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)

5-fluoro-3,4-dihydro-2,4-dioxo-N-[2-2- (dimethylphenylsilyl)ethylthioethyl]-1(2H)-pyrimidinocarb oxamide (SDK-12B-5), a novel antitumor agent, is covalently linked with 5-fluorouracil (5-FU) and 2-[(2-dimethylphenylsilyl)ethylthio] ethylamine(SDK-103) which possesses itself antitumor activity against murine solid tumors. It has a broad antitumor spectrum in experimental tumor systems including murine leukemias. Furthermore, SDK-12B-5 administered p.o. with various treatment schedules inhibited significantly the tumor growth of human breast cancer (MX-1), colon cancer (Co-4) and lung cancer (LX-1 and OAT) cells in BALB/c nu/nu mice and the chemotherapeutic index was about 10 for 4 different human cancer xenografts. In the Lewis lung carcinoma (LLC) metastasis model, SDK-12B-5 in combination with amputation of tumors inhibited significantly both the lymph node metastases and lung metastases of LLC and prolonged the life span (%ILS:91%) of BDF1 mice. We also found that the cell killing effect of SDK-12B-5 was affected by both concentration and exposure time in cultured human lung cancer (OAT) cells using soft-agar colony assay. A significant augmentation of delayed type hypersensitivity (DTH) response induced by SDK-12B-5 in comparison with the mixture of SDK-103 and 5-FU was seen when it was administered p.o. simultaneously with the immunization of sheep red blood cell (SRBC) in retired CD1 mice. From the studies on tissue distribution and pharmaco-kinetics of SDK-12B-5 by HPLC and ICP analysis. the persistence of SDK-12B-5 levels in serum and tumors was correlated with the findings that a maximum chemotherapeutic effect was obtained when SDK-12B-5 was administered p.o. repeatedly with every other day to avoid the cumulative toxicity.
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PMID:[Antitumor effects of 5-fluorouracil-bound organic silicon compound]. 278 16

Corticosteroid levels were studied in the plasma of athymic mice implanted with human breast tumor cells, either from MCF-7 or ZR-75-1 cell lines. There was a highly significant decrease in plasma corticosterone levels in the mice implanted with these tumor cells. There was no significant effect on corticosterone of GW 39 colon cancer cells, LS 174T colon cancer cells, or Calu-3 lung cancer cells.
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PMID:Diminished corticosterone levels in nude mice implanted with MCF-7 or ZR-75-1 human breast tumor cells. 280 57

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

A variety of musculoskeletal syndromes have been described in association with malignancy. The majority of such descriptions have dealt with the connective tissue disorder as a paraneoplastic syndrome, frequently the presenting feature of an otherwise occult malignancy. This may range from the well known syndrome of HOA, heralding lung cancer, to a lesser known association of pyogenic arthritis due to an unusual enteric pathogen, signaling colon cancer. Conversely, the connective tissue disorder may precede the malignancy, and by virtue of its pathophysiology or its therapy, foster the subsequent development of cancer. Awareness of these associations may lead to earlier cancer detection, and hence, potentially more effective therapy.
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PMID:Rheumatologic manifestations of cancer. 293 36

The incidence of cancer was studied in a cohort of 287 men who were exposed to asbestos at a nitric acid production plant from 1928 onwards. During the observation period from 1953 through 1980 all cancer cases among the cohort members were identified in The Cancer Registry. For the whole cohort 42 cases of cancer were observed versus 30.6 expected. The figures for cancer of the lungs and pleura combined were 17 observed versus 3.7 expected. The corresponding figures for a heavily exposed subcohort were 11 observed and 1.2 expected. In that group there was also an increased incidence of colon cancer with 3 cases observed against 0.8 cases expected. Within the whole cohort four cases of pleural and one case of peritoneal malignant mesothelioma were found. There was also an increased incidence of malignant melanoma of the skin with 3 cases observed against 0.6 expected. For cancer cases that were registered as of unknown origin there were 7 cases observed and 1.4 expected. There was no increased rate ratio for cancer at any site before 20 years after the first asbestos exposure. The smoking habits of all cohort members were recorded and the relative rates for lung cancer were calculated in relation to smoking habits. In common with previous studies the results indicate a multiplicative model for the interaction between asbestos exposure and smoking in regard to lung cancer risk.
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PMID:Asbestos exposure, smoking habits, and cancer incidence among production and maintenance workers in an electrochemical plant. 300 Jan 74

