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Query: UMLS:C0019829 (Hodgkin's disease)
 30,247 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The mortality of all 14,327 people who were known to have been employed at the Sellafield plant of British Nuclear Fuels at any time between the opening of the site in 1947 and 31 December 1975 was studied up to the end of 1983. The vital state of 96% of the workers was traced satisfactorily and 2277 were found to have died, 572 (25%) from cancer. On average the workers suffered a mortality from all causes that was 2% less than that of the general population of England and Wales and 9% less than that of the population of Cumberland (the area in which the plant is sited). Their mortality from cancers of all kinds was 5% less than that of England and Wales and 3% less than that of Cumberland. In the five years after their first employment Sellafield workers had an overall mortality that was 70% of that of England and Wales, probably due to healthier members of the population being selected for employment. Raised death rates from cancers of several specific sites were found, but only for those of ill defined and secondary sites was the excess statistically significant (30 observed, 19.7 expected). For cancers of the liver and gall bladder there was a significant deficit of deaths (four observed, 10.5 expected). Workers in areas of the plant where radiation exposure was likely were issued with dosimeters to measure their external exposure to ionising radiations. Personal dose records were maintained for workers who entered such areas other than infrequently. Workers with personal dose records ("radiation" workers) had lower death rates from all causes combined than other workers but the death rates from cancer in the two groups were similar. Compared with the general population radiation workers had statistically significant deficits of liver and gall bladder cancer, lung cancer, and Hodgkin's disease. There were excesses of deaths from myeloma (seven observed, 4.2 expected) and prostatic cancer (19 observed, 15.8 expected) but these were not significant and there was no evidence of an excess of leukaemia (10 deaths observed, 12.2 expected) or cancer of the pancreas (15 observed, 17.8 expected). Non-radiation workers had a significant deficit of leukaemia (one death observed, 5.1 expected) and a significant excess of cancers of ill defined and secondary sites (13 deaths observed, 5.8 expected). For no type of cancer was the ratio of observed to expected deaths significantly different between radiation and non-radiation workers.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Mortality of workers at the Sellafield plant of British Nuclear Fuels. 309 83

In 1982, the American Cancer Society enrolled over 1.2 million American men and women in a prospective mortality study of cancer and other causes in relation to different risk factors. The 2-year mortality of 461,981 males aged 40-79 years with known smoking habit has been analyzed in relation to exposure to diesel exhaust (DE) and to employment in selected occupations related to DE exposure. The relative risk (RR) for all causes of death for those exposed was 1.05 (95% confidence interval [CI]: 0.97-1.13). For lung cancer, the RR was 1.18 (95% CI: 0.97-1.44). A dose-response effect was present. Railroad workers, heavy equipment operators, miners, and truck drivers had a higher mortality both for all causes and for lung cancer when compared with subjects with other occupations and no exposure to DE. Truck drivers exposed to DE were not at excess risk of lung cancer if compared with truck drivers unexposed to DE, but a trend of increasing risk with duration of exposure was suggested. DE exposure was also associated with increase in mortality for accidents, cerebrovascular disease, arteriosclerosis, and cirrhosis of the liver. An association based on small numbers was also present for Hodgkin's disease and lymphoid leukemia. No association with chronic non-neoplastic pulmonary diseases or with bladder cancer was found.
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PMID:Diesel exhaust exposure and mortality among males in the American Cancer Society prospective study. 318 56

Cancer incidence trends from the late 1940s to 1983-84 were assessed among white residents of five geographic areas (Atlanta, Connecticut, Detroit, Iowa, San Francisco-Oakland) by means of data derived from several National Cancer Institute surveys, the Connecticut Tumor Registry, and the Surveillance, Epidemiology, and End Results Program. Incidence trends were compared with mortality trends for the entire United States and for the same five study areas. This study documented rising incidence and mortality rates for four cancers: lung cancer, melanoma of the skin, multiple myeloma, and non-Hodgkin's lymphomas. Increases in lung cancer continued through the early 1980s, but the rate of increase has been moderating during recent years, particularly among males and at younger ages for whom recent declines are evident. Overall, lung cancer incidence rates increased more than 220 and 400% among males and females, respectively. Although much rarer than lung cancer, melanoma of the skin and multiple myeloma increased greatly until the early 1980s among both males and females. The overall rate of increase in melanoma incidence among males was greater than that for lung cancer, and the rate of increase in multiple myeloma mortality among females was exceeded only by that for lung cancer. Increases of 70-120% were observed for non-Hodgkin's lymphomas. Increases in incidence and mortality rates for pancreatic cancer were apparent during the early years but less conspicuous in recent years. Laryngeal and kidney cancer rates generally increased substantially, although the changes were not remarkable for laryngeal cancer mortality among males and kidney cancer mortality among females. The rates for cancers of the mouth and pharynx increased among females but not males. Prostate, colon, and bladder cancer incidence rates increased more than 65% among males, whereas mortality rates changed only moderately. The incidence of thyroid cancer increased more than 75% among both sexes until the late 1970s, but mortality rates have declined during the period of study. Breast cancer incidence increased 30%, whereas mortality rates remained remarkably constant. The incidence of corpus uteri cancer increased dramatically during the mid-1970s and decreased substantially thereafter; these changes were not reflected in the mortality rates, which continually declined during the entire time period. The incidence of testicular cancer increased more than 90% and that of Hodgkin's disease did not change greatly; however, mortality rates for both cancers declined more than 50% since the late 1960s and early 1970s.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Cancer incidence and mortality trends among whites in the United States, 1947-84. 330 21

