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)

Lower prevalence of non-reproductive system cancers among former college athletes. Med. Sci. Sports Exerc., Vol. 21, No. 3, pp. 250-253, 1989. The prevalence (lifetime occurrence) rates of cancers of nonreproductive organs and tissues were determined for 5,398 living alumnae, 2,622 of whom were former college athletes and 2,776 who had been nonathletes, from data on medical history, reproductive history, athletic training, and diet. The non-reproductive system cancers were divided into two classes: class I, which included cancers of the digestive system, thyroid, bladder, lung, and other sites and hematopoietic cancers (lymphoma, leukemia, myeloma, and Hodgkin's disease), and class II, which included skin cancers and cutaneous melanoma. The former college athletes had a significantly lower prevalence of class I cancers compared to the nonathletes; the age-adjusted relative risk (RR) equals 3.34, 95% confidence limits (1.35, 8.33), P = 0.009. In contrast, the prevalence rates of malignant melanomas and skin cancers did not differ significantly between the former athletes and nonathletes. The age-adjusted RR did not differ from 1.0. The lower prevalence rate of class I cancers among the former athletes is in accord with previous findings of a significantly lower prevalence rate of breast cancer and cancers of the reproductive system among former college athletes compared to nonathletes.
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PMID:Lower prevalence of non-reproductive system cancers among female former college athletes. 278 2

Recently, the National Cancer Institute published a comprehensive monograph on multiple primary cancers in Connecticut and Denmark. This paper summarizes some of the observations made on the Connecticut population. Data compiled by the Connecticut Tumor Registry have extended our knowledge about the patterns of multiple primary cancers, especially among long-term survivors of cancer and among patients with relatively rare tumors about which little information currently exists. When compared with the general Connecticut population, cancer patients had a 31 percent (RR = 1.31) increased risk of developing a second cancer and a 23 percent (RR = 1.23) elevated risk of second cancer at a different site from the first. Common environmental exposures seemed responsible for the excess occurrence of many second cancers, particularly those related to cigarette smoking, alcohol consumption, or both. For example, persons with epithelial cancers of the lung, larynx, esophagus, buccal cavity, and pharynx were particularly prone to develop new cancers in the same or contiguous tissue throughout their lifetimes. Cancers of the colon, uterine corpus, breast, and ovary frequently occurred together, suggesting underlying hormonal or dietary influences. Only patients with prostate cancer were at significantly low risk for second cancer development; this might be an artifact of case finding, since advanced age at initial diagnosis was generally associated with an underascertainment of second cancers. Radiotherapy may have caused rectal and other cancer among patients with cancers of the female genital tract, and leukemia among patients with uterine corpus cancer. Chemotherapy with alkylating agents probably contributed to the excess of acute nonlymphocytic leukemia following multiple myeloma or cancers of the breast and ovary. Genetic susceptibility seemed to explain some tumor complexes, such as the multiple occurrences of cutaneous melanoma and the excess of bone cancer following retinoblastoma. Research into multiple cancer syndromes should enhance our understanding of carcinogenic factors and mechanisms and the development of strategies for cancer prevention and control.
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PMID:Multiple primary cancers in Connecticut, 1935-82. 354 9

A screening method is described to select monoclonal antibodies (Mabs) that bind to ocular melanoma-associated antigens (MAAs) retained in formalin-fixed, paraffin-embedded tissue sections. Small sections of epithelioid or spindle-cell-type uveal melanomas were cut into 2 mm cubes and reembedded in one block. Microslides were cut from this block and used to screen hybridoma supernatant fluid. Using this screening method, three MAbs were selected from two separate fusions of mouse myeloma cells with spleen cells of mice immunized previously with either ocular melanoma cells obtained fresh at enucleation or cells of a cutaneous melanoma cell line. Although all three MAbs showed similar specificities, MAb8-1H showed the strongest immunohistochemical reaction and was studied further in detail. MAb8-1H bound to 91% (71/79) of the choroidal or ciliochoroidal melanomas tested, indicating a high prevalence of this antigen in uveal melanomas. The antigen defined by MAb8-1H was isolated, purified, and partially characterized as a 40,000-50,000 dalton, highly glycosylated protein rich in glycine, serine, and glutamic acid, as is typical of a mucin-type glycoprotein.
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PMID:Tissue distribution and biochemical properties of an ocular melanoma-associated antigen. 390 53

