeation method, which was carried out together with indirect radioimmunoassay and quantitative absorption assay. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis and immunoblotting using melanosome preparations have revealed the antigen(s) reactive with the MoAb A4F11 in 3 bands corresponding to Mr 50,000, 18,000, and 17,000. Cell binding assay has shown the reactivity of the MoAb A4F11 with the cell surface of human normal melanocytes and melanoma cells, but not with other mammalian melanoma cells or with human nonpigment cells examined. Indirect immunofluorescence on cultured cells and frozen sections has revealed distinct granular reactivity not only with human melanotic melanoma, but also with junctional and intradermal nevi, cultured malignant blue nevus cells, as well as normal melanocytes. The above evidence has indicated the presence of an antigenic determinant common to the intracellular melanogenic compartments and to the cell surface of human pigment cells, regardless of their oncogenic differentiation status.
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PMID:Melanosomal antigenic expression on the cell surface and intracellular subunits within melanogenic compartments of pigment cells: analysis by antimelanosome-associated monoclonal antibody. 352 55

Human monoclonal antibodies were generated by fusing a nonsecretory variant of murine myeloma cells with lymphocytes obtained from the lymph nodes of patients with metastatic cutaneous malignant melanoma. Two human IgG monoclonal antibodies, designated 2-139-1 and 6-26-3, were extensively studied for their patterns of binding to cells in 64 specimens of formalin-fixed, paraffin-embedded tissue sections. These comprised: 23 cutaneous and 2 ocular melanomas; 4 specimens of lentigo maligna; 27 benign nevi; 2 basal and 2 squamous cell neoplasms of the skin; and 4 specimens of normal skin. A direct avidin-biotin-immunoperoxidase staining method was used. Under these conditions, the antibodies reacted with variable intensity to all 18 primary cutaneous malignant melanomas, 5 metastatic cutaneous melanomas, and both ocular melanomas. Antibody 2-139-1 reacted with 1 of 4 specimens and 6-26-3 with 3 of 4 specimens of lentigo maligna. Two of 5 dysplastic nevi reacted with both antibodies, each with a smaller proportion of cells than with melanomas. There was no reactivity with the 22 other nevi representing a spectrum of histologic types or with normal melanocytes. Basal cell and squamous cell carcinomas of the skin also were not stained. These human monoclonal antibodies appear to be useful in distinguishing malignant melanomas from benign nevi, with the exception of dysplastic nevi, and from basal and squamous cancers of the skin in routinely prepared tissue sections. They may also help to identify the cytoplasmic antigens that are immunogenic in humans.
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PMID:Human monoclonal antibodies that distinguish cutaneous malignant melanomas from benign nevi in fixed tissue sections. 352 8

Due to their specificity, constant properties and virtually unlimited supply monoclonal antibodies have given an important stimulus to almost every field of biomedical research within the last 10 years. The generation of mouse monoclonal antibodies includes immunisation of mice followed by fusion of mice spleen cells with a murine myeloma cell line. With this procedure hybridomas secreting monoclonal antibodies of a predefined specificity can be obtained. For three major reasons we worked on the establishment of human hybridomas secreting specific antibodies: human antibodies are less immunogenic when used for diagnostic or therapeutic purposes, only human monoclonal antibodies allow the analyses of the human B cell repertoire, there is evidence that human monoclonal antibodies recognise epitopes different from those seen by murine monoclonal antibodies. Therefore, we set out to generate human B cell hybridomas by cell fusion using the human lymphoblastoid B cell line Wi-L2-729 HF2 and lymphocytes from melanoma patients. The lymphocytes were isolated from tumour-draining cervical lymph nodes, stimulated with pokeweed mitogens plus the autologous tumour cells in an enriched tissue culture medium and fused in the presence of polyethylene glycol. Supernatants of hybridomas were screened in a single cell immunosorbent assay with either autologous melanoma cells or established melanoma cell lines fixed to the bottom of Terasaki plates or on cytospin preparations of these cells using the immunoperoxidase staining procedure. We could demonstrate that the tumour draining lymph nodes of these melanoma patients contained B lymphocytes capable of producing antibodies reacting with the tumour cells.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Attempts to produce human monoclonal antibodies to melanoma using the cervical lymph nodes]. 358 98


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