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)

Carcinosarcoma and pulmonary blastomas are rare biphasic tumors. Lung cancer pathogenesis is a multistep process. Proliferative activity, p53 accumulation and angiogenesis are of well-known relevance and ought to be evaluated in the epithelial and mesenchymal components of these tumors. Using antibodies against Ki-67 epitope MIB1 and proliferating cell nuclear antigen (PC 10) in 10 carcinosarcomas, tumors revealed a significantly higher proliferative activity in the epithelial component compared with the mesenchymal component in the MIB1 reaction (p = 0.013). In three pulmonary blastomas of the biphasic subtype, proliferative activity was similar in both parts. In five of 10 carcinosarcomas and in one of three pulmonary blastomas, accumulation of the p53 epitopes Pab 1801 and/or DO-1 was found. At the tumor front, a significantly higher vessel density was found compared with the central parts (p < or = 0.015) using a monoclonal antibody against human endothelium (CD 31). No differences were found between carcinosarcomas and pulmoblastomas. Higher proliferative activity in carcinosarcomas revealed a better prognosis regarding metastasis behavior (p = 0.05) and tumor-associated death in the follow-up (p < or = 0.017). p53 accumulation and microvessel density were of no prognostic value. This is in contrast to results in non-small cell lung cancer, pointing to a different biologic behavior.
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PMID:Proliferative activity, p53 accumulation and neoangiogenesis in pulmonary carcinosarcomas and pulmonary blastomas. 965 6

The proliferative rate of a tumor has been considered predictive of its clinical course. We evaluated the expression of the proliferative marker Ki-67 and its relationship to survival, disease-free survival and other clinicopathologic variables in both stage I and stage II non-small cell lung cancer (NSCLC). A total of 260 patients with surgically resected stage I (n = 193), and II (n = 67) NSCLC with at least 5 years follow-up were identified. The median survival for patients with low expression of Ki-67 (< or = 25%) was 54 months, while for those with high expression (> 25%), it was 45 months (P = 0.1). The disease-free survival in patients with low expression of Ki-67 was 59 months while it was only 32 months for patients with high Ki-67 (P = 0.1). Out of 136 patients, 84 (62%) had both increased S-phase (> 8%) and high Ki-67 (P = 0.001). A total of 28 of 30 patients who had loss of antigen A had high expression of Ki-67 (93.3%) (P = 0.03). Ki-67 expression was also higher in squamous cell (54/63, 85.7%) compared to nonsquamous cell cancer (70/108, 64%) (P = 0.03). We also analyzed for the presence of symptoms with survival. The presence of symptoms was not found to be statistically significant, for overall survival (P = 0.33) or disease-free survival (P = 0.72). When individual symptoms were analyzed, the presence of cough was statistically significant for both overall and disease-free survival. The median survival was 39 months for patients with cough, and 57 months for patients without cough (P = 0.04). Multivariate analysis showed higher N and T stages, presence of cough and loss of antigen A, predicted for poorer overall survival. Higher N and T stages, loss of antigen A, presence of mucin and cough and increased expression of Ki-67 predicted decreased disease-free survival. Although we did not find a statistically significant difference between low and high Ki-67, there was a trend for a poorer overall and disease-free survival in patients with high Ki-67 expression. Larger studies may be needed to prove a statistically significant effect of Ki-67 on survival. Future studies should assess the potential prognostic significance of the presence of symptoms (particularly cough) in addition to clinical-pathologic variables (such as T and N stage) and biological markers in patients with early stage NSCLC.
Lung Cancer 1998 May
PMID:Prognostic significance of Ki-67 immunostaining and symptoms in resected stage I and II non-small cell lung cancer. 971 28

