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)

A hospital-based case-control study was done to examine the hypothesis that persons with a family history of multiple myeloma (MM) or other cancers are at increased risk of multiple myeloma. Study members were 439 cases of multiple myeloma and 1317 matched controls seen at the Duke University Medical Center. Only 3 cases and 4 controls reported multiple myeloma in their families. The relative risk (RR) was 2.3, but the 95% confidence interval (CI) was 0.5-10.1, allowing no firm conclusion about the risk associated with familial MM. A family history of cancer of any type resulted in a relative risk of MM of 1.4 (CI: 1.1-1.8). This association was strongest (RR = 2.5, CI: 1.1-5.3) among young study members (age less than or equal to 49). A family history of hematologic malignancy (ICD 200-208) resulted in a RR of 2.4 (95% CI: 1.4-4.0). The data also suggested that a family history of lung cancer, breast cancer, and genitourinary cancer may be associated with increased risk of myeloma in older persons.
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PMID:Multiple myeloma and family history of cancer. A case-control study. 402 40

Erythrocyte mean corpuscular volume (MCV) evolution during cytotoxic therapy of Hodgkin's disease, lymphoma, multiple myeloma, ovarian cancer, and breast cancer was studied. The fastest and the highest MCV increases were observed in the diseases and with the therapies the most frequently involved in secondary leukemia: Hodgkin's disease treated with MOPP (mechlorethamine, vincristine, procarbazine, prednisone), and multiple myeloma and ovarian cancer treated with melphalan. On the contrary, with cytotoxic regimens not linked to a high frequency of secondary leukemia such as CMF (cyclophosphamide, methotrexate, 5-fluorouracil) used in ovarian or breast cancer, MCV increase was moderate. As the MCV increase reflects the bone marrow reaction to cytotoxic therapy, an unusually high increase could indicate bone marrow damages which could lead to secondary leukemia.
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PMID:Erythrocyte mean corpuscular volume during cytotoxic therapy and the risk of secondary leukemia. 403 78

In Denmark, approximately 5% of all malignant neoplasms occur within the lymphatic and hematopoietic tissues. Between 1943 and 1980, 23,367 persons with these diseases fulfilled the criteria for entering the study. The risk of developing a second primary cancer was significantly increased only after Hodgkin's disease [relative risk (RR) = 1.6], whereas no increase was found after non-Hodgkin's lymphoma [(NHL); RR = 1.0] or leukemia (RR = 1.1), and a significant deficit occurred after multiple myeloma (RR = 0.8). All initial cancer sites showed a higher incidence of second primary cancers among males than females. Significant elevated risks for acute non-lymphocytic leukemia occurred after Hodgkin's disease (RR = 17), NHL (3.8), and multiple myeloma (9.1). Among persons initially diagnosed with leukemia, NHL was significantly elevated (RR = 2.6). However, these RR should be regarded as minimum figures due to the likelihood of serious underreporting of second primary hematologic cancers in Denmark. The secondary leukemias were likely induced by the treatment of the first primary cancer (chemotherapy, radiotherapy), but common etiologies, misclassification, or progression of the initial cancer cannot be ruled out entirely. Other second primary cancers found to be above expectation following Hodgkin's disease were cancers of the pancreas, lung, and urinary bladder. The risk for bladder cancer increased with time, which suggested a causal relation to radiation or chemotherapy, or both. Cancers of the colon and rectum following NHL and female breast cancer following leukemia occurred below expectation and remain unexplained.
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PMID:Second cancer following lymphatic and hematopoietic cancers in Denmark, 1943-80. 408 11

