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1. Wang G, Ye Y, Zheng W, Ma W: [Identification of candidate genes for lung adenocarcinoma using Toppgene]. Zhongguo Fei Ai Za Zhi; 2010 Apr;13(4):282-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Identification of candidate genes for lung adenocarcinoma using Toppgene].
  • BACKGROUND AND OBJECTIVE: Lung adenocarcinoma (AC) is the most common type of lung cancer, however, its mechanism of oncongenesis is still unknown.
  • The aim of this study is to screen candidate genes of lung adenocarcinoma using bioinformatics strategy and elucidate the mechanism of lung adenocarcinoma.
  • Genes correlated with lung adenocarcinoma, obtained by data mining tools genecard and Fable were regarded as "train gene set".
  • Finally, candidate genes of lung adenocarcinoma were screened by the tool "Toppgene".
  • RESULTS: Three hundred and forty-four differential genes were defined as "test gene set", and 277 genes correlated with lung adenocarcinoma were regarded as "train gene set".
  • Thirty-six candidate genes were screened out by Toppgene, among them, 21 genes had nearly no report in cancer.
  • CONCLUSION: It is demonstrated that Toppgene is useful in identification of the candidate genes of lung adenocacinoma, which provides the proof for the discovery of the specific disease genes.
  • [MeSH-major] Adenocarcinoma / genetics. Computational Biology. Data Mining. Lung Neoplasms / genetics

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  • (PMID = 20677550.001).
  • [ISSN] 1009-3419
  • [Journal-full-title] Zhongguo fei ai za zhi = Chinese journal of lung cancer
  • [ISO-abbreviation] Zhongguo Fei Ai Za Zhi
  • [Language] chi
  • [Databank-accession-numbers] GEO/ GSE10072/ GSE7670
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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2. Barletta JA, Yeap BY, Chirieac LR: Prognostic significance of grading in lung adenocarcinoma. Cancer; 2010 Feb 1;116(3):659-69
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  • [Title] Prognostic significance of grading in lung adenocarcinoma.
  • BACKGROUND: Although grading has prognostic significance for many tumor types, a prognostically significant grading system for lung adenocarcinoma has not yet been established.
  • The aim of this study was to evaluate histologic characteristics included in tumor grading systems, establish optimal cutoff values that have the strongest association with overall survival, and develop a grading system incorporating the histopathologic characteristics that the authors found to have prognostic significance in patients with lung adenocarcinoma.
  • METHODS: The authors studied lung adenocarcinomas from 85 consecutive patients, and evaluated the percentage of solid pattern (as a reflection of tumor architecture), the degree of cytologic atypia, and the mitotic count.
  • A grading score, computed as the sum of the architecture score and cytologic atypia score (2 = well differentiated, 3 = moderately differentiated, 4 = poorly differentiated), was a significant predictor of overall survival in univariate analysis (median overall survival times, 72.4, 39.5, and 8.7 months for well, moderately, and poorly differentiated adenocarcinoma, respectively; P = .0001).
  • CONCLUSIONS: The authors describe a grading system that incorporates the percentage of solid pattern and degree of the cytologic atypia that is an independent predictor of survival in patients with lung adenocarcinoma.

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  • [Copyright] Copyright 2009 American Cancer Society.
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  • (PMID = 20014400.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P20 CA090578; United States / NCI NIH HHS / CA / P50 CA090578-079002; United States / NCI NIH HHS / CA / CA090578; United States / NCI NIH HHS / CA / P50 CA090578; United States / NCI NIH HHS / CA / CA090578-079002
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS161919; NLM/ PMC2846761
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3. Kondou M, Nagayasu T, Hidaka S, Tsuchiya T, Takeshita H, Yasutake T, Yano H, Minami H, Iwasaki K: Correlation between angiogenesis and p53 expression in lung adenocarcinoma of young patients. Tohoku J Exp Med; 2009 Feb;217(2):101-7
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  • [Title] Correlation between angiogenesis and p53 expression in lung adenocarcinoma of young patients.
  • Lung cancer commonly occurs in individuals who are 60 years of age or older.
  • Lung cancer in patients younger than 40 years of age is rare and is often advanced when discovered.
  • However, the biological features of lung cancer in young adults have not yet been fully elucidated.
  • This study was conducted to determine the role of p53 expression and neoangiogenesis in lung adenocarcinomas of young patients.
  • Lung adenocarcinomas, which were surgically resected from 20 patients younger than 40 years of age between 1977 and 1996, were compared with lung adenocarcinomas selected with random sampling from 45 patients older than 60 years of age.
  • The expression of p53, vascular endothelial growth factor (VEGF), CD34, a marker for vascular endothelial cells, and proliferating cell nuclear antigen (PCNA) were studied immunohistochemically in both young and elderly patient groups.
  • Lung adenocarcinomas with p53-positive staining showed higher expression of VEGF protein than p53-negative tumors in both the young and the elderly groups.
  • Lung adenocarcinoma occurring in young patients tends to have a poorer prognosis, and angiogenesis of lung adenocarcinoma in young patients is more closely correlated with p53 expression than in elderly patients.
  • [MeSH-major] Adenocarcinoma / blood supply. Adenocarcinoma / metabolism. Lung Neoplasms / blood supply. Lung Neoplasms / metabolism. Neovascularization, Pathologic / metabolism. Tumor Suppressor Protein p53 / metabolism
  • [MeSH-minor] Adult. Age Distribution. Aged. Antigens, CD34 / metabolism. Female. Humans. Immunohistochemistry. Male. Microvessels / metabolism. Microvessels / pathology. Middle Aged. Proliferating Cell Nuclear Antigen / metabolism. Regression Analysis. Survival Analysis. Vascular Endothelial Growth Factor A / metabolism

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  • (PMID = 19212102.001).
  • [ISSN] 1349-3329
  • [Journal-full-title] The Tohoku journal of experimental medicine
  • [ISO-abbreviation] Tohoku J. Exp. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Proliferating Cell Nuclear Antigen; 0 / Tumor Suppressor Protein p53; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A
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4. Maniwa Y, Yoshimura M, Bermudez VP, Okada K, Kanomata N, Ohbayashi C, Nishimura Y, Hayashi Y, Hurwitz J, Okita Y: His239Arg SNP of HRAD9 is associated with lung adenocarcinoma. Cancer; 2006 Mar 1;106(5):1117-22
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  • [Title] His239Arg SNP of HRAD9 is associated with lung adenocarcinoma.
  • BACKGROUND: It was previously reported that a functional human (h) Rad9 protein accumulated in the nuclei of non-small cell lung carcinoma (NSCLC) cells.
  • METHODS: The sequence of the HRAD9 was examined in tumor and peripheral normal lung tissues obtained from 50 lung adenocarcinoma patients during surgery.
  • RESULTS: No sequence alterations were detected in the HRAD9 gene, which was found to be normally transcribed in surgically resected lung carcinoma cells.
  • CONCLUSIONS: Whereas the capacity to produce a functional hRad9 protein was intact in lung adenocarcinoma cells, a nonsynonymous SNP of HRAD9 was detected that might be associated with the development of lung adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / genetics. Carcinoma, Non-Small-Cell Lung / genetics. Cell Cycle Proteins / genetics. Lung Neoplasms / genetics

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  • (PMID = 16444745.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 139691-42-2 / rad9 protein
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5. Weir BA, Woo MS, Getz G, Perner S, Ding L, Beroukhim R, Lin WM, Province MA, Kraja A, Johnson LA, Shah K, Sato M, Thomas RK, Barletta JA, Borecki IB, Broderick S, Chang AC, Chiang DY, Chirieac LR, Cho J, Fujii Y, Gazdar AF, Giordano T, Greulich H, Hanna M, Johnson BE, Kris MG, Lash A, Lin L, Lindeman N, Mardis ER, McPherson JD, Minna JD, Morgan MB, Nadel M, Orringer MB, Osborne JR, Ozenberger B, Ramos AH, Robinson J, Roth JA, Rusch V, Sasaki H, Shepherd F, Sougnez C, Spitz MR, Tsao MS, Twomey D, Verhaak RG, Weinstock GM, Wheeler DA, Winckler W, Yoshizawa A, Yu S, Zakowski MF, Zhang Q, Beer DG, Wistuba II, Watson MA, Garraway LA, Ladanyi M, Travis WD, Pao W, Rubin MA, Gabriel SB, Gibbs RA, Varmus HE, Wilson RK, Lander ES, Meyerson M: Characterizing the cancer genome in lung adenocarcinoma. Nature; 2007 Dec 6;450(7171):893-8
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  • [Title] Characterizing the cancer genome in lung adenocarcinoma.
  • The prospect of targeted therapies and the development of high-resolution, genome-wide approaches are now spurring systematic efforts to characterize cancer genomes.
  • Here we report a large-scale project to characterize copy-number alterations in primary lung adenocarcinomas.
  • Only six of these focal events are currently associated with known mutations in lung carcinomas.
  • On the basis of genomic and functional analyses, we identify NKX2-1 (NK2 homeobox 1, also called TITF1), which lies in the minimal 14q13.3 amplification interval and encodes a lineage-specific transcription factor, as a novel candidate proto-oncogene involved in a significant fraction of lung adenocarcinomas.
  • More generally, our results indicate that many of the genes that are involved in lung adenocarcinoma remain to be discovered.


6. Seth R, Athanassopoulos A, Mir S: First presentation of lung adenocarcinoma as a subungual metastasis. Hand (N Y); 2008 Mar;3(1):69-71

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] First presentation of lung adenocarcinoma as a subungual metastasis.
  • Subungual metastasis as a presenting feature of lung adenocarcinoma is rare and may be confused with a benign inflammatory disorder of the nail unit with subsequent diagnostic and management delay.
  • We discuss the case of a 46-year-old man with a subungual metastasis as a presenting feature of lung adenocarcinoma.

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  • (PMID = 18780124.001).
  • [ISSN] 1558-9447
  • [Journal-full-title] Hand (New York, N.Y.)
  • [ISO-abbreviation] Hand (N Y)
  • [Language] eng
  • [Publication-type] Case Reports
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2528977
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7. Shih JY, Tsai MF, Chang TH, Chang YL, Yuan A, Yu CJ, Lin SB, Liou GY, Lee ML, Chen JJ, Hong TM, Yang SC, Su JL, Lee YC, Yang PC: Transcription repressor slug promotes carcinoma invasion and predicts outcome of patients with lung adenocarcinoma. Clin Cancer Res; 2005 Nov 15;11(22):8070-8
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  • [Title] Transcription repressor slug promotes carcinoma invasion and predicts outcome of patients with lung adenocarcinoma.
  • PURPOSE: In a previous genome-wide gene expression profiling analysis using an invasion cancer cell lines model, we have identified Slug as selectively overexpressed in the highly invasive cancer cells.
  • Here, we investigated the clinical significance of Slug in lung adenocarcinoma and the role of Slug in the process of cancer cell invasion and metastasis.
  • EXPERIMENTAL DESIGN: Real-time quantitative reverse transcription-PCR was used to investigate Slug mRNA in surgically resected lung adenocarcinoma of 54 patients and its correlation with survival.
  • We overexpressed Slug in a lung adenocarcinoma cell line with very low Slug levels and investigated the in vitro and in vivo effects of Slug expression.
  • RESULTS: High expression of Slug mRNA in lung cancer tissue was significantly associated with postoperative relapse (P = 0.03) and shorter patient survival (P < 0.001).
  • CONCLUSIONS: Slug expression can predict the clinical outcome of lung adenocarcinoma patients.
  • Slug is a novel invasion-promoting gene in lung adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / pathology. Lung Neoplasms / pathology. Transcription Factors / genetics
  • [MeSH-minor] Aged. Animals. Blotting, Northern. Cadherins / metabolism. Cell Line, Tumor. Cell Movement. Cell Proliferation. Female. Gene Expression Regulation, Neoplastic. Humans. Male. Matrix Metalloproteinase 2 / metabolism. Mice. Mice, SCID. Middle Aged. Neoplasm Invasiveness. Neoplasm Recurrence, Local. Neoplasm Transplantation. Neoplasms, Experimental / blood supply. Neoplasms, Experimental / genetics. Neoplasms, Experimental / metabolism. Neovascularization, Pathologic / genetics. Neovascularization, Pathologic / metabolism. Neovascularization, Pathologic / pathology. Prognosis. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Survival Analysis. Transfection. Transplantation, Heterologous. Treatment Outcome

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  • (PMID = 16299238.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cadherins; 0 / RNA, Messenger; 0 / Transcription Factors; 0 / snail family transcription factors; EC 3.4.24.24 / Matrix Metalloproteinase 2
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8. Uchisaka N, Takahashi N, Sato M, Kikuchi A, Mochizuki S, Imai K, Nonoyama S, Ohara O, Watanabe F, Mizutani S, Hanada R, Morio T: Two brothers with ataxia-telangiectasia-like disorder with lung adenocarcinoma. J Pediatr; 2009 Sep;155(3):435-8
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  • [Title] Two brothers with ataxia-telangiectasia-like disorder with lung adenocarcinoma.
  • We report on 2 brothers with ataxia-telangiectasia-like disorder with lung adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / genetics. Ataxia Telangiectasia / genetics. Lung Neoplasms / genetics


9. Aida Y, Igarashi A, Inoue S, Abe S, Shibata Y, Kubota I: [A case of lung adenocarcinoma exhibiting Garcin syndrome]. Nihon Kokyuki Gakkai Zasshi; 2010 Jan;48(1):66-9
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  • [Title] [A case of lung adenocarcinoma exhibiting Garcin syndrome].
  • We report a rare case of lung adenocarcinoma exhibiting Garcin syndrome due to skull base metastasis.
  • A diagnosis of lung adenocarcinoma and intraperitoneal lymph node metastases was given to a 50-year-old man after pathological examination of a superclavicular lymph node biopsy.
  • However, facial paralysis occurred and his auditory nerve disorder progressed to deafness.
  • After intrathecal administration of methotrexate and cranial irradiation, the progression of facial paralysis and auditory nerve disorder were halted.
  • It is important to consider Garcin syndrome as a possible complication in lung cancer patients who have central nervous system symptoms.
  • [MeSH-major] Adenocarcinoma / complications. Cranial Nerve Diseases / etiology. Lung Neoplasms / complications

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  • (PMID = 20163025.001).
  • [ISSN] 1343-3490
  • [Journal-full-title] Nihon Kokyūki Gakkai zasshi = the journal of the Japanese Respiratory Society
  • [ISO-abbreviation] Nihon Kokyuki Gakkai Zasshi
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
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10. Martín Martorell P, Marí Cotino JF, Insa A: Choroidal metastases from lung adenocarcinoma. Clin Transl Oncol; 2009 Oct;11(10):694-7
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  • [Title] Choroidal metastases from lung adenocarcinoma.
  • Diagnostic workup revealed a lung mass and the biopsy was compatible with lung adenocarcinoma.
  • The intraocular lesion was the only metastatic site at the time of diagnosis.
  • Choroidal metastases are an infrequent site of systemic dissemination and associated with a poor prognosis, with a median survival of around 2 months if it is the first manifestation of a lung neoplasm.
  • [MeSH-major] Adenocarcinoma / secondary. Choroid Neoplasms / secondary. Lung Neoplasms / pathology

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  • (PMID = 19828413.001).
  • [ISSN] 1699-3055
  • [Journal-full-title] Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico
  • [ISO-abbreviation] Clin Transl Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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11. Shinmura K, Suzuki M, Yamada H, Tao H, Goto M, Kamo T, Nagura K, Kageyama S, Kato M, Ogawa S, Maekawa M, Takamochi K, Suzuki K, Nakamura T, Sugimura H: Characterization of adenocarcinoma of the lung in a familial adenomatous polyposis patient. Pathol Int; 2008 Nov;58(11):706-12
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  • [Title] Characterization of adenocarcinoma of the lung in a familial adenomatous polyposis patient.
  • The incidence of several extracolonic tumors, such as duodenal carcinoma, is higher in familial adenomatous polyposis (FAP) patients than in the general population, but there is little information about lung carcinoma in FAP.
  • A 43-year-old woman presented with a lung tumor 17 years after total colectomy for FAP.
  • Pathohistological analysis of the lung tumor demonstrated mixed adenocarcinoma consisting of a papillary adenocarcinoma component and a bronchioloalveolar carcinoma component.
  • The other APC allele in the lung carcinoma was not inactivated by somatic mutations, promoter methylation, or chromosomal deletion.
  • No somatic mutations in any of the coding regions of the p53 gene or in the mutation hot spot regions of the K-ras or EGFR genes were detected in the carcinoma.
  • The present results suggest that the chromosomal copy number alterations detected on SNP microarray were involved in the carcinogenesis of the adenocarcinoma of the lung in the present FAP patient.
  • [MeSH-major] Adenocarcinoma, Bronchiolo-Alveolar / pathology. Adenocarcinoma, Papillary / pathology. Adenomatous Polyposis Coli / pathology. Lung Neoplasms / pathology


12. Martín-Martorell P, Insa-Molla A, Chirivella-González MI, Cervera-Miguel JI: Nonbacterial thrombotic endocarditis associated with lung adenocarcinoma. Clin Transl Oncol; 2007 Nov;9(11):744-6
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  • [Title] Nonbacterial thrombotic endocarditis associated with lung adenocarcinoma.
  • Nonbacterial thrombotic endocarditis (NBTE) is a rather frequent neoplasic complication, most often occurring in adenocarcinomas of the lung and pancreas.
  • Diagnosis is frequently missed on transthoracic ultrasound, making transoesophagic ultrasound a more reliable diagnostic tool.
  • We present a case of NBTE associated with lung adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / complications. Endocarditis / etiology. Lung Neoplasms / complications. Thrombosis / etiology
  • [MeSH-minor] Adult. Diagnosis, Differential. Female. Humans

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  • (PMID = 18055331.001).
  • [ISSN] 1699-048X
  • [Journal-full-title] Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico
  • [ISO-abbreviation] Clin Transl Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Spain
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13. Dacic S, Finkelstein SD, Yousem SA: Clonal selection of adenocarcinoma of the lung as determined by loss of heterozygosity. Exp Mol Pathol; 2005 Apr;78(2):135-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clonal selection of adenocarcinoma of the lung as determined by loss of heterozygosity.
  • Although the most frequently altered oncogenes and tumor suppressor genes in non-small cell lung carcinoma (NSCLC) have been recognized, the exact mechanisms responsible for the progression and phenotypic expression of carcinoma, particularly adenocarcinoma of the lung are uncertain.
  • Fifty-six cases of adenocarcinoma of the lung (11 bronchioloalveolar carcinoma [BAC], 25 stage 1, 20 stage 2) and paired 19 lymph node metastases (LNM) of stage 2 adenocarcinomas were analyzed for loss of heterozygosity (LOH).
  • LOH on chromosomes 1p (P = 0.0209) and 17p (P = 0.0274) was more frequently present in stage 1 adenocarcinomas than in BAC.
  • There was no significant difference between BAC, stage 1 and stage 2 adenocarcinoma in the frequency of LOH at individual chromosomal arms.
  • The pattern of LOH in LNM of stage 2 adenocarcinoma was similar to the primary tumor.
  • Overall fractional allelic loss (FAL) was significantly different between BAC and stage 1 invasive adenocarcinoma (P = 0.0013), and it was significantly higher in stage 1 adenocarcinoma than in stage 2 adenocarcinoma (P = 0.0062) and their LNM (P = 0.0001).
  • Stage 2 adenocarcinomas showed significantly higher overall FAL than their LNM (P = 0.022).
  • Our study failed to identify a single target gene responsible for progression of lung adenocarcinoma.
  • A trend towards lower overall FAL in advanced stage tumors and in their metastases suggests that clonal selection may play a role in lung adenocarcinoma progression.
  • [MeSH-major] Adenocarcinoma / genetics. Loss of Heterozygosity / genetics. Lung Neoplasms / genetics. Lymphatic Metastasis / genetics

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  • (PMID = 15713439.001).
  • [ISSN] 0014-4800
  • [Journal-full-title] Experimental and molecular pathology
  • [ISO-abbreviation] Exp. Mol. Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
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14. Kuraishi H, Yamashita J, Tsuchiya Y, Kokubu F, Takizawa K: [A case of lung adenocarcinoma of pancoast type successfully treated with concurrent chemoradiotherapy]. Gan To Kagaku Ryoho; 2009 Feb;36(2):291-3

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [A case of lung adenocarcinoma of pancoast type successfully treated with concurrent chemoradiotherapy].
  • We reported a case of lung adenocarcinoma of Pancoast type that was successfully treated with chemoradiotherapy.
  • Using transbronchial needle aspiration, we diagnosed lung adenocarcinoma (cT3N0M0).
  • [MeSH-major] Adenocarcinoma / drug therapy. Adenocarcinoma / radiotherapy. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Pancoast Syndrome / drug therapy. Pancoast Syndrome / radiotherapy

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  • (PMID = 19223748.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
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15. Xu Y, Zhou Y, Huang M, Zou B, Zhang X, Zhang X, Zhou L, Zhu J, Gong Y, Hou M, Lu Y: Gefitinib versus platinum contained doublet chemotherapy in chemotherapy-naive patients with stage IIIb or IV non-small cell lung cancer of adenocarcinoma histology: A retrospective case control study. J Clin Oncol; 2009 May 20;27(15_suppl):e19070

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gefitinib versus platinum contained doublet chemotherapy in chemotherapy-naive patients with stage IIIb or IV non-small cell lung cancer of adenocarcinoma histology: A retrospective case control study.
  • : e19070 Background: The results of the ISEL study in non-small cell lung cancer (NSCLC) suggest greater benefit of gefitinib among Asian patients and non-smokers compared with the overall trial population.
  • METHODS: We conducted a retrospective case-control study to compare outcomes for gefitinib versus platinum doublet chemotherapy as first line treatment in selected NSCLC patients (stage IIIB/IV adenocarcinoma, PS 0-2).
  • RESULTS: 99 chemo-naïve adenocarcinoma patients treated in our institute from January 2006 to December 2007 were collected: 33 received gefitinib and 66 received chemotherapy.
  • Gefitinib as first-line treatment confers clinically relevant benefit in Asian NSCLC patients with adenocarcinoma histology versus platinum based chemotherapy.

