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Query: UMLS:C0001418 (adenocarcinoma)
 68,496 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Survival and histologic subtype were compared in 61 patients with small cell anaplastic lung cancer. Patients with lymphocyte-like (oat cell) and fusiform histologies treated with chemotherapy had longer median survivals than the polygonal and other varieties on the same treatment. Likewise, when detectable disease was confined to the chest and supraclavicular nodes, the patients with lymphocyte-like and fusiform types lived longer. The improved survival in the lymphocyte-like and fusiform categories accounted for most of our improved overall median survival rates with the COPP regimen in small cell lung cancer. Survival in the polygonal and other types was not appreciably different from that seen in non-small cell lung cancer (squamous and adenocarcinoma). It may be possible to refine treatment plans on the basis of cell type so as to further increase survival in small cell anaplastic lung carcinoma.
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PMID:Relationship between survival and histologic type in small cell anaplastic carcinoma of the lung. 22 3

The establishment and characterization of 11 human lung cancer cell lines are described in this article. Nine of these cell lines were established over a 5-year period, from 1983 to 1988, from patients treated at the Kingston Regional Cancer Centre. These include eight definite or probable small cell lung cancer (SCLC) lines and one adenocarcinoma line. In addition, two other SCLC cell lines were characterized. All of the lines have been in continuous culture for more than 2 years. The clinical histories of the patients from whom the cell lines were derived are outlined here. Several features of the cell lines are presented, including the following: (1) a comparison of the histologic features of the cell lines with the original biopsy specimens; (2) the expression of various markers, including cytokeratin, carcinoembryonic antigen, calcitonin, and neuron-specific enolase; (3) activities of the enzymes l-dopa decarboxylase and the brain isoenzyme of creatine kinase; (4) growth characteristics; (5) cloning efficiency in soft agar; (6) tumorigenicity in nude mice; and (7) cytogenetic studies. These cell lines, obtained directly from patients with a spectrum of drug-sensitive and drug-resistant tumors, will be valuable in vitro models of sensitivity and resistance to chemotherapy in lung cancer.
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PMID:Establishment and characterization of a panel of human lung cancer cell lines. 131 80

A study of 149 light microscopic tissue slides from 147 patients with recorded initial diagnoses of small cell lung cancer (SCLC) (114 cases) and undifferentiated carcinoma (35 cases) was undertaken to test the reproducibility and prognostic impact of a new histopathologic subclassification of SCLC proposed by the Pathology Panel of the International Association for the Study of Lung Cancer (IASLC). This study was further designed to test the impact of clinical stage, age, sex, and race on survival. The tissue slides were blindly reclassified as SCLC or non-SCLC by a panel of five pathologists with no knowledge of the initial diagnosis. The SCLCs were divided into the three subtypes outlined by the IASLC pathology panel: small (classic or pure), mixed (small cell/large cell), and combined (small cell/squamous carcinoma or small cell/adenocarcinoma). Small cell lung cancer was clinically staged as local, regional, or distant. Consensus diagnosis (defined as agreement by at least three of the five pathologists) was achieved in 144 (96.6%) of the 149 cases. Of these 144 cases, 124 were reclassified as SCLC (115 [92.8%] small, five [4.0%] mixed, and four [3.2%] combined) and 20 were classified as non-SCLC. The median lengths of survival for the small, mixed, and combined subtypes were 225, 1,110, and 203 days, respectively (P = .025). Adequate staging data were available in 123 of the 124 SCLC cases. Of the 123 SCLC cases, 27 (21.9%) were local, 22 (17.9%) were regional, and 74 (60.2%) were distant stage. The median lengths of survival for the local, regional, and distant stages were 428, 251, and 111 days, respectively. This association was highly significant (P = .0001). We conclude that stage is the major determinant of survival in SCLC. Mixed subtypes had significantly longer survival times than the small or combined subtypes (P = .025). Survival times were longer for women than for men, and the survival time difference between men and women was significant (P = .0028). We found no significant differences in survival according to age or race.
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PMID:Prognostic significance of histopathologic subtype and stage in small cell lung cancer. 131 77

