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

Three patients, two men and one woman, diagnosed as having adenocarcinoma of the lung were found to have changes in cholestatic biochemical values, and CT scan of the abdomen demonstrated dilation of the biliary tree. Upon further evaluation using ERCP marked dilation of the biliary tree was confirmed. There was no anatomic obstruction to bile flow, no neoplastic involvement of the liver or bile ducts and no evidence of any infiltrative process or disease to explain the dilation. A paraneoplastic syndrome is proposed as the etiology of the biliary tract abnormality. Along with other more common causes, this newly described paraneoplastic syndrome should be considered in the differential diagnosis of lung cancer in patients presenting with cholestasis and biliary tract dilation.
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PMID:Unexplained biliary tract dilatation in lung cancer patients. 800 96

The fact that routinely effective treatments for disseminated lung cancer are not available has prompted the search for effective early detection systems. It is important to identify lung cancer while it is still confined to the bronchial epithelium and is potentially curable with local modalities. We have previously reported on an immunologically based assay to identify antigens expressed on shed bronchial epithelial cells. This assay resulted in a statistically significant correlation of immunostaining with the eventual development of lung cancer 2-4 years prior to routine clinical detection. Attempts to further improve this approach require an understanding of the basis for its success. Based on the work of Hakomori and coworkers, this difucosylated Lewis X structure would be a likely marker of carcinogenic transformation of the bronchial epithelium. In fact, an antibody to this structure was useful for sputum immunocytochemistry analysis for early lung cancer detection. Other carbohydrate structures would also be reasonable markers to evaluate for early detection application, based on the known pattern of expression of these structures in fetal, dysplastic, and neoplastic lung tissue. Another antibody used for sputum immunostaining recognizes a 31-kd protein structure; the antibody is not a known member of a likely class of early detection targets. The reported cases of lung cancer missed by the immunostaining approach included principally adenocarcinoma of the lung, suggesting that the addition of a marker(s) of that type of morphologic differentiation should be considered. Markers to dissect the various forms of lung adenocarcinoma are being characterized and are available for evaluation in early detection applications.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Rational targets for the early detection of lung cancer. 138 92

A 75-year-old male presented with paraparesis and pain in the thighs, which progressed rapidly. Five days later, he was unable to stand or to void urine. A lung cancer was found in the right upper lobe. A spinal cord metastasis from the lung cancer was suspected from the neurologic and pulmonary findings. After 2 weeks, motor dysfunction and a total sensory deficit were observed below the lumbar region, and the patient developed pneumonia, which resulted in death. Autopsy showed an extensive intramedullary metastasis at the third lumbar segment of the spinal cord. Histology revealed poorly differentiated adenocarcinoma of the lung.
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PMID:Intramedullary spinal cord metastasis from lung cancer presenting with paraparesis: an autopsied case. 141 59

Cytosolic glutathione S-transferases (GSTs) are a supergene family of dimeric enzymes capable of detoxifying a number of carcinogenic electrophiles. Of the numerous components of tobacco smoke, the polycyclic aromatic hydrocarbons appear to be the principal compounds that yield substrates for these enzymes, GSTM1-1 being effective with those PAH derivatives so far studied; however, the gene locus for GSTM1 is polymorphic, containing two well-characterized expressing genes and a null allele. Use of cDNA for GSTM1-1 or appropriate fragments of genomic clones as probes in Southern blots indicated that the null allele is due to the absence of GSTM1. In preliminary experiments, described here, with lung tissue from smokers, levels of 32P-postlabeled nuclease P1-enhanced DNA adducts were inversely correlated with levels of antigen cross-reacting with antibody to GSTM1-1, suggesting that initiation depends on the expression of GSTM1-1. Since similar quantities of DNA adducts and GSTM1-1 activity have been shown to occur in bronchial and peripheral lung, however, the development of malignancy, which is usually in the bronchial region, presumably depends on additional factors that bring about promotion and progression, which are not necessarily affected by GSTM1 expression. Two epidemiological studies have been carried out in which a possible correlation between the absence of GSTM1 and lung cancer incidence is considered. In the first, involving a U.S. population sample, smokers with and without lung cancer were phenotyped, and a highly significant correlation between the absence of GSTM1-1 activity and adenocarcinoma of the lung was observed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The human glutathione S-transferase supergene family, its polymorphism, and its effects on susceptibility to lung cancer. 148 68

An 80-year-old man was admitted to our division because of hemosputum, cough, and chest pain for three months. A chest roentgenogram, chest CT scanning, and bronchoscopic examinations revealed adenocarcinoma of the lung with atelectasis of the right upper lobe. The patient developed radiation pneumonitis after receiving radiation therapy (5,100 cGy) for lung cancer. At the same time, the right upper lobe atelectasis improved and movement of infiltrates consistent with radiation pneumonitis to the middle lung fields occurred. A chest roentgenogram taken when the atelectasis had improved revealed the absence of pneumonitis shadows in the right upper lobe, suggesting that the atelectatic lung escaped radiation pneumonitis.
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PMID:Atelectatic lung escaping radiation pneumonitis. 154 Nov 73