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  • (PMID = 27962215.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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16. Benjamin H, Lebanony D, Tabak S, Barabash N, Gibori H, Morgenstern S, Meiri E, Bentwich Z, Rosenwald S, Cohen D: MicroRNA-based assay for differential diagnosis of mesothelioma. J Clin Oncol; 2009 May 20;27(15_suppl):e22079

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] MicroRNA-based assay for differential diagnosis of mesothelioma.
  • Mesothelioma can be difficult to differentiate from other tumors in the lung or pleura such as primary lung adenocarcinoma presenting with pleural effusion or metastatic adenocarcinoma from extrathoracic sites.
  • We addressed the increasing need for accurate differential diagnosis of these tumors by developing a diagnostic assay based on expression levels of microRNAs, a family of small, non-coding RNAs whose tissue-specificity has proven applicability for identification of cancer tissue type and histology.
  • RESULTS: We identified microRNAs that are differentially expressed between mesothelioma, lung adenocarcinoma, and other confounding tumor types.
  • A diagnostic assay (miRview™ meso) was developed, that utilizes qRT-PCR measurement of a small set of microRNAs to differentiate between mesothelioma and non-mesothelioma samples.
  • CONCLUSIONS: MicroRNAs are emerging as effective cancer biomarkers.
  • A robust and simple assay based on the expression level of a few microRNA biomarkers can accurately differentiate mesothelioma from other possible tumors in the lung and pleura.

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  • (PMID = 27963221.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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17. Castro C, Cardona AF, Reguart N, Carrasco-Chaumel E, Otero JM, Carranza H, Vargas C, Reveiz L, Torres D, Blumenschein G: Wood-smoke exposure (WSE) as a predictor of response and survival in erlotinib-treated advanced lung adenocarcinoma (ALA) patients (pts) (ONCOLGroup study). J Clin Oncol; 2009 May 20;27(15_suppl):e19052

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Wood-smoke exposure (WSE) as a predictor of response and survival in erlotinib-treated advanced lung adenocarcinoma (ALA) patients (pts) (ONCOLGroup study).
  • : e19052 Background: There is consistent information suggesting that long-term WSE constitutes a risk factor for lung cancer.
  • More than 50 years of WSE was associated with non-small cell lung cancer (NSCLC).
  • Retrospectively, we estimated overall response rates (ORR), time to progression (TTP) and overall survival (OS) in a subgroup of pts with significant WSE (exposure >5 years for at least 4 hours/day) treated with erlotinib, and compared them with the non-WSE population treated with the same compound.

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  • (PMID = 27962158.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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18. Jackman DM, Cioffredi L, Lindeman NI, Morse LK, Lucca J, Weckstein D, Huberman MS, Lynch TJ, Johnson BE, Janne PA: Phase II trial of erlotinib in chemotherapy-naive women with advanced pulmonary adenocarcinoma. J Clin Oncol; 2009 May 20;27(15_suppl):8065

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase II trial of erlotinib in chemotherapy-naive women with advanced pulmonary adenocarcinoma.
  • : 8065 Background: This single-arm phase II study explored the role of clinical characteristics (female gender, adenocarcinoma histology, no tobacco within 1 year) in selecting pts for 1st-line therapy w/ erlotinib.
  • METHODS: Eligible pts were chemotherapy-naïve women, stage IIIB/ IV, PS 0-2, adenocarcinoma, and w/ available tissue for analysis of EGFR mutation status.
  • 7 pts not evaluable (5 tox, 1 non-progression death, 1 withdrawn consent).

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  • (PMID = 27962638.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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19. Shih J, Yang C, Su W, Hsia T, Tsai C, Chen Y, Chang H, Terlizzi E, Shahidi M, Miller VA: A phase II study of BIBW 2992, a novel irreversible dual EGFR and HER2 tyrosine kinase inhibitor (TKI), in patients with adenocarcinoma of the lung and activating EGFR mutations after failure of one line of chemotherapy (LUX-Lung 2). J Clin Oncol; 2009 May 20;27(15_suppl):8013

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A phase II study of BIBW 2992, a novel irreversible dual EGFR and HER2 tyrosine kinase inhibitor (TKI), in patients with adenocarcinoma of the lung and activating EGFR mutations after failure of one line of chemotherapy (LUX-Lung 2).
  • A phase II trial evaluating the efficacy of BIBW 2992 (Tovok), a novel, potent, irreversible, dual EGFR and HER2 TKI with preclinical activity in cell lines harboring activating (H3255, IC<sub>50</sub>=0.7 nM) and resistant (H1975, IC<sub>50</sub>=99 nM) EGFR mutations, is reported.
  • Eligible pts have stage IIIB/IV lung adenocarcinoma, EGFR mutation in exons 18-21 (tested by direct sequencing), measurable disease, ECOG PS 0-2 and adequate end organ function.
  • An international Phase III trial program investigating BIBW 2992 in NSCLC, LUX-Lung, is now recruiting.

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  • (PMID = 27962806.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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20. Nakayama H, Kato Y, Tsuboi M, Okumura S, Daisaki H, Uehara H, Adachi S, Yoshimura M, Okada M: Value of FDG-PET/CT findings revised using an anthropomorphic body phantom for the evaluation of tumor malignancy grade in small-sized lung adenocarcinomas: A multicenter study. J Clin Oncol; 2009 May 20;27(15_suppl):7573

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Value of FDG-PET/CT findings revised using an anthropomorphic body phantom for the evaluation of tumor malignancy grade in small-sized lung adenocarcinomas: A multicenter study.
  • : 7573 Background: The malignant behavior of small lung adenocarinomas (AD), which have been detected with increasing frequency recently, has not yet been clearly evaluated, and an understanding of this biological characteristic is vital for selecting the appropriate therapeutic strategy.
  • We examined the malignancy grade of small lung ADs using FDG-PET/CT (PET), in addition to high-resolution CT (HRCT) and pathologic evaluation in a multicenter setting.
  • METHODS: A total of 204 patients with cT1N0M0 AD underwent PET and HRCT, followed by complete resection with lymph node dissection.
  • Assessment by PET in addition to HRCT is useful for selection of the appropriate treatment strategy for small lung AD.

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  • (PMID = 27963381.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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21. Strickler JH, Mostertz W, Kim W, Walters K, Stevenson M, Acharya C, Onaitis M, Nevins J, Potti A: Integration of mRNA and microRNA profiles as prognostic and predictive markers in lung adenocarcinoma. J Clin Oncol; 2009 May 20;27(15_suppl):7522

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Integration of mRNA and microRNA profiles as prognostic and predictive markers in lung adenocarcinoma.
  • : 7522 Background: Lung adenocarcinoma (ADC) is a distinct biologic entity with unique gene amplifications (Weir B, Nature 2008).
  • Yet, comprehensive transcriptomic analysis, including microRNAs, specific to lung ADC are lacking.
  • METHODS: Using mRNA expression data from a discovery cohort of 154 patients with histologically proven early stage (I and II) lung ADC, signatures of oncogenic pathway and tumor microenvironment status were applied and further organized by hierarchical clustering to develop a metagene model.
  • Further, using in vitro assays in a large cohort of lung ADC cell lines (n = 42) with corresponding mRNA and microRNA data, novel microRNAs associated with a poor prognosis and their relationship to cisplatin resistance was elucidated.
  • Utilizing the extremes of survival to identify cohorts of patients as high and low risk phenotypes, using bayesian regression, a 100 gene signature ('metagene') that captured the diversity of signaling pathways unique to patients at increased risk of recurrence was identified and validated in an independent cohort (n = 364) of lung ADC samples with 78.3% accuracy.
  • Using in vitro cell proliferation assays, predicted high risk lung ADC cell lines were identified as being more resistant to cisplatin therapy than those predicted to be low risk (p=0.001).
  • CONCLUSIONS: mRNA and microRNA profiles reflect unique aspects of individual tumors and may characterize histology-specific tumor heterogeneity in lung ADC, providing an opportunity to better characterize the oncogenic process and refine therapeutic options.

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  • (PMID = 27963289.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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22. Moreno-Vega A, Chavarría N, Rubio J, Villandiego I, Estepa R, Gordon M, Salvador J, Jimenez E: Primary breast sarcoma: Clinical and retrospective analysis of cases from Jerez General Hospital, Spain. J Clin Oncol; 2009 May 20;27(15_suppl):e21526

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Diagnosis and treatment is unclear.
  • RESULTS: Seven cases of PBS (1 male/6 female) were reviewed, from 790 BC diagnosed (0.8%): 2 angiosarcomas (AS), 1 malignant fibrous histiocytoma, 2 undifferentiated, one osteoclastic and other spindle-cell sarcoma.
  • Contralateral low grade AS in one woman, and lung adenocarcinoma in the man, had been diagnosed 2 years later.
  • CONCLUSIONS: PBS are rare and difficult diagnosis tumors.
  • There are few series published, without prospective studies to evaluate an adequate therapy, diagnosis and valuable prognostic factors.
  • Our incidence was high, but the independent pathology analysis confirmed all histopathological diagnosis.
  • This review included novel IHC and IRM images, considered necessary for diagnosis and personalized treatment.

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  • (PMID = 27963456.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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23. Yang C, Hirsh V, Cadranel J, Chen Y, Park K, Kim S, Chao T, Oberdick M, Shahidi M, Miller V: Phase IIb/III double-blind randomized trial of BIBW 2992, an irreversible, dual inhibitor of EGFR and HER2 plus best supportive care (BSC) versus placebo plus BSC in patients with NSCLC failing 1-2 lines of chemotherapy (CT) and erlotinib or gefitinib (LUX- Lung1): A preliminary report. J Clin Oncol; 2009 May 20;27(15_suppl):8062

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • METHODS: Pts with advanced adenocarcinoma of the lung (Stage IIIB/IV; ECOG 0-2), who have failed one or two lines of CT (including platinum) and progressed following at least 12 weeks of E or G are randomized in a 2:1 ratio to receive BSC plus either oral BIBW 2992 50 mg qd or placebo until disease progression or unacceptable toxicity.
  • Main prior EGFR-TKI was G in Asians (70%) and E in non-Asians (85%).

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  • (PMID = 27962637.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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24. Pengying L, Longbang C, Xiang H: The antitumor effects of CIK cells combined with docetaxel against drug-resistant lung adenocarcinoma cell line SPC-A1/DTX in vitro and in vivo. J Clin Oncol; 2009 May 20;27(15_suppl):3039

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The antitumor effects of CIK cells combined with docetaxel against drug-resistant lung adenocarcinoma cell line SPC-A1/DTX in vitro and in vivo.
  • Multidrug resistance (MDR) phenomenon is a major hindrance to the successful chemotherapy of cancer.
  • In this study, the anti-tumor activity of CIK cells combined with docetaxel (DTX) against multidrug resistance SPC-A1/DTX cell line was evaluated in vitro and in vivo.
  • CONCLUSIONS: CIK cells plused with docetaxel demonstrated a prominent augmentation of anti-tumor activity against MDR lung adenocarcinoma cell lines both in vitro and in vivo.

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  • (PMID = 27962075.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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25. Kim D, Lee S, Lee J, Lee M, Kang J, Kim S, Shin S, Kim H, Heo DS: A multicenter phase II study to evaluate efficacy and safety of gefitinib as the first-line treatment for Korean patients (pts) with advanced pulmonary adenocarcinoma harboring EGFR mutations. J Clin Oncol; 2009 May 20;27(15_suppl):8066

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A multicenter phase II study to evaluate efficacy and safety of gefitinib as the first-line treatment for Korean patients (pts) with advanced pulmonary adenocarcinoma harboring EGFR mutations.
  • : 8066 Background: This study (D7913L00056) was designed to prospectively evaluate the efficacy and safety of first-line gefitinib treatment in pts with advanced pulmonary adenocarcinoma harboring EGFR mutations and to explore the molecular factors affecting the efficacy of gefitinib.
  • METHODS: Chemo-naïve pts with advanced (stage IIIB/IV/recurrent disease) pulmonary adenocarcinoma underwent direct DNA sequencing of tumor EGFR exons 18, 19 and 21.
  • The most common EGFR mutations were in-frame exon 19 deletions (del 19, 29 pts, 64%) and L858R point mutations in exon 21 (L858R, 15 pts, 33%).
  • The ORR and DCR were higher in pts with del 19 than those with L858R (62.1% vs 33.3%; P=0.0705 and 96.6% vs 66.7%; P=0.0062, respectively).
  • In addition, PFS at 12 mo was significantly better in pts with del 19 than those with L858R (63.2% vs 23.8%, P=0.0034).
  • CONCLUSIONS: Gefitinib as the first-line treatment for Korean pts with advanced pulmonary adenocarcinoma harboring EGFR mutations was very effective and well tolerated.
  • Subgroup analysis suggests that the benefit from gefitinib treatment was more prominent in pts with the del 19 mutation.

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  • (PMID = 27962641.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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26. Li J, Zhou X, Liu Q, Wang Z, Li Y, Li Y: The correlation between the expression of ABH and Lewis A histo-blood group antigens and the biological behavior of primary pulmonary adenocarcinoma. J Clin Oncol; 2009 May 20;27(15_suppl):e19066

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The correlation between the expression of ABH and Lewis A histo-blood group antigens and the biological behavior of primary pulmonary adenocarcinoma.
  • : e19066 Objective: To investigate the correlation between the expression of ABH and Lewis A histo-blood group antigens and the differentiation, tumorigenesis, progression, metastasis and prognosis of primary pulmonary adenocarcinoma.
  • METHODS: The expression of ABH and Lewis A histo-blood group antigens were detected in normal tissue (n=30), primary adenocarcinoma (n=103) and corresponding metastatic lesion (n=41) with immunohistochemistry S-P method.
  • RESULTS: The positive expression of A, B, H antigens was found in normal corresponding pulmonary tissue.
  • While in cancer tissue, such expression was absent.
  • The absence in poorly differentiated tumor was significantly higher than in moderate and highly differentiated cell (P<0.001).
  • And the absent expression was statistically higher in tumor with metastasis than in without metastasis (P=0.036),higher in N<sub>2</sub> than in N<sub>1</sub> group, higher in secondary tumor in than primary focus(P=0.008).There was significantly statistical difference on the absent expression rates among normal pulmonary tissue, primary tumor and metastatic tumor (P<0.001), and having a tendency of increased absence rate.
  • The expression of Lewis A antigen was markedly higher in pulmonary adenocarcinoma than in normal tissue (P=0.024).
  • Concerning Lewis A expression, the significant difference was found in Stage I,II and III+IV cancers (P=0.001), while the positive expression rate in advanced cancer (StageII+III+IV) was remarkably higher than in early cancer (Stage I) .
  • CONCLUSIONS: The absence of ABH antigen is closely correlated with tumorigenesis, poor differentiation, and metastasis of primary adenocarcinoma.

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  • (PMID = 27962141.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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27. Gibbons DL, Lin W, Creighton C, Zhang S, Lozano G, Kurie J: Use of a murine model of NSCLC to evaluate the role of the microRNA-200 family in regulating EMT and metastasis. J Clin Oncol; 2009 May 20;27(15_suppl):11006

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : 11006 Background: Non-small cell lung cancer (NSCLC) is the leading cause of cancer death worldwide, primarily due to metastatic disease.
  • Unfortunately, we lack a clear understanding of the molecular and cellular basis for lung cancer metastasis, partly because the experimental study is hampered by lack of good models.
  • METHODS/RESULTS: To address this deficiency we have developed an experimental murine model of metastatic NSCLC using cell lines derived from a genetic mouse model of human lung adenocarcinoma that develops metastatic disease owing to the expression of K-ras<sup>G12D</sup> and p53<sup>R172H</sup>.
  • Combined mRNA and microRNA profiling of highly metastatic subcutaneous tumors versus non-metastatic tumors revealed a signature for the epithelial-to-mesenchymal transition (including increases in known EMT-inducing transcription factors and down-regulation of genes responsible for maintenance of epithelial polarity) and associated loss of the microRNA-200 family (miR-141, 200a, 200b, 200c & 429) expression.
  • Forced expression of the miR-200 family produced a more epithelial cell phenotype and associated changes in the ability of the cancer cells to respond to EMT-inducing stimuli such as TGFβ.
  • We believe this to be a mechanism whereby changes in the tumor microenvironment influence tumor cell state and ability to undergo metastasis.
  • This work should provide new insights into the cell biology of tumor progression and metastasis, while generating new potential targets for therapy of metastatic disease.

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  • (PMID = 27964037.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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28. Gong Y, Yao E, Arcila M, Frankel S, Teruya-Feldstein J, Zakowski M, Thomas R, Ladanyi M, Pao W: Expression levels of total IGF-1R and sensitivity of NSCLC cells in vitro to an anti-IGF-1R antibody (R1507). J Clin Oncol; 2009 May 20;27(15_suppl):8095

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : 8095 Background: The IGF-1R (IGF receptor type 1) pathway is frequently deregulated in human tumors and has become a target of interest for anti-cancer therapy.
  • METHODS: We examined the growth inhibitory effects of R1507, a fully-humanized IgG1 anti-IGF-1R monoclonal Ab (Roche), against a panel of 22 NSCLC cell lines using CellTiter Blue assays.
  • RESULTS: 5 of 22 NSCLC cell lines were moderately sensitive (25-50% growth inhibition) to R1507 alone.
  • In one EGFR mutant lung adenocarcinoma cell line, R1507 and erlotinib co-treatment induced apoptosis, whereas treatment with either drug alone induced only cell cycle arrest.
  • CONCLUSIONS: In NSCLC cell lines, high levels of total IGF-1R are associated with moderate sensitivity to R1507.

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  • (PMID = 27962673.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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29. Sugarbaker DJ, Tilleman TR, Swanson SJ, Jaklitsch MT, Mentzer SJ, Mujoomdar AA, Bueno R: The role of extrapleural pneumonectomy in the management of pleural cancers. J Clin Oncol; 2009 May 20;27(15_suppl):7577

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : 7577 Background: We report our experience with EPP for non-mesothelial malignancies.
  • Of these, 32 patients had mediastinoscopy negative T4 lung cancer, 11 had metastases to only one pleura from extrathoracic sites, 10 had unilateral lung sarcomas involving the pleural envelope, 8 had thymomas metastatic to a pleural space, 2 were preoperatively diagnosed as mesotheliomas but at final pathology were determined to be small cell lung cancer and sarcomatoid carcinoma, and 2 represented primary mucoepidermoid and neuroectodermal malignancies.
  • Twenty-eight patients had stage IIIB (T4-N0-1) lung adenocarcinoma representing the largest homogeneous group of patients by cell type and stage.

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  • (PMID = 27963385.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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30. Johnson ML, Rizvi NA, Ginsberg MS, Miller VA, Kris MG, Pao W, Riely GJ: A phase II trial of salirasib in patients with stage IIIB/IV lung adenocarcinoma enriched for KRAS mutations. J Clin Oncol; 2009 May 20;27(15_suppl):8012

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A phase II trial of salirasib in patients with stage IIIB/IV lung adenocarcinoma enriched for KRAS mutations.
  • : 8012 Background: KRAS mutations are present in 30% of lung adenocarcinomas and are associated with primary resistance to erlotinib and gefitinib.
  • Salirasib inhibits KRAS-dependent growth in cell lines and xenograft models.
  • The primary endpoint was rate of RECIST non-progression at 10 wks.
  • The successful enrollment over 15 months of 29 pts with tumors with known KRAS mutations demonstrates that trials of a KRAS-specific genotype in lung cancer are feasible, and should be standard in future studies targeting the KRAS pathway.