In the present study, K-ras mutation was investigated in 156 neogenetic epithelia that appeared in the lesion of subpleural fibrosis in order to elucidate the close relationship of lung cancer development with pulmonary interstitial pneumonia. The neogenetic epithelia were histologically subclassified into six types: (i) ciliated bronchial epithelium (CBE); (ii) squamous metaplastic epithelium (SME); (iii) cuboidal immature epithelium (CIE); (iv) stratified immature epithelium (SIE); (v) mucus cell epithelium (MCE); and (vi) intestinal metaplastic epithelium (IME). K-ras mutation was detected in 9.6% of neogenetic epithelia overall; 21% of CIE, 12% of SIE, 16% of SME, but not in other types of neogenetic epithelia. Immunohistochemically, CIE and SIE frequently expressed surfactant apoprotein and SME was characteristic to carcinoembryonic antigen expression. According to Ki-67 immunostain, CIE, SIE and SME are likely to grow faster than other histological types of epithelia. K-ras mutation was seen exclusively in codon 12 with predominant G to A and G to C substitutions without any G to T transversions, results which are somewhat different to previous studies in lung cancers. The present study clearly demonstrated that K-ras mutation appeared in certain histological types of neogenetic epithelia, but raised the question of whether K-ras mutation in neogenetic epithelia during the inflammatory reparative process might be an early genetic event in lung carcinogenesis.
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PMID:K-ras gene point mutation in neogenetic lesions of subpleural fibrotic lesions: either an early genetic event in lung cancer development or a non-specific genetic change during the inflammatory reparative process. 1041 84

Two cases of primitive neuroectodermal tumor of the lung are reported. The first case is a 41-year-old man with a tumor in the left upper lung, and the second case is a 30-year-old woman with a tumor in the right lower lung. In both cases, the tumors originated in the lung but not in the chest wall. No distant metastasis was detected. In case 1, transcutaneous fine-needle biopsy (TCNB) revealed small round cell proliferation, although bronchoscopic examination showed no abnormal findings. Both the expression of Mic2 protein and t(11;22)(q24;q12) translocation were proved in the tumor cells. The tumor cells were positive for periodic acid-Schiff (PAS), neuron-specific enolase (NSE), and vimentin, but negative for Leu7, chromogranin A, and pro-gastrin-releasing peptide (ProGRP). In case 2, bronchoscopic examination showed only compressive change in right lower lobe bronchi. TCNB revealed small round tumor cells expressing Mic2 protein. The tumor cells were negative for leukocyte common antigen, S100 protein, pankeratin, chromogranin A, and desmin, but weakly positive for NSE and moderately positive for Ki-67 (MIB1). Both patients were successfully treated by the combination of surgical resection and chemotherapy, and are alive with no sign of recurrence for approximately 22 months in case 1 and 16 months in case 2.
Lung Cancer 2000 Jan
PMID:Primary primitive neuroectodermal tumor of the lung: report of two cases. 1067 84

The promyelocytic leukemia (PML) gene, which encodes a transformation and growth suppressor, was first identified at the chromosomal translocation break point t(15;17) in acute promyelocytic leukemia (PML). To determine if the PML gene might be involved in other neoplasias such as lung cancer, PML expression was analyzed by immunohistochemical staining and in situ hybridization. Considerable PML protein expression in the PML-oncogenic domain (POD) structure was found in adenocarcinomas (ADC) and squamous cell carcinomas (SCC) of the lung, but was almost completely absent in all the small cell lung carcinomas (SCLC) examined. In situ hybridization showed that both mRNA and DNA of PML were present in SCLC and in normal lung, suggesting that the decreased protein expression was due to either a defect in translation or protein instability, rather than the consequence of decreased transcription or gene deletion. Double staining showed that PML expression was inversely correlated with the proliferation marker Ki-67 and positively correlated with levels of apoptotic cells in these tumors. To determine if the precursor cells of SCLC, the neuroendocrine-producing cells, express PML, double labeling was performed with PML and chromogranin A, a bio-marker for neuroendocrine cells. Neuroendocrine cells from normal tissues were found to be PML positive, indicating that the lack of PML protein in SCLC is associated with the tumorigenic phenotype and is not the result of cell-lineage specificity. Thus, the decreased PML expression may play an important role in SCLC development.
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PMID:Lack of expression for the suppressor PML in human small cell lung carcinoma. 1069 36