Evidence pertaining to the role of dietary factors in carcinogenesis comes from both epidemiological studies and laboratory experiments. In 1982, the Committee on Diet, Nutrition, and Cancer of the National Research Council conducted a comprehensive evaluation of this evidence. That assessment as well as recent epidemiological and laboratory investigations suggest that a high fat diet is associated with increased susceptibility to cancer of different sites, particularly the breast and colon, and to a lesser extent, the prostate. Current data permit no definitive conclusions about other dietary macroconstituents including cholesterol, total caloric intake, protein, carbohydrates and total dietary fiber. Specific components of fiber, however, may have a protective effect against colon cancer. In epidemiological studies, frequent consumption of certain fruits and vegetables, especially citrus fruits and carotene-rich and cruciferous vegetables, is associated with a lower incidence of cancers at various sites. The specific components responsible for these effects are not clearly identified, although the epidemiological evidence appears to be most consistent for a protective effect of carotene on lung cancer and less so for vitamins A and C and various cancer sites. The laboratory evidence is most consistent for vitamin A deficiency and enhanced tumorigenesis, and for the ability of various nonnutritive components in cruciferous vegetables to block in-vivo carcinogenesis. The data for minerals and carcinogenesis are extremely limited, although preliminary evidence from both epidemiological and laboratory studies suggests that selenium may protect against overall cancer risk. Frequent consumption of cured, pickled, or smoked foods, possibly because they may contain nitrosamines or polycyclic aromatic hydrocarbons, appears to increase the risk of esophageal or stomach cancer, however, the specific causative agents in these foods are not clearly identified. Excessive alcohol consumption among smokers appears to be associated with an elevated risk of cancers of the oral cavity, esophagus, larynx, and respiratory tract. The mechanisms of action of dietary factors on carcinogenesis are poorly understood. The NRC committee, and more recently, the National Cancer Institute and the American Cancer Society have proposed interim dietary guidelines to lower the risk of cancer. These guidelines are consistent with general dietary recommendations proposed by U.S. government agencies for maintenance of good health.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Diet, nutrition, and cancer. 301 Mar 79

Progestogens should be added to estrogen replacement therapy, not only to prevent endometrial cancer in women with a uterus, but also to reduce the risk of breast cancer in some women. Smoking should be discouraged to reduce the risk for both lung cancer and heart disease. Recommendations should be made to increase fiber intake to lessen the risk for carcinoma of the colon. Reducing fat intake also decreases risk for colon cancer, as well as carcinoma of the breast. Postmenopausal bleeding must be investigated for early diagnosis of endometrial cancer and, when endometrial hyperplasia is the finding, it should be treated with progestogens to prevent adenocarcinoma. The progestogen challenge test is recommended for all women with a uterus, and if bleeding occurs, the progestogen should be continued for 13 days each month. Use of mammograms and other diagnostic modalities should be increased to make the earliest possible diagnosis of breast cancer.
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PMID:Cancer in the older woman: diagnosis and prevention. 304 28

