Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study is to calculate a risk of lung cancer in a cohort of 1411 sarcoidosis cases which were followed for a 3 year period from 1984 to 1987. The physicians were requested to answer the questionnaire about progress of the disease by mail. Excess death was investigated using standardized mortality ratio (SMR). The expected number of deaths was calculated from Japanese sex-age specific mortality rate in 1985, using person-year method. Death from all causes and cancers did not show any excess. SMR being 0.98 and 0.97 respectively. The SMR of lung cancer was 3.26 (male: 5.56, female: 3.03), being statistically significant. The SMR of lung infection was 4.2, with statistical significance. The SMR of other main causes of death in Japan i.e., cerebrovascular accident, ischemic heart diseases and heart failure was less than 0.88. It is probably that sarcoidosis is a risk factor of lung cancer. The SMR of leukemia and uterine cancer was 5.88 and 8.70, respectively, though the observed number of leukemia was too small to conclude how high the cancer risk is among sarcoidosis patients. Gastric cancer, hepatic cancer and colon cancers were not observed.
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PMID:Excess death of lung cancer among sarcoidosis patients. 166 41

Cancer mortality in relation to radiation dose was evaluated among 4153 women treated with intrauterine radium (226Ra) capsules for benign gynecologic bleeding disorders between 1925 and 1965. Average follow up was 26.5 years (maximum = 59.9 years). Overall, 2763 deaths were observed versus 2687 expected based on U.S. mortality rates [standardized mortality ratio (SMR) = 1.03]. Deaths due to cancer, however, were increased (SMR = 1.30), especially cancers of organs close to the radiation source. For organs receiving greater than 5 Gy, excess mortality of 100 to 110% was noted for cancers of the uterus and bladder 10 or more years following irradiation, while a deficit was seen for cancer of the cervix, one of the few malignancies not previously shown to be caused by ionizing radiation. Part of the excess of uterine cancer, however, may have been due to the underlying gynecologic disorders being treated. Among cancers of organs receiving average or local doses of 1 to 4 Gy, excesses of 30 to 100% were found for leukemia and cancers of the colon and genital organs other than uterus; no excess was seen for rectal or bone cancer. Among organs typically receiving 0.1 to 0.3 Gy, a deficit was recorded for cancers of the liver, gall bladder, and bile ducts combined, death due to stomach cancer occurred at close to the expected rate, a 30% excess was noted for kidney cancer (based on eight deaths), and there was a 60% excess of pancreatic cancer among 10-year survivors, but little evidence of dose-response. Estimates of the excess relative risk per Gray were 0.006 for uterus, 0.4 for other genital organs, 0.5 for colon, 0.2 for bladder, and 1.9 for leukemia. Contrary to findings for other populations treated by pelvic irradiation, a deficit of breast cancer was not observed (SMR = 1.0). Dose to the ovaries (median, 2.3 Gy) may have been insufficient to protect against breast cancer. For organs receiving greater than 1 Gy, cancer mortality remained elevated for more than 30 years, supporting the notion that radiation damage persists for many years after exposure.
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PMID:Cancer mortality following radium treatment for uterine bleeding. 221 30

The lipophilic antitumor alkaloid acronycine (ACRO) was solubilized in the cosolvent system used for etoposide. ACRO in this etoposide diluent (VPD) was found to be cytotoxic (less than or equal to 50% colony formation in soft agar) in fresh human tumors from patients with renal cell cancer, ovarian cancer, uterine cancer, and metastatic tumors of unknown primary. In P-glycoprotein-positive, multidrug-resistant (MDR) cell lines, ACRO in VPD was active in MDR Chinese hamster ovary cells but not against MDR L1210 murine leukemia cells, 8226 human myeloma cells, or human CCRF-CEM lymphoblasts. In mice, ACRO in VPD was active in two solid tumor models and an i.p. MOPC-315 plasmacytoma model. ACRO i.p. in 10% VPD (v/v%) produced significant tumor growth delays in (a) nude mice bearing human MCF-7 breast cancer xenografts and (b) C57BL mice bearing colon 38 tumor. In MOPC-315-bearing mice, a single i.p. ACRO dose of 25 mg/kg was as effective as melphalan (15 mg/kg) at prolonging life span. Finally, ACRO pharmacokinetics was evaluated in mice given single 25-mg/kg doses i.p. or p.o. The oral bioavailability of an ACRO solution in VPD was only 50% but both i.p. and p.o. regimens achieved plasma levels greater than 1.0 micrograms/ml. The plasma half-life was just under 2 h. These results show that parenteral ACRO in VPD comprises a cytotoxic antitumor agent with improved bioavailability over p.o. administration. ACRO is active in vitro against several human solid tumors but is cross-resistant in 3 of 4 MDR tumor cell lines. The prior clinical activity of p.o. ACRO in myeloma and the new results in MOPC-315 plasmacytomas in mice suggest that ACRO in VPD could have activity against human multiple myeloma.
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PMID:Antitumor activity and murine pharmacokinetics of parenteral acronycine. 291 Apr 53

