Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242379 (lung cancer)
 71,905 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

rTNF was administered to 28 patients with advanced metastatic cancers by continuous intravenous infusion for 5 consecutive days every 2 weeks. The dose levels were 30, 40, 70, 110, 180 and 290 micrograms/M2/day. Groups of 3 patients were started at each successive dose level and then on subsequent courses treated with the next dose level through 4 escalations as tolerated. Tumor types were: colon cancer 14; adenocarcinoma of unknown primary, 2; renal cancer, 2; leiomyosarcoma, 2; lung cancer, 1; prostate cancer, 1; thymona, 1; bladder cancer; 1; parotid, 1; Kaposi's sarcoma 2; ovarian 1. Toxicities included fever and chills (usually within the first 8 hours of infusion), fatigue, headache, decreased performance status, hypotension and CNS. All patients experienced leukopenia and thrombocytopenia within 24 hours or less after start of infusion with return of baseline by 72 hours after rTNF was stopped. The fall in these counts averaged 50% and was not dose related. No major changes in liver or renal function, coagulation or blood lipids were seen. Major dose limiting toxicities were fatigue, confusion, thrombocytopenia, seizures, hypotension and decreased performance status. NK cell activity measured against K562 target cells was augmented from about 30% target cell lysis to about 70% target cell lysis over the first 7 days of treatment. Two patients, both with metastatic colon cancer showed transient, objective tumor regression which did not qualify as a partial response. One patient with ovarian cancer had a stable partial response but progressed after 13 courses of treatment. Continuous infusion of TNF can be safely administered to patients with a maximum tolerated dose of only between 30 and 40 micrograms/M2/day.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A phase I trial of recombinant tumor necrosis factor (rTNF) administered by continuous intravenous infusion in patients with disseminated malignancy. 264 24

Metal cutting/grinding fluids are of three basic types: straight oil (insoluble), oil-in-water emulsions (soluble) and synthetic/semisynthetic. All contain a variety of additives to improve performance. Human exposure occurs primarily by direct skin contact with the liquid or by skin and respiratory contact after fluid misting. Dermatitis caused by primary or direct skin irritation is the most prevalent health effect of exposure to cutting fluids. Occasionally allergic dermatitis is seen which is related to the development of sensitization to one or more of the additive components. Recent studies indicate that long-term exposure to cutting fluids does not result in increased incidences of lung cancer, urinary bladder cancer, gastrointestinal cancer, or death from non-malignant respiratory diseases. Long-term exposure to certain cutting fluids, however, is believed to have resulted in certain types of skin cancer, especially scrotal cancer. It is likely that these carcinogenic responses were caused by contact with polycyclic aromatic compounds (PCA) of 3-7 rings. Modern base oils which are severely refined have very low levels of PCA, are not carcinogenic in animal bioassays, and are unlikely to be carcinogenic in man. This is not necessarily true for re-refined oils which may contain significant levels of PCA and polychlorinated biphenyls derived from comingling used cutting oils with used engine oils and transformer oils. Cutting oils, themselves, generally do not accumulate significant levels of carcinogenic PCA during use. Additives, in theory, can cause a variety of health effects either directly or through the generation of reaction products such as nitrosamines. In actual use, adverse health effects appear to be limited to occasional instances of allergic contact dermatitis. Nitrosamines are extremely carcinogenic in test animals; although no human cancer cases directly attributable to nitrosamine contamination have been observed, nitrosating agents and amines should not be combined in cutting fluid formulations. It is difficult to anticipate or predict the potential toxicity of a particular cutting fluid formulation because of the presence of variable amounts of proprietary additives which, themselves, are often complex reaction mixtures. Thus, each additive and final formulation must be evaluated on a case by case basis to appropriately assess potential health hazards.
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PMID:Health effects of oil mists: a brief review. 266 32

Tumour markers are often circulating tumour-associated indicators of tumour development. As such they are not suitable for tumour screening and localization, but valuable as adjuncts for medical follow-up care of tumour patients, where their serum level alterations may anticipate the clinical detection of tumour behaviour by a lead time of 1 to 6 months before other methods. The following tumour may be controlled by established markers: endocrine tumours by NSE, calcitonin, parathormone, 5-HIAA, catecholamines/metabolites etc.; head-neck tumours: SCC, CEA; thyroid carcinoma: TG, calcitonin; lung cancer: CEA, NSE, SCC; liver cancer: AFP (PLC), CA 19-9 (cholangiocell.), CEA (secondary): biliary tract and pancreatic cancer: CA 19-9; colorectal carcinoma: CEA, CA 19-9; squamous cell carcinoma (ENT, oesophagus, anal): SCC; breast cancer: CEA and CA 15-3; ovarian cancer: CA 125 (epithelial), CA 19-9 (mucinous); germ cell tumours (ovary including trophoblastic tumours/testes): AFP and HCG; prostatic cancer: PAP and PSA; bladder cancer: TPA.
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PMID:[Clinical relevance of tumor markers]. 267 6