Eighteen small cell lung cancers (SCLCs), 108 non-SCLCs (67 adenocarcinomas, 29 squamous cell carcinomas and 12 large cell carcinomas) were immunohistochemically examined for expressions of cluster 1 SCLC antigen/N-CAM and chromogranin A with monoclonal antibodies NCC-Lu-243 and anti-chromogranin A. The cell membranes of all the SCLCs and three of the 67 adenocarcinomas (4.5%) were stained for cluster 1 SCLC antigen/N-CAM. Eight of the 18 SCLCs (44.4%), and three of the 67 adenocarcinomas (4.5%) were stained for chromogranin A, but no squamous cell carcinoma or large cell carcinoma was stained for both antigens. Two of the three adenocarcinomas which expressed cluster 1 SCLC antigen/N-CAM had been suspected of being either SCLC or poorly-differentiated adenocarcinoma cytologically, and were resected after chemotherapy and radiotherapy. Histologically, they were poorly-differentiated adenocarcinoma with rosette-like tubules. The remaining one was moderately-differentiated papillary adenocarcinoma resembling bronchial surface epithelial cells without mucin (BSE type adenocarcinoma). The three adenocarcinomas which expressed chromogranin A were well- to moderately-differentiated BSE type adenocarcinomas, and stained tumor cells were distributed sparsely as neuroendocrine cells in the normal bronchial mucosa. One of them also expressed cluster 1 SCLC antigen/N-CAM. In the present study, we demonstrated the usefulness of NCC-Lu-243 in the immunohistochemical detection of adenocarcinomas with neuroendocrine features.
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PMID:Immunohistochemical detection of cluster 1 small cell lung cancer antigen and chromogranin A in lung carcinomas. 131 1

The efficacy of combined high-dose etoposide with standard dose cisplatin was evaluated in patients who had refractory lung cancer after standard chemotherapy. Each patient was given etoposide at 500 mg/m2/day on day 1 to 3 continuously (total dose 1,500 mg/m2) and cisplatin at 80 mg/m2 on day 1. Fifteen patients (7 adenocarcinoma, 5 small cell lung cancer, 2 squamous cell lung cancer and 1 sarcoma, which latter was difficult to distinguish from giant cell carcinoma) were entered in this study. The overall response was 41.7% (5 of 12); five partial response, 6 no change, and 1 progressive disease. Three treatment-related deaths were observed; one resulted from sepsis and two from respiratory failure because of tumor progression. All of the patients developed severe myelosuppression; the mean nadir white blood cell count was 400, and the mean nadir platelet count was 24,000 in 28 evaluable courses. The range of maximum concentration of etoposide determined by HPLC was from 17.4 to 39.1 micrograms/ml. These results suggest that high-dose etoposide combined with a standard dose of cisplatin is effective against refractory lung cancer.
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PMID:[Pilot phase II trial of high-dose etoposide combined with cisplatin in the treatment of refractory lung cancer]. 131 97

Encouraging response rates have been observed with long-term daily administration of oral etoposide to treat lung cancer. Reasons why EP (etoposide/cisplatin) has been used to treat non-small cell lung cancer (NSCLC), despite the fact that etoposide has demonstrated only a modest degree of activity against this disease, are preclinical suggestions of cisplatin/etoposide synergism and successful results for the combination in treating small cell lung cancer (SCLC). We evaluated a long-term daily oral etoposide regimen in combination with cisplatin for NSCLC. One course consisted of cisplatin on day 1 and etoposide from day 1 through day 21. The course was repeated, beginning at day 29. We concluded that the maximum tolerated dose in this schedule was 50 mg/m2/day oral etoposide for 21 days plus 80 mg/m2 intravenous (i.v.) cisplatin on day 1. The major dose-limiting toxic effect was myelosuppression, and mucositis was also significant in some patients. During this phase I study of 22 patients (18 evaluable), we observed partial responses (PRs) in 4 patients, 1 each with uterine cancer and SCLC, and 2 with squamous cell lung cancers. We then designed a phase II pilot study in patients with advanced NSCLC. The recommended treatment schedule is 80 mg/m2 i.v. cisplatin on day 1 plus 40 mg/m2/day oral etoposide for 21 consecutive days. Of the 13 evaluable patients, PRs were observed in 4 (30.8%), in 2 patients with adenocarcinoma and 2 with squamous cell carcinoma. None of the side effects were severe or life-threatening. Nearly all of the projected doses were given, with delays of 7-10 days. In this pilot phase II study, the response rate of advanced NSCLC was above 30%. Future studies should combine long-term administration of oral etoposide with radiation therapy or surgery to treat stage III NSCLC.
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PMID:Platinum/oral etoposide therapy in non-small cell lung cancer. 132 14