Increasing attention is being given to the occurrence of second primary tumours among survivors of childhood cancer. Our aims are to examine the risk of a subsequent primary, particularly in relation to chemotherapy, in a well-defined cohort; and to examine interesting associations between first and second primary tumours in relation to therapy generally and chemotherapy in particular among a less well-defined group of cases developing at least two primary tumours. There is suggestive evidence from our data that chemotherapy is involved either directly or indirectly in the development of secondary leukaemia, and this confirms previous work. Our data, although based on small numbers, indicate consistent evidence of an association between cyclophosphamide and an increased risk of a second primary tumour following retinoblastoma; this may be due to cyclophosphamide, radiotherapy or an interaction between the two. Two cases of uterine cancer were observed among three patients given oestrogen replacement therapy.
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PMID:Second primary tumours among survivors of childhood cancer treated with anticancer drugs. 347 36

Second malignancies were observed in 181 cases after treatment of antecedent breast cancer, among 5,302 primary breast cancer cases. The accumulated incidence of double cancer was as follows: 2.8% for 5 years, 5.2% for 10 years, 7.6% for 15 years, and 10.0% for 20 years. The observed incidence of second malignancy for all sites was 1.58 times as frequent as in the normal group. Statistically significant increased risks were observed for opposite breast cancer (O/E ratio 5.92), ovarian cancer (O/E ratio 4.47), corpus uterine cancer (O/E ratio 5.97) and thyroid cancer (O/E ratio 5.07). Among 5,302 cases, 2,431 (45.9%) underwent adjuvant chemotherapy. In chemotherapy groups, significantly increased risk of stomach cancer, thyroid cancer, leukemia and hepatoma was observed, but there were no remarkable differences between the MMC group and the CPA group. However, in the MMC + CPA combination treatment group, the risk of stomach cancer and leukemia was higher than in the single drug treatment groups. When multiple drugs were administered in large doses as long-term adjuvants, the risk of second malignancy seemed to become greater.
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PMID:[Effects of surgery and adjuvant chemotherapy of breast cancer on the incidence of a second malignancy]. 372 65

In an effort to establish a survival curve model which could help to evaluate adjuvant therapy, two equations were presented to approximate the various clinical curves. These curves usually show three different segments, describing high-risk, intermediate-risk and low-risk groups. The percentage of patients and the annual mortality in each risk group can be calculated from the coefficients of the equation. The present study analysed the survival curves of variously treated uterine cancer and stomach cancer after resection on the one hand, and of adjuvant therapy of breast cancer, malignant melanoma and acute lymphoid leukaemia on the other hand. This method of analysis should be useful for understanding and comparison of curves of phase III trials.
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PMID:Comparison of clinical protocols through the mathematical results analysis of survival curves. 373 55

We calculated sex- and age-specific familial relative risks (FRRs) of cancer in offspring of cancer probands at 19 male and 20 female cancer sites, based on the nationwide Family Cancer Database from Sweden. The proportion of familial cancers among all cancers was also determined. The database contained 550,000 primary cancers. The familial risk at known sites: colon, breast, ovary, testis, skin (melanoma), nervous system, thyroid and other endocrine glands were confirmed. The FRR of thyroid cancer exceeded any other cancer and was over twice as high for male as for female offspring, and appeared to constitute an early- and late-onset component. Novel register-based findings were familial risks in cervical and uterine cancer, and in male offspring of male probands kidney and skin (mainly squamous cell) cancer. Familial risks were noted also for lung cancer, lymphoma and leukaemia but they may have largely environmental causes. The proportion of familial cancers depended on the site, ranging from 11% in prostate to 8.7% in female breast and to well below 1% at many sites.
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PMID:Familial cancers in a nationwide family cancer database: age distribution and prevalence. 1053 56

Nitrate contamination of drinking water may increase cancer risk, because nitrate is endogenously reduced to nitrite and subsequent nitrosation reactions give rise to N-nitroso compounds; these compounds are highly carcinogenic and can act systemically. We analyzed cancer incidence in a cohort of 21,977 Iowa women who were 55-69 years of age at baseline in 1986 and had used the same water supply more than 10 years (87% > 20 years); 16,541 of these women were on a municipal supply, and the remainder used a private well. We assessed nitrate exposure from 1955 through 1988 using public databases for municipal water supplies in Iowa (quartile cutpoints: 0.36, 1.01, and 2.46 mg per liter nitrate-nitrogen). As no individual water consumption data were available, we assigned each woman an average level of exposure calculated on a community basis; no nitrate data were available for women using private wells. Cancer incidence (N = 3,150 cases) from 1986 through 1998 was determined by linkage to the Iowa Cancer Registry. For all cancers, there was no association with increasing nitrate in drinking water, nor were there clear and consistent associations for non-Hodgkin lymphoma; leukemia; melanoma; or cancers of the colon, breast, lung, pancreas, or kidney. There were positive associations for bladder cancer [relative risks (RRs) across nitrate quartiles = 1, 1.69, 1.10, and 2.83] and ovarian cancer (RR = 1, 1.52, 1.81, and 1.84), and inverse associations for uterine cancer (RR = 1, 0.86, 0.86, and 0.55) and rectal cancer (RR = 1, 0.72, 0.95, and 0.47) after adjustment for a variety of cancer risk/protective factors, agents that affect nitrosation (smoking, vitamin C, and vitamin E intake), dietary nitrate, and water source. Similar results were obtained when analyses were restricted to nitrate level in drinking water from 1955 through 1964. The positive association for bladder cancer is consistent with some previous data; the associations for ovarian, uterine, and rectal cancer were unexpected.
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PMID:Municipal drinking water nitrate level and cancer risk in older women: the Iowa Women's Health Study. 1133 13