It has been 5 years since the National Research Council (NRC) Committee on Diet, Nutrition and Cancer published "Interim Dietary Guidelines" for the nutritional prevention of cancer. The term "interim" implies that these recommendations should be regarded as temporary, pending more definitive findings from additional scientific research. This article reviews findings relevant to the connections between diet and cancer that have emerged from nutritional epidemiology subsequent to the 1982 the NRC report. Some recent research has supported the earlier work which served as a basis for the interim recommendations, some has not, and additional hypotheses have emerged. There continues to be evidence, although it is inconsistent, that dietary fat may be an important factor in colon cancer, and that something related to fruits and vegetables, perhaps carotene, may lower the risk of lung cancer. However, the hypothesized relationships between dietary fat and breast cancer and between dietary fiber and colon cancer have been less consistently supported by new findings. Meanwhile, a new hypothesis has emerged relating alcohol intake to breast cancer risk, although many important questions remain regarding the age at which alcohol use may affect risk, and the dose above which risk is increased. The last 5 years seem to have been characterized by only slow progress in our understanding of the relationship between diet and cancer. It is clear that in 1988 we are still very much in the interim. Critical methodologic assessments of the reasons for the discrepancies in findings among the various studies, and meta analytic approaches may be helpful in increasing our understanding of the set of epidemiologic research conducted to date. More important, however, are the many types of studies now underway, including more rigorously designed observational studies and chemo-preventive and dietary-preventive trials. These studies will likely provide more definitive future answers to the questions we still face in the interim.
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PMID:Diet and cancer. Any progress in the interim? 304 34

The purpose of this paper is to clarify the short-term and long-term objectives of screening for various cancers, and to indicate the kinds of data that are needed to determine whether or not the objectives are met. Cancers at various sites differ with respect to their innate suitability for screening. Criteria that enhance screening suitability include the potential for serious complications and a high rate of mortality (applicable to most cancers), a prolonged preclinical phase, and an existing therapy that is simpler and more effective in reducing the mortality rate when applied to preclinical disease than to clinically evident cancer. Tests and procedures suitable for screening are simple to perform, inexpensive, acceptable to patients and physicians, safe, relatively painless, and accurate, as measured by the test's sensitivity and specificity. The actual yield of previously undiagnosed cancer arising from a screening program will depend heavily on prevalence of disease in the screened population, specificity of the screening test, and successful follow-up of screen-positive patients with diagnosis and treatment. These issues are discussed in the context of four cancers and their respective screening modalities: cervical cancer and cytologic studies, breast cancer and mammography, colon cancer and fecal occult blood tests, and lung cancer and sputum cytologic studies. The quality of data on which screening decisions have been made for each of these cancers and tests varies. The cancers vary in terms of their relevant biologic characteristics and treatment effectiveness. Similarly, each screening procedure has its own particular advantages and disadvantages. Current American Cancer Society Guidelines for early detection of three of the cancers are presented.
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PMID:Cancer screening. Degrees of proof and practical application. 304 38

Sensitivities to sister chromatid exchange (SCE) induction by chemicals of peripheral lymphocytes from 26 cancer patients were estimated under conditions identical to those for healthy humans which had been reported (Cancer Res., 43: 439-442, 1983). The sensitive individual was defined as one whose cells give a mean induced SCE frequency more than 2 standard deviation units above the population mean of induced SCEs in cells from the healthy humans. When cells were treated with 3-amino-1-methyl-5H-pyrido[4, 3-b]indole in the presence of rat liver S9 mix, 8 in 10 stomach cancer patients, 4 in 4 colon cancer patients, 3 in 9 lung cancer patients, 0 in 3 patients bearing other cancers, and 0 in 9 non-cancerous individuals were sensitive. The corresponding frequency of individuals in the healthy population, reported previously, was 1 in 33 persons. Thus, the frequency of sensitive individuals in the combined group of stomach and colon cancer patients was very significantly higher than were frequencies in control groups. Three in 10 patients with stomach cancer and 4 in 16 patients with other cancers were sensitive to induction of SCE by methyl methanesulfonate. Six in these 7 methyl methanesulfonate-sensitive patients were also 3-amino-1-methyl-5H-pyrido[4,3-b]indole sensitive. The frequency of methyl methanesulfonate-sensitive individuals in the healthy populations was 2 in 50. There was no patient who was sensitive to SCE induction by 4-nitroquinoline 1-oxide. The frequency was not significantly different from the healthy population, in which 3 in 50 persons were sensitive. These results suggest that a particular cancer correlates with the sensitivity of peripheral lymphocytes to SCE induction by particular chemicals.
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PMID:Novel responses of peripheral lymphocytes of cancer patients to chemical induction of sister chromatid exchanges. 307 70


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