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)

This work has for aim to suggest coefficients of adjustment applicable to the statistics of malignant tumours refunded through the health insurance as long-term diseases. Those coefficients would allow to evaluate the morbidity rate of cancer in the general population in France. To reach this target, we compared the figures of health insurance to those of the registers of cancers in six french departments, after we made the necessary adjustments to make the comparison possible. We showed that, for each cancer, the coefficient of adjustment is equal to the median of the relative differences that we noticed between the figures of the registers and those of the health insurance. We calculated the adjustment coefficients for bladder cancers (1.07), colon-rectum cancers (1.36), womb cancers (1), kidney cancers (0.83), lung cancers (1.33), oesophagus cancers (1.56) and prostate cancers (1.37). The comparison between the incidences adjusted on the basis of the figures of the health insurance, the incidences estimated by the Inserm and those released in the literature allowed us to confirm the validity of the coefficient we propose, except for the kidney cancer and the lung cancer by women, for whom we can't make any conclusions. Our work shows that the statistics of health insurance builds up a basis of information that can be used to study the morbidity rate of some malignant tumours in France.
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PMID:[Estimation of the incidence of eight malignant tumours in France, on the basis of health insurance's statistics]. 1006 48

Routinely collected data for New South Wales were used to analyse cancer mortality in migrants from the British Isles, southern Europe and eastern Europe according to duration of residence in Australia. A case-control approach compared deaths from cancer at one site with deaths from all other cancers, adjusting for age, sex and calendar period. Compared with the Australia-born, migrants had a significantly lower risk of dying from cancers of the mouth/pharynx and prostate (migrants from each region), colon/rectum (from the British Isles and southern Europe) and lung (female southern European migrants), evident from the time of migration and maintained for 30 years after migration. Whereas a deficit of deaths from colorectal cancer remained in migrants from southern Europe, a clear gradient of increasing risk with duration of stay in Australia was apparent. A similar trend was seen with respect to kidney cancer in southern European migrants. Persistent excess risks of death from stomach cancer were seen in all migrant groups, from lung cancer in British migrants and from liver cancer in southern and eastern European migrants. Although the risk of death from breast cancer increased significantly with duration in Australia in southern European migrants, the increase was not monotonic, as the relative risk in the first 10 years after migration was almost the same as that after more than 30 years. The pattern of risk for cancers of the prostate and mouth/pharynx suggests some protective role for inheritance or maintained cultural factors.
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PMID:Cancer mortality in migrants from the British Isles and continental Europe to New South Wales, Australia, 1975-1995. 1047 24

We conducted a retrospective cohort study of 6107 aerospace workers to examine whether exposure to chemicals--primarily hydrazine fuels--during rocket-engine fueling and testing affects cancer mortality. When conditional logistic regression analysis was applied and adjusted for confounding variables, the estimated rate ratio for lung cancer mortality, comparing exposed to unexposed workers from the same facility, ranged from 1.68 (95% confidence interval, 1.12 to 2.52) to 2.10 (95% confidence interval, 1.36 to 3.25), depending on job-duration threshold (6 or 24 months) and lag (0 to 15 years). Similar results were obtained for hemato- and lymphopoietic cancer and for bladder and kidney cancer mortality, but estimates for these cancers were imprecise. We concluded that occupational exposure to hydrazine or other chemicals associated with rocket-engine testing jobs increased the risk of dying from lung cancer, and possibly other cancers, in this population of aerospace workers; however, our results need to be replicated in other populations.
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PMID:Chemical exposures of rocket-engine test-stand personnel and cancer mortality in a cohort of aerospace workers. 1052 46

Currently used rodent tumor models, including transgenic tumor models, or subcutaneously-growing human tumors in immunodeficient mice, do not sufficiently represent clinical cancer, especially with regard to metastasis and drug sensitivity. In order to obtain clinically accurate models, we have developed the technique of surgical orthotopic implantation (SOI) to transplant histologically-intact fragments of human cancer, including tumors taken directly from the patient, to the corresponding organ of immunodeficient rodents. It has been demonstrated in 70 publications describing 10 tumor types that SOI allows the growth and metastatic potential of the transplanted tumors to be expressed and reflects clinical cancer. Unique clinically-accurate and relevant SOI models of human cancer for antitumor and antimetastatic drug discovery include: spontaneous SOI bone metastatic models of prostate cancer, breast cancer and lung cancer; spontaneous SOI liver and lymph node ultra-metastatic model of colon cancer, metastatic models of pancreatic, stomach, ovarian, bladder and kidney cancer. Comparison of the SOI models with transgenic mouse models of cancer indicate that the SOI models have more features of clinical metastatic cancer. Cancer cell lines have been stably transfected with the jellyfish Aequorea victoria green fluorescent protein (GFP) in order to track metastases in fresh tissue at ultra-high resolution and externally image metastases in the SOI models. Effective drugs can be discovered and evaluated in the SOI models utilizing human tumor cell lines and patient tumors. These unique SOI models have been used for innovative drug discovery and mechanism studies and serve as a bridge linking pre-clinical and clinical research and drug development.
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PMID:Orthotopic metastatic mouse models for anticancer drug discovery and evaluation: a bridge to the clinic. 1075 2

