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Query: UMLS:C0684249 (lung carcinoma)
 23,830 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Some dysplasias in the bronchial epithelium are thought to be precancerous lesions that can develop into squamous cell carcinomas. In this investigation, we assessed the biological behavior of bronchial squamous dysplasia in order to define which dysplasias have the potential to progress to squamous cell carcinoma. Using autofluorescence bronchoscopy, we followed up periodically localized dysplasias and examined for correlation between histological outcome and smoking status during the follow-up period, telomerase activity, Ki-67 labeling index, and p53 immunoreactivity of initial biopsy specimens. Ninety-nine dysplasias from 50 participants mainly with sputum cytology suspicious or positive for malignancy were followed up. Of 99 dysplasias, 3 dysplasias progressed to squamous cell carcinoma, 41 dysplasias remained as dysplasia, 6 dysplasias changed to metaplasia, 14 dysplasias changed to hyperplasia, and 35 dysplasias regressed to bronchitis or normal bronchial epithelium. There were no significant associations between histological outcome and smoking status. Mean initial telomerase activity and Ki-67 labeling index values in the dysplasias increased in proportion to the severity of the histological outcome at the second biopsy. There was also a significant difference between p53-positive and p53-negative dysplasia in terms of histological outcome at the second biopsy. Our results suggested that dysplasias with high telomerase activity, increased Ki-67 labeling index, and p53-positivity tended to remain as dysplasia and might have the potential to progress to squamous cell carcinoma. Patients with dysplastic lesions with these characteristics should be carefully followed up.
Lung Cancer 2004 Nov
PMID:Biological features of bronchial squamous dysplasia followed up by autofluorescence bronchoscopy. 1589 14

The cancerization field concept implies that lung cancer multicentricity may be a frequent event and primary studies using white-light bronchoscopy (WLB) have reported a high prevalence of multicentricity in patients with roentgenographically occult lung cancer. We have used autofluorescence bronchoscopy (AFB) to reassess the prevalence of synchronous lesions in patients referred for the staging and/or treatment of occult lesions initially detected during WLB. All the patients referred with high-grade preinvasive lesions (severe dysplasia, DYS S and carcinoma in situ, CIS) and occult invasive squamous cell carcinoma (CIV) of the bronchus initially detected during WLB at other centers, underwent AFB. Data were prospectively collected and retrospectively analyzed to assess the prevalence of synchronous occult lesions. From January 1996 to December 2001, 28 patients (26 males, 2 females; mean age: 65 +/- 11) were assessed. After re-evaluation, in two cases, the referred lesions corresponded only to metaplasia and were discarded from analysis. The 26 other patients were referred for 28 lesions (3 DYS S, 19 CIS and 6 CIV; 2 patients were referred with two synchronous lesions). AFB revealed, in these 26 patients, six additional lesions (1 DYS S, 4 CIS and 1 CIV). Multicentricity in this group, initially estimated to amount to 7% with WLB alone, raised to 23% by using AFB. The high prevalence of synchronous lesions in this series of patients with occult DYS S, CIS and occult CIV suggests that AFB may be a useful adjunct in the pretreatment evaluation.
Lung Cancer 2004 Dec
PMID:Synchronous lesions detected by autofluorescence bronchoscopy in patients with high-grade preinvasive lesions and occult invasive squamous cell carcinoma of the proximal airways. 1554 19

World Health Organisation (WHO) defined three types of preinvasive epithelial lesions, one of which is preinvasive bronchial squamous lesions consisting of dysplasia and carcinoma in situ (CIS). It is not clear whether or not CIS at the bronchial resection margin is to be considered as incomplete resection in the literature. Follow-up data of such patients using autofluorescence bronchoscopy proved that CIS regresses without further treatment in significant number of patients. It is therefore reasonable to accept any reported CIS lesion on frozen-section examination as complete clearance of the tumor and thus further resection may not be warranted.
Lung Cancer 2004 Dec
PMID:Carcinoma in situ from the view of complete resection. 1554 27

Angiogenesis is an important factor in the development of epithelial neoplasias and is useful in the study of progression and metastasis. Neoplastic cells produce angiogenic factors that overtake the antiangiogenic capacity of autoimmune cells. The vascular endothelial growth factor (VEGF) is the most important factor in the neoplastic angiogenesis. In colo-rectal carcinoma the expression of VEGF is parallel with genetic alterations and Duke's grade. In non-small cell lung carcinoma it is possible to define the angiogenic squamous dysplasia that evolves to invasive epidermoid carcinoma. In invasive gastric and lung cancer, the stromal molecules: COX 2, metalloproteinasis and adhesion molecules develop angeogenesis and their validation is important either in and therapy. In breast cancer there is a correlation between the growing of microvessels density, VEGF expression and p53 alterations, pointing to prognosis. Serological values of VEGF may also be used to monitorise the follow up of sarcomas and its reccurrence but vascular metastatic process is not yet completely understood.
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PMID:[Angiogenesis and cancer: from biopathology to therapy]. 1563 32