Among 41,109 women diagnosed with breast cancer between 1935 and 1982 in Connecticut, 3,984 developed a second cancer, whereas 2,426 were expected [relative risk (RR) = 1.64; 95% CI = 1.6-1.7]. This increased risk persisted for 30 years and was highest in women under 55 years of age at the time of breast cancer diagnosis. Second primary breast cancers (RR = 3.0) accounted for almost one-half of all new neoplasms. However, if subsequent breast cancers were excluded, the risk for all other second cancers was only 1.15 (95% CI = 1.10-1.20), and no excess risk was seen among women over age 55 at initial breast cancer. Significant risks were found for cancers of the ovary (RR = 1.7) and uterine corpus (RR = 1.4), possibly linked with shared reproductive factors such as nulliparity or late age at menopause. Malignant melanoma (RR = 1.5), thyroid cancer (RR = 1.6), and colon cancer (RR = 1.2) were also significantly elevated; possible shared risk factors remain to be elucidated. Significant deficits of multiple myeloma and chronic lymphocytic leukemia were noted. Women who received initial radiotherapy compared with those who did not were at slightly higher risk of developing a second cancer, most notably acute nonlymphocytic leukemia, non-Hodgkin's lymphoma, and cancers of the esophagus, kidney, and connective tissue, although the nature of the associations was not always clear. Some of the soft tissue sarcomas were lymphangiosarcomas of the arm, a consequence of the lymphedema that may complicate radical mastectomy (Stewart-Treves syndrome). Women treated with radiation were at higher risk of developing a second breast neoplasm (RR = 3.9) than nonirradiated women (RR = 2.8). Further investigation should focus on the mechanisms underlying the relationships between breast, genital tract, and colon cancers, and on the effects of treatment modalities on the risk of subsequent neoplasms.
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PMID:Second cancer following cancer of the breast in Connecticut, 1935-82. 408 15

Four cases of acute myelodysplastic-non-lymphocytic leukemia secondary to cytotoxic agents were reported. Primary diseases were breast cancer (1 patient), ovarian cancer (2 patients) and multiple myeloma (1 patient). All except one (with multiple myeloma) were in clinical remission of their primary diseases. Common cytotoxic agent used was melphalan. Median total drug dose and median latent period from diagnosis of primary diseases were 1299 mg and 63 months respectively. None with the exception of one received specific treatment. All died except one who is in a very poor condition. Survival from the diagnosis of hematologic diseases ranged from 3-9 months. Clinical features, cytogenetic findings, pathogenetic mechanism and risk of the disease were briefly discussed.
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PMID:Therapy related acute non-lymphocytic leukemia: report of 4 cases. 409 7

Hybridomas secreting monoclonal antibodies specific for human lung cancer were produced by fusing immunized mouse spleen cells with mouse myeloma line X63-Ag8.653. Prior to fusion, BALB/c mice were immunized with two different histological types of human lung cancer (Squamous cell carcinoma and adenocarcinoma) obtained from surgery. An immunocytoadherence test was used to select hybridomas secreting antibodies that bound the patient's lung tumor, but did not bind to a B-lymphoblastoid cell line derived from the same patient. Five stable antibody-producing hybrids have been established and cloned. The antibodies produced by these clones have been characterized according to their light and heavy chain isotypes and for their specificity. In addition to binding to the tumor used for immunization, the antibodies bound to other lung tumors of the same histological type (i.e., squamous cell or adenocarcinoma). This reactivity was observed with both established lung tumor cell lines and with fresh tumors obtained from biopsy of patients in our clinic. Some significant reactivity was also observed with large cell carcinoma but the antibodies did not react with small cell carcinomas of the lung, bronchiolo-alveolar cell carcinoma, cancer of the esophagus and stomach, melanomas, several types of leukemias, normal human lung tissue, fibroblasts, or erythrocytes of type A, B, or O. Two of the five antibodies, 5C7 and 5E8 cross-reacted with one breast cancer obtained from surgery, and 5C7 also cross-reacted with one melanoma biopsy specimen. These results suggest that we have generated monoclonal antibodies that recognize a set of antigenic determinants that are commonly expressed on a portion of human lung tumors that are not detectable on a variety of other human tumors or normal human tissue.
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PMID:Monoclonal antibodies specific for two different histological types of human lung carcinoma. 609 Mar 7

