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Primary Lung Adenocarcinoma (primary + lung_adenocarcinoma)

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Medical Sciences	100%

Selected Abstracts

Epidermal growth factor receptor targeted therapy with gefitinib in locally advanced and metastatic primary lung adenocarcinoma

RESPIROLOGY, Issue 3 2006
Chong-Kin LIAM
Objective: To describe the efficacy of monotherapy with the epidermal growth factor receptor-tyrosine kinase inhibitor, gefitinib in patients with locally advanced and metastatic primary lung adenocarcinoma. Methods: A retrospective analysis was undertaken of patients who had locally advanced or metastatic lung adenocarcinoma treated with gefitinib 250 mg orally once daily until disease progression. All patients had either been previously treated with systemic cytotoxic chemotherapy and/or radiotherapy or had declined chemotherapy or were medically not fit for cytotoxic chemotherapy. Results: A total of 23 patients (13 men) (15 never smokers) with a median age of 51 years (range 35,79 years) received gefitinib monotherapy. Disease control occurred in 14 patients (61%); there was a reduction in the size of the primary and/or metastatic tumours (partial response (PR)) in 11 patients (48%), and 3 patients (13%) had stable disease. The response rate was significantly higher in those who had never smoked (10 of 15 (67%)) compared with that of smokers (1 of 8 (13%)) (odds ratio (95% confidence interval), 14.0 (1.33,147.43) P = 0.027). In total, 11 of 18 patients (61%) with a WHO performance status 1 or 2 showed a PR, whereas none with a performance status 3 or 4 responded (P = 0.037). Response was not affected by the patient's age, gender, disease stage, prior chemotherapy treatment, interval between diagnosis and commencement of gefitinib or the development of skin toxicity. The median time to symptom improvement was 1.5 (range 0.5,6) weeks. The median progression-free survival time was: 60 (range 15,138) weeks in patients with PR and 34 (range 7,38) weeks in patients with stable disease (P = 0.368). Conclusion: When given alone, gefitinib showed significant antitumour activity in patients with locally advanced and metastatic primary lung adenocarcinoma. An objective response was observed more frequently in never smokers and exclusively in patients with good performance status. [source]

Human Tissue Distribution of TA02, Which is Homologous with a New Type of Aspartic Proteinase, Napsin A

CANCER SCIENCE, Issue 10 2000
Takashi Hirano
The N-terminal amino acid sequence of TA02 (molecular weight 35.0 kDa, isoelectric point 5.29), which is associated with primary lung adenocarcinoma, was determined and a fragment peptide was used to generate mouse monoclonal antibodies (mAbs) against TA02. The amino acid sequence suggested that TA02 might be homologous with napsin A, a new type of aspartic proteinase. In this context, we confirmed the expression of napsin A in primary lung adenocarcinoma using reversetranscription polymerare chain reaction (RT-PCR) and showed that the TA02 mAbs reacted with glutathione-S-transferase (GST)-napsin A fusion protein. We concluded that TA02 is the same molecule as napsin A, and showed immunohistochemically that it is distributed mainly in type II pneumocytes, alveolar macrophages, renal tubules and exocrine glands and ducts in the pancreas. In particular, type II pneumocytes and alveolar macrophages showed high expression of TA02 among human normal tissues. In primary lung adenocarcinoma, 47 out of 58 (81.0%) primary lesions were positive. All well-differentiated adenocarcinomas except those of goblet cell type showed high expression of TA02. In addition, two out of seven (28.6%) large cell carcinomas showed low expression of TA02. The other histopathological types of primary lung cancer did not express TA02 at all. A few cases of renal cell cancer, pancreatic cancer, breast cancer, thyroid cancer, colon cancer and ovarian cancer showed low expression, but the staining patterns were completely different from that of primary lung adenocarcinoma, which showed a granular staining pattern. Our novel mAbs should be valuable for immunochemical detection of TA02/napsin A. [source]

Lung adenocarcinoma associated with atypical adenomatous hyperplasia.

PATHOLOGY INTERNATIONAL, Issue 12 2003
A clinicopathological study with special reference to smoking, cancer multiplicity
Atypical adenomatous hyperplasia (AAH) of the lung has been proposed as a possible precursor lesion of adenocarcinoma of the lung. In the present study, we sought to clarify the clinicopathological characteristics of lung adenocarcinoma cases associated with AAH, with special reference to tobacco smoking and the presence of multiple primary carcinomas of pulmonary and extrapulmonary organs. We examined 123 surgically resected lung adenocarcinomas and conducted histopathological diagnoses for AAH and multiple primary pulmonary carcinomas. Clinicopathological characteristics such as age, sex, smoking index, survival, and the presence of extrapulmonary primary carcinomas were obtained from clinical records, and the associations among these factors were examined statistically. Sixteen lung adenocarcinoma patients had accompanying AAH (the AAH group) and 107 cases did not (the NAAH group). The incidence of primary carcinomas in extrapulmonary organs was higher in the AAH group (37.5%; 6/16) than in the NAAH group (12.5%; 13/107) (P = 0.01). Multiple primary lung cancers tended to be more frequent in the AAH group, but the difference was not statistically significant (P = 0.07). Although there was no difference in tobacco smoking between the two groups, all eight cases with multiple primary lung carcinomas were smokers. Furthermore, multiple primary lung carcinomas were found more frequently in smokers of the AAH group (37.5%; 3/8) than in the smokers of the NAAH group (7.2%; 5/69) (P = 0.04). The results suggested that constitutional or genetic factors might predispose patients to the development of AAH together with extrapulmonary primary carcinomas, and that smoking might contribute to the development of multiple primary lung adenocarcinomas, especially in patients with pre-existing AAH. [source]