This article analyzes phenotype and genotype alterations of the lung in association with lung cancer. The frequency of phenotype preneoplastic lesions (atypical adenomatoid hyperplasia (AAH) and squamous cell dysplasia (SCD)) was analyzed at distinct distances from the tumor boundary in 150 lung carcinomas. AAH was noted in 19/150 (13%) cases and more frequently seen in adeno carcinomas, squamous cell dysplasia was noted in 46/150 (31%) cases and more frequently seen in squamous cell carcinomas. The degree of cellular atypia decreased with increasing distance from tumor boundary in both AAH and SCD. At similar distances, genotype (chromosome) alterations of surrounding bronchial mucosa were studied in additional 55 primary and secondary lung tumors by karyotype analysis. Numerical chromosome aberrations occur frequently in primary lung carcinomas and adjacent bronchial mucosa, and affect at average 4.5/10 metaphases in primary lung cancer and 2/10 metaphases in metastases. Most abnormal metaphases were induced by chromosome losses, only few by additional copies, i.e. trisomy, etc. Losses of y chromosome were seen in both malignancy and adjacent bronchial mucosa, and interpreted as "tumor related", losses of chromosome 21 in adjacent bronchial mucosa were non-tumor related in adenocarcinoma and metastases, losses of chromosome 19 in adjacent bronchial mucosa occurred independently in squamous cell and large cell carcinomas. The data suggest the hypothesis that preneoplastic lesions in the lung might be partly induced by the tumor itself.
Lung Cancer 2005 Feb
PMID:Lung carcinoma-associated atypical adenomatoid hyperplasia, squamous cell dysplasia, and chromosome alterations in non-neoplastic bronchial mucosa. 1563 19

Neoangiogenesis is required for the growth of invasive lung carcinoma, however, the role of angiogenesis in the progression of premalignant changes to carcinoma of the lung is less clear. We have evaluated vascular endothelial growth factor (VEGF) expression and microvessel densities (MVDs) in 62 bronchoscopic biopsies from normal, reactive (basal cell hyperplasia (BCH)) and dysplastic bronchial epithelium and in tissue from twenty-seven invasive lung carcinomas in an effort to demonstrate angiogenic activity in these preneoplastic lesions and determine whether it is associated with increased bronchial epithelial VEGF expression. MVDs and VEGF RNA expression measured by quantitative RT-PCR were found to be elevated in comparison to normal bronchial tissue in bronchial dysplasias and invasive lung carcinomas but not in basal cell hyperplasias. Immunohistochemical (IHC) analyses revealed that expression of VEGF arose predominantly from bronchial epithelium. ELISA analysis of lung tumor tissue showed that elevated VEGF protein expression correlated with VEGF RNA levels (r=0.59, p=0.004). Increased expression of VEGF RNA was also found in histologically normal bronchial mucosa from patients with either dysplasia at other sites or a history of heavy tobacco use suggesting a possible field effect in regard to the elaboration of VEGF. Furthermore, analysis of VEGF isoforms and VEGF receptors by semi-quantitative RT-PCR in dysplastic and invasive lesions revealed characteristic altered patterns of expression in dysplasia and early cancer as compared to normal tissue. These results indicate that angiogenesis develops early in lung carcinogenesis and is associated with overexpression of VEGF.
Lung Cancer 2005 Apr
PMID:Overexpression of vascular endothelial growth factor and its receptors in bronchial dypslasia demonstrated by quantitative RT-PCR analysis. 1577 69

Circulating cell-free nucleic acids are noninvasive diagnostic tools for cancer detection. Heterogeneous nuclear ribonucleoprotein (hnRNP) B1, an RNA binding protein, has been found overexpressed in the early stage of lung cancer, including bronchial dysplasia, a premalignant lesion of lung squamous cell carcinoma. To determine the utility of plasma hnRNP B1 RNA and as cancer detection markers for lung cancer, we analyzed plasma hnRNP B1 mRNA of lung cancer patients by real-time RT-PCR. Plasma RNA was extracted from plasma of 44 lung cancer patients, 7 lung neoplasm patients, 24 benign lung diseases and 25 healthy volunteers. Mean concentration of plasma hnRNP B1 mRNA in lung cancer patients was 0.99 pg/microg RNA, whereas that in healthy volunteers and in benign lung diseases was 0.23 pg/microg RNA and 0.30 pg/microg RNA, respectively (p<0.05). Twenty of 44 (45.5%) lung cancer patients showed more than 0.70 pg/microg RNA of plasma hnRNP B1 mRNA, compared with only 3 of 25 (12.0%) healthy volunteers. Looking at histological subtype, squamous cell carcinoma patients showed higher hnRNP B1 mRNA in the plasma than did adenocarcinoma patients, which is consistent with our previous immunohistochemistry results. These results indicate that plasma hnRNP B1 mRNA is a useful non-invasive markers for detection of lung cancer.
Lung Cancer 2005 Apr
PMID:Detection of plasma hnRNP B1 mRNA, a new cancer biomarker, in lung cancer patients by quantitative real-time polymerase chain reaction. 1577 73