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  • (PMID = 27962781.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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31. Zhu Y, Chen L: Identification and characterization of SP cells in human lung adenocarcinoma SPC-A1 cells. J Clin Oncol; 2009 May 20;27(15_suppl):e22230

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification and characterization of SP cells in human lung adenocarcinoma SPC-A1 cells.
  • With an extensive understanding of their biology, a major role for stem cells in the malignant process has been proposed and the existence of cancer stem cells(CSCs) has been confirmed in hematopoietic malignancies, brain cancer, and solid organ malignancies including breast, prostate, colon, and pancreatic cancer.
  • Lung cancer is the leading cause of cancer mortality in most large cities of China.
  • It is possible that lung cancer contains cancer stem cells responsible for its malignancy.
  • The aim of this study is to identify, characterize and enrich the CSC population that drives and maintains lung adenocarcinoma growth and metastasis.
  • METHODS: Side population (SP) cell analysis and sorting were applied to established human lung adenocarcinoma cell line and an attempt to further enrich them by preliminary serum-free culture before fluorescence activated cell sorting(FACS) was done.
  • Stem cell properties of SP cells were evaluated by their proliferative index, colony-forming efficiency, tumorigenic potential, bi-differentiation capacity and the expression of common stem cell surface markers.
  • RESULTS: Lung cancer cells could grow in a serum-free Medium (SFM) as non-adherent spheres similar to neurospheres or mammospheres.
  • The proportion of SP cells in cell spheres was significantly higher than that in cells grown as monolayers.
  • SP cells were both CCA positive and SP-C positive while non-SP cells were only SP-C positive.
  • Flow cytometric analysis of cell phenotyping showed that SP cells expressed CD133 and CD44, the common cell surface markers of cancer stem cells, while non-SP cells only expressed CD44.
  • CONCLUSIONS: SP cells existed in human lung adenocarcinoma cell lines and they could be further enriched by preliminary serum-free culture before FACS sorting.
  • SP cells possessed the properties of cancer stem cells.

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  • (PMID = 27964107.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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32. Stevenson MM, Mostertz W, Acharya C, Walters K, Barry W, Tuchman S, Ready N, Onaitis M, Crawford J, Potti A: Characterizing the clinical relevance of an embryonic stem cell phenotype in lung adenocarcinoma. J Clin Oncol; 2009 May 20;27(15_suppl):11001

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Characterizing the clinical relevance of an embryonic stem cell phenotype in lung adenocarcinoma.
  • : 11001 Background: Cancer cells possess traits reminiscent of those ascribed to normal stem cells.
  • It is unclear whether these phenotypic similarities between normal/embryonic stem cells and mature tumor cells, specific to lung cancer, are a result of underlying biologic processes, such as specific molecular pathways and regulatory networks.
  • METHODS: Using a large cohort of lung cancer cell lines with associated gene expression data, genes associated with an embryonic stem cell identity were used to develop a 'signature' representative of embryonic stemness (ES) activity specific to lung adenocarcinoma.
  • The ES signature was applied to three independent early (stage I - IIIa) lung adenocarcinoma data sets (N = 634) with clinically annotated gene expression data.
  • RESULTS: Using Bayesian regression analysis, a 100 gene signature representative of ES activity in lung adenocarcinoma was developed and validated in a leave-one-out-analysis.
  • GSEA identified gene sets significantly represented in the ES signature: signature of neoplastic transformation, signature of undifferentiated cancer, BRCA pathway, and fibroblast serum response pathway, all associated with cancer invasiveness.
  • Adenocarcinomas with ES demonstrated increased activation of RAS (p = 0.0002), MYC (p = 0.0057), wound healing (angiogenesis) (p < 0.0001), chromosomal instability (p < 0.0001), and invasiveness (p < 0.0001) gene signatures.
  • Adenocarcinomas (N= 634) with ES had a decreased survival (p<0.04).
  • The ES signature was not prognostic in prostate, ovarian, or breast adenocarcinomas.
  • Lung tumors (N=634) and adenocarcinoma cell lines (N=31) with ES were more resistant to cisplatin (p<0.0001 and p=0.0063, respectively).
  • CONCLUSIONS: Lung adenocarcinomas that share a common gene expression pattern with normal stem cells were associated with decreased survival and increased likelihood of resistance to cisplatin, indicating the aggressiveness of lung tumors with a stem cell phenotype.

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  • (PMID = 27964049.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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33. Reinersman M, Riely GJ, Nicastri A, Soff GA, Getinet A, Schwartz AG, Zakowski MF, Rusch VW, Kris MG, Ladanyi M: EGFR and KRAS mutation status of lung adenocarcinomas in African Americans. J Clin Oncol; 2009 May 20;27(15_suppl):11065

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] EGFR and KRAS mutation status of lung adenocarcinomas in African Americans.
  • : 11065 Background: The 2004 discovery of the tyrosine kinase inhibitor-sensitizing mutations in the epidermal growth factor receptor (EGFR) represents a major advance in the study and management of non-small cell lung cancer.
  • EGFR mutations occur almost exclusively in adenocarcinoma, and are more common in never smokers, women, and people born in East Asian (compared to Whites).
  • No comprehensive studies exist of EGFR and KRAS mutations in lung cancers from African-American patients.
  • METHODS: We collected formalin-fixed paraffin-embedded material from 121 resected lung adenocarcinomas from African-American patients for DNA extraction.
  • These data were compared to Memorial Sloan-Kettering data for EGFR and KRAS mutations in all resected adenocarcinomas in white patients.
  • When compared to data from Memorial Sloan-Kettering for White patients (81/273, 30%), the 17% rate of KRAS mutations in lung adenocarcinomas from African-Americans was significantly lower (p=0.01).
  • CONCLUSIONS: This is the first large series reporting results of mutation testing in lung adenocarcinoma specimens from African-Americans.
  • African-American patients are less likely than Whites to harbor KRAS mutations in their lung adenocarcinomas.

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  • (PMID = 27963141.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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34. Walker M, Peltz G, Houts A, Pohl G, Schwartzberg L, Stepanski E, Marciniak M: Psychosocial impact of cancer-related symptoms among patients with lung cancer. J Clin Oncol; 2009 May 20;27(15_suppl):6621

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Psychosocial impact of cancer-related symptoms among patients with lung cancer.
  • : 6621 Background: Patients with lung cancer may experience adverse physical symptoms due to cancer, cancer treatment, or comorbid medical conditions.
  • These cancer-related symptoms (CRS) may be associated with functional impairment (FI), and may affect psychosocial functioning.
  • METHODS: We conducted a retrospective analysis of self reported symptom burden with the 38-item Patient Care Monitor survey (PCM), collected as part of routine clinical care in 1,384 lung cancer patients identified by ICD-9 codes at 8 community oncology practices in the US.
  • Histological type was 36% adenocarcinoma, 18% squamous cell, 37% unspecified, and 9% other.
  • Depressive disorder was recorded for < 5% of patients.
  • CONCLUSIONS: Cancer related symptoms are associated with FI and with psychosocial outcomes in lung cancer patients.

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  • (PMID = 27961795.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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35. Kristeleit R, Calvert H, Arkenau H, Olmos D, Adam J, Plummer ER, Lock V, Squires M, Fazal L, Judson I: A phase I study of AT9283, an aurora kinase inhibitor, in patients with refractory solid tumors. J Clin Oncol; 2009 May 20;27(15_suppl):2566

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Exposure of solid tumour cell lines to AT9283 in vitro induces an "aurora inhibitory" phenotype.
  • Cell survival decreases with increased duration of exposure.
  • An additional 4 patients received at least six cycles of therapy (squamous cell carcinoma of the lung, adenocarcinoma of the esophagus and colorectal carcinoma [2]) with a best response of stable disease.

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  • (PMID = 27961883.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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36. Janjigian YY, Park BJ, Kris MG, Miller VA, Riely GJ, Zheng J, Dycoco JP, Shen R, Azzoli CG: Impact on disease-free survival of adjuvant erlotinib or gefitinib in patients with resected lung adenocarcinomas that harbor epidermal growth factor receptor (EGFR) mutations. J Clin Oncol; 2009 May 20;27(15_suppl):7523

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Impact on disease-free survival of adjuvant erlotinib or gefitinib in patients with resected lung adenocarcinomas that harbor epidermal growth factor receptor (EGFR) mutations.
  • : 7523 Background: Patients with stage IV adenocarcinoma whose tumors harbor EGFR mutations have high rates of response (∼ 75%) and prolonged progression free survival after EGFR tyrosine kinase inhibitor (TKI) treatment.
  • To see if adjuvant treatment with EGFR TKI (gefitinib or erlotinib) improves DFS in patients with EGFR mutation NSCLC, we conducted a retrospective review of patients with resected lung adenocarcinoma harboring EGFR mutations, some of whom received EGFR TKIs postoperatively.
  • METHODS: With Institutional Review Board approval, clinical information was obtained on all patients with stage I-III lung adenocarcinoma harboring EGFR exon 19 or 21 mutations that underwent resection at MSKCC between May 2002 and August 2008.
  • RESULTS: We studied 150 patients (112 women, 38 men) with completely resected stage I-III lung adenocarcinoma whose resection specimens contained EGFR activating mutations in exon 19 or 21.
  • After controlling for stage, individuals who received adjuvant gefitinib or erlotinib had a better DFS (HR=0.38, 95%CI: 0.16-0.90) than the non-TKI group (p=0.03).
  • CONCLUSIONS: These data indicate that the adjuvant use of either gefitinib or erlotinib improves DFS in patients with completely resected stage I -III lung adenocarcinomas with mutations in EGFR exons 19 and 21.

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  • (PMID = 27963290.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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37. Otero JM, Cardona AF, Carrasco-Chaumel E, Carranza H, Vargas C, Carlos C, Diana T, Ludovic R, Reguart N, Cuello M: Survival of patients (pts) with advanced lung adenocarcinoma (ALA) treated in four hospitals from Bogotá D.C., Colombia, and report of a novel alteration in the epidermal growth factor receptor (EGFR) (ONCOLGroup study). J Clin Oncol; 2009 May 20;27(15_suppl):e19097

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Survival of patients (pts) with advanced lung adenocarcinoma (ALA) treated in four hospitals from Bogotá D.C., Colombia, and report of a novel alteration in the epidermal growth factor receptor (EGFR) (ONCOLGroup study).
  • The brain was the dominant site for metastasis (38%) followed by the lungs (38%).
  • Three pts with EGFR alterations were identified in this cohort; two presented a non- described change in E19 which may have corresponded to a novel alteration in our region, with possible increased sensitivity to E.

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  • (PMID = 27962247.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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38. Sánchez-Romero A, Oliver I, Costa D, Orduña A, Lacueva J, Pérez-Vicente F, Arroyo A, Calpena R: Giant splenic metastasis due to lung adenocarcinoma. Clin Transl Oncol; 2006 Apr;8(4):294-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Giant splenic metastasis due to lung adenocarcinoma.
  • Lung cancer is the most prevalent malignancy in western countries and most of the patients present at advanced stages, but single splenic metastasis is exceptional instead.
  • We report on a case of a seventy- three-year old male presenting with non-hemoptoic productive cough, constitutional syndrome and pain in the left lower quadrant.
  • Physical examination and complementary radiological and histological procedures revealed the presence of an adenocarcinoma of the left lung with probable splenic metastasis.
  • The patient underwent splenectomy, which confirmed the diagnose of splenic metastasis of lung adenocarcinoma and, secondly, lung resection was performed.
  • Topics about lung cancer metastasis are discussed.
  • [MeSH-major] Adenocarcinoma / secondary. Lung Neoplasms / pathology. Splenic Neoplasms / secondary

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  • (PMID = 16648107.001).
  • [ISSN] 1699-048X
  • [Journal-full-title] Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico
  • [ISO-abbreviation] Clin Transl Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Spain
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39. De Stefani E, Boffetta P, Brennan P, Deneo-Pellegrini H, Ronco A, Gutiérrez LP: Occupational exposures and risk of adenocarcinoma of the lung in Uruguay. Cancer Causes Control; 2005 Sep;16(7):851-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Occupational exposures and risk of adenocarcinoma of the lung in Uruguay.
  • OBJECTIVES: To investigate occupational risks of lung adenocarcinoma in Uruguay and to confirm a previously reported increased risk among butchers.
  • METHODS: We conducted a case-control study among men in four major hospitals in Montevideo, based on interviews to 338 cases of lung adenocarcinoma and 1014 hospital-based controls.
  • We calculated odds ratios (ORs) of lung adenocarcinoma for employment in 22 jobs, after adjustment for tobacco smoking and other potential confounders.
  • Long-term employment as mason, glass worker or textile worker resulted in an increased OR.
  • CONCLUSIONS: Occupational exposures seem to play a limited role in causing lung adenocarcinoma among men in Uruguay.
  • [MeSH-major] Adenocarcinoma / epidemiology. Adenocarcinoma / etiology. Lung Neoplasms / epidemiology. Lung Neoplasms / etiology. Occupational Exposure / adverse effects

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  • (PMID = 16132795.001).
  • [ISSN] 0957-5243
  • [Journal-full-title] Cancer causes & control : CCC
  • [ISO-abbreviation] Cancer Causes Control
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Dust; 1332-21-4 / Asbestos; 7631-86-9 / Silicon Dioxide
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40. Fujita A, Kameda Y, Goya T: Clinicopathology of stromal invasion in lung adenocarcinoma. Pathol Int; 2009 Jan;59(1):1-6
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  • [Title] Clinicopathology of stromal invasion in lung adenocarcinoma.
  • In the World Health Organization classification, lung adenocarcinoma with mixed subtypes is defined as invasive carcinoma with evidence of vascular, pleural, or stromal invasion.
  • A total of 157 peripheral pure bronchioloalveolar carcinoma (BAC) or lung adenocarcinoma with mixed BAC and others were reviewed.
  • Survival of patients with adenocarcinoma without DAF (n = 41) was 100%.
  • Even when adenocarcinoma involved DAF and lacked EAAI (n = 21), survival was 100%.
  • [MeSH-major] Adenocarcinoma / pathology. Lung Neoplasms / pathology. Neoplasm Invasiveness / pathology

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  • (PMID = 19121086.001).
  • [ISSN] 1440-1827
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Australia
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41. Falvella FS, Galvan A, Frullanti E, Spinola M, Calabrò E, Carbone A, Incarbone M, Santambrogio L, Pastorino U, Dragani TA: Transcription deregulation at the 15q25 locus in association with lung adenocarcinoma risk. Clin Cancer Res; 2009 Mar 1;15(5):1837-42
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Transcription deregulation at the 15q25 locus in association with lung adenocarcinoma risk.
  • PURPOSE: We characterized the candidacy of the six candidate genes mapping in the chromosome 15q25 locus, which was previously reported as associated with lung cancer risk, and confirmed the locus association with lung cancer risk in an Italian population of lung adenocarcinoma patients and controls.
  • EXPERIMENTAL DESIGN: We did a quantitative analysis of mRNA levels of IREB2 (iron-responsive element-binding protein 2), LOC123688, PMSA4 [proteasome (prosome, macropain) subunit alpha type 4], CHRNB4 (cholinergic receptor nicotinic beta 4), CHRNA3 (cholinergic receptor nicotinic alpha 3), and CHRNA5 (cholinergic receptor nicotinic alpha 5) genes in paired normal lung and lung adenocarcinoma tissue, and an immunohistochemical localization of CHRNA3- and CHRNA5-encoded proteins.
  • We also examined the association of CHRNA5 D398N polymorphism with lung cancer risk and with CHRNA5 mRNA levels in the normal lung.
  • RESULTS: Expression analysis of the six candidate genes mapping in the lung cancer risk-associated chromosome 15q25 locus revealed a 30-fold up-regulation of the gene encoding the CHRNA5 subunit and a 2-fold down-regulation of the CHRNA3 subunit in lung adenocarcinoma as compared with the normal lung.
  • The carrier status of the 398N allele at the D398N polymorphism of the CHRNA5 gene was associated with lung adenocarcinoma risk (odds ratio, 1.5; 95% confidence interval, 1.2-2.0) in a population-based series of lung adenocarcinoma patients (n=467) and healthy controls (n=739).
  • Analysis of a family-based series of nonsmoker lung cancer cases (n=80) and healthy sib controls (n=80) indicated a similar trend.
  • In addition, the same D398N variation correlated with CHRNA5 mRNA levels in normal lung of adenocarcinoma patients.
  • [MeSH-major] Adenocarcinoma / genetics. Chromosomes, Human, Pair 15 / genetics. Iron Regulatory Protein 2 / genetics. Lung Neoplasms / genetics. Nerve Tissue Proteins / genetics. Proteasome Endopeptidase Complex / genetics. Receptors, Nicotinic / genetics
  • [MeSH-minor] Adult. Aged. Carcinoma, Squamous Cell / genetics. Carcinoma, Squamous Cell / metabolism. Carcinoma, Squamous Cell / secondary. Case-Control Studies. DNA / genetics. DNA / metabolism. Female. Genotype. Humans. Immunoenzyme Techniques. Lung / metabolism. Lung / pathology. Male. Middle Aged. Polymerase Chain Reaction. Polymorphism, Single Nucleotide / genetics. RNA, Messenger / genetics. RNA, Messenger / metabolism. Risk Factors

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  • [CommentIn] Clin Cancer Res. 2009 Sep 1;15(17):5599; author reply 5599 [19706810.001]
  • (PMID = 19223495.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CHRNA5 protein, human; 0 / CHRNB4 protein, human; 0 / Nerve Tissue Proteins; 0 / RNA, Messenger; 0 / Receptors, Nicotinic; 0 / nicotinic receptor subunit alpha3; 9007-49-2 / DNA; EC 3.4.25.1 / Proteasome Endopeptidase Complex; EC 4.2.1.3 / Iron Regulatory Protein 2
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42. Kubota Y, Chihara Y, Date K, Yamada T, Hara H: [Case of thymic carcinoid accompanied by adenocarcinoma of the lung]. Nihon Kokyuki Gakkai Zasshi; 2010 Dec;48(12):950-4
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  • [Title] [Case of thymic carcinoid accompanied by adenocarcinoma of the lung].
  • A 71-year-old man was found to have growing nodules in his right lung, and an anterior mediastinal tumor.
  • The rapid intraoperative pathological diagnosis was adenocarcinoma from the lung nodules and low grade malignancy from an anterior mediastinal tumor.
  • Postoperative pathological examination revealed the coexistence of lung cancer and a typical carcinoid of the thymus.
  • To the best of our knowledge, we report the first case of thymic carcinoid accompanied with adenocarcinoma of the lung.
  • [MeSH-major] Adenocarcinoma / diagnosis. Carcinoid Tumor / diagnosis. Lung Neoplasms / diagnosis. Mediastinal Neoplasms / diagnosis. Neoplasms, Multiple Primary. Thymus Neoplasms / diagnosis

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  • (PMID = 21226303.001).
  • [ISSN] 1343-3490
  • [Journal-full-title] Nihon Kokyūki Gakkai zasshi = the journal of the Japanese Respiratory Society
  • [ISO-abbreviation] Nihon Kokyuki Gakkai Zasshi
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
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43. Houseni M, Chamroonrat W, Zhuang J, Gopal R, Alavi A, Zhuang H: Prognostic implication of dual-phase PET in adenocarcinoma of the lung. J Nucl Med; 2010 Apr;51(4):535-42
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  • [Title] Prognostic implication of dual-phase PET in adenocarcinoma of the lung.
  • The purpose of this study was to determine whether dual-phase (18)F-FDG PET could be a prognostic factor for adenocarcinoma of the lung.
  • METHODS: One hundred patients with histologically proven adenocarcinoma of the lung were included in this retrospective analysis.
  • The percentage change in the maximal standardized uptake values (SUVmax) of the cancer between the early and the delayed images was calculated.
  • RESULTS: Statistical analysis showed that SUVmax change over time between the early and the delayed PET was a strong independent predictor of outcome for lung adenocarcinoma.
  • Our findings suggest that the percentage SUVmax change over time is a strong prognostic factor in patients with lung adenocarcinoma and can be complementary to the other well-known factors.
  • [MeSH-major] Adenocarcinoma / diagnosis. Adenocarcinoma / radionuclide imaging. Lung Neoplasms / diagnosis. Lung Neoplasms / radionuclide imaging. Positron-Emission Tomography

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  • (PMID = 20237037.001).
  • [ISSN] 1535-5667
  • [Journal-full-title] Journal of nuclear medicine : official publication, Society of Nuclear Medicine
  • [ISO-abbreviation] J. Nucl. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0Z5B2CJX4D / Fluorodeoxyglucose F18
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44. Alexandrescu C, Civaia F, Dor V: Tumor thrombus in right atrium from lung adenocarcinoma. Ann Thorac Surg; 2009 Feb;87(2):e11-2
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  • [Title] Tumor thrombus in right atrium from lung adenocarcinoma.
  • The patient underwent surgical excision of the mass because he would have a high risk of sudden death, pulmonary embolism, or tricuspid obstruction.
  • A histologic examination established the diagnosis of lung adenocarcinoma metastases.
  • [MeSH-major] Adenocarcinoma / secondary. Heart Neoplasms / secondary. Lung Neoplasms / pathology. Neoplasm Invasiveness / pathology. Neoplastic Cells, Circulating / pathology

