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[PMID]:24150851
[Au] Autor:Petersen I
[Ad] Endereço:Institut für Pathologie, Universitätsklinikum Jena Deutschland.
[Ti] Título:[The new classification of lung adenocarcinoma].
[Ti] Título:Adenokarzinome der Lunge--die neue Klassifikation..
[So] Source:Zentralbl Chir;138 Suppl 1:S16-24, 2013 Oct.
[Is] ISSN:1438-9592
[Cp] País de publicação:Germany
[La] Idioma:ger
[Ab] Resumo:The new, interdisciplinary IASLC/ATS/ERS classification of lung adenocarcinoma has achieved a considerable impact since its publication in the year 2011. It separates tumours into preinvasive, minimally invasive and invasive subtypes. The preinvasive lesions atypical, adenomatous hyperplasia (AAH) and adenocarcinoma in situ (AIS) together with the minimally invasive adenocarcinoma (MIA), have an excellent prognosis after complete resection with 100 % survival. It enables a reproducible tumour grading by the determination of the predominant histological growth pattern which could be confirmed in several follow-up studies. Thereby the mixed subtype was eliminated which formerly represented about 80 % of all adenocarcinomas. Similarly, the terms bronchioloalveolar adenocarcinoma and bronchioloalveolar tumour growth were eliminated because they represented several distinct entities, specifically the in-situ lesions AAH and ACIS as well as the non-in-situ/invasive tumours like minimally invasive adenocarcinoma, lepidic predominant adenocarcinoma (LPA) and invasive mucinous adenocarcinoma (IMA). Although the classification is based on data from tumour resections it accommodates the fact that most tumours are diagnosed on biopsies and cytological specimens and includes recommendations for an efficient work-up to preserve tissue for molecular testing. Furthermore, the morphological analysis may provide hints for molecular changes including mutations with therapeutic relevance that may enable targeted molecular diagnostics. This review presents essentials facts of the new classification that will be part of the next WHO classification of lung tumors and its follow-up publications.
[Mh] Termos MeSH primário: Adenocarcinoma/classificação
Comportamento Cooperativo
Comunicação Interdisciplinar
Neoplasias Pulmonares/classificação
[Mh] Termos MeSH secundário: Adenocarcinoma/patologia
Adenocarcinoma Bronquíolo-Alveolar/classificação
Adenocarcinoma Bronquíolo-Alveolar/patologia
Adenocarcinoma Mucinoso/classificação
Adenocarcinoma Mucinoso/patologia
Adenomatose Pulmonar/classificação
Adenomatose Pulmonar/patologia
Biópsia
Carcinoma in Situ/classificação
Carcinoma in Situ/patologia
Seres Humanos
Pulmão/patologia
Neoplasias Pulmonares/patologia
Técnicas de Diagnóstico Molecular
Gradação de Tumores
Invasividade Neoplásica
Lesões Pré-Cancerosas/classificação
Lesões Pré-Cancerosas/patologia
Prognóstico
[Pt] Tipo de publicação:ENGLISH ABSTRACT; JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1406
[Cu] Atualização por classe:131023
[Lr] Data última revisão:
131023
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:131024
[St] Status:MEDLINE
[do] DOI:10.1055/s-0033-1350878


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[PMID]:22033683
[Au] Autor:Bubendorf L
[Ad] Endereço:Institut für Pathologie, Universitätsspital Basel, Schönbeinstr. 40, 4031, Basel, Schweiz. lbubendorf@uhbs.ch
[Ti] Título:[Preneoplastic lesions of pulmonary carcinoma].
[Ti] Título:Vorläuferläsionen des Lungenkarzinoms..
[So] Source:Pathologe;32 Suppl 2:218-23, 2011 Nov.