Since the nuclear accumulation of p53 protein is known to correspond well with mutation of the p53 tumor suppressor gene, the authors examined 88 primary lung cancer specimens immunohistochemically using anti-p53 mouse monoclonal antibody, pAb1801, and analyzed the relationship between the immunohistochemical results and clinicopathological features. Nuclear localization of p53 protein was found in 43/88 (49%) tumor specimens, but not in the corresponding normal lung tissues. The percentage of cases showing nuclear p53 localization varied according to the histological type. In squamous cell carcinoma, nuclear p53 localization was found in 15/26 (57%), appearing more frequently than in other histologic types. However, no obvious correlation was observed between nuclear p53 localization and patients' age, sex, history of smoking, TNM factor, degree of differentiation, or any other clinicopathological features analyzed. In adenocarcinoma, nuclear p53 localization was found in 20/46 (43%). Incidence of positive cases was significantly correlated with regional lymph node metastasis, distant metastasis, and pathological stage (P less than 0.05). These results indicate that mutation of the p53 tumor suppressor gene plays an important role in the development of primary lung cancer, and that nuclear accumulation of p53 protein is a potential prognostic factor in adenocarcinoma of the lung.
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PMID:Clinicopathological significance of nuclear accumulation of tumor suppressor gene p53 product in primary lung cancer. 154 66

Activation of ras oncogenes is commonly found in human neoplasms. We have investigated 280 human lung cancer specimens for ras activation, including 38 that have not been reported previously, using an oligonucleotide detection assay. From a total of 141 adenocarcinoma samples from smokers, 41 tested positive for a point mutation in codon 12 of K-ras (30%), while three tumors had another type of ras activation. Only two of 40 cases from nonsmokers had a K-ras mutation (5%), suggesting that K-ras mutations may be directly caused by exposure to carcinogens in tobacco smoke. The majority of the point mutations in adenocarcinomas were guanine to thymine transversions in codon 12 of the K-ras oncogene. Occasional point mutations in ras oncogenes were detected in adenosquamous carcinomas (one of five cases) and large cell carcinoma (one of 24 cases), but no ras activations were found in small cell carcinomas (six cases), squamous carcinomas (48 cases), carcinoid carcinomas (15 cases), or thymoma (one case). Analysis of the clinical and pathological features of the adenocarcinoma cases showed no apparent associations between the K-ras activation and age at diagnosis, sex, disease stage, and the occurrence of other neoplasms. K-ras-positive adenocarcinomas tended to be less differentiated than the K-ras-negative ones (P = 0.044, chi 2 test for trend). K-ras mutations identify a subgroup of patients with adenocarcinoma of the lung who have a very poor prognosis despite radical resection of their tumor. Although K-ras has been proposed as a target for antitumor therapy, its major clinical significance could be to aid in the selection of patients for specific therapeutic interventions, such as adjuvant chemotherapy.
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PMID:Clinical significance of ras oncogene activation in human lung cancer. 156 97

Myc gene abnormalities were studied in 30 human lung cancer cell lines. N-myc gene amplification was found in an adenocarcinoma cell line, VMRC-LCD. Neither c- or L-myc gene amplifications nor K-ras codon 12, 13, 61 point mutations were observed in this tumor. Cytomorphologically the VMRC-LCD cells had positive characteristics of typical adenocarcinoma, and the carcinoembryonic antigen in the culture medium was strongly positive. N-myc gene amplification in adenocarcinoma of the lung is extremely rare, therefore we report herein on this case.
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PMID:Amplification of the N-myc oncogene in an adenocarcinoma cell line of the lung. 162 16

Implantation of malignant cells along the needle tract is an extremely rare but potential complication following percutaneous needle aspiration biopsy of malignant lesions. Percutaneous fine-needle aspiration biopsy (FNAB) has recently received more attention for cytologic diagnosis of bronchogenic carcinoma because of its high diagnostic yield, simplicity, and low morbidity. On the other hand, dissemination of cancer cells by needle aspiration biopsy can change a potentially resectable localized lung cancer to an unresectable one. We report two cases: one patient underwent FNAB of a metastatic left adrenal mass that seeded a paraspinal muscle implantation of malignant cells that subsequently developed a tumor mass, and the second patient had tumor cell implantation in the chest wall after FNAB of a pleural-based adenocarcinoma of the lung. The theoretical and practical importance of tumor cell spread along the needle tract is discussed. Because of its rare incidence, however, this complication should not affect the use of needle aspiration biopsy in bronchogenic carcinoma, although care should be undertaken during the procedure.
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PMID:Implantation metastasis of carcinoma after percutaneous fine-needle aspiration biopsy. 162 81

A patient presenting with marked inflammatory lymphadenitis and Jaccoud's arthritis was found to have a rearranged gene for the beta-chain of the T-cell receptor (TCR-beta) antigen in the lymph node DNA digests and normal germ line DNA in the peripheral blood lymphocytes. Four months later, the patient was diagnosed to have poorly differentiated adenocarcinoma of the lung with small foci of metastatic tumor in lymph nodes that contained the same extensive lymphocytic and inflammatory cell infiltrates noted earlier. Rearranged TCR-beta chain genes were detected in both lymph node and peripheral blood lymphocyte DNA at this time. The most likely explanation for the florid lymph node reaction and the unusual arthropathy appears to be a paraneoplastic immune response. The rearranged TCR-beta genes indicate a clonal T-cell expansion that most likely resulted from the aberrant immunologic response to the lung cancer.
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PMID:Clonal rearrangement of the T-cell receptor beta-chain gene in hyperplastic lymphadenopathy associated with lung cancer. 165 14


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