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Query: UMLS:C0242379 (lung cancer)
 71,905 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The risk of second cancers (SCs) was assessed in 744 patients with Hodgkin's disease (HD) admitted to The Netherlands Cancer Institute from 1966 to 1983. Sixty-nine SCs were observed one month or more after start of first treatment. These included 14 cases of lung cancer, nine cases of non-Hodgkin's lymphoma (NHL), 16 cases of leukemia, and six cases of the myelodysplastic syndrome (MDS). The median interval between the diagnosis of HD and that of second lung cancer, NHL, and leukemia was 8.1, 13.3, and 5.7 years, respectively. The overall relative risks (RR) (observed/expected [O/E] ratios) of developing lung cancer, NHL, and leukemia were 4.9 (95% confidence limit [CL], 2.7 to 8.2), 31.0 (95% CL, 14.2 to 58.9) and 45.7 (95% CL, 26.1 to 74.2), respectively. At 15 years the cumulative risk of developing an SC amounted to 20.6% +/- 2.9%. The 15-year estimates of lung cancer, NHL, and leukemia were 6.2% +/- 1.9%, 5.9% +/- 2.1% and 6.3% +/- 1.7%, respectively. Increased lung cancer risk following HD has not frequently been clearly demonstrated before; that we were able to demonstrate such risk may be due to the completeness of follow-up over long periods that could be achieved in this study. Excess lung cancer risk was only noted in treatment regimens with radiotherapy (RT); also, all lung cancers arose in irradiation fields. Excess risk of leukemia was only found in treatment regimens involving chemotherapy (CT). For NHL, combined modality treatment was shown to be the most important risk factor. Risk of lung cancer and NHL increased with time since diagnosis. A time-dependent covariate analysis (Cox model) performed on leukemia and MDS showed an increasing risk with intensity of CT, age (greater than 40 years), and a splenectomy.
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PMID:Increased risk of lung cancer, non-Hodgkin's lymphoma, and leukemia following Hodgkin's disease. 275 47

The surname analysis of over 40,000 Wisconsin cancer mortalities for the period 1979 through 1985 partially reveals the relative genetic component of various major cancers. The surname frequencies and frequency distributions indicate that both tumor-promoting and tumor-suppressing genes may be involved. A number of cancers exhibit some probable genetic component, but genetic involvement seems marked in male and female leukemia and male lung cancer. Evidence is found for autosomal and sex-linked, dominant and recessive patterns. Most surprising is the strong evidence for tumor-suppressing genes for most cancers. Clustering of surnames across cancers evinces a number of Wisconsin surnames that may be involved in a cancer family syndrome.
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PMID:Surnames and cancer genes. 276 70

Cause specific mortality was analysed among 883 white male workers from a paper company in Berlin, New Hampshire. Subjects were assigned to different exposure groups on the basis of their having worked in the pulp mill, the paper mill, or elsewhere in the paper company. A standardised mortality ratio (SMR) analysis was used to compare death rates for each of the exposure groups with United States national rates. For all the subjects, deaths due to all causes, all malignant neoplasms, and lung cancer were close to the number expected and excesses were noted for cancers of the digestive system and leukaemia. Among pulp mill workers, the number of cancers of the digestive system was raised and the SMR for pancreatic cancer was especially high (SMR = 305, 95% CI = 98-712). Among paper mill workers, more deaths were due to leukaemia and cancers of the digestive system than expected. These results are consistent with the findings from other studies that employment in pulp and paper mills is associated with excess mortality due to digestive and lymphopoietic cancers.
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PMID:Mortality among pulp and paper workers in Berlin, New Hampshire. 278 69

The mortality experience of 13,385 tuberculosis patients treated between 1925 and 1954 in Massachusetts was determined through August 1986. Among 6,285 patients examined by X-ray fluoroscopy an average of 77 times during lung collapse therapy and followed for up to 50 yr (average = 25 yr), no increase in the total number of cancer deaths occurred [standardized mortality ratio (SMR) = 1.05, n = 424]. In contrast, the 7,100 patients treated by other means were at significant risk of dying from cancer (SMR = 1.3), especially of sites linked to cigarette smoking and alcohol use. Among the irradiated patients, estimates of mean radiation doses to the breast, lung, esophagus, and active bone marrow were 0.75, 0.84, 0.80, and 0.09 Gy, respectively. Cancers of the breast (SMR = 1.4, n = 62) and esophagus (SMR = 2.1, n = 14) were significantly increased. The risk of esophageal cancer, however, decreased with time since exposure. Lung cancer (SMR = 0.8, n = 69) and leukemia (SMR = 1.2, n = 17) were not elevated. Despite a wide range of doses to the lung, reaching over 8 Gy, there was no evidence of a dose response. Lung cancer risk also did not vary by time since exposure or age at exposure. Adjustment for smoking and the amount of lung tissue at risk did not appreciably modify these findings. These data suggest that frequent exposures to low doses of radiation over a period of several years increase the occurrence of cancer of the breast. When compared with studies of atomic bomb survivors, however, the fractionated exposures experienced by this cohort appear less effective in causing lung cancer than single exposures of the same total dose.
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PMID:Cancer mortality in a radiation-exposed cohort of Massachusetts tuberculosis patients. 279 Aug 25