We have developed panels of human lung cancer cell lines with acquired and inherent resistance to cisplatin. Three parental cell lines, NCI-H69/P (small cell), COR-L23/P (large cell), and MOR/P (adenocarcinoma), were grown in increasing concentrations of cisplatin over a period of 6-9 months. This resulted in the development of sublines, H69/CPR, L23/CPR, and MOR/CPR which were 3- to 8-fold resistant to cisplatin as determined by a 6-day 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. None of the resistant sublines showed a significant change in cellular glutathione content or sensitivity to cadmium chloride (an indicator of metallothionein content), although changes in glutathione-S-transferase activity were seen. The sublines each showed cross-resistance to melphalan. Cisplatin accumulation was unchanged in H69/CPR, 1.3-fold reduced in L23/CPR, and 2.0-fold reduced in MOR/CPR compared with their respective parent lines. In a panel of 10 small cell lung cancer cell lines, there was a 16-fold range of sensitivities to cisplatin. The panels have been used to examine cross-resistance between cisplatin, carboplatin, iproplatin, tetraplatin, and a series of 10 novel ammine/amine dicarboxylate platinum(IV) compounds. Whereas H69/CPR and MOR/CPR showed little or no cross-resistance to any of the other compounds, L23/CPR was generally cross-resistant to all of them. In the panel of small cell lines, whereas the ranking of sensitivity to carboplatin and cisplatin were similar, each of the other compounds provided individual patterns of sensitivity. There was always a wide range of sensitivities among the panel, ranging from 8- to 28-fold. Among the dicarboxylate compounds, there was a great range of potencies, with two compounds (JM273 and JM274) being approximately 100-fold more potent than cisplatin.
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PMID:Sensitivity to novel platinum compounds of panels of human lung cancer cell lines with acquired and inherent resistance to cisplatin. 132 13

Small cell lung cancer (SCLC) cells express several characteristics of neuronal cells, including synthesis of neuropeptides and expression of the respective receptors. Establishment and maintenance of the neuronal phenotype of SCLC may depend on expression of gene transcription factors inherent to the central nervous system. The present study shows the nervous system-specific transcription factor N-Oct 3 (brain-2) to be expressed in all 13 SCLC cell lines investigated. Furthermore, N-Oct 3 (brain-2) was also found in SCLC-derived skin metastasis. In contrast, in extracts and RNA of non-SCLC cell lines and non-SCLC tumor tissues, such as lung squamous, large cell, and adenocarcinoma, expression of N-Oct 3 (brain-2) was not detectable. These data support the concept that SCLC cells derive from the neuroectodermal cell lineage since expression of N-Oct 3 (brain-2) protein is highly abundant at the neural tube stage and in the adult restricted to the neuroectodermal cell lineage.
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PMID:Human small cell lung cancer expresses the octamer DNA-binding and nervous system-specific transcription factor N-Oct 3 (brain-2). 132 24

The aim of this study was to investigate anti-elastin antibodies of the IgG and IgM types in sera of patients suffering from lung cancer, using the DOT immunobinding assay. We studied 96 pathological and 40 control sera. Anti-elastin antibodies were found to be present in 45% of patients with small cell lung cancer, 19% of subjects with adenocarcinoma and not-identified lung tumor and 15% of patients with squamous cell lung cancer. They circulated in 5% of control persons only. The highest values of their titers were observed in the advanced stages of disease. In 55% of anti-elastin antibody positive small cell lung cancer patients, antibodies were of the IgM type, suggesting the initial step of the autoimmunization to elastin.
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PMID:Anti-elastin antibodies in patients with lung cancer. 133 26

The histopathology criteria which could be taken into account in devising the best strategy in tumor extension search in non small cell lung carcinoma (NSCLC), were examined. First, the differential diagnosis between primary and metastatic carcinoma is impossible on histological basis in squamous carcinomas, and in mucinous adenocarcinoma which share several features with tumors from digestive tract including mucus secretion, morphological pattern and ultrastructural signs. The recognition of cells which are unique in the lung (Clara cells, pneumonocytes II) guarantees the pulmonary origin of a non mucinous adenocarcinoma. In other cases such as large cell carcinomas, the diagnosis of metastasis can be achieved in some instances in using a large panel of immunohistochemical markers. Secondly, the expression of neuroendocrine markers in NSCLC could lead to an extension search procedure identical to that of SCLC, if it can be confirmed that they share their poor prognosis and chemosensibility. Finally, there is no statistical evidence of a difference in the extrathoracic extension between well and poorly differentiated forms of squamous carcinoma and adenocarcinoma. Only one exception should be made for the recently described basaloid carcinoma of the lung which extension and prognosis are more severe than in other NSCLC.
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PMID:[Do pathologic-anatomic data influence the staging of non-small cell bronchial cancer?]. 133 79


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