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

A comparison is made of the immunohistochemistry at the ultrastructural level of three monoclonal antibodies directed against surface components of DNS cells. Hybridomas secreting these antibodies were obtained from two cell fusions of a rat myeloma cell line and immune splenocytes derived from rats immunized either with primary mouse brain cultured cells or membrane components. In cultures one antibody, anti-BSP2 (Brain Surface Protein-2), was preferentially directed against neurons while another, anti-BSP-3 (Brain Surface Protein-3), preferentially labeled astrocytes. In mouse cerebellar sections, both labeled the surface of Purkinje cells, granule cells and astrocytes. In addition a cytoplasm localization was apparent in granule cells and astrocytes. Another antibody anti-MESA-1 (Mouse Endothelial Surface Antigen-1) reacted exclusively with the surface of endothelial cells lining blood vessels. These data are discussed with reference to the biochemical nature of the corresponding antigens and to known glycoproteins of neural cell membranes.
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PMID:Monoclonal antibodies as neural cell surface markers. 705 Jul 55

Risk of cancer mortality from 1973 to 1985 in persons born in the Indian subcontinent who migrated to England and Wales was analysed by ethnicity, and compared with cancer mortality in the England and Wales native population, using data from England and Wales death certificates. There were substantial highly significant raised risks in Indian ethnic migrants for cancers of the mouth and pharynx, gall bladder, and liver in each sex, larynx and thyroid in males, and oesophagus in females. There were also substantial raised risks in these migrants of each sex for non-Hodgkin's lymphoma and myeloma. For the mouth and pharynx, and liver in each sex, and gall bladder in females, there were also raised risks of lesser magnitude in British ethnic migrants. For colon and rectal cancer and cutaneous melanoma in each sex, ovarian cancer in women and bladder cancer in men, there were appreciable significantly reduced risks in the Indian ethnic migrants not shared by those of British ethnicity. Appreciable raised risks in British ethnic migrants not shared by those of Indian ethnicity occurred for nasopharyngeal cancer in males, soft tissue malignancy in both sexes and non-melanoma skin cancer in males. In migrants of both ethnicities there were appreciable significantly raised risks in each sex for leukaemia and decreased risks in each sex for gastric cancer, for lung cancer except in females of British ethnicity and in males for testicular cancer. The results suggest the need for public health measures to combat the high risks of oral and pharyngeal cancers and liver cancer in the Indian ethnic immigrant population of England and Wales, by prevention of betel quid chewing and hepatitis transmission respectively. The data also imply that early exposures or early acquired behaviours in India, or exposures during migration, may increase the risk of leukaemia and reduce the risks of gastric and testicular cancers in the migrants irrespective of their ethnicity. Aetiological studies would be worthwhile to investigate the reasons for the sizeable decreased risk of colon and rectal cancer and increased risk of gall bladder cancer in each sex and the increased risk of thyroid and laryngeal cancer in males and oesophageal cancer in females of Indian ethnicity but not of British ethnicity who have migrated from the Indian subcontinent.
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PMID:Cancer mortality in Indian and British ethnic immigrants from the Indian subcontinent to England and Wales. 757 89

We calculated the short-term and long-term risks of developing cancer among 3,766 patients with a diagnosis of cutaneous melanoma in situ in Sweden from 1958 to 1992. In total, 393 patients developed a primary cancer at any site compared with an expected number of 177 [standardized incidence ratio (SIR) = 2.2, 95% confidence interval (CI) = 2.0-2.4]. Patients below 60 years of age at diagnosis had the highest SIR (2.7, 95% CI = 2.3-3.2). The overall risks were similar between men and women. The highest risk was seen during the first year of follow-up, though the risk remained elevated also after 15 or more years of follow-up. For specific sites, the highest SIR was found for developing invasive cutaneous malignant melanoma (SIR = 22.2). The risk of subsequent primary non-melanoma skin cancer was elevated 8-fold in men and almost 7-fold in women. An elevated risk was also found for female breast cancer (SIR = 1.4). Especially among women, other sites with increased cancer risk (though not significant) were non-Hodgkin's lymphoma (SIR = 1.9), multiple myeloma (3.2) and cancers of the colon (1.6) and pancreas (1.6). In conclusion, patients with melanoma in situ run a generally increased risk of developing primary cancers, especially cutaneous malignant melanoma and non-melanoma skin cancer. The increased long-term risk of cancer after diagnosis of melanoma in situ may be due to continuing carcinogenic exposure or to intrinsic tumor susceptibility.
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PMID:Cancer risk in patients with earlier diagnosis of cutaneous melanoma in situ. 1049 22

