Bronchial Lung Cancer Research Articles

The Correlation between Bronchostenosis and Changes in the Levels of Interferon-γ and Transforming Growth Factor-β during the Treatment in patients with Endobronchial Tuberculosis

Background : Endobronchial tuberculosis often complicates bronchostenosis, which can cause dyspnea due to an airway obstruction, and can be misdiagnosed as bronchial asthma or lung cancer. This study investigated the possible correlation between the () and transforming growth () levels in the serum and bronchial washing fluid and the treatment results in endobronchial tuberculosis patients. Methods : Sixteen patients, who were diagnosed as endobronchial tuberculosis using bronchoscopy, and 10 healthy control subjects were enrolled in this study. The and levels were measured in the serum and bronchial washing fluid of 16 endobronchial tuberculosis patients before and after treatment using the ELISA method. The endobronchial tuberculosis patients were divided into those who showed bronchial fibrostenosis after treatment and those who did not. Results : The and levels in the bronchial washing fluid in endobronchial tuberculosis patients were elevated comparing to the control (p level was lower than the patients without fibrostenosis after treatment (p level after treatment further decreased comparing to the patients without fibrostenosis after treatment(p and levels in the bronchial washing fluid in endobronchial tuberculosis patients are believed to be related to the pathogenesis of endobronchial tuberculosis. The decreased initial serum level and the change in the serum level after treatment are believed to be involved in bronchial fibrostenosis during the course of the disease.

P-269 Angiogenic activity in bronchial dysplasia and invasive lung cancer: Features of vascular endothelial growth factor (VEGF) expression

P-269 Angiogenic activity in bronchial dysplasia and invasive lung cancer: Features of vascular endothelial growth factor (VEGF) expression

The relationship between caspase-3 expression and cell proliferation in rat lung squamous cell carcinoma

To analyse the relationship between caspase-3 expression and cell proliferation, and to find molecular-biology markers to adjust canceration during rat lung squamous cell carcinogenesis. The 3-methylcholanthrene(MCA) and diethyinitrosamine (DEN) were used to induce lung squamous cell carcinoma by intra-left lobar-bronchial instillation in 50 Wistar rats, and 10 normal rats as controls. Expression of caspase-3 and PCNA were evaluated by immunohistochemistry (IHC). Caspase-3 protein positive rate was 44.12% in 34 rat lung squamous cell carcinomas, and positive coefficient value was 1.38±0.95, which were significantly lower than that of normal bronchial epithelium (P=0.007, P < 0.01) and premalignant lesions (P < 0.05, P < 0.05). The mean PCNA-labeling indexes (PCNA-LI) of normal rat bronchial epithelium, premalignant lesions and lung cancer were 14.10±5.02, 28.13±8.72 and 41.88±14.24 (P < 0.05), respectively. There was a negative correlation between caspase 3 and PCNA LI (r=-0.730 6, P < 0.01). Loss expression of caspase-3 may promote tumor cell growth, and it may be important in rat lung squamous cell carcinogenesis. Detection of caspase-3 and PCNA proteins can be regarded as major markers in the diagnosis of lung canceration.

Clinical Experience with Lung-Imaging Fluorescence Endoscope (LIFE) in Patients with Lung Cancer

Abstract: British Columbia Cancer Research Center developed a new technique for detection of lung cancer with a device called the lung-imaging fluorescence endoscope (LIFE). Our aim was to confirm whether LIFE system would be useful in diagnosis of dysplasia of bronchial mucosa and lung cancer. Thirty patients with suspected lung cancer were included in this study. All patients underwent bronchoscopic examination by LIFE following examination by the conventional white-light bronchoscope. Pathological examination was performed for the abnormal areas detected by white-light or fluorescence bronchoscopic examination. Malignant tumors were diagnosed in 12 patients by both conventional bronchoscopy and LIFE; one dysplasia was also diagnosed by conventional bronchoscopy. The LIFE system diagnosed malignancy in four regions and one dysplasia that conventional bronchoscopy could not. Malignant lesions diagnosed by conventional bronchoscopy at three locations were proved later by the LIFE system to be benign. The sensitivity and specificity of the conventional bronchoscope for detection of dysplasia and cancer were 65% and 71%, respectively. The LIFE system's sensitivity was 90% and its specificity was 77.4%. No complications related to the LIFE system were detected throughout the course of this study. We conclude that the LIFE system can detect minute malignant lesions which are commonly non-detectable by conventional bronchoscopy without any complications. This method may be applicable in the screening of high risk groups for lung cancer.

Molecular cytogenetic alterations in the early stage at human bronchial epithelial cell carcinogenesis

Lung carcinogenesis is a multi-step process involving activation of oncogenes and inactivation of tumor suppress genes. Many molecular and cytogenetic alterations occur in the early stages of carcinogenesis. We have developed an effective culture system for human bronchial epithelial cells and lung cancer cells. Four immortalized human bronchial epithelial cell lines were established by transfecting the epithelial cells with plasmid DNA containing the early region of SV40. Some molecular and cytogenetic alterations, such as 3p-, 2q-, 9p-, c-myc translocation t(8;14) (q23; q32), were found in one immortalized bronchial epithelial cell line M when approaching malignant transformation. An increase in cell proliferation and decrease of apoptosis were noted in the late passages of the immortalized cell line M. Some molecular cytogenetic alterations were also observed in human primary non-small cell lung cancers. Molecular cytogenetic alterations during the early stage of carcinogenesis of human bronchial epithelial cells may be useful as biomarkers for both diagnosis and intermediate endpoint of chemoprevention of lung cancer.