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  • (PMID = 19161731.001).
  • [ISSN] 1552-6259
  • [Journal-full-title] The Annals of thoracic surgery
  • [ISO-abbreviation] Ann. Thorac. Surg.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Netherlands
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45. Kushitani K, Takeshima Y, Amatya VJ, Furonaka O, Sakatani A, Inai K: Immunohistochemical marker panels for distinguishing between epithelioid mesothelioma and lung adenocarcinoma. Pathol Int; 2007 Apr;57(4):190-9
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  • [Title] Immunohistochemical marker panels for distinguishing between epithelioid mesothelioma and lung adenocarcinoma.
  • The distinction between epithelioid mesothelioma and lung adenocarcinoma remains an important diagnostic challenge for surgical pathologists.
  • The aim of the present study was to select a limited and appropriate panel of antibodies that can differentiate between epithelioid mesothelioma and lung adenocarcinoma.
  • Specimens of 90 epithelioid mesotheliomas and 51 lung adenocarcinomas obtained from Japanese cases were examined using calretinin, WT1, AE1/AE3, CAM5.2, cytokeratin (CK) 5/6, vimentin, epithelial membrane antigen (EMA), thrombomodulin, CEA, CA19-9, and CA125.
  • In contrast, 33% of lung adenocarcinomas were positive for calretinin; 16% for WT1; 100% for AE1/AE3, CAM5.2, and EMA; 41% for CK 5/6; 47% for vimentin; 20% for thrombomodulin; 69% for mesothelin; 98% for CEA; 73% for CA19-9; and 80% for CA125.
  • For distinguishing between epithelioid mesothelioma and lung adenocarcinoma, the combination of CEA, calretinin and each WT1 or thrombomodulin was suggested to be the best panel of immunohistochemical markers.
  • [MeSH-major] Adenocarcinoma / diagnosis. Biomarkers, Tumor / metabolism. Epithelioid Cells / pathology. Lung Neoplasms / diagnosis. Mesothelioma / diagnosis
  • [MeSH-minor] Calbindin 2. Carcinoembryonic Antigen / analysis. Carcinoembryonic Antigen / metabolism. Diagnosis, Differential. Humans. Immunohistochemistry. S100 Calcium Binding Protein G / analysis. S100 Calcium Binding Protein G / metabolism. Sensitivity and Specificity. Thrombomodulin / analysis. Thrombomodulin / metabolism. WT1 Proteins / analysis. WT1 Proteins / metabolism

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  • [CommentIn] Pathol Int. 2009 Apr;59(4):274; author reply 274 [19351375.001]
  • (PMID = 17316414.001).
  • [ISSN] 1320-5463
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CALB2 protein, human; 0 / Calbindin 2; 0 / Carcinoembryonic Antigen; 0 / S100 Calcium Binding Protein G; 0 / Thrombomodulin; 0 / WT1 Proteins
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46. Kalogeraki A, Tzardi M, Zoras O, Giannikaki E, Papadakis M, Tamiolakis D, Petraki PE, Diamantis A, Siafakas N, Stathopoulos E: Apoptosis and cell proliferation correlated with tumor grade in patients with lung adenocarcinoma. In Vivo; 2010 Sep-Oct;24(5):667-70
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Apoptosis and cell proliferation correlated with tumor grade in patients with lung adenocarcinoma.
  • BACKGROUND: Apoptosis and cell proliferation in patients with adenocarcinoma of the lung have not been well described with relation to fine-needle aspiration biopsies (FNABs).
  • To investigate the contribution of apoptosis to the growth of adenocarcinoma of the lung, both apoptosis and cell proliferation were analysed for correlation with the grade of the tumor.
  • PATIENTS AND METHODS: Fifty tumors from 50 patients with adenocarcinoma of the lung were studied.
  • The detection of DNA fragments in situ using the terminal deoxyribonucleotidyl transferase-mediated dUTP-digoxigenin nick-end labeling (TUNEL) assay was applied to investigate active cell death (apoptosis) and the MIB-1 antigen was used to investigate cell proliferation.
  • RESULTS: The TUNEL indices were 0.55±0.09, 0.90±0.33 and 3.1±0.99 in well-, moderately and poorly differentiated adenocarcinoma of the lung respectively.
  • The differences in both TUNEL and MIB-1 labeling indices were significant between well-, moderately and poorly differentiated adenocarcinoma of the lung and a positive correlation was found between the TUNEL indices and the MIB-1 indices.
  • CONCLUSION: Apoptosis (cell death) and cell proliferation increases as the grade of differentiation decreases in adenocarcinoma of the lung, suggesting a rapid turn over of the tumor cells in tumors with a lower grade of differentiation.
  • [MeSH-major] Adenocarcinoma / pathology. Apoptosis / physiology. Lung Neoplasms / pathology. Severity of Illness Index
  • [MeSH-minor] Biomarkers, Tumor / metabolism. Biopsy, Fine-Needle. Cell Differentiation / physiology. Cell Division / physiology. Humans. In Situ Nick-End Labeling. Ki-67 Antigen / metabolism. Prognosis. Tumor Cells, Cultured

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  • (PMID = 20952731.001).
  • [ISSN] 1791-7549
  • [Journal-full-title] In vivo (Athens, Greece)
  • [ISO-abbreviation] In Vivo
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Ki-67 Antigen
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47. Oda T, Tian T, Inoue M, Ikeda J, Qiu Y, Okumura M, Aozasa K, Morii E: Tumorigenic role of orphan nuclear receptor NR0B1 in lung adenocarcinoma. Am J Pathol; 2009 Sep;175(3):1235-45
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tumorigenic role of orphan nuclear receptor NR0B1 in lung adenocarcinoma.
  • Cancer stem cells are a limited population of tumor cells that are thought to reconstitute whole tumors.
  • The Hoechst dye exclusion assay revealed that tumors are composed of both a main population and a side population of cells, which are rich in cancer stem cells.
  • NR0B1 is an orphan nuclear receptor that is expressed to a greater extent in the side population, as compared with the main population, of a lung adenocarcinoma cell line.
  • In this study, we investigated the role of NR0B1 in lung adenocarcinoma cells.
  • Reduction of NR0B1 expression levels in lung adenocarcinoma cell lines resulted in vulnerability to anti-cancer drugs and decreased abilities for invasion, in vitro colony formation, and tumorigenicity in non-obese diabetic/severe compromised immunodeficient mice.
  • When 193 cases of lung adenocarcinoma were immunohistochemically examined, higher levels of NR0B1 expression correlated with higher rates of lymph node metastasis and recurrence.
  • In clinical samples, NR0B1 expression levels inversely correlated to the proportion of methylated CpG sequences around the transcription initiation site of the NR0B1 gene, suggesting the epigenetic control of NR0B1 transcription in lung adenocarcinoma.
  • In conclusion, NR0B1 might play a role in the malignant potential of lung adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / metabolism. Biomarkers, Tumor. DAX-1 Orphan Nuclear Receptor / biosynthesis. Lung Neoplasms / metabolism
  • [MeSH-minor] Animals. Cell Line, Tumor. Disease-Free Survival. Female. Gene Expression Regulation, Neoplastic. Humans. Lymphatic Metastasis / genetics. Methylation. Mice. Mice, Inbred NOD. Mice, SCID. Neoplasm Invasiveness / genetics. Neoplasm Transplantation. Prognosis. Promoter Regions, Genetic. Recurrence. Transcription, Genetic

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  • (PMID = 19644015.001).
  • [ISSN] 1525-2191
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DAX-1 Orphan Nuclear Receptor; 0 / NR0B1 protein, human
  • [Other-IDs] NLM/ PMC2731142
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48. Van Hul I, Cools P, Rutsaert R: Solitary splenic metastasis of an adenocarcinoma of the lung 2 years postoperatively. Acta Chir Belg; 2008 Jul-Aug;108(4):462-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Solitary splenic metastasis of an adenocarcinoma of the lung 2 years postoperatively.
  • We report a case of an asymptomatic, isolated splenic metastasis in a 67-year-old man diagnosed 2 years after resection of an adenocarcinoma of the lung.
  • [MeSH-major] Adenocarcinoma / secondary. Lung Neoplasms / pathology. Splenic Neoplasms / secondary
  • [MeSH-minor] Aged. Diagnosis, Differential. Follow-Up Studies. Humans. Laparotomy. Male. Pneumonectomy. Splenectomy / methods. Tomography, X-Ray Computed

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  • (PMID = 18807605.001).
  • [ISSN] 0001-5458
  • [Journal-full-title] Acta chirurgica Belgica
  • [ISO-abbreviation] Acta Chir. Belg.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Belgium
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49. Lu J, Li J, Ji C, Yu W, Xu Z, Huang S: Expression of lipoprotein lipase associated with lung adenocarcinoma tissues. Mol Biol Rep; 2008 Mar;35(1):59-63
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of lipoprotein lipase associated with lung adenocarcinoma tissues.
  • Herein cDNA microarray and Northern blots analysis were used to study the expression of lipoprotein lipase in lung adenocarcinoma tissues.
  • LPL gene is expressed lowly at the average ratio 0.26 (Cy5/Cy3) in lung adenocarcinoma tissues over controls.
  • Northern blots confirmed those changes detected from the cDNA microarray and suggested that low expression of LPL may play an important role in the lung adenocarcinoma development.
  • [MeSH-major] Adenocarcinoma / enzymology. Adenocarcinoma / genetics. Lipoprotein Lipase / genetics. Lung Neoplasms / enzymology. Lung Neoplasms / genetics

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  • (PMID = 17347923.001).
  • [ISSN] 0301-4851
  • [Journal-full-title] Molecular biology reports
  • [ISO-abbreviation] Mol. Biol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] EC 3.1.1.34 / Lipoprotein Lipase
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50. Miki D, Kubo M, Takahashi A, Yoon KA, Kim J, Lee GK, Zo JI, Lee JS, Hosono N, Morizono T, Tsunoda T, Kamatani N, Chayama K, Takahashi T, Inazawa J, Nakamura Y, Daigo Y: Variation in TP63 is associated with lung adenocarcinoma susceptibility in Japanese and Korean populations. Nat Genet; 2010 Oct;42(10):893-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Variation in TP63 is associated with lung adenocarcinoma susceptibility in Japanese and Korean populations.
  • Lung cancer is the most common cause of death from cancer worldwide, and its incidence is increasing in East Asian and Western countries.
  • To identify genetic factors that modify the risk of lung adenocarcinoma, we conducted a genome-wide association study in a Japanese cohort, with replication in two independent studies in Japanese and Korean individuals, in a total of 2,098 lung adenocarcinoma cases and 11,048 controls.
  • The combined analyses identified two susceptibility loci for lung adenocarcinoma: TERT (rs2736100, combined P = 2.91 × 10⁻¹¹), odds ratio (OR) = 1.27) and TP63 (rs10937405, combined P = 7.26 × 10⁻¹²), OR = 1.31).
  • Our results suggest that genetic variation in TP63 may influence susceptibility to lung adenocarcinoma in East Asian populations.
  • [MeSH-major] Adenocarcinoma / genetics. Genetic Predisposition to Disease. Lung Neoplasms / genetics. Polymorphism, Single Nucleotide / genetics. Trans-Activators / genetics. Tumor Suppressor Proteins / genetics

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  • (PMID = 20871597.001).
  • [ISSN] 1546-1718
  • [Journal-full-title] Nature genetics
  • [ISO-abbreviation] Nat. Genet.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / TP63 protein, human; 0 / Trans-Activators; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins
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51. Kato T, Nakashima M, Yoshimura K, Imao M, Goto H, Yasuda S, Sano K: [A case of lung adenocarcinoma of the lung with disappearance of brain metastasis by re-treatment with gefitinib]. Nihon Kokyuki Gakkai Zasshi; 2005 Nov;43(11):700-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [A case of lung adenocarcinoma of the lung with disappearance of brain metastasis by re-treatment with gefitinib].
  • BACKGROUND: Tumor response rate to gefitinib by previously treated patients with advanced non-small-cell lung cancer was approximately 20%.
  • CASE: A 40-year-old man was given a diagnosis of adenocarcinoma of lung (c-T2N3M1).
  • Reduction of the primary tumor, brain metastasis, pulmonary metastasis and liver metastasis was seen.
  • Recurrence of pulmonary metastasis and liver metastasis was discovered 8 months after treatment with gefitinib.
  • However, primary tumor, pulmonary metastasis and liver metastasis progressed.
  • [MeSH-major] Adenocarcinoma / drug therapy. Antineoplastic Agents / therapeutic use. Brain Neoplasms / drug therapy. Lung Neoplasms / pathology. Quinazolines / therapeutic use

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  • (PMID = 16366371.001).
  • [ISSN] 1343-3490
  • [Journal-full-title] Nihon Kokyūki Gakkai zasshi = the journal of the Japanese Respiratory Society
  • [ISO-abbreviation] Nihon Kokyuki Gakkai Zasshi
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Quinazolines; S65743JHBS / gefitinib
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52. Castadot P, Magné N, Berghmans T, Drowart A, Baeyens L, Smets D, Van Houtte P: [Ovarian metastasis and lung adenocarcinoma: a case report]. Cancer Radiother; 2005 May;9(3):183-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Ovarian metastasis and lung adenocarcinoma: a case report].
  • [Transliterated title] Métastase ovarienne et adénocarcinome pulmonaire: observation d'un cas clinique.
  • Ovarian metastasis as first dissemination site of a lung adenocarcinoma has not been described in the literature.
  • We report the case of a 61-year-old woman who had a pneumectomy for a centrally located lung adenocarcinoma, which was discovered on a routine chest X-Ray.
  • Pathology reported an adenocarcinoma.
  • Clinical course, pathological and immunohistochemical data concluded to the diagnosis of ovarian metastasis of the lung adenocarcinoma.
  • In conclusion, in the differential diagnosis of an ovarian metastasis, clinicians should not forget the lung as primary site since epidemiologic data of lung cancer in women show progressive incidence.
  • [MeSH-major] Adenocarcinoma / secondary. Carcinoma, Non-Small-Cell Lung / secondary. Lung Neoplasms / pathology. Ovarian Neoplasms / secondary
  • [MeSH-minor] Diagnosis, Differential. Female. Humans. Immunohistochemistry. Middle Aged. Pneumonectomy. Positron-Emission Tomography

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  • (PMID = 16023045.001).
  • [ISSN] 1278-3218
  • [Journal-full-title] Cancer radiothérapie : journal de la Société française de radiothérapie oncologique
  • [ISO-abbreviation] Cancer Radiother
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
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53. Su Y, Zhu L, Jin Y, Zhang X, Zhou Q, Bai M: Impact of siRNA targeting pirh2 on proliferation and cell cycle control of the lung adenocarcinoma cell line A549. Front Med China; 2007 Oct;1(4):359-63
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Impact of siRNA targeting pirh2 on proliferation and cell cycle control of the lung adenocarcinoma cell line A549.
  • The aim of this study was to investigate the role of pirh2 (p53-induced RING-H2) protein in the proliferation, apoptosis and cell cycle control of the lung cancer cell line A549.
  • Cell proliferation was assessed by cell counting kit-8 (CCK-8).
  • Cell cycle control and apoptosis were analyzed by flow cytometry.
  • The inhibition of pirh2 expression by siRNA (psiRNA-pirh2) resulted in reduced cell proliferation and increased apoptosis.
  • Taken together, the inhibition of pirh2 expression in the lung adenocarcinoma cell line A549 resulted in reduced tumor cell growth via the inhibition of cell proliferation, the activation of apoptosis and the interruption of cell cycle transition.

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  • (PMID = 24573925.001).
  • [ISSN] 1673-7342
  • [Journal-full-title] Frontiers of medicine in China
  • [ISO-abbreviation] Front Med China
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China
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54. Kuroda N, Hamaguchi N, Takeuchi E, Ohara M, Hirouchi T, Mizuno K: Lung adenocarcinoma with a micropapillary pattern: a clinicopathological study of 25 cases. APMIS; 2006 May;114(5):381-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Lung adenocarcinoma with a micropapillary pattern: a clinicopathological study of 25 cases.
  • Lung adenocarcinoma with a micropapillary pattern has recently been described, but its biological behavior is as yet uncertain.
  • In this article we present a clinicopathological study of lung adenocarcinoma with micropapillary morphology.
  • We selected 25 patients with lung adenocarcinoma with micropapillary morphology from the 2001-2004 pathology files (age range 54 to 81 years; mean 64.5 years).
  • Micropapillary carcinoma is predominantly located at the periphery of the tumor nodule or mass and occurs irrespective of the subtype of the adenocarcinoma.
  • Four cases showed intensive invasive growth such as micropapillary adenocarcinoma of the breast and 21 showed alveolar type morphology with piling-up of the neoplastic cells with or without stromal invasion.
  • Regarding clinical outcome, 14 patients were alive without disease, 5 were alive with disease, and 5 died of the lung adenocarcinoma.
  • Lung micropapillary carcinoma of breast type may behave more aggressively than the alveolar type.
  • [MeSH-major] Adenocarcinoma / pathology. Lung Neoplasms / pathology
  • [MeSH-minor] Adenocarcinoma, Bronchiolo-Alveolar / pathology. Adenocarcinoma, Papillary / pathology. Aged. Aged, 80 and over. Calcinosis / pathology. Carcinoma, Acinar Cell / pathology. Female. Humans. Lymph Nodes / pathology. Lymphatic Metastasis. Male. Middle Aged. Neoplasm Invasiveness. Neoplasm Staging. Pleura / pathology. Survival Analysis

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  • (PMID = 16725015.001).
  • [ISSN] 0903-4641
  • [Journal-full-title] APMIS : acta pathologica, microbiologica, et immunologica Scandinavica
  • [ISO-abbreviation] APMIS
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Denmark
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55. Hiroi N, Yanagisawa R, Yoshida-Hiroi M, Endo T, Kawase T, Tsuchida Y, Toyama K, Shibuya K, Nakata K, Yoshino G: Retroperitoneal hemorrhage due to bilateral adrenal metastases from lung adenocarcinoma. J Endocrinol Invest; 2006 Jun;29(6):551-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Retroperitoneal hemorrhage due to bilateral adrenal metastases from lung adenocarcinoma.
  • A 56-yr-old man was admitted to our university hospital for severe back pain one month after a resection for lung adenocarcinoma (stage IIIA) without evidence of the adrenal mass.
  • Core-needle biopsy was performed on the right adrenal tumor and revealed adenocarcinoma cells mimicking a primary lung tumor previously examined.
  • We diagnosed retroperitoneal hemorrhage due to bilateral adrenal gland metastasis from lung adenocarcinoma with adrenal insufficiency.
  • Adrenal metastases most commonly originate from a primary lung tumor, followed by stomach, esophagus and liver/bile ducts.
  • Clinically significant adrenal hemorrhage by metastasis is exceedingly rare and non-specific symptoms, such as abdominal, chest or back pain, nausea and vomiting, confusion, weakness, hypotension, shock and high fever, are often observed in these patients.
  • We present a case of massive retroperitoneal hemorrhage and adrenal insufficiency due to adrenal gland metastasis from adenocarcinoma of lung.
  • [MeSH-major] Adenocarcinoma / secondary. Adrenal Gland Neoplasms / secondary. Adrenal Insufficiency / etiology. Hemorrhage / etiology. Lung Neoplasms / pathology

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  • (PMID = 16840834.001).
  • [ISSN] 0391-4097
  • [Journal-full-title] Journal of endocrinological investigation
  • [ISO-abbreviation] J. Endocrinol. Invest.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
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56. Ueshima Y, Kurioka H, Yamada R, Takumi C, Hiraoka N, Ono S: [Stromal bone formation by lung adenocarcinoma]. Nihon Kokyuki Gakkai Zasshi; 2005 Sep;43(9):523-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Stromal bone formation by lung adenocarcinoma].
  • We report a case of lung adenocarcinoma with stromal bone formation.
  • A 73-year-old woman was incidentally found to have a coin lesion in the left lower lung field on a chest roentgenogram and computed tomography showed a nodular lesion containing a few coarse high density areas in the left lower lobe.
  • Since transbronchial cytology revealed adenocarcinoma, left lower lobectomy was performed.
  • Histologically, the tumor was a papillary-tubular adenocarcinoma, and fragments of osseous tissue were found within abundant fibrous stroma.
  • Bone formation in primary lung adenocarcinoma is a very rare condition, and only 7 other cases have been reported in the literature.
  • [MeSH-major] Adenocarcinoma, Papillary / physiopathology. Lung Neoplasms / physiopathology. Osteogenesis

