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)

The specific detection of tumors in vivo using a radiolabeled syngeneic monoclonal antibody made by fusion of P3U1 (BALB/c myeloma cells) and C57BL/6 spleen cells primed with syngeneic B16 melanoma cells was investigated by color imaging, autoradiography, and biodistribution. The radiolabeled antimelanoma antibody specifically accumulated only in the tumor lesions, whereas no radioactivity was observed in normal tissues or organs. The distribution patterns of the radioactive antibody in the tumor lesions depended on the sizes of the tumor. Almost the entire region of the small metastatic tumor in lymph nodes was labeled, whereas the radioactive antibody was irregularly localized mainly in the center of the medium-sized tumor. However, only the peripheral region of the large primary tumor was labeled. The highest uptake of radioactivity (tumor:blood ratio) was observed in the small lymph node metastatic tumor lesions rather than in the large primary tumor. Furthermore, high resolution color imaging of B16 melanoma was also obtained by using 125I-labeled monoclonal antibody. Tumor location was specifically visible without subtraction or enhancement methods 3-5 days after injection of the radiolabeled antibody.
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PMID:Specific biodetection of B16 mouse melanoma in vivo by syngeneic monoclonal antibody. 362 96

Four stable IgM monoclonal antibody-producing hybridomas were generated by fusing mouse myeloma cells with spleen lymphocytes from C57BL/6 mice hyperimmunized against the syngeneic B16 melanoma. All four monoclonal antibodies (R31/15, R37/4, R37/6, and R37/7), in common with polyclonal antiserum from immunized mice, recognized antigens on the same complex of related cell surface molecules specified by endogenous AKR-type murine leukemia virus, designated the B16-gp/70/80/85 antigen complex. Reactivity with this antigen complex was demonstrated by radioimmunoprecipitation. Specificity for viral Mr 70,000 glycoprotein-related antigens was indicated by absorption of antibody activity by endogenous AKR virus and by inhibition of antibody binding to B16 melanoma cells by monospecific antiserum to murine leukemia virus Mr 70,000 glycoprotein. Neither polyclonal nor monoclonal antibodies recognized antigens on fish, guinea pig, swine, or human melanoma cell lines. Polyclonal antiserum reacted with several other mouse melanomas and with certain mouse lymphoma lines induced by, or harboring, endogenous murine leukemia viruses, but the monoclonal antibodies were unreactive except for recognition of antigens on Harding-Passey mouse melanoma cells by antibody R37/4 and on RL male 1 mouse lymphoma cells by antibody R37/7. Only monoclonal R37/7 was cytotoxic for cultured B16 melanoma cells in an antibody- and complement-dependent assay with guinea pig complement, although all antibodies were cytotoxic with rabbit complement. In reflecting the predominant humoral immune response to the B16 melanoma detected in syngeneic mice during tumor growth, these monoclonal antibodies will permit experimental amplification of that response to help determine how that immunity influences tumor growth and metastatic dissemination.
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PMID:Syngeneic monoclonal antibodies to B16 melanoma viral antigens. 365 42

To analyze the humoral immune response to melanoma, human-mouse hybridomas were generated by the fusions of regional lymph node lymphocytes of patients with the mouse myeloma cell line M5. Six stable hybridomas were cloned from six separate lymphocyte parents obtained from three patients. Ascites were obtained from nude mice after i.p. injection with cultured hybridoma cells. The monoclonal antibodies, four immunoglobulin Gs and two pentameric immunoglobulin Ms, were partially purified to remove mouse immunoglobulin and then conjugated to biotin for immunocytochemical and immunohistochemical studies. With the avidin:biotin:peroxidase complex method to detect and amplify binding by the biotin-conjugated human monoclonal antibodies, we found the six antibodies to be reactive against cytoplasmic determinants in five short-term melanoma cultures and formalin-fixed paraffin-embedded melanoma tumors from four patients. The antigenic target of the antibodies identified was not carcinoembryonic antigen. Two antibodies, 2-139-1 and 6-26-3, were studied in more detail. Each stained 25 of 25 specimens of melanomas. Little or no reactivity was detected against fixed sections of normal skin, which included tissues such as epidermis, dermis, monocytes, lymphocytes, and vascular endothelium. More striking was the absence of binding to melanocytes in the basal layer of the skin or to pigmented nevus cells. Both antibodies showed cross-reactivity against other tumors, in particular colonic and prostatic carcinomas. In the normal colon, reactivity was restricted to the surface of the columnar epithelium; no reactivity was detected against normal prostatic epithelium. Reactivity was also not observed against liver and lung. However, the epithelia of the renal tubules, pancreatic ducts, and salivary ducts were all reactive. These human monoclonal antibodies identify cytoplasmic melanoma-associated tumor antigens that appear different from the membrane antigens defined by serological approaches and by most mouse monoclonal antibodies.
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PMID:Human monoclonal antibodies directed against melanoma tumor-associated antigens. 369 90