A retrospective cohort study was carried out in 1982-1983 among 28,460 benzene-exposed workers (15,643 males, 12,817 females) from 233 factories and 28,257 control workers (16,621 males, 12,366 females) from 83 factories in 12 large cities in China. All-cause mortality was significantly higher among the exposed (265.46/100,000 person-years) than among the unexposed (139.06/100,000 person-years), as was mortality from all malignant neoplasms (123.21/100,000 versus 54.7/100,000, respectively). For certain cancers, increased mortality was noted among benzene-exposed males in comparison with that among unexposed males; the standardized mortality ratios (SMR) were elevated for leukemia (SMR = 5.74), lung cancer (SMR = 2.31), primary hepatocarcinoma (SMR = 1.12), and stomach cancer (SMR = 1.22). For females only leukemia occurred in excess among the exposed. Risk of leukemia rose as duration to exposure to benzene increased up to 15 years, and then declined with additional years of exposure. Leukemia occurred among some workers with as little as 6 to 10 ppm average exposure and 50 ppm-years (or possibly less) cumulative lifetime exposure (based on all available measurements for the exposed work units). Among the 30 leukemia cases identified in the exposed cohort, the proportion of subjects with acute lymphocytic leukemia was substantially lower and the proportion with acute nonlymphocytic leukemias was higher than in the general population. During 1972 to 1981, the annual incidence of leukemia ranged from 5.83 to 28.33 per 100,000 with higher rates occurring in the interval 1977 to 1981 than in the earlier years of the study period.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A retrospective cohort study of leukemia and other cancers in benzene workers. 279 42

A series of case-control studies was conducted to investigate cancer risks among farmers. These studies were based on Missouri Cancer Registry data for 15,000 white male patients, including 1720 subjects classified as farmers, registered between 1984 and 1988. For each cancer site, all other cancer registrations formed the control group. The largest risks among farmers were found for lip cancer (odds ratio [OR], 3.07; 95% confidence interval [CI], 1.99 to 4.73) and cancer of the bone (OR, 2.02; 95% CI, 0.66 to 5.81). Elevated risks were observed for several other sites, including the nasal cavity and sinuses (OR, 1.66; 95% CI, 0.54 to 4.70), prostate (OR, 1.33; 95% CI, 1.18 to 1.51), non-Hodgkin's lymphoma (OR, 1.40; 95% CI, 1.04 to 1.85), and multiple myeloma (OR, 1.40; 95% CI, 0.87 to 2.24). Other smaller elevations in risk were noticed for cancer of the rectum (OR, 1.21; 95% CI, 0.95 to 1.53), liver (OR, 1.19; 95% CI, 0.58 to 2.37), malignant melanoma (OR, 1.26; 95% CI, 0.63 to 2.45), kidney (OR, 1.21; 95% CI, 0.89 to 1.65), and leukemia (OR, 1.12; 95% CI, 0.81 to 1.55); however, some of these estimates were imprecise due to small numbers. The overall OR for lymphatic and hematopoietic cancers was 1.28 (95% CI, 1.06 to 1.56). Consistent with previous studies, a decreased risk of lung cancer was observed among farmers (OR, 0.67; 95% CI, 0.60 to 0.76). The current findings are presented in the context of other recent studies, including discussions of possible causes of farming-associated excess cancer risk and possible sources of bias.
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PMID:Cancer risks among Missouri farmers. 280 30