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  • (PMID = 16218421.001).
  • [ISSN] 1343-3490
  • [Journal-full-title] Nihon Kokyūki Gakkai zasshi = the journal of the Japanese Respiratory Society
  • [ISO-abbreviation] Nihon Kokyuki Gakkai Zasshi
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Number-of-references] 13
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57. Suzuki M, Iizasa T, Nakajima T, Kubo R, Iyoda A, Hiroshima K, Nakatani Y, Fujisawa T: Aberrant methylation of IL-12Rbeta2 gene in lung adenocarcinoma cells is associated with unfavorable prognosis. Ann Surg Oncol; 2007 Sep;14(9):2636-42
MedlinePlus Health Information. consumer health - Lung Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Aberrant methylation of IL-12Rbeta2 gene in lung adenocarcinoma cells is associated with unfavorable prognosis.
  • BACKGROUND: Interleukin-12 receptor beta2 (IL-12Rbeta2) knock-out mice develop lung adenocarcinoma, and epigenetic silencing by CpG methylation leads to loss of this gene in B-cell malignancies.
  • The aim of this study was to determine whether IL-12Rbeta2 methylation is a common feature in human lung cancer.
  • METHODS: We examined mRNA expression of IL-12Rbeta2 in lung cancer cell lines, and normal bronchial, and tracheal epithelial cells using RT-PCR, and we examined the methylation status of IL-12Rbeta2 in primary lung cancers.
  • RESULTS: Loss of expression was found in 10 of 13 (77%) NSCLC cell lines, and 2 of 5 (40%) SCLC cell lines compared with normal bronchial or tracheal cells.
  • Treatment of 11 expression-negative cell lines with a demethylating agent restored expression in all cases.
  • IL-12Rbeta2 methylation correlated with poorer prognosis in lung adenocarcinomas (hazard ratio = 2.33, P = 0.0059).
  • CONCLUSIONS: We conclude that epigenetic silencing of IL-12Rbeta2 is a frequent event in lung cancers.
  • Aberrant methylation of this gene seems to be a useful predictor of long-term outcome for adenocarcinoma of the lung.
  • [MeSH-major] Adenocarcinoma / genetics. Gene Expression Regulation, Neoplastic. Interleukin-12 / genetics. Lung Neoplasms / genetics
  • [MeSH-minor] Carcinoma, Non-Small-Cell Lung / genetics. DNA Methylation. Gene Silencing. Humans. Prognosis. Proportional Hazards Models. Reverse Transcriptase Polymerase Chain Reaction. Statistics, Nonparametric. Tumor Cells, Cultured

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  • (PMID = 17602269.001).
  • [ISSN] 1068-9265
  • [Journal-full-title] Annals of surgical oncology
  • [ISO-abbreviation] Ann. Surg. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 187348-17-0 / Interleukin-12
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58. Li X, Zhang Q, Lu B, Qiu X, Luo Y, Zhang W, Xu S: [Expression of DLL4 and VEGF in Lung Adenocarcinoma and their Relationship with Angiogenesis in Tumor.]. Zhongguo Fei Ai Za Zhi; 2009 Feb 20;12(2):117-21

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Expression of DLL4 and VEGF in Lung Adenocarcinoma and their Relationship with Angiogenesis in Tumor.].
  • This experiment investigates the expression of Notch ligand DLL4 and VEGF in lung adenocarcinoma and their relationship with angiogenesis in tumor.
  • METHODS: Immunohistochemical method was used to detect DLL4, VEGF and CD34 protein expression in 80 cases of lung adenocarcinoma (including bronchioloalveolar carcinoma and common lung adenocarcinoma) paraffin section tissues.
  • RESULTS: The expression of DLL4 and VEGF was closely related to tumor diameter, clinical stage, histological grade and lymph node metastasis, the VEGF expression rate in DLL4 positive expression cases was significantly more than the DLL4 negative cases, the correlation between microvascular density and DLL4, VEGF co-expression was more significant, the expression of DLL4 in common lung adenocarcinoma was significantly higher than that in bronchioloalveolar carcinoma.
  • CONCLUSIONS: The prognosis of lung adenocarcinoma is significant correlated with the angiogenesis, high expression of DLL4 is closely related to the metastasis and the prognosis.

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  • (PMID = 20716403.001).
  • [ISSN] 1999-6187
  • [Journal-full-title] Zhongguo fei ai za zhi = Chinese journal of lung cancer
  • [ISO-abbreviation] Zhongguo Fei Ai Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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59. Wang C, Yang R, Yue D, Zhang Z: Expression of FAK and PTEN in bronchioloalveolar carcinoma and lung adenocarcinoma. Lung; 2009 Mar-Apr;187(2):104-9
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  • [Title] Expression of FAK and PTEN in bronchioloalveolar carcinoma and lung adenocarcinoma.
  • Bronchioloalveolar carcinoma (BAC) is classified as a subset of lung adenocarcinoma but has a distinct clinical presentation, tumor biology, response to therapy, and prognosis compared with other subtypes of lung adenocarcinoma.
  • This study was designed to investigate the clinicopathological differences between BAC and adenocarcinoma and the expression of focal adhesion kinase (FAK) and phosphatase and tensin homologue (PTEN) and their clinical significance in BAC and adenocarcinoma.
  • A retrospective analysis was performed on 77 patients with BAC and 172 patients with pure adenocarcinoma seen during the period from January 1998 to December 2000.
  • Clinicopathological characteristics and survival outcome were reviewed and compared between patients with BAC and adenocarcinoma.
  • Lymph node status, clinical symptoms, CT appearance and expression of FAK were different between BAC and adenocarcinoma.
  • The overall survival of BAC was better than that of adenocarcinoma.
  • In patients with FAK(-), the overall survival was not different between BAC and adenocarcinoma.
  • In patients with adenocarcinoma, the overall survival was better for FAK(-) compared with FAK(+).
  • Expression of PTEN had a prognostic significance in patients with BAC and adenocarcinoma.
  • BAC and adenocarcinoma have different clinicopathological presentations.
  • Expression of FAK has some effect on such differences and affects survival of lung adenocarcinoma.
  • Expression of PTEN can predict outcome of resected lung adenocarcinoma and BAC.
  • [MeSH-major] Adenocarcinoma / enzymology. Adenocarcinoma, Bronchiolo-Alveolar / enzymology. Biomarkers, Tumor / analysis. Focal Adhesion Kinase 1 / analysis. Lung Neoplasms / enzymology. PTEN Phosphohydrolase / analysis

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  • [CommentIn] Lung. 2009 May-Jun;187(3):207-8 [19408043.001]
  • (PMID = 19242756.001).
  • [ISSN] 1432-1750
  • [Journal-full-title] Lung
  • [ISO-abbreviation] Lung
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 2.7.10.2 / Focal Adhesion Kinase 1; EC 2.7.10.2 / PTK2 protein, human; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase
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60. Asahina H, Yamazaki K, Kinoshita I, Yokouchi H, Dosaka-Akita H, Nishimura M: Non-responsiveness to gefitinib in a patient with lung adenocarcinoma having rare EGFR mutations S768I and V769L. Lung Cancer; 2006 Dec;54(3):419-22
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  • [Title] Non-responsiveness to gefitinib in a patient with lung adenocarcinoma having rare EGFR mutations S768I and V769L.
  • Mutations in the tyrosine kinase (TK) domain of the epidermal growth factor receptor (EGFR) are associated with clinical responsiveness to EGFR-tyrosine kinase inhibitors (EGFR-TKIs) in patients with non-small cell lung cancers (NSCLCs).
  • Here, we report the first case of adenocarcinoma of the lung in which the patient had rare mutations S768I and V769L and was treated with gefitinib.
  • [MeSH-major] Adenocarcinoma / genetics. Drug Resistance, Neoplasm / genetics. Lung Neoplasms / genetics. Quinazolines / therapeutic use. Receptor, Epidermal Growth Factor / genetics

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  • (PMID = 17045698.001).
  • [ISSN] 0169-5002
  • [Journal-full-title] Lung cancer (Amsterdam, Netherlands)
  • [ISO-abbreviation] Lung Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Quinazolines; 04Y7590D77 / Isoleucine; 452VLY9402 / Serine; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; GMW67QNF9C / Leucine; HG18B9YRS7 / Valine; S65743JHBS / gefitinib
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61. Okamoto J, Onda M, Hirata T, Miyamoto S, Akaishi J, Mikami I, Hirai K, Haraguchi S, Koizumi K, Shimizu K: Dissimilarity in gene expression profiles of lung adenocarcinoma in Japanese men and women. Gend Med; 2006 Sep;3(3):223-35
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  • [Title] Dissimilarity in gene expression profiles of lung adenocarcinoma in Japanese men and women.
  • BACKGROUND: Although clinical differences in lung cancer between men and women have been noted, few studies have examined the sex dissimilarity using gene expression analysis.
  • OBJECTIVE: The purpose of this study was to determine the different molecular carcinogenic mechanisms involved in lung cancers in Japanese men and women.
  • METHODS: Patients who received surgery for stage I lung adenocarcinoma were included.
  • RESULTS: In a microarray analysis of tissue from 13 men and 6 women, 12 genes were under-expressed and 24 genes were overexpressed in lung adenocarcinoma in women compared with men.
  • Genes related to cell cycle were present in underexpressed genes, and genes related to apoptosis, ubiquitination, and metabolism were observed in overexpressed genes.
  • CONCLUSION: Thirty-six genes that characterize lung adenocarcinoma by sex were selected.
  • This information may contribute to the development of novel diagnostic techniques and treatment modalities that consider sex differences in lung adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / genetics. Biomarkers, Tumor / genetics. Gene Expression Regulation, Neoplastic. Lung Neoplasms / genetics. RNA, Neoplasm / genetics

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  • (PMID = 17081955.001).
  • [ISSN] 1550-8579
  • [Journal-full-title] Gender medicine
  • [ISO-abbreviation] Gend Med
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / RNA, Neoplasm
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62. Jiang SS, Fang WT, Hou YH, Huang SF, Yen BL, Chang JL, Li SM, Liu HP, Liu YL, Huang CT, Li YW, Jang TH, Chan SH, Yang SJ, Hsiung CA, Wu CW, Wang LH, Chang IS: Upregulation of SOX9 in lung adenocarcinoma and its involvement in the regulation of cell growth and tumorigenicity. Clin Cancer Res; 2010 Sep 1;16(17):4363-73
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  • [Title] Upregulation of SOX9 in lung adenocarcinoma and its involvement in the regulation of cell growth and tumorigenicity.
  • PURPOSE: SOX9 is an important transcription factor required for development and has been implicated in several types of cancer.
  • However, SOX9 has never been linked to lung cancer to date.
  • Here, we show that SOX9 expression is upregulated in lung adenocarcinoma and show how it is associated with cancer cell growth.
  • EXPERIMENTAL DESIGN: Data mining with five microarray data sets containing 490 clinical samples, quantitative reverse transcription-PCR validation assay in 57 independent samples, and immunohistochemistry assay with tissue microarrays containing 170 lung tissue cores were used to profile SOX9 mRNA and protein expression.
  • Short interference RNA suppression of SOX9 in cell lines was used to scrutinize functional role(s) of SOX9 and associated molecular mechanisms.
  • RESULTS: SOX9 mRNA and protein were consistently overexpressed in the majority of lung adenocarcinoma.
  • Knockdown of SOX9 in lung adenocarcinoma cell lines resulted in marked decrease of adhesive and anchorage-independent growth in concordance with the upregulation of p21 (CDKN1A) and downregulation of CDK4.
  • In agreement with higher SOX9 expression level in lung adenocarcinoma, the p21 mRNA level was significantly lower in tumors than that in normal tissues, whereas the opposite was true for CDK4, supporting the notion that SOX9 negatively and positively regulated p21 and CDK4, respectively.
  • CONCLUSIONS: Our data suggest that SOX9 is a new hallmark of lung adenocarcinoma, in which SOX9 might contribute to gain of tumor growth potential, possibly acting through affecting the expression of cell cycle regulators p21 and CDK4.
  • [MeSH-major] Adenocarcinoma / genetics. Cell Proliferation. Lung Neoplasms / genetics. SOX9 Transcription Factor / genetics
  • [MeSH-minor] Animals. Blotting, Western. Cell Line, Tumor. Cyclin-Dependent Kinase 4 / genetics. Cyclin-Dependent Kinase 4 / metabolism. Cyclin-Dependent Kinase Inhibitor p21 / genetics. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. Down-Regulation. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. Liver Neoplasms, Experimental / genetics. Liver Neoplasms, Experimental / metabolism. Liver Neoplasms, Experimental / pathology. Mice. Mice, SCID. Oligonucleotide Array Sequence Analysis. RNA Interference. Reverse Transcriptase Polymerase Chain Reaction. Transplantation, Heterologous. Tumor Burden. Up-Regulation

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  • (PMID = 20651055.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CDKN1A protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / SOX9 Transcription Factor; 0 / SOX9 protein, human; EC 2.7.11.22 / Cyclin-Dependent Kinase 4
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63. Ohtaki Y, Ishii G, Nagai K, Ashimine S, Kuwata T, Hishida T, Nishimura M, Yoshida J, Takeyoshi I, Ochiai A: Stromal macrophage expressing CD204 is associated with tumor aggressiveness in lung adenocarcinoma. J Thorac Oncol; 2010 Oct;5(10):1507-15
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  • [Title] Stromal macrophage expressing CD204 is associated with tumor aggressiveness in lung adenocarcinoma.
  • BACKGROUND: Tumor tissue is composed of variable numbers of cancer cells and stromal cells, and tumor-associated macrophages are recruited into cancer-induced stroma and produce a specific microenvironment.
  • METHODS: To investigate whether CD204-positive macrophages reflect tumor aggressiveness in adenocarcinoma of the lung, we investigated the relationships between the numbers of CD204-positive stromal macrophages and both clinicopathological features and outcome in 170 consecutive resected cases.
  • We evaluated associations between the levels of expression of the cytokines IL-6, IL-10, IL-12a, IL-12b, M-colony-stimulating factor, IFN-gamma-., and monocyte chemoattractant protein-1 in cancer tissue and the numbers of CD204-positive macrophages.
  • CONCLUSION: These findings demonstrated that CD204-positive macrophages clearly reflect the tumor-promoting phenotype of tumor-associated macrophages in lung adenocarcinoma.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Lung Neoplasms / metabolism. Macrophages / metabolism. Scavenger Receptors, Class A / metabolism. Stromal Cells / metabolism
  • [MeSH-minor] Adenocarcinoma / metabolism. Adenocarcinoma / secondary. Adult. Aged. Aged, 80 and over. Cell Differentiation. Cytokines / metabolism. Female. Humans. Immunoenzyme Techniques. Lymphatic Metastasis. Male. Middle Aged. Prognosis. Retrospective Studies

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  • (PMID = 20802348.001).
  • [ISSN] 1556-1380
  • [Journal-full-title] Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer
  • [ISO-abbreviation] J Thorac Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cytokines; 0 / MSR1 protein, human; 0 / Scavenger Receptors, Class A; Adenocarcinoma of lung
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64. Nakao M, Ishii G, Nagai K, Kawase A, Kenmotsu H, Kon-No H, Hishida T, Nishimura M, Yoshida J, Ochiai A: Prognostic significance of carbonic anhydrase IX expression by cancer-associated fibroblasts in lung adenocarcinoma. Cancer; 2009 Jun 15;115(12):2732-43
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  • [Title] Prognostic significance of carbonic anhydrase IX expression by cancer-associated fibroblasts in lung adenocarcinoma.
  • BACKGROUND: Cancer tissue is comprised of cancer cells and several types of stromal cells, including cancer-associated fibroblasts (CAFs).
  • Carbonic anhydrase (CA) IX has been used as an endogenous hypoxia marker, and although its expression by cancer cells has been reported to be associated with a poor outcome in a board range of tumors, to the authors' knowledge, the biologic significance of its expression by CAFs remains unclear.
  • METHODS: The authors investigated CA IX expression by CAFs and cancer cells immunohistochemically in 158 consecutive resected cases of lung adenocarcinoma.
  • RESULTS: CA IX was expressed by CAFs in 39 (24.7%) of the 158 cases and by cancer cells in 40 (25.3%) cases.
  • A univariate analysis and the log-rank test demonstrated a significant association between CA IX expression by CAFs (P = .006 and P = .0052, respectively) and by cancer cells (P = .020 and P = .0179, respectively) with lower survival rate.
  • A multivariate analysis of these 2 factors indicated a statistically significant association between CA IX expression by CAFs and a lower survival rate (hazards ratio [HR], 1.797; P = .032), but not between expression by cancer cells and lower survival rate (HR, 1.561; P = .102).
  • CONCLUSIONS: The findings of the current study indicate that CA IX expression by CAFs was a better predictor of outcome than CA IX expression by cancer cells and provides new insights into the biologic significance of CAFs in the hypoxic microenvironment of the lung adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / metabolism. Antigens, Neoplasm / metabolism. Carbonic Anhydrases / metabolism. Fibroblasts / metabolism. Lung Neoplasms / metabolism

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  • [Copyright] (c) 2009 American Cancer Society.
  • (PMID = 19365853.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; EC 4.2.1.1 / CA9 protein, human; EC 4.2.1.1 / Carbonic Anhydrases
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65. Lin DM, Ma Y, Zheng S, Liu XY, Zou SM, Wei WQ: Prognostic value of bronchioloalveolar carcinoma component in lung adenocarcinoma. Histol Histopathol; 2006 06;21(6):627-32
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  • [Title] Prognostic value of bronchioloalveolar carcinoma component in lung adenocarcinoma.
  • BAC is a common pattern in conventional lung adenocarcinoma.
  • As a result, it was difficult to evaluate the prognosis on this type of lung adenocarcinoma.
  • Though the 1999 WHO classification of BAC provides a useful framework, it does not provide detailed enough information to predict prognosis in lung adenocarcinomas with BAC feature.
  • The aim of this study was to address the prognostic value of bronchioloalveolar carcinoma (BAC) component in lung adenocarcinoma.
  • Ninety-one consecutive surgically treated patients with adenocarcinoma exhibiting various degrees of BAC features and complete follow-up records were retrospectively studied.
  • In lung adenocarcinoma, the BAC component may prove to be useful to predict the outcome of the patients, and the percentage of BAC pattern and pathological stage appear to be two independent prognostic factors.
  • [MeSH-major] Adenocarcinoma, Bronchiolo-Alveolar / diagnosis. Adenocarcinoma, Bronchiolo-Alveolar / pathology. Lung Neoplasms / diagnosis. Lung Neoplasms / pathology
  • [MeSH-minor] Adult. Age Factors. Aged. Cell Proliferation. Female. Histocytochemistry. Humans. Male. Middle Aged. Multivariate Analysis. Neoplasm Staging. Outcome Assessment (Health Care). Prognosis. Retrospective Studies. Sex Factors. Smoking. Survival Rate. World Health Organization

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  • (PMID = 16528673.001).
  • [ISSN] 1699-5848
  • [Journal-full-title] Histology and histopathology
  • [ISO-abbreviation] Histol. Histopathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Spain
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66. Yuan Y, Wang F, Liu XH, Gong DJ, Cheng HZ, Huang SD: Angiogenin is involved in lung adenocarcinoma cell proliferation and angiogenesis. Lung Cancer; 2009 Oct;66(1):28-36
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  • [Title] Angiogenin is involved in lung adenocarcinoma cell proliferation and angiogenesis.
  • It was found in the present study that 67 out of 100 lung adenocarcinomas exhibited angiogenin nuclear expression, and this nuclear expression correlated with vascular and pleural invasion as well as positive lymph node metastasis.
  • ELISA, real-time qPCR and immunocytochemical staining demonstrated that adenoviral-vector based siRNA decreased angiogenin mRNA level and protein secretion, and inhibited angiogenin nuclear expression in A549 cells, resulting in marked inhibition on ribosomal RNA transcription, in vitro cell proliferation, soft agar colony formation, and xenograft tumor proliferation and angiogenesis.
  • Based on these data, we concluded that angiogenin nuclear expression played a dual role in the growth of lung adenocarcinoma with respect to cancer cell proliferation and angiogenesis.
  • [MeSH-major] Adenocarcinoma / blood supply. Adenocarcinoma / metabolism. Angiogenesis Inducing Agents / metabolism. Lung Neoplasms / blood supply. Lung Neoplasms / metabolism. Neovascularization, Pathologic / metabolism. Ribonuclease, Pancreatic / metabolism
  • [MeSH-minor] Aged. Cell Line, Tumor. Cell Proliferation. Disease Progression. Female. Humans. Male. Middle Aged. RNA Interference. RNA, Messenger / metabolism. Ribosomes / metabolism