We previously reported elevated levels of TGF-beta1 in patients with renal carcinoma. Certain aspects led us to ask whether they might be caused by chronic damage to the kidney(s). Here we report on an extended set of patients with various renal diseases, lung cancer, humoral immunodeficiency and controls. For latent TGF-beta1 in plasma, we find that the control, immunodeficiency, lung cancer and kidney transplant groups do not differ significantly (means, 7.0-8.8 ng/ml). Also, acute short-term renal stress (extracorporal lithotrypsy) does not lead to an increase of TGF-beta1. However, the pyelonephritis patients present with levels of 19.0 ng/ml, chronic extracorporal dialysis patients with 15.5 ng/ml, and renal cell carcinoma patients with 22.8 ng/ml. For active TGF-beta1 these findings are exactly recovered. For serum levels, only the renal carcinoma group presents with significantly elevated levels of TGF-beta1. Kidney transplantation seems to normalize TGF-beta1 levels, while in the kidney cancer patients surgery has an effect only in part of the group. We conclude that elevated plasma TGF-beta1 levels are common in at least two chronic renal disease conditions, and that it normalizes with restoration of renal function. It is tempting to speculate that chronic elevation of TGF-beta1 in these patients may be critically involved in these conditions predisposing to renal cancer.
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PMID:Elevated plasma TGF-beta1 in renal diseases: cause or consequence? 1088 Feb 55

A literature search was conducted aiming at all empirical studies from Germany till mid 1997 containing data on the association between environmentally-related diseases and the socio-economic status (education, occupation, income, social class) and/or on the association between the exposure to harmful substances and the socio-economic status. With respect to the exposures, a clear picture becomes visible: the concentration of harmful substances in the ambient air as well as indoors is considerably higher with regard to the lower social class as compared with the higher social class. This applies to children as well as to adults and to West Germany as well as to East Germany. However, with respect to environmentally-related diseases, no such clear picture becomes visible. For example, several studies indicate that allergies, atopic eczema and croup occur less frequently in the lower social class than in the higher social class. Malignant tumours (lung cancer, kidney cancer or bladder cancer), however, seem to occur more frequently in the lower social class than in the higher social class. Environmental-epidemiological studies should increasingly integrate socio-epidemiological study approaches and explicitly present their results.
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PMID:Social inequality and environmentally-related diseases in Germany: review of empirical results. 1093 33

In 1989 we published a critical review of cancer epidemiology in petroleum workers, which included as a component of the review a meta-analysis by cancer site. Subsequently we have completed three additional reviews and meta-analyses on cell-type-specific leukemias (1995), multiple myeloma (1997), and non-Hodgkin's lymphoma (2000). The objective of the present investigation was to update our 1989 review and meta-analysis of nonlymphohematopoietic cancers in cohort studies of petroleum workers. Included in the present investigation were cohort studies of petroleum workers from the United States, the United Kingdom, Canada, Australia, Finland, Sweden, and Italy. Individual studies were reviewed with regard to specific cancer sites. For each cancer of interest, risk ratios from the individual studies were presented. In some studies, subcohort analyses stratified by exposure parameters such as length of employment, job category, and hire year were also reported. These subcohort or stratified analyses were reviewed and the results of these analyses were taken into consideration in our interpretation. In addition to the qualitative review of individual studies, a meta-analysis was performed to combine data from individual cohort studies of petroleum workers. The primary purpose of the meta-analysis was to provide a summary measure of risk for each cancer site. Based on a review and meta-analyses of cohort studies of more than 350,000 petroleum workers in the United States, the United Kingdom, Canada, Australia, Finland, Sweden, and Italy, we concluded that there was no increased mortality from digestive cancers (stomach, large intestine, liver, or pancreas), lung cancer, bladder cancer, kidney cancer, or brain cancer. The summary standardized mortality ratios for these cancer sites were all below unity. Significant increases of melanoma mortality were reported in some small groups of refinery workers in the United Kingdom and upstream operation workers in Canada, but no responsible agent(s) had been identified. The observed mortality from skin cancer in all other studies was similar to the expected. In particular, no significant increase of skin cancer mortality was reported in any of the U.S. studies. Elevated mortality from prostate cancer was noted in short-term workers at a U.S. refinery and in short-term workers employed in certain crafts at U.S. crude oil operations. However, the absence of an upward trend by length of employment in these workers argued against an association between exposure to petroleum products and prostate cancer. For all petroleum workers as a whole, mortality from prostate cancer was as expected.
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PMID:A critical review of cancer epidemiology in the petroleum industry, with a meta-analysis of a combined database of more than 350,000 workers. 1102 72