A review is made of studies on occupational cancer conducted in different countries in order to compare estimates of the attributable risks (i.e., the proportion of cancers occurring in the general population due to occupational exposure), and to identify the sources of variation. Estimates vary according to several factors, including different study designs and chiefly, different proportions of exposed workers in the geographical areas that have been investigated. For lung cancer, estimates ranged between 1 and 35%, with values of 10-15% occurring frequently; for bladder cancer, the range was between 1 and 19%. The implications of this variability in prevention programmes are discussed and the problems encountered in the identification and compensation of occupational cancer are examined.
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PMID:[Prevention of occupational tumors: an update]. 269 1

Cancer incidence among 8,004 patients hospitalized for epilepsy between 1933 and 1962 in the Filadelfia treatment community in Denmark was compared to that of the general population. Patients received powerful and prolonged treatment with phenobarbital, phenytoin, and other anticonvulsants. This new survey extends the follow-up from 1976 through 1984. Among 7,864 patients with epilepsy not known to have received radioactive Thorotrast, record linkage with national cancer incidence files identified 789 cancers, compared to 664 expected [relative risk (RR) = 1.19; 95% confidence interval = 1.11-1.27]. Significant risks were found for cancers of the brain and central nervous system (RR = 5.7; n = 118) and the lung (RR = 1.4; n = 106). The excess numbers of brain cancer were concentrated within 10 years of hospitalization (RR = 20.7; n = 80) and decreased significantly over time, which suggests that brain tumors account for the seizure disorder and are not due to phenobarbital exposure as suggested by some epidemiologic studies. No overall risk was apparent when brain cancers were excluded (RR = 1.03). Because bladder cancer was significantly decreased (RR = 0.6; n = 18), the excess risk of lung cancer may not have been related to the "anecdotal" heavy smoking reported among confined groups of epileptic patients in the early years of the study period. The incidence of malignant melanoma was also significantly low (RR = 0.5; n = 7), which suggested limited exposure to sunlight among confined patients. The risk of non-Hodgkin's lymphoma was increased, but not significantly (RR = 1.4; n = 16), which is interesting in view of previous reports suggesting an association with phenytoin. Overall, these data provide little evidence that phenobarbital and phenytoin are carcinogenic to humans, but the excess risks of lung cancer and non-Hodgkin's lymphoma among epileptic patients in our study deserve further evaluation.
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PMID:Cancer among epileptic patients exposed to anticonvulsant drugs. 250 19

A series of 1,438 parents and 2,663 other relatives of retinoblastoma patients have been followed up to ascertain the incidence among them of non-ocular cancer. Among 117 of these relatives who were known carriers of the mutation of the retinoblastoma gene 23 cases of non-ocular cancer developed during the follow-up period of the study. This compares with an expected number of 2.3, a relative risk of 9.9. A total of 25 deaths among these carriers included 21 from non-ocular cancer; the expected number was 1.8, a relative risk of 11.6. Relatives who are carriers are about 15 times more likely to die from lung cancer than the general population. Previous findings of an association of melanoma and bladder cancer with retinoblastoma are borne out in this study. The incidence of non-ocular cancer among relatives of hereditary cases who are not definitely known to be carriers shows an excess risk of 1.6: it is concluded that a proportion of these relatives are in fact carriers of the mutated retinoblastoma gene. For relatives who are not gene carriers there appears to be no excess risk of developing cancer. Carriers relatives who are not themselves affected with retinoblastoma may be inherently less liable than affected carriers to the further genetic changes which lead to the development of both retinoblastoma and subsequent non-ocular cancer.
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PMID:Non-ocular cancer in relatives of retinoblastoma patients. 278 42