[Is] ISSN:1432-1963
[Cp] País de publicação:Germany
[La] Idioma:ger
[Ab] Resumo:The World Health Organization (WHO) 2004 classification includes 3 categories of pulmonary preneoplastic lesions, including squamous dysplasia and carcinoma in situ (CIS) for squamous cell carcinoma, atypical adenomatous hyperplasia (AAH) for the majority of adenocarcinomas and diffuse idiopathic pulmonary neuroendocrine cell hyperplasia (DIPNECH) for carcinoids. The distinction of the 3 grades of squamous dysplasia and CIS is mainly based on the degree by which the basal cell zone is expanded, the degree of cellular atypia and the level of mitoses. The category AAH consists of a proliferation of atypical epithelial cells with Clara cells or type 2 pneumocyte features. They grow along the alveolar septae in a lepidic fashion, sometimes reaching into the terminal bronchioles. In contrast to the newly described adenocarcinoma in situ (AIS), AAH is smaller (≤ 5 mm), has a lower cell density and a lower degree of cellular atypia. The putative cancer stem cells of peripheral adenocarcinomas reside in the bronchioloalveolar duct junction, while those of central squamous cell carcinomas are located in the basal cell compartment of the bronchi. This review provides an overview of the current knowledge on preneoplastic lesions of the lungs and their clinical impact.
[Mh] Termos MeSH primário: Adenocarcinoma/genética
Adenocarcinoma/patologia
Adenomatose Pulmonar/genética
Adenomatose Pulmonar/patologia
Tumor Carcinoide/genética
Tumor Carcinoide/patologia
Carcinoma de Células Escamosas/genética
Carcinoma de Células Escamosas/patologia
Transformação Celular Neoplásica/genética
Transformação Celular Neoplásica/patologia
Neoplasias Pulmonares/genética
Neoplasias Pulmonares/patologia
Lesões Pré-Cancerosas/genética
Lesões Pré-Cancerosas/patologia
[Mh] Termos MeSH secundário: Proliferação Celular
Seres Humanos
Hiperplasia
Pulmão/patologia
Índice Mitótico
[Pt] Tipo de publicação:ENGLISH ABSTRACT; JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1203
[Cu] Atualização por classe:170928
[Lr] Data última revisão:
170928
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:111029
[St] Status:MEDLINE
[do] DOI:10.1007/s00292-011-1527-y


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[PMID]:21474972
[Au] Autor:Hirooka S; Akashi T; Ando N; Suzuki Y; Ishida N; Kurata M; Takizawa T; Kayamori K; Sakamoto K; Fujiwara N; Kojima M; Eishi Y
[Ad] Endereço:Department of Pathology, Tokyo Medical and Dental University, Japan.
[Ti] Título:Localization of the invadopodia-related proteins actinin-1 and cortactin to matrix-contact-side cytoplasm of cancer cells in surgically resected lung adenocarcinomas.
[So] Source:Pathobiology;78(1):10-23, 2011.
[Is] ISSN:1423-0291
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: Actin-associated proteins at cell-matrix-contact sites form invadopodia in cancer cells and participate in migration, matrix degradation and invasion. We investigated an alteration of subcellular localization of invadopodia-related actin-associated proteins, actinin-1 and cortactin, in lung adenocarcinomas, its clinical significance, and its possible regulatory factors. METHODS: Invadopodia-related proteins, actinin-1 and cortactin, were immunohistochemically examined in 90 cases of lung adenocarcinomas. Expression of invadopodia-associated proteins and their possible regulators in lung adenocarcinomas were examined by real-time RT-PCR, database search, and immunohistochemistry. RESULTS: Actinin-1 and cortactin showed matrix-contact-side localization in adenocarcinoma cells, but rarely in normal bronchiolar epithelial cells, alveolar cells, or precursor lesion atypical adenomatous hyperplasia cells. Immunoelectron-microscopic examination of adenocarcinoma cells revealed actinin-1 localization to matrix-contact-side cytoplasm with cytoplasmic protrusions. Matrix-contact-side localization of actinin-1 and cortactin was correlated with tumor stages, lymph node metastasis, vascular permeation, and loss of basement membrane. The tumor-specific survival rate was worse for the group in which matrix-contact-side localization of cortactin was high than for the low group. mRNA of the Rho guanine exchange factor epithelial cell transforming sequence-2 (Ect2) tended to be overexpressed in lung adenocarcinomas and cytoplasmic expression of Ect2 tended to be correlated with matrix-contact-side localization of actinin-1. CONCLUSION: Matrix-contact-side localization of invadopodia-related proteins in the lung adenocarcinoma cells were correlated with invasion, metastasis, and poor prognosis. Ect2 was a possible regulator of matrix-contact-side localization of invadopodia-related proteins.