PSK is a protein-bound polysaccharide prepared from cultured mycelium of the Basidiomycete Coriolus versicolor. Effects of PSK on the immunologic responsiveness in tumor-bearing animals were investigated using syngeneic or allogeneic tumors in mice (Lewis lung carcinoma, B16 melanoma, Meth A fibrosarcoma, adenocarcinoma 755, X5563 plasmacytoma, colon 26, MOPC 31C myeloma, sarcoma 180 and Ehrlich carcinoma), rats (BC47 bladder carcinoma, Walker 256 sarcoma and AH7974 hepatoma), hamsters (HA-1T tumor and RPMI 1846 melanoma), guinea pigs (line-10 hepatoma) and rabbit (VX2 and VX7 tumor). Oral or intraperitoneal administration of PSK restored the depressed delayed hypersensitivity against sheep erythrocytes to a normal level in these tumor-host systems. Also, oral administration of PSK lowered the activity of immunosuppressive substances in the serum of tumor-bearing animals. These results suggest that PSK exhibits antitumor effects by restoring the depressed immunologic responsiveness in tumor-bearing animals.
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PMID:[Restoration of immunologic responsiveness by PSK in tumor-bearing animals]. 378 58

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

The numbers of second cancers among 182,040 women treated for cervical cancer that were reported to 15 cancer registries in 8 countries were compared to the numbers expected had the same risk prevailed as in the general population. A small 9% excess of second cancers (5,146 observed vs. 4,736 expected) occurred 1 or more years after treatment. Large radiation doses experienced by 82,616 women did not dramatically alter their risk of developing a second cancer; at most, about 162 of 3,324 second cancers (approximately equal to 5%) could be attributed to radiation. The relative risk (RR = 1.1) for developing cancer in organs close to the cervix that had received high radiation exposures--most notably, the bladder, rectum, uterine corpus, ovary, small intestine, bone, and connective tissue--and for developing multiple myeloma increased with time since treatment. No similar increase was seen for 99,424 women not treated with radiation. Only a slight excess of acute and non-lymphocytic leukemia was found among irradiated women (RR = 1.3), and substantially fewer cases were observed than expected on the basis of current radiation risk estimates. The small risk of leukemia may be associated with low doses of radiation absorbed by the bone marrow outside the pelvis, inasmuch as the marrow in the pelvis may have been destroyed or rendered inactive by very large radiotherapy exposures. There was little evidence of a radiation effect for cancers of the stomach, colon, liver, and gallbladder, for melanoma and other skin cancers, or for chronic lymphocytic leukemia despite substantial exposures. An excess of thyroid cancer possibly was related to the low dose received by this organ. Ovarian damage caused by radiation may have been responsible for a low breast cancer risk (RR = 0.7), which was evident even among postmenopausal women. A substantial excess of lung cancer (RR = 3.7) largely may be due to misclassification of metastases and the confounding influence of cigarette smoking. Women who were under 30 or over 50 years of age when irradiated were at greatest absolute risk for developing a second cancer. The RR, however, was higher among those under age 30 years at exposure (RR = 3.9) than among older women. The expression period for radiation-induced solid tumors appeared to continue to the end of life.
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PMID:Second cancers following radiation treatment for cervical cancer. An international collaboration among cancer registries. 385 84

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

Alpha interferons are biological response modifiers that regulate immune function, slow cell proliferation, and inhibit virus replication. Large supplies of purified preparations are now available for clinical trials. Common toxicity includes an influenza-like syndrome to which tolerance occurs after several doses, and chronic fatigue and anorexia that may be dose-limiting. Myelosuppression is mild. Alpha interferons have established clinical activity against several human cancers, including melanoma, Kaposi's sarcoma, multiple myeloma, non-Hodgkin's lymphoma, hairy cell leukemia, and renal cell carcinoma. These data and alpha interferon nomenclature are summarized in table form. Intranasal alpha interferon is effective in prophylaxis of common viral upper respiratory tract infections, although toxicity in long-term use is prohibitive. Short-term administration to high risk populations may be most useful. Optimal doses and schedules need to be determined for all indications.
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PMID:The new alpha interferons. 391 Mar 84

Female BALB/c mice were immunized with human melanoma (Mewo) cells containing ganglioside GD3 as a surface antigen. Immune splenocytes were fused with syngeneic P3-X63.Ag 8 myeloma cells. Antibodies produced by hybrid clones were analyzed by solid phase immunoassay. B, C, D and Q clones producing antibodies against Raja clavata brain gangliosides were obtained. Monoclonal B and C antibodies bound monosialogangliosides. Monoclonal D antibody bound a number of gangliosides but reacted predominantly with GD1a. Monoclonal Q antibody reacted selectively with GQ1c. It is assumed that ganglioside GQ1c is expressed on the melanoma cell surface and may be found only in the early stage of ontogenesis of high vertebrates.
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PMID:[Isolation and analysis of monoclonal antibodies against various gangliosides]. 394 18

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


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