Thirty-eight patients with advanced breast cancer, multiple myeloma, and malignant lymphoma were treated with partially purified (about 0.1%) leukocyte interferon. Patients were treated with a remission-induction schedule of 3 million to 9 million antiviral units daily intramuscularly for 4 to 26 weeks. Responding patients were maintained on a schedule of 3 million U three times weekly. Tumor regression was observed in seven of 17 patients with breast cancer. Six of 10 patients with multiple myeloma responded with a decrease of at least 50% in serum myeloma protein levels or Bence Jones protein excretion. Six of the 11 lymphoma patients achieved tumor regression. Complete remissions occurred in two patients. Of the 19 responding patients, five remain on study for 52 to 63 weeks. Toxicity included low-grade fever, fatigue, anorexia, and partial alopecia. Myelosuppression (lowest median leukocyte count, 2500/mm3; granulocytes, 1300/mm3) occurred in most patients. On the basis of this pilot study, we conclude that leukocyte interferon can induce tumor regression in patients with advanced cancer.
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PMID:Leukocyte interferon-induced tumor regression in human metastatic breast cancer, multiple myeloma, and malignant lymphoma. 615 12

Radioimmunological assays of carcino-embryonic antigen (CEA) and beta 2 microglobulin were carried out in 61 cases of malignant bone disease, including myeloma and metastases from carcinomas of the breast and prostate. CEA assays seemed to be of greater interest in mammary cancer metastases and beta 2 microglobulin assays in prostatic cancer metastases and myeloma. The correlation which appeared between CEA levels of the outcome of breast cancer metastases was of assistance in adjusting treatment. Combining CEA and beta 2 microglobulin assays would enhance their usefulness in current practice.
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PMID:[Carcino-embryonic antigen and beta 2 microglobulin in malignant bone diseases. 61 cases (author's transl)]. 617 40

Fusion of splenic lymphocytes from Lewis rats, immunized with affinity-purified estrogen receptor from the cytosol of MCF-7 human breast cancer cells, with two different mouse myeloma lines, has provided 13 monoclonal hybridoma lines secreting antiestrophilin antibodies, each of which (with one possible exception) recognizes a different antigenic determinant in the human receptor molecule. Of this library of monoclonal antibodies, some react with estrophilin from all sources tested, some react with mammalian but not avian receptors, whereas one preparation appears specific for estrophilin from primate sources. By proteolytic digestion under controlled conditions with mercury-deactivated papain, chymotrypsin, and trypsin, respectively, it is possible to remove sequentially the determinants recognized by one, two or three of the monoclonal antibodies, leaving the epitopes for the six remaining antibodies investigated on the steroid-binding portion of the receptor. The proteolytic fragment containing the epitope most readily removed (by mercuripapain) also contains the DNA-binding domain of the activated receptor molecule. Immunocytochemical staining, using the peroxidase procedure with various monoclonal antibody preparations, of frozen sections of human breast cancer tissue, fixed in ethanol or in picric acid-formaldehyde reagent, shows clearly that the majority of the native receptor, which appears in the cytosol after tissue homogenization, is actually localized within the nuclear compartment in the intact cell. The immunocytochemical technique also permits the identification of mixed populations of receptor-containing and non-containing cells in human breast cancers.
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PMID:Immunochemical studies of estrogen receptors. 620 Jul

Fusion of spleen cells, from mice immunized against the human hormone-dependent breast cancer cell line ZR-75-1, with murine myeloma cells resulted in the establishment of a hybridoma cell line, HY59-H10 (H59). The purified monoclonal IgM produced by the hybridoma reacts with the most differentiated human breast tumor cell lines but not with cells derived from normal breast secretions or with numerous other malignant cell lines. Of 106 biopsy specimens examined, H59 bound to 54% of malignant breast specimens, to 83% of fibroadenomas, and to 82% of specimens containing fibrocystic disease.
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PMID:Characterization of a monoclonal antibody reactive with a subset of human breast tumors. 627 51


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