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  • (PMID = 19423182.001).
  • [ISSN] 1872-8332
  • [Journal-full-title] Lung cancer (Amsterdam, Netherlands)
  • [ISO-abbreviation] Lung Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Angiogenesis Inducing Agents; 0 / RNA, Messenger; EC 3.1.27.- / angiogenin; EC 3.1.27.5 / Ribonuclease, Pancreatic
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67. Wang R, Geng J, Wang JH, Chu XY, Geng HC, Chen LB: Overexpression of eukaryotic initiation factor 4E (eIF4E) and its clinical significance in lung adenocarcinoma. Lung Cancer; 2009 Nov;66(2):237-44
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  • [Title] Overexpression of eukaryotic initiation factor 4E (eIF4E) and its clinical significance in lung adenocarcinoma.
  • However, the clinical significance of eIF4E expression in lung adenocarcinoma (AdC) remains unclear.
  • The aim of this study was to explore the expression of eIF4E gene in lung adenocarcinoma cell lines and tissues, and to investigate its relationship with clinical characteristics and prognosis of patients with lung adenocarcinoma in combination with p53 status.
  • METHODS: Semi-quantitative RT-PCR and Western blotting assays were performed to detect the expression of eIF4E mRNA and protein in normal human lung epithelial cell line, immortalized lung epithelial cell line and lung adenocarcinoma cell lines.
  • Additionally, the expression of eIF4E gene was also detected in 32 cases of lung adenocarcinoma tissues, tumor adjacent tissues and tumor surrounding normal tissues by the same methods.
  • Moreover, expression of eIF4E and the status of p53 in specimens from 76 patients with lung adenocarcinoma were examined by immunohistochemical staining.
  • Correlations between eIF4E expression and clinicopathological features, and the effect of eIF4E on prognosis of patients with lung adenocarcinoma were evaluated by statistical analysis.
  • RESULTS: The levels of eIF4E mRNA and protein expression were higher in lung adenocarcinoma cell lines and in telomerase-immortalized lung epithelial cell line than in the normal lung epithelial cell line.
  • Moreover, the higher levels of eIF4E expression were correlated with poorer differentiation (P=0.012), higher pathological stage (P<0.0001) and clinical stage (P=0.002), a higher incidence of hematogenous metastasis (P=0.007) and cancer-related death (P=0.036).
  • CONCLUSION: High eIF4E expression was correlated with poorer overall survival in lung adenocarcinoma patients. eIF4E might be a better clinical marker predicting the prognosis for lung adenocarcinoma patients in combination with p53 status.
  • [MeSH-major] Adenocarcinoma / diagnosis. Biomarkers, Tumor / metabolism. Eukaryotic Initiation Factor-4E / metabolism. Lung Neoplasms / diagnosis
  • [MeSH-minor] Cell Line, Tumor. Female. Gene Expression. Genetic Predisposition to Disease. Humans. Male. Middle Aged. RNA, Messenger / metabolism

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  • (PMID = 19261348.001).
  • [ISSN] 1872-8332
  • [Journal-full-title] Lung cancer (Amsterdam, Netherlands)
  • [ISO-abbreviation] Lung Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Eukaryotic Initiation Factor-4E; 0 / RNA, Messenger
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68. Kim Y, Kim HS, Cui ZY, Lee HS, Ahn JS, Park CK, Park K, Ahn MJ: Clinicopathological implications of EpCAM expression in adenocarcinoma of the lung. Anticancer Res; 2009 May;29(5):1817-22
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  • [Title] Clinicopathological implications of EpCAM expression in adenocarcinoma of the lung.
  • BACKGROUND: The frequency of epithelial cell adhesion molecule (EpCAM) expression was investigated in non-small cell lung cancer (NSCLC) cells and human tissues, and its clinicopathological significance in adenocarcinoma of the lung was evaluated.
  • EpCAM protein expression was evaluated in 234 adenocarcinoma tissues using immunohistochemistry.
  • EpCAM overexpression was detected in 120/234 (51.3%) surgically resected adenocarcinoma tissues.
  • EpCAM overexpression occurred significantly more frequently in adenocarcinoma than in bronchioloalveolar carcinoma (p=0.02).
  • CONCLUSION: These findings suggest EpCAM plays a role in the carcinogenesis of adenocarcinoma of the lung and might provide a promising molecule for targeted therapy in NSCLC.
  • [MeSH-major] Adenocarcinoma / metabolism. Antigens, Neoplasm / metabolism. Cell Adhesion Molecules / metabolism. Lung Neoplasms / metabolism
  • [MeSH-minor] Base Sequence. Cell Line, Tumor. DNA Primers. Flow Cytometry. Humans. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 19443410.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Cell Adhesion Molecules; 0 / DNA Primers; 0 / EPCAM protein, human
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69. Maekawa S, Iwasaki A, Shirakusa T, Kawakami T, Yanagisawa J, Tanaka T, Shibaguchi H, Kinugasa T, Kuroki M, Kuroki M: Association between the expression of chemokine receptors CCR7 and CXCR3, and lymph node metastatic potential in lung adenocarcinoma. Oncol Rep; 2008 Jun;19(6):1461-8
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  • [Title] Association between the expression of chemokine receptors CCR7 and CXCR3, and lymph node metastatic potential in lung adenocarcinoma.
  • Chemokines and their receptors are essential for leukocyte trafficking, and are also involved in cancer metastasis to specific organs.
  • Although the migration of tumor cells into the lymph nodes is an important aspect of cancer, the processes involved are poorly understood.
  • Chemokine receptors CCR7 and CXCR3 have been shown to play an important role in tumor cell migration and lymph node metastasis.
  • Therefore, the assessment of chemokine receptor expression on lung adenocarcinomas may improve the prediction of the spread of this carcinoma to the lymph nodes.
  • In this study, we examined the expression and function of these two chemokine receptors (CCR7 and CXCR3) in lung adenocarcinoma.
  • By using flow cytometry, they were detected in all of the lung adenocarcinoma cell lines examined.
  • In clinical lung adenocarcinoma samples, we found the expression of CCR7 and CXCR3 in 65 and 90% cases, respectively, most of which had lymph node metastasis.
  • These results suggest that the activation of CCR7 and CXCR3 with their ligands preferentially stimulates lung adenocarcinoma metastasis to the draining lymph nodes.
  • [MeSH-major] Adenocarcinoma / metabolism. Lung Neoplasms / metabolism. Lymph Nodes / metabolism. Receptors, CCR7 / metabolism. Receptors, CXCR3 / metabolism

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  • (PMID = 18497951.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / CCR7 protein, human; 0 / CXCR3 protein, human; 0 / Chemokine CCL21; 0 / Receptors, CCR7; 0 / Receptors, CXCR3
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70. Zhang X, Han B, Huang J, Zheng B, Geng Q, Aziz F, Dong Q: Prognostic significance of OCT4 expression in adenocarcinoma of the lung. Jpn J Clin Oncol; 2010 Oct;40(10):961-6
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  • [Title] Prognostic significance of OCT4 expression in adenocarcinoma of the lung.
  • OBJECTIVE: The purpose of this study was to detect the presence of cancer stem-like cells with bronchioalveolar stem cells (BASCs) properties and investigate the clinicopathological role of expression of OCT4 as well as the correlation with clinical outcomes in adenocarcinoma of the lung.
  • METHODS: Specimens of 112 cases of Stage IB-IIIA lung adenocarcinoma after radical surgery were collected from June 1999 to June 2002.
  • The putative cancer stem cells in tumor sections were visualized immunofluorescently by using the antibodies against three bronchioalveolar stem cells markers: surfactant protein C (SPC), Clara cell secretary protein (CCSP) and Octamer-4 (OCT4).
  • Cancer stem-like cells with bronchioalveolar stem cell properties in human lung adenocarcinoma were subdivided into two phenotypes: OCT4(+)BASC (SPC(+)CCSP(+)OCT4(+)) and OCT4(-)BASC (SPC(+)CCSP(+)OCT4(-)).
  • RESULTS: Cancer cells with CCSP(+)SPC(+)BASC phenotype were detected in 107 cases, 80 cases with OCT4(+)BASC phenotype (SPC(+)CCSP(+)OCT4(+)) and 27 cases with SPC(+)CCSP(+)OCT4(-).
  • The pattern of survival curves shows the expected trend of decreasing survival with increasing stage at diagnosis (P = 0.015) and with OCT4(+)BASC expression (P = 0.019).
  • CONCLUSIONS: The cancer cells with bronchioalveolar stem cells phenotype are detectable in adenocarcinoma of the lung and the expression of self-renewal regulatory gene OCT4 in these cells indicated the worse clinical outcomes.
  • [MeSH-major] Adenocarcinoma / metabolism. Lung Neoplasms / metabolism. Neoplastic Stem Cells / metabolism. Octamer Transcription Factor-3 / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cisplatin. Female. Fluorescent Antibody Technique / statistics & numerical data. Humans. Kaplan-Meier Estimate. Male. Middle Aged. Multivariate Analysis. Prognosis. Proportional Hazards Models. Pulmonary Surfactant-Associated Protein C / metabolism. Uteroglobin / metabolism. Vinblastine / administration & dosage. Vinblastine / analogs & derivatives. Young Adult

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  • (PMID = 20462980.001).
  • [ISSN] 1465-3621
  • [Journal-full-title] Japanese journal of clinical oncology
  • [ISO-abbreviation] Jpn. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Octamer Transcription Factor-3; 0 / POU5F1 protein, human; 0 / Pulmonary Surfactant-Associated Protein C; 0 / SCGB1A1 protein, human; 5V9KLZ54CY / Vinblastine; 9060-09-7 / Uteroglobin; Q20Q21Q62J / Cisplatin; Q6C979R91Y / vinorelbine
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71. Job B, Bernheim A, Beau-Faller M, Camilleri-Broët S, Girard P, Hofman P, Mazières J, Toujani S, Lacroix L, Laffaire J, Dessen P, Fouret P, LG Investigators: Genomic aberrations in lung adenocarcinoma in never smokers. PLoS One; 2010;5(12):e15145
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  • [Title] Genomic aberrations in lung adenocarcinoma in never smokers.
  • BACKGROUND: Lung cancer in never smokers would rank as the seventh most common cause of cancer death worldwide.
  • METHODS AND FINDINGS: We performed high-resolution array comparative genomic hybridization analysis of lung adenocarcinoma in sixty never smokers and identified fourteen new minimal common regions (MCR) of gain or loss, of which five contained a single gene (MOCS2, NSUN3, KHDRBS2, SNTG1 and ST18).
  • NSD1 and FUS are oncogenes hitherto not known to be associated with lung cancer.
  • Other cancer genes present in aberrations included ARNT, BCL9, CDK4, CDKN2B, EGFR, ERBB2, MDM2, MDM4, MET, MYC and KRAS.
  • CONCLUSIONS: The present study has uncovered new aberrations containing cancer genes.
  • Multiple genetic pathways defined by gains of MYC, deletions of RB1 and WRN or gains on 7p and 7q are involved in lung adenocarcinoma in never smokers.
  • [MeSH-major] Adenocarcinoma / genetics. Chromosome Aberrations. Genomics. Lung Neoplasms / genetics

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  • (PMID = 21151896.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
  • [Other-IDs] NLM/ PMC2997777
  • [Investigator] Dartevelle P; Dulmet E; Leroy-Ladurie F; de Montpreville V; Monnet I; Bernard A; Piard F; Alifano M; Camilleri-Broët S; Régnard JF; Hofman P; Hofman V; Mouroux J; Trédaniel J; Beau-Faller M; Massard G; Neuville A; Antoine M; Cadranel J; Brouchet L; Mazières J; Rouquette I; Saint-Blancard P; Vaylet F; Berhneim A; Dessen P; Dufour F; Dorvault N; Fouret P; Job B; Lacroix L; Lazar V; Richon C; Roux V; Saulnier P; Taranchon E; Toujani S; Valent A; Girard P; Gossot D; Validire P; Laffaire J
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72. Iwakawa R, Kohno T, Anami Y, Noguchi M, Suzuki K, Matsuno Y, Mishima K, Nishikawa R, Tashiro F, Yokota J: Association of p16 homozygous deletions with clinicopathologic characteristics and EGFR/KRAS/p53 mutations in lung adenocarcinoma. Clin Cancer Res; 2008 Jun 15;14(12):3746-53
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  • [Title] Association of p16 homozygous deletions with clinicopathologic characteristics and EGFR/KRAS/p53 mutations in lung adenocarcinoma.
  • PURPOSE: The p16 gene is frequently inactivated in lung adenocarcinoma.
  • In particular, homozygous deletions (HD) have been frequently detected in cell lines; however, their frequency and specificity is not well-established in primary tumors.
  • The purpose of this study was to elucidate the prevalence and the timing for the occurrence of p16 HDs in lung adenocarcinoma progression in vivo.
  • EXPERIMENTAL DESIGN: Multiple ligation-dependent probe amplification was used for the detection of p16 HDs in 28 primary small-sized lung adenocarcinomas and 22 metastatic lung adenocarcinomas to the brain.
  • Cancer cells were isolated from primary adenocarcinoma specimens by laser capture microdissection.
  • HDs were detected with similar frequencies (17-29%) among adenocarcinomas with epidermal growth factor receptor (EGFR) mutations, with KRAS mutations, and without EGFR/KRAS mutations, and with similar frequencies (22-28%) between adenocarcinomas with and without p53 mutations.
  • CONCLUSIONS: p16 HDs occur early in the development of lung adenocarcinomas and with similar frequencies among EGFR type, KRAS type, and non-EGFR/KRAS type lung adenocarcinomas.
  • Tobacco carcinogens would not be a major factor inducing p16 HDs in lung adenocarcinoma progression.
  • [MeSH-major] Adenocarcinoma / genetics. Gene Deletion. Genes, erbB-1. Genes, p16. Genes, p53. Genes, ras. Lung Neoplasms / genetics

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  • (PMID = 18559592.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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73. Yoshida Y, Kokubu A, Suzuki K, Kuribayashi H, Tsuta K, Matsuno Y, Kusumoto M, Kanai Y, Asamura H, Hirohashi S, Shibata T: Molecular markers and changes of computed tomography appearance in lung adenocarcinoma with ground-glass opacity. Jpn J Clin Oncol; 2007 Dec;37(12):907-12
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  • [Title] Molecular markers and changes of computed tomography appearance in lung adenocarcinoma with ground-glass opacity.
  • BACKGROUND: High-resolution computed tomography (HRCT) of lung adenocarcinoma at early stage shows pure ground-glass opacity (GGO) and most cases of pure GGO remain stable during follow-up.
  • Identification of the molecular mechanisms that are associated with the natural history of lung adenocarcinoma should provide useful information.
  • METHODS: Twenty-three lung adenocarcinomas that were followed-up for more than 6 months pre-operatively by HRCT were included in this study.
  • CONCLUSIONS: EGFR mutations were frequently found in lung adenocarcinoma with GGO on HRCT in this study.
  • [MeSH-major] Adenocarcinoma / pathology. Biomarkers, Tumor / metabolism. Lung Neoplasms / pathology. Mutation. Receptor, Epidermal Growth Factor / genetics. Tomography, Spiral Computed. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 18089646.001).
  • [ISSN] 1465-3621
  • [Journal-full-title] Japanese journal of clinical oncology
  • [ISO-abbreviation] Jpn. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Tumor Suppressor Protein p53; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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74. Stoll LM, Johnson MW, Gabrielson E, Askin F, Clark DP, Li QK: The utility of napsin-A in the identification of primary and metastatic lung adenocarcinoma among cytologically poorly differentiated carcinomas. Cancer Cytopathol; 2010 Dec 25;118(6):441-9
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  • [Title] The utility of napsin-A in the identification of primary and metastatic lung adenocarcinoma among cytologically poorly differentiated carcinomas.
  • BACKGROUND: New developments in the treatment of lung cancer have necessitated the further histologic and cytologic subtyping of nonsmall cell lung carcinomas.
  • Thyroid transcription factor-1 (TTF-1) long has served as the predominant marker for demonstrating lung origin.
  • However, it is also expressed in a variety of other tumors, particularly neuroendocrine neoplasms and, to a much lesser degree, squamous cell carcinoma of the lung.
  • Napsin-A, which is expressed in lung tissue, is a relatively new marker for lung adenocarcinoma.
  • In this study, the authors examined the utility of napsin-A compared with TTF-1 in cytologic specimens of primary and metastatic, poorly differentiated lung adenocarcinomas.
  • METHODS: The archives of the Department of Pathology at The Johns Hopkins Hospital were searched for cytologic cases of poorly differentiated lung adenocarcinoma that were histologically confirmed.
  • In total, 75 patients (cases) along with 95 controls were included, each of whom had adequate cell block material for TTF-1 and napsin-A staining.
  • Tissue microarrays of lung adenocarcinoma also were examined.
  • Napsin-A was not detected in small cell carcinomas or in other carcinomas of nonlung origin except for renal cell carcinoma.
  • CONCLUSIONS: Although TTF-1 had a higher sensitivity, napsin-A was useful as a surrogate marker when encountering a poorly differentiated lung adenocarcinoma or an unknown primary tumor, particularly in cytologic specimens and difficult cases.
  • [MeSH-major] Adenocarcinoma / diagnosis. Aspartic Acid Endopeptidases / analysis. Biomarkers, Tumor / analysis. Lung Neoplasms / diagnosis. Nuclear Proteins / analysis. Transcription Factors / analysis
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cell Differentiation. Female. Humans. Immunohistochemistry. Male. Middle Aged. Neoplasm Metastasis. Sensitivity and Specificity

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  • [Copyright] Copyright © 2010 American Cancer Society.
  • (PMID = 20830690.001).
  • [ISSN] 1934-662X
  • [Journal-full-title] Cancer cytopathology
  • [ISO-abbreviation] Cancer Cytopathol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Nuclear Proteins; 0 / Transcription Factors; 0 / thyroid nuclear factor 1; EC 3.4.23.- / Aspartic Acid Endopeptidases; EC 3.4.23.- / NAPSA protein, human
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75. Park JA, Park HJ, Lee JS, Ha JO, Lee GK, Park BK, Ghim TT: Adenocarcinoma of lung in never smoked children. Lung Cancer; 2008 Aug;61(2):266-9
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  • [Title] Adenocarcinoma of lung in never smoked children.
  • Except in developed countries, the incidence of lung cancer notably in women and non-smokers is rising in most parts of the world.
  • Here, we report two children diagnosed with pulmonary adenocarcinoma at a very early age.
  • Furthermore, one had preceding pulmonary tuberculosis.
  • In the literature, the possible association of pulmonary tuberculosis and adenocarcinoma of lung especially in non-smokers has long been debated.
  • The two children, by far the youngest with EGFR negative adenocarcinoma of lung, form the basis of this report.
  • [MeSH-major] Adenocarcinoma / complications. Lung Neoplasms / complications. Tuberculosis, Pulmonary / complications
  • [MeSH-minor] Adolescent. Cough. Diagnosis, Differential. Fatal Outcome. Female. Humans. Male. Neoplasm Metastasis. Radiography, Thoracic. Risk Factors. Smoking. Weight Loss

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  • (PMID = 18394748.001).
  • [ISSN] 0169-5002
  • [Journal-full-title] Lung cancer (Amsterdam, Netherlands)
  • [ISO-abbreviation] Lung Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Ireland
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76. Wislez M, Antoine M, Rabbe N, Gounant V, Poulot V, Lavolé A, Fleury-Feith J, Cadranel J: Neutrophils promote aerogenous spread of lung adenocarcinoma with bronchioloalveolar carcinoma features. Clin Cancer Res; 2007 Jun 15;13(12):3518-27
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  • [Title] Neutrophils promote aerogenous spread of lung adenocarcinoma with bronchioloalveolar carcinoma features.
  • PURPOSE: Adenocarcinoma with bronchioloalveolar carcinoma (BAC) features is a subtype of non-small cell lung cancers characterized by an intense inflammatory reaction composed of macrophages and neutrophils and by a distinct natural history with intrapulmonary spread leading to death due to respiratory failure.
  • We hypothesized that neutrophils could promote aerogenous spread of lung adenocarcinoma with BAC features.
  • EXPERIMENTAL DESIGN: We examined the effect of neutrophils on A549 cell line detachment in vitro and we quantified desquamation of tumor cells on tumor tissue (n = 25) and on matched bronchioloalveolar lavage (n = 17) in vivo in a series of patients with adenocarcinoma with BAC features.
  • RESULTS: Neutrophils induced A549 detachment mediated by signals through cell-to-cell contact.
  • The shedding cell percentage was a significant factor in shorter survival (P = 0.034, univariate Cox analysis).
  • It is a significant factor of shorter survival and may be an important event in adenocarcinoma progression.
  • [MeSH-major] Adenocarcinoma / pathology. Adenocarcinoma, Bronchiolo-Alveolar / pathology. Lung Neoplasms / pathology. Neoplasm Invasiveness / pathology. Neutrophils / metabolism
  • [MeSH-minor] Cell Adhesion / physiology. Cell Communication / physiology. Cell Line, Tumor. Cell Proliferation. Coculture Techniques. Female. Flow Cytometry. Humans. Immunohistochemistry. Male

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  • (PMID = 17575214.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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77. Ding L, Getz G, Wheeler DA, Mardis ER, McLellan MD, Cibulskis K, Sougnez C, Greulich H, Muzny DM, Morgan MB, Fulton L, Fulton RS, Zhang Q, Wendl MC, Lawrence MS, Larson DE, Chen K, Dooling DJ, Sabo A, Hawes AC, Shen H, Jhangiani SN, Lewis LR, Hall O, Zhu Y, Mathew T, Ren Y, Yao J, Scherer SE, Clerc K, Metcalf GA, Ng B, Milosavljevic A, Gonzalez-Garay ML, Osborne JR, Meyer R, Shi X, Tang Y, Koboldt DC, Lin L, Abbott R, Miner TL, Pohl C, Fewell G, Haipek C, Schmidt H, Dunford-Shore BH, Kraja A, Crosby SD, Sawyer CS, Vickery T, Sander S, Robinson J, Winckler W, Baldwin J, Chirieac LR, Dutt A, Fennell T, Hanna M, Johnson BE, Onofrio RC, Thomas RK, Tonon G, Weir BA, Zhao X, Ziaugra L, Zody MC, Giordano T, Orringer MB, Roth JA, Spitz MR, Wistuba II, Ozenberger B, Good PJ, Chang AC, Beer DG, Watson MA, Ladanyi M, Broderick S, Yoshizawa A, Travis WD, Pao W, Province MA, Weinstock GM, Varmus HE, Gabriel SB, Lander ES, Gibbs RA, Meyerson M, Wilson RK: Somatic mutations affect key pathways in lung adenocarcinoma. Nature; 2008 Oct 23;455(7216):1069-75
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  • [Title] Somatic mutations affect key pathways in lung adenocarcinoma.
  • Determining the genetic basis of cancer requires comprehensive analyses of large collections of histopathologically well-classified primary tumours.
  • Here we report the results of a collaborative study to discover somatic mutations in 188 human lung adenocarcinomas.
  • DNA sequencing of 623 genes with known or potential relationships to cancer revealed more than 1,000 somatic mutations across the samples.
  • These data provide evidence of somatic mutations in primary lung adenocarcinoma for several tumour suppressor genes involved in other cancers--including NF1, APC, RB1 and ATM--and for sequence changes in PTPRD as well as the frequently deleted gene LRP1B.
  • Our findings shed further light on several important signalling pathways involved in lung adenocarcinoma, and suggest new molecular targets for treatment.