Autocrine Growth Loop of The Epidermal Growth Factor Receptor in Normal and Immortalized Human Bronchial Epithelial Cells

Epidermal growth factor (EGF) is a potent growth factor for human normal bronchial epithelial (HBE) cells and lung cancer cells, which often demonstrate an EGF receptor (EGFR) autocrine loop. We have found that HBE cells are capable of proliferating in basal medium without EGF supplementation, and this suggests the probable presence of an active EGFR autocrine loop in non-neoplastic HBE cells. Northern blot hybridization shows that the parental and immortalized HBE cells express comparable and high levels of mRNA for EGFR, transforming growth factor-alpha (TGF-α), and amphiregulin (AR), but not EGF. Incubation with neutralizing monoclonal antibodies (mAb) against EGFR partially inhibits the growth of these cells. Immunohistochemistry shows that HBE cells express the TGF-α peptidein vitroandin vivo,however, neutralizing mAbs against TGF-α fail to inhibit their proliferation. In contrast, AR stimulates the growth of HBE cells. Thus, several EGF-family ligands appear to be involved functionally in the EGFR autocrine growth loop in HBE cells.

Biology of small cell lung cancer

The bombesin-like peptides can function as autocrine growth factors in lung cancer and candidate tumor suppressor genes on chromosomes 3 and 9 play important roles in lung cancer. Bombesin-like peptides can function as mitogens for normal bronchial epithelial cells and lung cancer cell lines. The monoclonal antibody directed against gastrin releasing peptide and bombesin, 2A11, can inhibit the growth of small cell lung cancer in vitro and in vivo and intravenous administration has induced a clinical remission in a patient with relapsed small cell lung cancer. The loss of a portion of one of the two short arms of chromosome 3 (3p) is identified in nearly 100%of tumor cell lines and tumors from patients with small cell lung cancer. Introduction of chromosome 3 into tumor cell lines suppresses their tumorigenicity in athymic nude mice, one of the characteristics of the cancer phenotype. Both copies of the candidate tumor suppressor gene on chromosome 9, CDKN2, are deleted in approximately one-fourth of lung cancer cell lines examined and the protein product of CDKN2, p16 is undetectable in one-third of the lung cancer cell lines studied. The CDKN2 gene is inactivated more commonly in non-small cell lung cancer than small cell lung cancer while the retinoblastoma gene is inactivated more commonly in small cell lung cancer than non-small cell lung cancer. It appears that a single defect in this cell cycle pathway is necessary for unregulated growth in lung cancer and current evidence suggests these defects differ between small cell and non-small cell lung cancer.

Combined effect of CYP1A1 inducibility and GSTM1 polymorphism on histological type of lung cancer.

The combinations of the CYP1A1 inducibility and GSTM1 polymorphism have been investigated in relation to the histological type and peripheral or bronchial location of lung cancer in 54 surgically treated, current smoker lung cancer patients. The induced CYP1A1 was detected in 46 patients (85%) and the homozygous GSTM1 null genotype in 32 patients (59%). The role of CYP1A1 inducibility was found to be more important than that of GSTM1 polymorphism, because the non-inducible CYP1A1 was associated solely with bronchial tumours (P = 0.001), mainly squamous cell carcinomas. In patients with inducible CYP1A1, the expressing GSTM1 gene appeared to have a protective effect against contracting bronchial lung cancer, since 88% (14/16) of the lung tumours in this patient group were peripheral, whereas almost equal numbers of peripheral and bronchial tumours were observed in those patients lacking the gene (P = 0.037).

Characterization of genetic lesions in non malignant bronchial epithelium, preneoplastic lesions and lung cancer

Characterization of genetic lesions in non malignant bronchial epithelium, preneoplastic lesions and lung cancer

Neuroendocrine and epithelial markers in diagnostic bronchial lung cancer biopsy specimens

The incidence of neuroendocrine and epithelial markers was investigated by immunocytochemistry in archival, lung cancer, bronchial biopsy specimens ( n = 48). No correlation of antigenicity with histological type was observed. 79% non-small cell lung carcinoma (NSCLC) and 61% small cell lung carcinoma (SCLC) were positive for epithelial markers. HuTu-m3 did not discriminate adenocarcinomas and squamous cell carcinomas from SCLC. 83% SCLC and 93% NSCLC were positive for one or more neuroendocrine marker. Multiple neuroendocrine markers were found in 61% SCLC, 83% NSCLC and 83% squamous cell carcinomas, this incidence being greater in the NSCLC group, and in the squamous carcinomas in particular, than previously reported.

Endobronchial tuberculosis simulating exacerbation of bronchial asthma

Despite extensive global efforts, pulmonary tuberculosis is still a major health problem worldwide. Endobronchial tuberculosis (EBTB) is seen in 10-40% of patients with active pulmonary tuberculosis. It commonly mimics the common lung diseases like bronchial asthma, pneumonia and lung cancer. Endobronchial stenosis is a common complication of EBTB. It requires early detection and prompt administration of anti-tuberculosis chemotherapy to prevent this complication. We are reporting an interesting case of a young male with bronchial asthma who presented with features of acute exacerbation and was diagnosed to have EBTB.