We studied familial risks in invasive and in situ cutaneous melanoma by comparing the occurrence of melanoma, or discordant cancer, between parents and offspring, and between siblings, based on the Swedish Family Cancer Database of over 10 million individuals. Offspring were 0-66 y of age. Cancers were obtained from the Swedish Cancer Registry from 1961 to 1998. The study was based on 24,818 invasive and 5510 in situ cases of melanoma. Standardized incidence ratios were calculated for familial risk. The standardized incidence ratios for offspring was 2.40 (95% confidence intervals: 2.10-2.72) when only the parent had melanoma and it was 2.98 (95% confidence intervals: 2.54-3.47) when only a sibling was affected; when both a parent and a sibling were affected the standardized incidence ratios was 8.92 (95% confidence intervals: 4.25-15.31). The respective population attributable risks were 1.38, 1.20, and 0.10%. The familial risk showed a clear age dependence and somewhat higher risk in in situ melanoma than in the invasive counterpart. The highest standardized incidence ratio of 61.78 (5.82-227.19) was noted for offspring whose parent had multiple melanomas. Superficially spreading melanoma showed the highest familial risk both among invasive and in situ tumors. Melanoma associated with breast, nervous system, and skin cancers, and in situ melanoma possibly also with connective tissue and thyroid tumors and multiple myeloma.
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PMID:Familial and attributable risks in cutaneous melanoma: effects of proband and age. 1508 79

Using the unique Utah Population Database, which links Utah genealogical data with Utah cancer data, we examined risks for other cancers among relatives of 4,079 melanoma cases. Age- and sex-specific rates for 35 different cancer sites were calculated, and used to estimate relative risks among relatives. In addition to the well-recognized risk for melanoma among first-degree relatives, we found significantly increased risks for prostate, breast, and colon cancers, non-Hodgkin's lymphoma, and multiple myeloma, ranging from 32 to 72% increased risk. Among second-degree relatives, in addition to increased risk for melanoma, we identified significantly increased risks for prostate cancer and multiple myeloma (27 and 53% increase, respectively). Among first-degree relatives of melanoma cases diagnosed before the age of 40 years, we found significantly elevated risks for cutaneous melanoma (380% increase) and prostate cancer (83% increase). Significantly increased risks for prostate cancer and multiple myeloma in both first- and second-degree relatives of melanoma cases are suggestive of heritable cancer syndromes. The increased risks for five additional cancer types in first-degree relatives of melanoma cases suggest that individuals with a family history of melanoma should strictly adhere to recommended screenings for all cancers.
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PMID:Population-based assessment of non-melanoma cancer risk in relatives of cutaneous melanoma probands. 1690 18

Ocular melanoma is a rare neoplasm with a poorly understood etiology, especially concerning its link with ultraviolet-light exposure. Studying the risk of second primary cancers may help to formulate causal hypotheses. We used data from 13 cancer registries, including 10,396 first occurring ocular melanoma cases, and 404 second occurring cases. To compare the second cancer incidence in ocular melanoma patients to that in noncancer population, we calculated standardized incidence ratios (SIRs) of 32 types of cancer. We also calculated SIRs of second ocular melanoma after other primaries. Ocular melanoma patients had significantly increased risk of cutaneous melanoma (SIR = 2.38, 95% CI 1.77-3.14), multiple myeloma (SIR = 2.00, 1.29-2.95), and of liver (SIR = 3.89, 2.66-5.49), kidney (SIR = 1.70, 1.22-2.31), pancreas (SIR = 1.58, 1.16-2.11), prostate (SIR = 1.31, 1.11-1.54), and stomach (SIR = 1.33, 1.03-1.68) cancers. Risks of cutaneous melanoma were highly variable between registries and were mainly increased in females, in younger patients, in first years following diagnosis, and for patients diagnosed after 1980. The risk of ocular melanoma was significantly increased only after prostate cancer (SIR = 1.41, 1.08-1.82). Risk of cutaneous melanoma after ocular melanoma had epidemiological patterns, similar to cutaneous melanoma screening in the general population. The increased risk of cutaneous melanoma would be largely due to greater skin cancer surveillance in ocular melanoma patients, and not to common etiological factors. The high SIR found for liver cancer may be explained by misclassification bias. Common etiological factors may be involved in ocular and prostate cancers.
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PMID:Associations between ocular melanoma and other primary cancers: an international population-based study. 1703 22


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