Atypical adenomatous hyperplasia (AAH) is a possible precursor lesion of adenocarcinoma of the lung, but there have been no reports of AAH focusing on autopsy studies of the lungs of elderly patients, who have higher lung cancer mortality rates. We intended to clarify the characteristics of AAH in the general elderly population on the basis of the findings in autopsy cases. A total of 19 AAH lesions were found microscopically in 16 out of 241 autopsy cases (6.6%). AAH was found in only two cases of adenocarcinoma among 28 lung cancer cases. p53 immunoreactivity was observed in one of 11 low-grade AAH lesions (9.1%), but in three of four high-grade AAH lesions (75%, P=0.03) and the cases of high-grade AAH were more frequently positive for Ki-67 and CEA than the low-grade cases and less positive for pro-surfactant apoprotein C. Four of 123 patients without malignant neoplasms (3.4%) and 12 of 118 patients with malignant neoplasms (11.1%) had AAH (P=0.03). The finding that AAH was more common in the cases with malignancy than in those without malignancy indicated that genesis of AAH may be closely associated with that of malignant neoplasms.
Lung Cancer 2000 Aug
PMID:High prevalence of atypical adenomatous hyperplasia of the lung in autopsy specimens from elderly patients with malignant neoplasms. 1096 42

CD44, belongs to the cell adhesion molecule family and is expressed on cell surfaces in several isoforms which are generated by alternative splicing of messenger RNA. These splice variants have been shown in several cancer cell types and are thought to be involved in tumor progression. The aim of the current study was to evaluate the expression of selected CD44 variants on lung cancer cells of various histology and to compare these with other markers of tumor spread. Surgical samples of primary lung carcinoma of various histology were subjected to alkaline phosphatase-anti-alkaline phosphatase complex immunohistochemistry using a panel of monoclonal antibodies: anti-CD44 v5, v6, v7/8, v10, anti-Ki-67, anti-Bcl-2 and anti-p53. Positive cells were scored in a semiquantitative way. The patients were subdivided into groups with and without metastases, as found during surgery. All CD44 variants tested could be demonstrated on lung cancer cells, but the incidence of particular isoforms varied, depending on lung cancer histology. In general, CD44 expression was highest in squamous cell tumors and lowest in anaplastic small cell carcinomas. Squamous cell cancers had high expression of v5 and v6 variants, while in anaplastic large cell and small cell carcinomas v10 was abundant. When Ki-67, Bcl-2 and p53 protein expression was compared to the incidence of CD44 variants, coincidence was found for v10 only. Most of the cases positive for v10 were also Ki-67 positive (p = 0.0146). In 12 cases with metastases, tumor cells had high v6 and Ki-67 expression, but these data were not significant compared to cases without metastases. Overall, these data suggest that v5 and v6 variants are of significance in squamous cell lung carcinoma, presumably in the promotion of metastasis, while in anaplastic small cell or large cell cancers only v10 expression seems to correlate with proteins associated with tumor growth and progression.
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PMID:Isoform expression of CD44 adhesion molecules, Bcl-2, p53 and Ki-67 proteins in lung cancer. 1105 26