A family history (FH) of breast cancer (BC) is a long recognized risk factor for developing the disease. Also, there have been some reports of links between an FH and some other malignancies (mostly uterus, ovary, and prostate cancers), and an increased risk of developing BC. In this paper we present descriptive report of the occurrence pattern of malignancies in families of BC afflicted patients through 4 generations. Patients included 542 Iranian primary BC cases, presenting at an outpatient clinic for treatment and follow-up. Detailed pedigrees were drawn for each patient, and data for a total of 6220 relatives were gathered. Among the probands, 29.9% and 53.9% had a positive FH of BC and other malignancies (OM) respectively. Mean number of breast cancers was nearly double in maternal-lines versus paternal-line relatives. Also, occurrence of brain, uterus, and colorectal cancers was significantly higher in maternal-line relatives, but conversely, liver cancer showed a tendency toward paternal-line relatives (1st degree relatives excluded). The highest frequency of BC involvement was noted in 2nd degree/2nd generation, and 3rd degree/3rd generation relatives. For OMs, although gastric cancer was by far the most frequent OM across pedigrees, uterus cancer, and hematopoeitic system lesions (leukemia) predominated over gastric cancer through the 3rd and 4th generations respectively. We did not find any relation between having a positive FH of BC, and developing early-onset BC. The findings discussed in this paper were partially presented at the 18th UICC International Cancer Congress, Oslo-Norway, 30 June-5 July 2002.
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PMID:Laddering through pedigrees: family history of malignancies in primary breast cancer patients. 1450 37

The survivors of the atomic bombings in Hiroshima and Nagasaki are a general population of all ages and sexes and, because of the wide and well characterised range of doses received, have been used by many scientific committees (International Commission on Radiological Protection (ICRP), United Nations Scientific Committee on the Effects of Atomic Radiation (UNSCEAR), Biological Effects of Ionizing Radiations (BEIR)) as the basis of population cancer risk estimates following radiation exposure. Leukaemia was the first cancer to be associated with atomic bomb radiation exposure, with preliminary indications of an excess among the survivors within the first five years after the bombings. An excess of solid cancers became apparent approximately ten years after radiation exposure. With increasing follow-up, excess risks of most cancer types have been observed, the major exceptions being chronic lymphocytic leukaemia, and pancreatic, prostate and uterine cancer. For most solid cancer sites a linear dose response is observed, although in the latest follow-up of the mortality data there is evidence (p = 0.10) for an upward curvature in the dose response for all solid cancers. The only cancer sites which exhibit (upward) curvature in the dose response are leukaemia, and non-melanoma skin and bone cancer. For leukaemia the dose response is very markedly upward curving, indeed largely describable as a pure quadratic dose response, particularly in the low dose (0-2 Sv) range. Even 55 years after the bombings over 40% of the Life Span Study cohort remain alive, so continued follow-up of this group is vital for completing our understanding of long-term radiation effects in people. In general, the relative risks per unit dose among the Japanese atomic bomb survivors are greater than those among comparable subsets in studies of medically exposed individuals. Cell sterilisation largely accounts for the discrepancy in relative risks between these two populations, although other factors may contribute, such as the generally higher underlying cancer risks in the medical series than in the Japanese atomic bomb survivors. Risks among occupationally exposed groups such as nuclear workforces and underground miners are generally consistent with those observed in the Japanese atomic bomb survivors. In general, consistent patterns of variation of risk with age at exposure are also seen in all studies-risks for all cancer types diminish with increasing age at exposure. There are also excess risks of various types of non-malignant disease in the Japanese atomic bomb survivors, in particular cardiovascular, respiratory and digestive diseases. Indeed, risks are elevated to much the same degree for a number of non-malignant disease endpoints, suggestive of bias. However, in contrast with the cancer data, there is much less consistency in the pattern of risk between the atomic bomb survivors and other exposed groups; for example, radiation-associated respiratory and digestive diseases have not been seen in these other groups. Although cardiovascular risks have been seen elsewhere, particularly in medically exposed groups, in contrast with the cancer data there is much less consistency in risk between studies: risks per unit dose in epidemiological studies vary over at least two orders of magnitude, possibly as a result of confounding factors. In the absence of a convincing mechanistic explanation of epidemiological evidence, at present a cause-and-effect interpretation of the reported statistical associations for cardiovascular disease is unreliable but cannot be excluded. Further epidemiological and biological evidence will allow a firmer conclusion to be drawn.
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PMID:Cancer and non-cancer effects in Japanese atomic bomb survivors. 1945 4


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