Proton therapy was developed as one of the most promising radiation therapy techniques and it has shown remarkable improvement of the local cure rate of cancer lesions and decrease of late injury. However, cooperation with chemotherapy is to be considered as a reasonable way to further improve the radical cure rate, because the indication of proton therapy is limited to a single primary lesion. Thereupon, combined chemotherapy before or after completion of the proton therapy of the primary lesion to control latent metastases of lung cancer, esophageal cancer, to control multicentric lesions of liver cancer, urinary bladder cancer, or to diminish the size of the lesions with too much volume, could well contribute to improved clinical results.
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PMID:[Cooperation of proton therapy and chemotherapy]. 283 99

Two monoclonal antibodies (MAbs) were tested for their reactivity with antigens of exfoliated malignant cells in respiratory secretions of lung cancer patients. MAb CE 407 was developed from tissue culture cell line SW 756, derived from human uterine cervical squamous cell carcinoma; MAb BL 99-57 was developed from cell line T-24, derived from human transitional cell bladder cancer. MAb CE 407 reacted preferentially with squamous cell carcinomas (80%) and with some (44%) of the adenocarcinomas of the lung; BL 99-57 reacted with 76% of the adenocarcinomas, but only with 27% of the squamous cell carcinomas of the lung. The reactivity of BL 99-57 was more apparent in well-differentiated adenocarcinomas (89% positive), but less in poorly differentiated adenocarcinomas (65% positive). Neither of these antibodies reacted with antigens of small cell anaplastic carcinoma. These two MAbs may be useful in differentiating histologic types of lung cancer in cases that are difficult to diagnose morphologically and/or in which tissue is not available for study.
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PMID:The potential usefulness of monoclonal antibodies in the determination of histologic types of lung cancer in cytologic preparations. 284 47

In a Danish cohort of schizophrenics consisting of 6,168 patients followed during 1957-1980, the incidence of certain types of cancer has been shown to be significantly decreased (5). From this cohort 30 males with lung cancer, 21 males with bladder cancer, 17 females with cancer of the uterine cervix and 40 females with breast cancer, were each matched to two "healthy" schizophrenic controls from the same cohort. A range of social, demographic and nosocomial factors were registered from the individual case files, and statistical analysis was carried out, using Cox's regression model. Neuroleptic treatment with various drugs other than reserpine reduced the risk of developing all four cancer types studied. In contrast reserpine treatment increased the risk of developing cancer of the breast and uterine cervix. Furthermore, cancer risk was found to be modified by other well-known risk factors.
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PMID:Neuroleptic treatment and other factors modifying cancer risk in schizophrenic patients. 288 88

The 1916 painters and the 1948 electricians who resided in the Canton of Geneva at the time of the 1970 census were identified and followed up to 1984. During the study period 121 disability pensions were awarded to painters and 59 to electricians. Age standardised incidence of disability per 1000 man-years at risk was higher among painters than among electricians for all neuropsychiatric causes (1.23/1000 and 0.68/1000, respectively) and for all other causes (5.50/1000 and 3.41/1000, respectively). No case of presenile dementia was diagnosed among painters. There was inadequate evidence to indicate that the higher risk of neuropsychiatric disability for painters might have been due to their occupational exposure to organic solvents. A possible toxic effect of these substances on the central nervous system was confounded with alcoholism which was associated with disability from neuropsychiatric disease in 12 of 20 painters and in only one of 10 electricians. Mortality and incidence of cancer were assessed among both cohorts and compared with the expected figures calculated from Geneva rates. Among painters there was a significant increase in overall mortality (O = 254, E = 218.5), in mortality from all cancers (O = 96, E = 75.4), and in incidence from all cancers (O = 159, E = 132.0). For the specific cancer sites, there was a significant excess risk for lung cancer (mortality: O = 40, E = 23.0), which was possibly related to occupational exposure to asbestos and to zinc chromate, although cigarette smoking was not controlled. The significant excesses of biliary tract cancer and of bladder cancer were in accordance with previous observations among painters from other countries. There was also a significant increase in incidence from testicular cancer (O=5, E=1.6), which has not been reported before. For causes of death other than cancer the excesses for alcoholism (O=5, E=0.8). for liver cirrhosis (O=14, E=8.8), for motor vehicle accidents (O=12, E=5.9), and for cerebrovascular disease when allowing for ten years of latency (O=8, E=4.0), were consistent with a probable increased risk of alcohol abuse. Among electricians overall mortality was similar to that expected (O=137, E=139.0). No significant excess risk was found for all cancers or for any specific cancer site. Because of the small number of expected deaths the statistical power was low for the assessment of a possible risk for leukaemia or for brain tumour.
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PMID:Disability, mortality, and incidence of cancer among Geneva painters and electricians: a historical prospective study. 292 Jan 39


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