Purpose: At the University Of Pittsburgh Medical Center, over 100 oncology studies have been performed using a combined PET/CT scanner. The scanner is a prototype, which combines clinical PET and clinical CT imaging in a single unit. The sensitivity achieved using three-dimensional PET imaging as well as the use of the CT for attenuation correction and image fusion make the device ideal for clinical oncology. Clinical indications imaged on the PET/CT scanner include, but are not limited to, tumor staging, solitary pulmonary nodule evaluation, and evaluation of tumor reoccurrence in melanoma, lymphoma, colorectal cancer, lung cancer, pancreatic cancer, head and neck cancer, and renal cancer.Methods: For all studies, seven millicuries of F(18)-fluorodeoxyglucose is injected and a forty-five minute uptake period is allowed prior to positioning the patient in the scanner. A helical CT scan is acquired over the region, or regions of interest followed by a multi-bed whole body PET scan for the same axial extent. The CT scan is used to correct the PET data for attenuation. The entire imaging session lasts 1-1.5 hours depending on the number of beds acquired, and is generally well tolerated by the patient.Results and Conclusion: Based on our experience in over 100 studies, combined PET/CT imaging offers significant advantages, including more accurate localization of focal uptake, distinction of pathology from normal physiological uptake, and improvements in evaluating therapy. These benefits will be illustrated with a number of representative, fully documented studies.
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PMID:7. Survey of Results of Whole Body Imaging Using the PET/CT at the University of Pittsburgh Medical Center PET Facility. 1115 Jul 64

VIP/PACAP are autocrine growth factors for lung cancer. VIP and/or PACAP mRNA is present in most lung cancer cell lines examined. Although mRNA for VPAC2-R is not common, VPAC1-R and PAC1-R mRNA is present in many lung cancer cell lines. 125I-VIP binds with high affinity to lung cancer cells and specific 125I-VIP binding is inhibited with high affinity by (Lys15, Arg16, Leu27)VIP1-7 GRF8-27, the VPAC1-R specific agonist, but not by Ro25-1553(18), the VPAC2-R specific agonist. VIP elevates cAMP and increases c-fos gene expression. The increase in cAMP and c-fos mRNA caused by VIP is inhibited by SN(VH). (SH)VH inhibited the proliferation of NCIH1299 cells in the MTT assay, which is based on cytotoxicity. In a recent cell line screen, (SN)VH inhibited the growth of 51 of 56 cancer cell lines including leukemia, lung cancer, colon cancer, CNS cancer, melanoma, ovarian cancer, renal cancer, breast cancer, and prostate cancer (T. Moody, unpublished). It remains to be determined if (SN)VH will be useful for treatment of a wide variety of cancers.
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PMID:VPAC1 receptors and lung cancer. 1119 32

The diagnostic value of pyruvate-kinase type tumor M2 (Tumor M2-PK) has been investigated in different tumors, and showed interesting results in cases of renal cancer, pancreatic cancer, lung cancer and some cases of gastric cancer. In this study we investigated EDTA-plasma of 68 patients with gastrointestinal cancer, 22 patients with inflammatory bowel disease (IBD) and 60 healthy controls. Sensitivity of Tumor M2-PK was 70.6% for all GI-tumors, that of CA19-9 was 55.4% and that of CEA was 53.3%. In pancreatic cancer CA19-9 showed the best sensitivity. In oesophageal/gastric cancer Tumor M2-PK was most sensitive and in colorectal cancer CEA and Tumor M2-PK showed the best results. The specificity of Tumor M2-PK was 90-96, 7%. In IBD some individuals showed elevated Tumor M2-PK levels but there was no correlation to CRP or to the clinical activity score. The results indicated that Tumor M2-PK might be a valuable marker in gastrointestinal cancer.
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PMID:Tumor M2-pyruvate kinase: a promising tumor marker in the diagnosis of gastro-intestinal cancer. 1132 48


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