A seventy-year-old woman was admitted for an abnormal chest shadow on a routine radiograph. She had undergone left upper lobectomy with mediastinal lymph node resection (R2a) for lung cancer (stage I), eight years before. We diagnosed this cancer as well differentiated papillary adenocarcinoma, and it coexisted with a focus of atypical adenomatous hyperplasia (AAH) in the resected material. We had been following up this patient with chest radiography, CT scanning, and tumor marker tests, but eight years after her first operation, we found a small nodular lesion in the left upper field (S6). This nodule was not diagnosed with fiberoptic bronchoscopy. Because we could not exclude primary lung cancer or intrapulmonary metastasis (eight years ago), we performed partial lung resection on the left S6 nodule. Histopathologically, the diagnosis was well differentiated papillary adenocarcinoma of the lung, coexisting with a small hyperplastic focus in the resected material. It was very difficult to diagnose whether these two cancers were metachronous multiple primary lung cancers, or one primary and its intrapulmonary metastasis. In a retrospective study, an immunohistochemical examination employing Ki-67, PCNA, p 27 and p 53 was performed in order to differentiate between metachronous multiple primary lung cancer and intrapulmonary metastasis. But we found AAH in the same resected lung eight years ago, and suggested the possibility that another small, atypical focus had developed into a malignancy. We report a case of metachronous multiple primary lung cancers and review the relevant literature.
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PMID:[A case of metachronous multiple primary lung cancers coexistent with atypical adenomatous hyperplasia]. 1132 21

Resistance to chemotherapy is common in non-small cell lung cancer. The aim of this study was to investigate the prognostic impact of in vitro established drug resistance markers on the response to chemotherapy in patients with advanced non-small cell lung cancer. Samples of 38 patients were analyzed by immunohistochemical staining, for topoisomerase IIalpha and IIbeta, Ki-67, MRP and LRP. In addition, mutation analysis of the topoisomerase IIalpha gene, the B/DNBS and the Tyr804 region, was performed. Lung tumor biopsies were taken prior for treatment with one of the following regimens; cisplatin/paclitaxel, cisplatin/VM26 or VP16, or carboplatin/VP16/ifosfamide. Seventeen patients obtained a partial response, 12 had stable disease and nine patients had progressive disease. None of the investigated markers was related with overall response rate. In one sample a point mutation in the B/DNBS region of the topo IIalpha gene was detected which substitutes IIe(510) with Val. This tumor had a partial response to four courses of cisplatin/VP16 treatment. The survival analysis showed that the patients with high topo IIalpha expressing tumors had a significantly worse survival compared with the patients with low or intermediate topo IIalpha expressing tumors. In conclusion, no relation was observed between expression of topoisomerase IIalpha, IIbeta, Ki-67, MRP or LRP and response rate. Furthermore, worse survival was seen in patients with high topoisomerase IIalpha expressing tumors. In one tumor sample, a newly described mutation in the B/DNBS region of the topo IIalpha gene was detected, which does not appear to be related to drug resistance.
Lung Cancer 2001 May
PMID:Topoisomerase IIalpha and other drug resistance markers in advanced non-small cell lung cancer. 1132 82

Squamous cell carcinomas of the esophagus, a disease with poor prognosis, are especially frequent in China and South Africa. To initiate the study of endogenous lectins in this tumor class we employed synthetic neoglycoconjugates and focused on galectins as markers. Histological sections of 43 cases of esophageal carcinomas were analyzed with labeled galectins-1 and -3 and their specific antibodies, neoglycoconjugates exposing chemically prepared histo-blood group A-, B- and H-trisaccharides and the antibody MIB-1 (Ki-67). Features of structural and numerical staining intensities determined quantitatively were correlated to clinical data sets of pTN stages, sex and age of patients. Low tumor stages (pT1/T2) were seen in 10/43 cases (23%) and 65% of the carcinomas surgically treated lacked notable lymph node involvement (pN0). The women were younger than the men (47 years versus 54 years). The proliferation activity of the tumor cells was high and amounted to 75% at average. The presence of galectin-1 and the structural entropy of distribution of staining with carrier-immobilized A-trisaccharide were associated with pN stages. These initial data indicate that distinct glycohistochemical features appear to have prognostic significance in this tumor class, adding to the emerging significance of this marker class in lung cancer.
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PMID:Expression of endogenous lectins (galectins, receptors for ABH-epitopes) and the MIB-1 antigen in esophageal carcinomas and their syntactic structure analysis in relation to post-surgical tumor stage and lymph node involvement. 1139 28


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