78. Lim WT, Chuah KL, Leong SS, Tan EH, Toh CK: Assessment of human papillomavirus and Epstein-Barr virus in lung adenocarcinoma. Oncol Rep; 2009 Apr;21(4):971-5
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  • [Title] Assessment of human papillomavirus and Epstein-Barr virus in lung adenocarcinoma.
  • The association of human papillomavirus (HPV) and Epstein-Barr virus (EBV) infection with non-small cell lung cancer is controversial.
  • HPV and EBV prevalence in a uniform population of lung adenocarcinoma was investigated, hypothesizing that there would be differences seen between smokers and non-smokers and between sexes.
  • Patients involved in this study were selected from a single institution database of lung cancer.
  • In total 497 patients with adenocarcinoma were identified and 110 patients had sufficient tissue for analysis with an in situ hybridization method that probed for high-risk and low-risk HPV and EBV.
  • There were similar number of smokers and non-smokers.
  • It is unlikely that HPV or EBV is an important etiological agent in adenocarcinoma of the lung, even among the never-smokers.
  • [MeSH-major] Adenocarcinoma / virology. Herpesvirus 4, Human / isolation & purification. Lung Neoplasms / virology. Papillomaviridae / isolation & purification

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  • (PMID = 19287995.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Differentiation, T-Lymphocyte; 0 / CD69 antigen; 0 / DNA, Viral; 0 / Lectins, C-Type; 0 / RNA, Viral
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79. Weiler-Bisig D, Ettlin G, Brink T, Arnold W, Glatz-Krieger K, Fischer A: Henoch-schonlein purpura associated with esophagus carcinoma and adenocarcinoma of the lung. Clin Nephrol; 2005 Apr;63(4):302-4
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  • [Title] Henoch-schonlein purpura associated with esophagus carcinoma and adenocarcinoma of the lung.
  • Henoch-Schönlein purpura (HSP) is known to exist in association with a variety of malignant diseases including squamous and small cell lung cancer and hematological malignancies.
  • We report the first cases of HSP associated with carcinoma of the esophagus and adenocarcinoma of the lung, respectively.
  • [MeSH-major] Adenocarcinoma / complications. Carcinoma, Squamous Cell / complications. Esophageal Neoplasms / complications. Lung Neoplasms / complications. Purpura, Schoenlein-Henoch / etiology

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  • (PMID = 15847258.001).
  • [ISSN] 0301-0430
  • [Journal-full-title] Clinical nephrology
  • [ISO-abbreviation] Clin. Nephrol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Immunoglobulin A
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80. Spinola M, Leoni V, Pignatiello C, Conti B, Ravagnani F, Pastorino U, Dragani TA: Functional FGFR4 Gly388Arg polymorphism predicts prognosis in lung adenocarcinoma patients. J Clin Oncol; 2005 Oct 10;23(29):7307-11
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  • [Title] Functional FGFR4 Gly388Arg polymorphism predicts prognosis in lung adenocarcinoma patients.
  • The Gly388Arg polymorphism in the FGFR4 gene was reported to modulate cancer cell migration in vitro and to be associated with breast, colon, and prostate cancer prognostic parameters.
  • The purpose of this study was to investigate the involvement of the FGFR4 polymorphism in lung tumorigenesis.
  • PATIENTS AND METHODS: A case-control study was performed including 274 patients with histologically confirmed lung adenocarcinoma and 401 healthy control subjects from general population. mRNA expression analysis was carried out in healthy lung of cancer patients.
  • RESULTS: Patients with the Arg/Arg or Gly/Arg genotype compared to those with a Gly/Gly genotype had an earlier age at cancer onset (median age, 60.2 v 63.4 years), higher proportion of poor clinical stage disease (hazard ratio [HR], 2.3; 95% CI, 1.4 to 3.9; P = .002), of nodal involvement (HR, 1.9; 95% CI, 1.1 to 3.2; P = .027), or of short-term survivors (HR, 1.6; 95% CI, 1.1 to 2.3; P = .008).
  • In healthy lungs, FGFR4 did not show allele-specific expression and mRNA levels were not associated with genotype.
  • CONCLUSION: This study suggests that FGFR4 Gly388Arg polymorphism may predict prognosis in lung adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / genetics. Lung Neoplasms / genetics. Receptor, Fibroblast Growth Factor, Type 4 / genetics

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  • (PMID = 16061909.001).
  • [ISSN] 0732-183X
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.1 / FGFR4 protein, human; EC 2.7.10.1 / Receptor, Fibroblast Growth Factor, Type 4
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81. Riely GJ, Kris MG, Rosenbaum D, Marks J, Li A, Chitale DA, Nafa K, Riedel ER, Hsu M, Pao W, Miller VA, Ladanyi M: Frequency and distinctive spectrum of KRAS mutations in never smokers with lung adenocarcinoma. Clin Cancer Res; 2008 Sep 15;14(18):5731-4
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  • [Title] Frequency and distinctive spectrum of KRAS mutations in never smokers with lung adenocarcinoma.
  • PURPOSE: KRAS mutations are found in approximately 25% of lung adenocarcinomas in Western countries and, as a group, have been strongly associated with cigarette smoking.
  • EXPERIMENTAL DESIGN: We determined the frequency and type of KRAS codon 12 and 13 mutations and characterized their association with cigarette smoking history in patients with lung adenocarcinomas.
  • RESULTS: KRAS mutational analysis was done on 482 lung adenocarcinomas, 81 (17%) of which were obtained from patients who had never smoked cigarettes.
  • CONCLUSIONS: Based on our data, KRAS mutations are not rare among never smokers with lung adenocarcinoma and such patients have a distinct KRAS mutation profile.
  • The etiologic and biological heterogeneity of KRAS mutant lung adenocarcinomas is worthy of further study.

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  • (PMID = 18794081.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA129243-01; United States / NCI NIH HHS / CA / P01 CA129243; United States / NCI NIH HHS / CA / NIH P01 CA129243; United States / NCI NIH HHS / CA / P01 CA129243-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / KRAS protein, human; 0 / Proto-Oncogene Proteins; EC 3.6.5.2 / ras Proteins
  • [Other-IDs] NLM/ NIHMS141466; NLM/ PMC2754127
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82. Yasuda H, Nakayama K, Watanabe M, Suzuki S, Fuji H, Okinaga S, Kanda A, Zayasu K, Sasaki T, Asada M, Suzuki T, Yoshida M, Yamanda S, Inoue D, Kaneta T, Kondo T, Takai Y, Sasaki H, Yanagihara K, Yamaya M: Nitroglycerin treatment may enhance chemosensitivity to docetaxel and carboplatin in patients with lung adenocarcinoma. Clin Cancer Res; 2006 Nov 15;12(22):6748-57
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  • [Title] Nitroglycerin treatment may enhance chemosensitivity to docetaxel and carboplatin in patients with lung adenocarcinoma.
  • PURPOSE: Nitroglycerin may improve the response to chemotherapy in advanced non-small cell lung cancer.
  • The effects and mechanisms of nitroglycerin on the enhancement of chemosensitivity to docetaxel and carboplatin regimen (DCb) in patients with lung adenocarcinoma have not been reported.
  • EXPERIMENTAL DESIGN: Seventeen patients with operable lung adenocarcinoma and stable angina pectoris were selected to investigate the effects of nitroglycerin on immunoreactivity for hypoxia-inducible factor 1alpha (HIF-1alpha), vascular endothelial growth factor (VEGF), P-glycoprotein (P-gp), the production of which is regulated by HIF-1, and p53 proteins in their resected tumor by semiquantitative immunohistochemical analyses.
  • Furthermore, to study the relationship between changes in plasma VEGF levels by nitroglycerin treatment and response to DCb, 29 patients with advanced lung adenocarcinoma were treated with nitroglycerin for 3 days before chemotherapy using DCb.
  • The magnitude of decrease in plasma VEGF levels after treatment with nitroglycerin was significantly associated with response to DCb in patients with advanced lung adenocarcinoma.
  • CONCLUSIONS: Nitroglycerin treatment may improve response to DCb in patients with lung adenocarcinoma, partly through decreasing VEGF and P-gp production via reduction of HIF-1alpha.
  • [MeSH-major] Adenocarcinoma / drug therapy. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carboplatin / administration & dosage. Lung Neoplasms / drug therapy. Nitroglycerin / pharmacology. Taxoids / administration & dosage

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  • (PMID = 17121895.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Controlled Clinical Trial; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / P-Glycoprotein; 0 / Taxoids; 0 / Tumor Suppressor Protein p53; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; 15H5577CQD / docetaxel; BG3F62OND5 / Carboplatin; G59M7S0WS3 / Nitroglycerin
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83. Larsen JE, Pavey SJ, Passmore LH, Bowman RV, Hayward NK, Fong KM: Gene expression signature predicts recurrence in lung adenocarcinoma. Clin Cancer Res; 2007 May 15;13(10):2946-54
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  • [Title] Gene expression signature predicts recurrence in lung adenocarcinoma.
  • PURPOSE: Improving outcomes for early-stage lung cancer is a major research focus at present because a significant proportion of stage I patients develop recurrent disease within 5 years of curative-intent lung resection.
  • EXPERIMENTAL DESIGN: To identify a gene signature predictive of recurrence in primary lung adenocarcinoma, we analyzed gene expression profiles in a training set of 48 node-negative tumors (stage I-II), comparing tumors from cases who remained disease-free for a minimum of 36 months with those from cases whose disease recurred within 18 months of complete resection.
  • RESULTS: Cox proportional hazards modeling with leave-one-out cross-validation identified a 54-gene signature capable of predicting risk of recurrence in two independent validation cohorts of 55 adenocarcinomas [log-rank P=0.039; hazard ratio (HR), 2.2; 95% confidence interval (95% CI), 1.1-4.7] and 40 adenocarcinomas (log-rank P=0.044; HR, 3.3; 95% CI, 1.4-7.9).
  • In a subset of earliest stage adenocarcinomas, generally expected to have good outcome, the signature predicted samples with significantly poorer survival.
  • CONCLUSIONS: We describe a 54-gene signature that predicts the risk of recurrent disease independently of tumor stage and which therefore has potential to refine clinical prognosis for patients undergoing resection for primary adenocarcinoma of the lung.
  • [MeSH-major] Adenocarcinoma / pathology. Biomarkers, Tumor / genetics. Gene Expression Profiling. Lung Neoplasms / pathology. Neoplasm Recurrence, Local / diagnosis

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  • (PMID = 17504995.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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84. MacDermed DM, Khodarev NN, Pitroda SP, Edwards DC, Pelizzari CA, Huang L, Kufe DW, Weichselbaum RR: MUC1-associated proliferation signature predicts outcomes in lung adenocarcinoma patients. BMC Med Genomics; 2010 May 06;3:16
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  • [Title] MUC1-associated proliferation signature predicts outcomes in lung adenocarcinoma patients.
  • BACKGROUND: MUC1 protein is highly expressed in lung cancer.
  • We characterized MUC1-CD-induced transcriptional changes and examined their significance in lung cancer patients.
  • METHODS: Using DNA microarrays, we identified 254 genes that were differentially expressed in cell lines transformed by MUC1-CD compared to control cell lines.
  • We then examined expression of these genes in 441 lung adenocarcinomas from a publicly available database.
  • The MAPS was further validated for prognostic significance in 84 lung adenocarcinoma patients from an independent database.
  • RESULTS: MAPS genes were found to be associated with proliferation and cell cycle regulation and included CCNB1, CDC2, CDC20, CDKN3, MAD2L1, PRC1 and RRM2.
  • MAPS expressors (MAPS+) had inferior survival compared to non-expressors (MAPS-).
  • CONCLUSIONS: The MAPS signature, comprised of MUC1-CD-dependent genes involved in the control of cell cycle and proliferation, is associated with poor outcomes in patients with adenocarcinoma of the lung.
  • These data provide potential new prognostic biomarkers and treatment targets for lung adenocarcinoma.

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  • (PMID = 20459602.001).
  • [ISSN] 1755-8794
  • [Journal-full-title] BMC medical genomics
  • [ISO-abbreviation] BMC Med Genomics
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA097098; United States / NCI NIH HHS / CA / (R01) CA111423; United States / NCI NIH HHS / CA / (R01) CA97098
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Mucin-1
  • [Other-IDs] NLM/ PMC2876055
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85. McDonald JM, Pelloski CE, Ledoux A, Sun M, Raso G, Komaki R, Wistuba II, Bekele BN, Aldape K: Elevated phospho-S6 expression is associated with metastasis in adenocarcinoma of the lung. Clin Cancer Res; 2008 Dec 1;14(23):7832-7
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  • [Title] Elevated phospho-S6 expression is associated with metastasis in adenocarcinoma of the lung.
  • PURPOSE: The primary objective of this study was to determine whether markers of differentiation and activation of the Akt pathway are associated with metastasis in adenocarcinoma of the lung.
  • EXPERIMENTAL DESIGN: Paired primary and metastatic tumor samples were obtained from 41 patients who had undergone resection of both primary lung adenocarcinoma and brain metastatic lesions.
  • Biomarkers that showed relative discordance in expression between the matched pairs were then assessed in a cohort of 77 primary lung adenocarcinomas.
  • Validation was done in an independent cohort of 82 primary lung adenocarcinomas.
  • The expression of E-cadherin, p-S6, and TTF-1 was evaluated in 77 primary lung adenocarcinomas, in which high p-S6 expression was associated with shorter time to metastasis.

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  • (PMID = 19047111.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA070907-040007; United States / NCI NIH HHS / CA / P50 CA070907; United States / NCI NIH HHS / CA / P50 CA070907-040007; United States / NCI NIH HHS / CA / P50CA70907
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cadherins; 0 / DNA-Binding Proteins; 0 / Ribosomal Proteins; 0 / TTF1 protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
  • [Other-IDs] NLM/ NIHMS83486; NLM/ PMC2614348
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86. Li M, Yin Z, Cui Z, He Q, Zhou B: [Association of genetic polymorphism in DNA repair gene XRCC1 with risk of lung adenocarcinoma in nonsmoking women]. Zhongguo Fei Ai Za Zhi; 2005 Oct 20;8(5):431-4

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Association of genetic polymorphism in DNA repair gene XRCC1 with risk of lung adenocarcinoma in nonsmoking women].
  • The aim of this study is to assess the relationship between XRCC1 polymorphism and susceptibility to lung adenocarcinoma in nonsmoking female via a hospital-based case-control study.
  • METHODS: Cases were 126 female patients with lung adenocarcinoma from January 2002 to October 2004 in China Medical University Hospital and Liaoning Tumor Hospital.
  • Controls were selected from patients with other pulmonary diseases in the hospitals at the same time.
  • The frequencies of Arg/Arg, Arg/Gln and Gln/Gln in lung adenocarcinoma group (32.54%, 42.86%, 24.60%) were significantly different from those in controls (54.76%, 40.48%, 4.76%) (P < 0.05).
  • The individual carrying Gln/Gln genotype was at a significantly increased risk of lung adenocarcinoma compared with those with Arg/Arg genotype (OR=8.695, 95%CI 3.343-22.614, adjusted for age and oil smoke exposure).
  • Furthermore, the OR of lung adenocarcinoma for the variant XRCC1 399Gln allele combined with exposure to oil smoke was 5.21 (95%CI 1.85-14.70, P < 0.001).
  • CONCLUSIONS: The results indicate that the Arg399Gln polymorphism in XRCC1 is associated with the risk of lung adenocarcinoma in nonsmoking women.

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  • (PMID = 21205527.001).
  • [ISSN] 1009-3419
  • [Journal-full-title] Zhongguo fei ai za zhi = Chinese journal of lung cancer
  • [ISO-abbreviation] Zhongguo Fei Ai Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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87. Tsuta K, Ishii G, Kim E, Shiono S, Nishiwaki Y, Endoh Y, Kodama T, Nagai K, Nagai K: Primary lung adenocarcinoma with massive lymphocyte infiltration. Am J Clin Pathol; 2005 Apr;123(4):547-52
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  • [Title] Primary lung adenocarcinoma with massive lymphocyte infiltration.
  • We report 6 cases of adenocarcinoma with massive lymphocyte infiltration.
  • This adenocarcinoma is found in 0.7% of surgically resected primary lung adenocarcinomas.
  • Histologically, the tumors revealed an acinar and glandular structure, and the cancer epithelium was destroyed by infiltrating lymphocytes.
  • The lung parenchyma was destroyed by the severe inflammatory cell infiltration without dense fibrosis.
  • This type of adenocarcinoma occurs in old age, and good outcome and distinctive histologic features were observed.
  • We refer to it as primary lung adenocarcinoma with massive lymphocyte infiltration.
  • [MeSH-major] Adenocarcinoma / pathology. Lung Neoplasms / pathology. Lymphocyte Subsets / pathology. Lymphocytes, Tumor-Infiltrating / pathology

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  • (PMID = 15743751.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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88. Li R, Wang H, Bekele BN, Yin Z, Caraway NP, Katz RL, Stass SA, Jiang F: Identification of putative oncogenes in lung adenocarcinoma by a comprehensive functional genomic approach. Oncogene; 2006 Apr 27;25(18):2628-35
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  • [Title] Identification of putative oncogenes in lung adenocarcinoma by a comprehensive functional genomic approach.
  • We used a functional genomic approach that integrated simultaneous genomic and transcript microarray, proteomics, and tissue microarray analyses to directly identify putative oncogenes in lung adenocarcinoma.
  • We first identified 183 genes with increases in both genomic copy number and transcript in six lung adenocarcinoma cell lines.
  • Next, we used two-dimensional polyacrylamide gel electrophoresis and mass spectrometry to identify 42 proteins that were overexpressed in the cancer cells relative to normal cells.
  • Specific inhibition of EEF1A2 and KCIP-1 expression with siRNA in the four cell lines tested suppressed proliferation and induced apoptosis.
  • Parallel fluorescence in situ hybridization and immunohistochemical analyses of EEF1A2 and KCIP-1 in tissue microarrays from patients with lung adenocarcinoma showed that gene amplification was associated with high protein expression for both genes and that protein overexpression was related to tumor grade, disease stage, Ki-67 expression, and a shorter survival of patients.
  • The amplification of EEF1A2 and KCIP-1 and the presence of overexpressed protein in tumor samples strongly suggest that these genes could be oncogenes and hence potential targets for diagnosis and therapy in lung adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / genetics. Gene Expression Regulation, Neoplastic. Lung Neoplasms / genetics. Neoplasm Proteins / genetics. Oncogenes / genetics