We reported a rare case of triple cancers with acute lymphoblastic leukemia (ALL) associated with disseminated intravascular coagulopathy (DIC) after the operations of colon cancer and primary lung cancer. A 78-year-old Japanese male, who had been operated upon for colon cancer (adenocarcinoma) on March 1981, metastatic brain tumor (adenocarcinoma) on December 1986, and primary lung cancer (squamous cell carcinoma) on February 1987, was admitted to our hospital because of severe general malaise on December 6 1987. On admission, he had mild hepatosplenomegaly and hemorrhage diathesis such as purpura. Serum LDH increased to 2,515 mU/ml. The white blood cell count was 6,210/microliters with 53% leukemia cells, and the platelet count was 12,000/microliters. A bone marrow was infiltrated with 96.0% leukemia cells. The leukemia cells stained positively for PAS and negatively for peroxidase. Immunological examination of leukemia cells showed that HLA-DR, TdT, B1 and J5 were positive and cytoplasmic Igmu and surface Ig were negative, indicating common ALL. The coagulation studies revealed that the activated partial thromboplastin time was prolonged to 42.0 seconds, FDP increased to 79.9 micrograms/ml, and antithrombin-III decreased to 62%. Chromosome analysis showed a 48, XY, +2, +21q-, t(9;22) karyotype. He was diagnosed as having Ph1 positive ALL associated with DIC. He was treated with vindesine, prednisolone, L-asparaginase, and adriamycin and complete remission (CR) was achieved after two months. But on August 1988, 8 months after CR, ALL and brain tumor relapsed and he died of pneumonia on September 19, 1988.
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PMID:[Ph1 positive acute lymphoblastic leukemia with DIC after operation of colon and lung cancer]. 281 Jul 93

Combination chemotherapy is frequently used in the therapy of advanced non-small-cell lung cancer (NSCLC), but late complications are rarely recognized because of the short survival of most patients. Of 119 patients with advanced NSCLC treated with cisplatin and other drugs, four patients developed acute nonlymphocytic leukemia (ANLL). All four patients received etoposide and cisplatin with or without vindesine. Leukemia was diagnosed at 13, 19, 28, and 35 months after start of treatment. Three patients had morphologic and/or cytogenetic features of acute leukemia with significant monoblastic involvement; the fourth patient had trilineage dysplasia and cytogenetic abnormalities more commonly associated with therapy-related leukemia. Detailed analysis of the subgroup who survived longer than 1 year (24 patients) suggests that high cumulative doses of etoposide are leukemogenic; the median etoposide dose was 6,795 mg/m2 (first year only) in the four leukemic patients compared with 3,025 mg/m2 in the 20 nonleukemic patients (P less than .01). The rate of ANLL was 0.30 per person-year after the first year (95% confidence limits 0.11 to 0.90), with a cumulative risk of 15% +/- 11% at 2 years, and 44% +/- 24% at 2.5 years. We conclude that high doses of etoposide are potentially leukemogenic, and can induce a syndrome with features of acute monoblastic leukemia de novo that is distinct from other secondary leukemias.
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PMID:Acute nonlymphocytic leukemia following etoposide and cisplatin combination chemotherapy for advanced non-small-cell carcinoma of the lung. 282 73

While the carcinogenicity of asbestos has been established in malignant mesotheliomas and lung cancers, and has recently been suspected in several other types of cancer, asbestos has not been implicated in the pathogenesis of acute leukemias. This article includes two cases of acute myelocytic leukemia in individuals with a long history of exposure to asbestos. Significant numbers of asbestos bodies were detected in specimens of their lungs and bone marrow. In addition, the kind of asbestos in both organs was crocidolite, which is implicated in carcinogenesis. No asbestos bodies were detected in the bone marrow specimens from a control group consisting of ten patients with lung cancer with similar occupational histories. The role of asbestos exposure in the development of leukemia requires further study.
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PMID:Acute myelocytic leukemia after exposure to asbestos. 284 Jan 93

Cytogenetic studies were done on the leukemia cells of two patients with small cell lung cancer (SCLC) who developed erythroleukemia (acute nonlymphocytic leukemia, French-American-British M6) after combined modality chemotherapy and radiotherapy for their lung cancer. Surprisingly, both erythroleukemias exhibited the del(3)(p14p23) predominantly found in SCLC. In four other patients who had secondary erythroleukemias associated with other cancers, no deletions of 3p were found. These findings could be accounted for by one of three possible mechanisms: (a) an inherited recessive gene (anti-oncogene or tumor suppressor gene) in this region of 3p was uncovered by the combined modality therapy, (b) an inherited predisposition to damage of both chromosomes at 3p14 leads to SCLC and erythroleukemia after exposure to carcinogens and/or chemotherapy-radiotherapy, or (c) the finding of lineage specificity for the 3p deletion with the presence of the 3p deletion in SCLC and erythroleukemia suggests a common bone marrow precursor.
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PMID:Deletion of 3(p14p23) in secondary erythroleukemia arising in long-term survivors of small cell lung cancer. 284 53


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