We observed nine cases of transitional-cell carcinoma of the urinary bladder among patients who had had long-term treatment of other cancers with cyclophosphamide. Seven of the bladder carcinomas occurred within a cohort of 471 patients treated for non-Hodgkin's lymphomas. In this cohort the relative risk of bladder cancer was 6.8 (95 percent confidence interval, 3.2 to 14.2). The cumulative risk (mean +/- SE) was 3.5 +/- 1.8 percent 8 years after the start of treatment with cyclophosphamide and 10.7 +/- 4.9 percent after 12 years. Three of the nine patients were 50 years of age or younger; seven died with progressive bladder cancer. Subsequently, an additional patient had acute nonlymphocytic leukemia. Hemorrhagic cystitis was observed in 33 patients (cumulative risk, 11.8 +/- 2.1 percent after five years). Development of carcinoma of the urinary bladder was not related to previous hemorrhagic cystitis. The results caution against long-term treatment with cyclophosphamide for diseases with a favorable prognosis.
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PMID:Carcinoma of the urinary bladder after treatment with cyclophosphamide for non-Hodgkin's lymphoma. 335 96

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

Mitoxantrone is an anthraquinone antineoplastic agent with structural similarities to doxorubicin. It has a mechanism of action similar to the anthracyclines. Its primary elimination route is hepatic metabolism (only seven percent renal excretion) and it has a terminal half-life of approximately 40 hours. Mitoxantrone has significant activity in the treatment of metastatic breast cancer, acute leukemias, and non-Hodgkin's lymphoma. Some activity is reported in head and neck cancer, Hodgkin's, myeloma, bladder cancer, prostate cancer, non-small-cell lung cancer, and liver cancer. There is a suggestion of incomplete cross-resistance between mitoxantrone and the anthracyclines in certain neoplasms. Some activity is reported with mitoxantrone in patients refractory to the anthracyclines in breast cancer, acute leukemias, and non-Hodgkin's lymphomas. The usual doses used in solid tumors and in lymphomas are mitoxantrone 12-14 mg/m2 iv q3-4wk and in leukemias is mitoxantrone 12 mg/m2/d X 5 d iv for initial induction.
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PMID:Mitoxantrone. 351 24

Eleven population-based cancer registries tabulated second cancers among 133,411 patients diagnosed with testicular cancer, ovarian cancer or Hodgkin's disease between 1945 and 1984. Overall, 3,157 second cancers were observed, as compared with 2,420 expected at least one year after the first cancer. Survivors of testicular and ovarian cancer experienced 30% and 20% more cancers respectively than the general population comparison group, and patients previously diagnosed with Hodgkin's disease had an 80% excess of cancer. No information was available either on treatment for the first cancer, or other risk factors. However, temporal patterns in the risk of specific second cancers were analysed, with particular reference to the possible role of therapy for the first cancer. Leukaemia of the acute or non-lymphatic type, which has been previously linked to alkylating agent therapy, occurred in excess following all 3 first cancers, as did non-Hodgkin's lymphoma (overall relative risks of 6.1 and 1.8 respectively, with considerably higher relative risks following Hodgkin's disease). Other cancers for which important and plausibly therapy-induced excesses occurred were lung cancer following Hodgkin's disease (relative risk 1.9), breast cancer following Hodgkin's disease (relative risk 1.4) and bladder cancer following ovarian cancer and Hodgkin's disease (relative risks 1.7 and 2.2 in women, respectively). Rarer sites at which striking excesses occurred were the salivary gland, thyroid, bone and connective tissue. There were smaller, but clear excesses for cancers of the rectum and colon following ovarian cancer and testicular cancer, skin cancer following Hodgkin's disease, and kidney cancer following ovarian cancer. Overdiagnosis, misclassification of metastases and confounding by other risk factors were all considered as explanations of observed excesses. Nonetheless, it appeared that there are clear excess risks for cancers other than acute leukaemia which must be ascribed to therapy for the first cancer, especially in view of the possible under-reporting in registry material. Case-control studies are under way to provide information on the role of specific aspects of therapy.
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PMID:Second malignancies following testicular cancer, ovarian cancer and Hodgkin's disease: an international collaborative study among cancer registries. 357 May 50

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

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

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


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