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  • (PMID = 16369491.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA113707-01; United States / NCI NIH HHS / CA / P50 CA70907
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / EEF1A2 protein, human; 0 / Neoplasm Proteins; 0 / Peptide Elongation Factor 1; 0 / RNA, Small Interfering
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89. Bischiniotis TS, Lafaras CT, Platogiannis DN, Moldovan L, Barbetakis NG, Katseas GP: Intrapericardial cisplatin administration after pericardiocentesis in patients with lung adenocarcinoma and malignant cardiac tamponade. Hellenic J Cardiol; 2005 Sep-Oct;46(5):324-9
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  • [Title] Intrapericardial cisplatin administration after pericardiocentesis in patients with lung adenocarcinoma and malignant cardiac tamponade.
  • INTRODUCTION: Patients with lung adenocarcinoma often suffer from metastatic pericardial effusion that may eventually cause cardiac tamponade.
  • We evaluated the safety and effectiveness of the intrapericardial infusion of cisplatin, a substance with antineoplastic and sclerosing properties, after pericardiocentesis in patients with lung adenocarcinoma and malignant cardiac tamponade.
  • METHODS: Twenty-five patients (19 males and 6 females, median age 55 years) with lung adenocarcinoma confirmed by cytological examination and cardiac tamponade were studied.
  • Paroxysmal atrial fibrillation was detected in three patients (12%) and non-sustained ventricular tachycardia in two (8%).
  • CONCLUSIONS: Intrapericardial administration of cisplatin is safe and effective in preventing the reaccumulation of malignant pericardial effusion in the majority of patients with lung adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / surgery. Cisplatin / administration & dosage. Lung Neoplasms / surgery. Pericardiocentesis. Pleural Effusion, Malignant / drug therapy

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  • (PMID = 16295940.001).
  • [ISSN] 1109-9666
  • [Journal-full-title] Hellenic journal of cardiology : HJC = Hellēnikē kardiologikē epitheōrēsē
  • [ISO-abbreviation] Hellenic J Cardiol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents; Q20Q21Q62J / Cisplatin
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90. Liu S, Chen B, Li Y, Zhao W, Wu J: [Effect of sCD40L combined with vinorelbine on lung adenocarcinoma cell A549]. Zhongguo Fei Ai Za Zhi; 2010 Jul;13(7):686-90
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  • [Title] [Effect of sCD40L combined with vinorelbine on lung adenocarcinoma cell A549].
  • BACKGROUND AND OBJECTIVE: The results of published data on the effect of CD40 signal related to cancer cell sensitivity to chemotherapy are inconclusive.
  • The aim of this study is to investigate the effect of soluble CD40 ligand (sCD40L) combined with vinorelbine on lung adenocarcinoma cell line A549.
  • METHODS: Lung adenocarcinoma A549 cells were chosen as target cells and CD40 signal was stimulated by sCD40L.
  • MTT assay and flow cytometry were used to determine the changes of cell proliferation, cell cycle and apoptosis of A549 cells treated by vinorelbine after CD40 was stimulated.
  • RESULTS: After CD40 stimulation, an increase of inhibition on CD40 positive cell line A549 proliferation was confirmed when vinorelbine was added (P < 0.05).
  • However, no significant changes were shown in apoptosis and cell cycle (P > 0.05).
  • CONCLUSIONS: Stimulation of CD40 can increase lung adenocarcinoma cell line A549 sensitivity to vinorelbine, which may be through a non-apoptosis, Caspase independent mechanism, and not associated with the inhibition of cell cycle.
  • [MeSH-major] Antigens, CD40 / metabolism. CD40 Ligand / pharmacology. Cell Proliferation / drug effects. Vinblastine / analogs & derivatives
  • [MeSH-minor] Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Antineoplastic Agents, Phytogenic / pharmacology. Apoptosis / drug effects. Caspase 3 / metabolism. Cell Cycle / drug effects. Cell Line, Tumor. Cell Survival / drug effects. Drug Synergism. Flow Cytometry. Humans. Lung Neoplasms / metabolism. Lung Neoplasms / pathology. Solubility

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  • (PMID = 20673484.001).
  • [ISSN] 1999-6187
  • [Journal-full-title] Zhongguo fei ai za zhi = Chinese journal of lung cancer
  • [ISO-abbreviation] Zhongguo Fei Ai Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD40; 0 / Antineoplastic Agents, Phytogenic; 147205-72-9 / CD40 Ligand; 5V9KLZ54CY / Vinblastine; EC 3.4.22.- / Caspase 3; Q6C979R91Y / vinorelbine
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91. Wu SG, Chang YL, Hsu YC, Wu JY, Yang CH, Yu CJ, Tsai MF, Shih JY, Yang PC: Good response to gefitinib in lung adenocarcinoma of complex epidermal growth factor receptor (EGFR) mutations with the classical mutation pattern. Oncologist; 2008 Dec;13(12):1276-84
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  • [Title] Good response to gefitinib in lung adenocarcinoma of complex epidermal growth factor receptor (EGFR) mutations with the classical mutation pattern.
  • BACKGROUND: Epidermal growth factor receptor (EGFR) mutations are usually detected in lung adenocarcinoma and are associated with a response to EGFR tyrosine kinase inhibitors (TKIs).
  • This study aimed to investigate the clinical characteristics and response to gefitinib in lung adenocarcinoma patients with complex EGFR mutations.
  • MATERIALS AND METHODS: Three hundred thirty-nine specimens of lung adenocarcinoma from patients treated with gefitinib were collected for EGFR sequencing.
  • EGFR TKIs may be the choice of treatment for this type of lung adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / drug therapy. Antineoplastic Agents / therapeutic use. Lung Neoplasms / drug therapy. Mutation. Protein Kinase Inhibitors / therapeutic use. Quinazolines / therapeutic use. Receptor, Epidermal Growth Factor / genetics

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  • (PMID = 19060236.001).
  • [ISSN] 1549-490X
  • [Journal-full-title] The oncologist
  • [ISO-abbreviation] Oncologist
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Protein Kinase Inhibitors; 0 / Quinazolines; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; S65743JHBS / gefitinib
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92. Amatya VJ, Takeshima Y, Kohno H, Kushitani K, Yamada T, Morimoto C, Inai K: Caveolin-1 is a novel immunohistochemical marker to differentiate epithelioid mesothelioma from lung adenocarcinoma. Histopathology; 2009 Jul;55(1):10-9
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  • [Title] Caveolin-1 is a novel immunohistochemical marker to differentiate epithelioid mesothelioma from lung adenocarcinoma.
  • There is difficulty in the accurate diagnosis of mesothelioma and its differentiation from lung adenocarcinoma.
  • Therefore, the use of a immunohistochemical panel that includes both positive and negative mesothelial markers has become a general rule for its accurate diagnosis.
  • METHODS AND RESULTS: An immunohistochemical study of 80 cases of epithelioid mesothelioma and 80 cases of lung adenocarcinoma was performed for the analysis of the expression of Cav-1 and other markers.
  • In contrast, only six cases (7.5%) of lung adenocarcinoma showed focal Cav-1 expression in the cytoplasm of the tumour cells.
  • The sensitivity and specificity of Cav-1 expression for the differentiation of epithelioid mesothelioma from lung adenocarcinoma were 100 and 92.5%, respectively.
  • CONCLUSIONS: Cav-1 is a novel immunohistochemical marker for the differentiation of epithelioid mesothelioma from lung adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / diagnosis. Biomarkers, Tumor / metabolism. Caveolin 1 / metabolism. Lung Neoplasms / diagnosis. Mesothelioma / diagnosis
  • [MeSH-minor] Diagnosis, Differential. Epithelioid Cells / pathology. Humans. Sensitivity and Specificity

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  • (PMID = 19614762.001).
  • [ISSN] 1365-2559
  • [Journal-full-title] Histopathology
  • [ISO-abbreviation] Histopathology
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Caveolin 1
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93. Hsiung CA, Lan Q, Hong YC, Chen CJ, Hosgood HD, Chang IS, Chatterjee N, Brennan P, Wu C, Zheng W, Chang GC, Wu T, Park JY, Hsiao CF, Kim YH, Shen H, Seow A, Yeager M, Tsai YH, Kim YT, Chow WH, Guo H, Wang WC, Sung SW, Hu Z, Chen KY, Kim JH, Chen Y, Huang L, Lee KM, Lo YL, Gao YT, Kim JH, Liu L, Huang MS, Jung TH, Jin G, Caporaso N, Yu D, Kim CH, Su WC, Shu XO, Xu P, Kim IS, Chen YM, Ma H, Shen M, Cha SI, Tan W, Chang CH, Sung JS, Zhang M, Yang TY, Park KH, Yuenger J, Wang CL, Ryu JS, Xiang Y, Deng Q, Hutchinson A, Kim JS, Cai Q, Landi MT, Yu CJ, Park JY, Tucker M, Hung JY, Lin CC, Perng RP, Boffetta P, Chen CY, Chen KC, Yang SY, Hu CY, Chang CK, Fraumeni JF Jr, Chanock S, Yang PC, Rothman N, Lin D: The 5p15.33 locus is associated with risk of lung adenocarcinoma in never-smoking females in Asia. PLoS Genet; 2010 Aug 05;6(8)
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  • [Title] The 5p15.33 locus is associated with risk of lung adenocarcinoma in never-smoking females in Asia.
  • Genome-wide association studies of lung cancer reported in populations of European background have identified three regions on chromosomes 5p15.33, 6p21.33, and 15q25 that have achieved genome-wide significance with p-values of 10(-7) or lower.
  • These studies have been performed primarily in cigarette smokers, raising the possibility that the observed associations could be related to tobacco use, lung carcinogenesis, or both.
  • Since most women in Asia do not smoke, we conducted a genome-wide association study of lung adenocarcinoma in never-smoking females (584 cases, 585 controls) among Han Chinese in Taiwan and found that the most significant association was for rs2736100 on chromosome 5p15.33 (p = 1.30 x 10(-11)).
  • This finding was independently replicated in seven studies from East Asia totaling 1,164 lung adenocarcinomas and 1,736 controls (p = 5.38 x 10(-11)).
  • In summary, our results show that genetic variation in the CLPTM1L-TERT locus of chromosome 5p15.33 is directly associated with the risk of lung cancer, most notably adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / genetics. Chromosomes, Human, Pair 5 / genetics. Genetic Predisposition to Disease. Lung Neoplasms / genetics

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  • (PMID = 20700438.001).
  • [ISSN] 1553-7404
  • [Journal-full-title] PLoS genetics
  • [ISO-abbreviation] PLoS Genet.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R37 CA70837; United States / Intramural NIH HHS / / ; United States / NCI NIH HHS / CA / R03 CA133939; United States / NCI NIH HHS / CA / R03 CA133939-01; United States / NCI NIH HHS / CP / N02CP11010
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2916850
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94. Jiang L, Zhang L, Wang Q, Wang S: [Down-regulation of GRP78 Enhances Chemotherapy Sensitivity to VP-16 in Lung Adenocarcinoma.]. Zhongguo Fei Ai Za Zhi; 2009 Nov 20;12(11):1159-63
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  • [Title] [Down-regulation of GRP78 Enhances Chemotherapy Sensitivity to VP-16 in Lung Adenocarcinoma.].
  • To investigate the relationship between the expression of GRP78 and resistance to anti-cancer drug VP-16 in vitro in lung adenocarcinoma SPCA-1 cell line.
  • Cell apoptosis was analyzed by flow cytometry in order to evaluate the therapeutic sensitivity to VP-16.
  • CONCLUSIONS: BAPTA-AM is highly effective in the inhibition of GRP78, down-regulation of GRP78 can significantly increase the sensitivity of adenocacinoma lung cancer to VP-16.
  • All these suggest that inhibition of the expression of GRP78 by chemicals such as BAPTA-AM or anti-sense RNA may be a new therapeutic strategies to lung cancer.

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  • (PMID = 20723363.001).
  • [ISSN] 1999-6187
  • [Journal-full-title] Zhongguo fei ai za zhi = Chinese journal of lung cancer
  • [ISO-abbreviation] Zhongguo Fei Ai Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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95. Kamiya K, Hayashi Y, Douguchi J, Hashiguchi A, Yamada T, Izumi Y, Watanabe M, Kawamura M, Horinouchi H, Shimada N, Kobayashi K, Sakamoto M: Histopathological features and prognostic significance of the micropapillary pattern in lung adenocarcinoma. Mod Pathol; 2008 Aug;21(8):992-1001
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  • [Title] Histopathological features and prognostic significance of the micropapillary pattern in lung adenocarcinoma.
  • We investigated the histopathobiological properties of the micropapillary pattern with immunohistochemistry, serial sections, and electron microscopy in lung adenocarcinoma.
  • The subjects included 383 adenocarcinoma cases, of which 184 (48%) were micropapillary pattern-positive and 199 (52%) were micropapillary pattern-negative.
  • Negative staining for laminin and loss of basement membrane as determined by electron microscopy suggest a loss of cell-matrix contact.
  • [MeSH-major] Adenocarcinoma, Papillary / pathology. Lung Neoplasms / pathology

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  • (PMID = 18516041.001).
  • [ISSN] 1530-0285
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CTNNB1 protein, human; 0 / Cadherins; 0 / Ki-67 Antigen; 0 / Laminin; 0 / beta Catenin
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96. Chen XJ, Xiao W, Qu X, Zhou SY: NS-398 enhances the efficacy of gemcitabine against lung adenocarcinoma through up-regulation of p21WAF1 and p27KIP1 protein. Neoplasma; 2008;55(3):200-4
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  • [Title] NS-398 enhances the efficacy of gemcitabine against lung adenocarcinoma through up-regulation of p21WAF1 and p27KIP1 protein.
  • Gemcitabine is a chemotherapeutic drug widely used in the treatment of non-small cell lung carcinoma, especially in advanced lung adenocarcinoma.
  • However, many patients with advanced lung adenocarcinoma show a resistance to gemcitabine.
  • Overexpression of COX-2 has been found in human non-small cell lung cancer tissues and itA s cell lines.
  • However, It is unknown whether COX-2 inhibitor can augment the efficacy of gemcitabine against lung adenocarcinoma.
  • The cell viability was examined by MTT assay.
  • The cell cycle distribution and apoptotic ratio were tested by flow cytometry.
  • It can be concluded that NS-398 enhances the efficacy of gemcitabine against lung adenocarcinoma and the efficacy is associated with up-regulation of p21WAF1 and p27KIP1protein.
  • [MeSH-major] Adenocarcinoma / drug therapy. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. Cyclin-Dependent Kinase Inhibitor p27 / metabolism. Cyclooxygenase 2 Inhibitors / pharmacology. Deoxycytidine / analogs & derivatives. Lung Neoplasms / drug therapy. Nitrobenzenes / pharmacology. Sulfonamides / pharmacology
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / pharmacology. Apoptosis / drug effects. Cell Line, Tumor. Drug Synergism. Humans. Up-Regulation

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  • (PMID = 18348652.001).
  • [ISSN] 0028-2685
  • [Journal-full-title] Neoplasma
  • [ISO-abbreviation] Neoplasma
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Slovakia
  • [Chemical-registry-number] 0 / CDKN1A protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Cyclooxygenase 2 Inhibitors; 0 / Nitrobenzenes; 0 / Sulfonamides; 0W860991D6 / Deoxycytidine; 123653-11-2 / N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; B76N6SBZ8R / gemcitabine
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97. Ruppert AM, Beau-Faller M, Neuville A, Guerin E, Voegeli AC, Mennecier B, Legrain M, Molard A, Jeung MY, Gaub MP, Oudet P, Quoix E: EGFR-TKI and lung adenocarcinoma with CNS relapse: interest of molecular follow-up. Eur Respir J; 2009 Feb;33(2):436-40
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] EGFR-TKI and lung adenocarcinoma with CNS relapse: interest of molecular follow-up.
  • The epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) erlotinib improves survival of lung cancer as second- or third-line therapy.
  • The present study reports the case of a 27-yr-old nonsmoking male presenting with a metastatic lung adenocarcinoma with EGFR exon 19 deletion, associated with sensitivity to EGFR-TKI.
  • The present report underscores the interest of molecular monitoring in lung cancer.
  • [MeSH-major] Adenocarcinoma / pathology. Adenocarcinoma / therapy. Central Nervous System Neoplasms / secondary. Central Nervous System Neoplasms / therapy. Lung Neoplasms / pathology. Lung Neoplasms / therapy. Receptor, Epidermal Growth Factor / antagonists & inhibitors. Receptor, Epidermal Growth Factor / metabolism

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  • (PMID = 19181917.001).
  • [ISSN] 1399-3003
  • [Journal-full-title] The European respiratory journal
  • [ISO-abbreviation] Eur. Respir. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Quinazolines; DA87705X9K / Erlotinib Hydrochloride; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; S65743JHBS / gefitinib
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98. Hongsachart P, Huang-Liu R, Sinchaikul S, Pan FM, Phutrakul S, Chuang YM, Yu CJ, Chen ST: Glycoproteomic analysis of WGA-bound glycoprotein biomarkers in sera from patients with lung adenocarcinoma. Electrophoresis; 2009 Apr;30(7):1206-20
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Glycoproteomic analysis of WGA-bound glycoprotein biomarkers in sera from patients with lung adenocarcinoma.
  • Differential protein expression profiles in the serum samples from patients with lung adenocarcinoma may be associated with glycosylation during cancer development.
  • In this study, we used various glycoproteomic approaches to investigate the different glycoproteomic profiles of human normal and lung adenocarcinoma serum samples and to investigate putative altered glycoprotein biomarkers.
  • We enriched for glycoproteins in the serum samples using WGA lectin affinity and then performed co-immunoprecipitation with anti-haptoglobin and 2-DE, 2-D difference in-gel electrophoresis and MS analyses.
  • In addition, three up-regulated glycoproteins (adiponectin, cerulolasmin and glycosylphosphatidyl-inositol-80) and two down-regulated glycoproteins (cyclin H and Fyn) that were found to be correlated with lung cancer development were validated by Western blot analysis.
  • We suggest that these altered glycoproteins may be useful as biomarkers for lung cancer development and progression.
  • [MeSH-major] Adenocarcinoma / diagnosis. Glycoproteins / blood. Lung Neoplasms / diagnosis. Proteome / analysis. Proteomics / methods. Wheat Germ Agglutinins / metabolism

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  • (PMID = 19294700.001).
  • [ISSN] 1522-2683
  • [Journal-full-title] Electrophoresis
  • [ISO-abbreviation] Electrophoresis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Validation Studies
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Glycoproteins; 0 / Proteome; 0 / Wheat Germ Agglutinins; I223NX31W9 / Fluorescein-5-isothiocyanate
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99. Wen C, Ying B, Zhang Y, Zhang J, Fan H: [Effect of quercetin on the expression and growth of caspase-3 in lung adenocarcinoma cancer cell line A549.]. Zhongguo Fei Ai Za Zhi; 2008 Apr 20;11(2):194-7

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Effect of quercetin on the expression and growth of caspase-3 in lung adenocarcinoma cancer cell line A549.].
  • BACKGROUND: To study the influence of Quercetin in the expression of caspase-3 in Lung Adenocarcinoma Cancer cell line A549.

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  • (PMID = 20731900.001).
  • [ISSN] 1999-6187
  • [Journal-full-title] Zhongguo fei ai za zhi = Chinese journal of lung cancer
  • [ISO-abbreviation] Zhongguo Fei Ai Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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100. Saito H, Kiuchi R, Demura Y, Yashiki N, Masuda S, Kitagawa K: [Intentional limited resection for lung adenocarcinoma of 2 cm in size or less according to intraoperative frozen section and high-resolution computed tomography]. Kyobu Geka; 2008 Jun;61(6):444-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Intentional limited resection for lung adenocarcinoma of 2 cm in size or less according to intraoperative frozen section and high-resolution computed tomography].
  • One hundred twenty-six cases of resected lung adenocarcinoma of 2 cm in size or less were studied about intra and postoperative Noguchi's classification, high-resolution computed tomography (HRCT) findings and lymph node metastases in cases of lobectomy.
  • Intentional limited resection for lung adenocarcinoma of 2 cm in size or less was recommended for selected patients with tumors of type A of Noguchi's classification diagnosed by intraoperative frozen diagnosis or tumors of intraoperative type B of 0.5 in ground-glass opacity (GGO) diameter ratio or more of HRCT.
  • This GGO diameter ratio of 0.5 is easily available as a criteria of intentional limited resection for lung adenocarcinoma of 2 cm in size or less.
  • [MeSH-major] Adenocarcinoma / diagnosis. Adenocarcinoma / surgery. Frozen Sections. Lung Neoplasms / diagnosis. Lung Neoplasms / surgery. Minimally Invasive Surgical Procedures. Pneumonectomy. Radiographic Image Enhancement. Tomography, X-Ray Computed

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  • (PMID = 18536290.001).
  • [ISSN] 0021-5252
  • [Journal-full-title] Kyobu geka. The Japanese journal of thoracic surgery
  • [ISO-abbreviation] Kyobu Geka
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Japan
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