A urine tumor marker, diacetylspermine, was examined in patients with recurrent pancreato-biliary carcinoma, liver tumor, lung carcinoma and gynecologic malignancies. The urine marker increased together with recurrence, suggesting a recurrence monitoring marker at the outpatient ward. Regarding hepatocellular carcinoma, the sensitivity of the urine marker was as high as conventional markers such as AFP and PIVKA II. Synchronous examination of serum and urine markers showed a higher sensitivity than the single serum or urine marker for hepatocellular carcinoma. The sensitivity for non-advanced hepatocellular carcinoma was 50%, while that for advanced hepatocellular carcinoma was 83%. The urine marker may be useful to detect non-advanced hepatocellular carcinoma. The sensitivity for lung cancer was 83% and that for Stage I or II was 82%. Concerning uterine cervical tumor, the value of the urine marker increased with the grade of dysplasia. The sensitivity for ovarian carcinoma was 100%, while that for benign ovarian tumor was 0%. These findings suggest that urine diacetylspermine is a useful tumor marker in hepatocellular carcinoma, lung cancer and gynecologic malignancy as well as pancreatobiliary carcinoma.
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PMID:[Urine diacetylspermine as a novel tumor marker]. 1579 46

A histological classification should provide guidelines for tumor diagnosis in order to evaluate patient prognosis and therapy. Pre-invasive lesions identified as precursors of invasive lung carcinoma are: squamous dysplasia/carcinoma in situ, atypical adenomatous hyperplasia and idiopatic pulmonary neuroendocrine cell hyperplasia. Squamous carcinoma and adenocarcinoma are the commonest types of lung carcinoma with the latter increasing in many countries mainly for changed smoking habits. Bronchioloalveolar carcinomas include exclusively noninvasive mucinous or non-mucinous tumors. Neuroendocrine tumors range from well differentiated neuroendocrine carcinoma (typical carcinoid) to intermediate grade (atypical carcinoma) to very aggressive poorly differentiated lesions (large cell neuroendocrine carcinoma and small cell carcinoma).
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PMID:Histological classification of lung cancer. 1585 19

It is generally assumed that squamous cell carcinoma develops in a stepwise manner from normal bronchial epithelium towards cancer by the accumulation of (epi)genetic alterations. Several mechanisms including mutations and homozygous deletions or hypermethylation of the p16(INK4a) promoter region can cause loss of p16 expression. Recent studies suggest overexpression of the polycomb-group gene BMI-1 might also down-regulate p16 expression. In this study, we analyzed the p16 expression in relation to the methylation status of the p16 promoter region of the p16(INK4a) gene and the expression of BMI-1 in bronchial squamous cell carcinomas (SCC) and its premalignant lesions. Nine (69%) SCC showed loss of p16 expression and 10 (77%) showed expression of BMI-1. Of four p16 positive samples two (50%) were BMI-1 positive, whereas among nine p16 negative samples, eight (89%) revealed BMI-1 staining. Four (44%) p16 negative samples were hypermethylated at the p16(INK4a) promoter region; the other p16 negative tumors that showed no hypermethylation revealed BMI-1 staining. Only two premalignant lesions showed absence of p16 expression, of which one (carcinoma in situ) was hypermethylated at the p16(INK4a) promoter region and the other (severe dysplasia) showed BMI-1 expression. In total, 11 precursor lesions (48%) revealed BMI-1 expression. In conclusion, the results of this study suggest that loss of p16 expression by promoter hypermethylation is inconsistently and occurs late in the carcinogenic process at the level of severe dysplasia. To what extent overexpression of the polycomb-group protein BMI-1 attributes to down regulating of p16 expression remains unclear.
Lung Cancer 2005 Jun
PMID:Expression of the p16(INK4a) gene product, methylation of the p16(INK4a) promoter region and expression of the polycomb-group gene BMI-1 in squamous cell lung carcinoma and premalignant endobronchial lesions. 1589 97


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