[Mh] Termos MeSH primário: Actinina/metabolismo
Adenocarcinoma/metabolismo
Cortactina/metabolismo
Neoplasias Pulmonares/metabolismo
[Mh] Termos MeSH secundário: Adenocarcinoma/genética
Adenocarcinoma/patologia
Adenomatose Pulmonar/genética
Adenomatose Pulmonar/metabolismo
Adenomatose Pulmonar/patologia
Biomarcadores Tumorais/metabolismo
Matriz Extracelular/metabolismo
Matriz Extracelular/patologia
Feminino
Expressão Gênica
Seres Humanos
Neoplasias Pulmonares/genética
Neoplasias Pulmonares/patologia
Masculino
Invasividade Neoplásica
Estadiamento de Neoplasias
Pneumonectomia
Proteínas Proto-Oncogênicas/genética
Proteínas Proto-Oncogênicas/metabolismo
RNA Mensageiro/metabolismo
Taxa de Sobrevida
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (ACTN1 protein, human); 0 (Biomarkers, Tumor); 0 (CTTN protein, human); 0 (Cortactin); 0 (ECT2 protein, human); 0 (Proto-Oncogene Proteins); 0 (RNA, Messenger); 11003-00-2 (Actinin)
[Em] Mês de entrada:1107
[Cu] Atualização por classe:151119
[Lr] Data última revisão:
151119
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:110409
[St] Status:MEDLINE
[do] DOI:10.1159/000322734


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[PMID]:20512074
[Au] Autor:Yoo SB; Chung JH; Lee HJ; Lee CT; Jheon S; Sung SW
[Ad] Endereço:Department of Pathology, Seoul National University College of Medicine, Seoul National University Bundang Hospital, Seongnam, Korea.
[Ti] Título:Epidermal growth factor receptor mutation and p53 overexpression during the multistage progression of small adenocarcinoma of the lung.
[So] Source:J Thorac Oncol;5(7):964-9, 2010 Jul.
[Is] ISSN:1556-1380
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: A progression model of atypical adenomatous hyperplasia (AAH) to bronchioloalveolar carcinoma (BAC) to invasive adenocarcinoma (ADC) has been proposed. However, the genetic alterations of the AAH-BAC-ADC sequence are not clearly established. We examined the mutation of the epidermal growth factor receptor (EGFR) gene and p53 protein overexpression in the AAH, BAC, and small ADC to understand their role in the pulmonary ADC pathogenesis. METHODS: Twenty AAH, 43 BAC (21 Noguchi type A and 22 type B), and 47 small ADC (Noguchi type C) were enrolled in this study. EGFR mutations at exons 18-21 and p53 protein overexpression were examined by polymerase chain reaction-direct sequencing and immunohistochemistry, respectively. RESULTS: Mutations of the EGFR gene were noted in 45 (40.9%) lesions, which included 7 (35.0%) of AAH, 15 (34.9%) of BAC, and 23 (48.9%) of ADC. Twenty-six (23.6%) of the mutations were detected as exon 19 deletion, 18 (16.4%) as exon 21 point mutation, and 1 (0.9%) as exon 18 point mutation. Overexpression of p53 protein was found in 19 (17.2%) lesions, none of AAH, 4 (9.8%) of BAC, and 15 (31.9%) of ADC. Multivariate analysis showed that p53 overexpression was associated with invasive ADC (P = 0.003). CONCLUSIONS: High frequency and similar incidence of EGFR mutation in AAH, BAC, and ADC support that EGFR gene mutation occurs in the early stage of pulmonary ADC development and tumor initiation from the preneoplastic lung parenchyma to neoplastic conditions. On the contrary, p53 overexpression is a late event during tumor development and plays a role in the progression of the peripheral pulmonary ADC.
[Mh] Termos MeSH primário: Neoplasias Pulmonares/genética
Neoplasias Pulmonares/metabolismo
Mutação/genética
Receptor do Fator de Crescimento Epidérmico/genética
Proteína Supressora de Tumor p53/metabolismo
[Mh] Termos MeSH secundário: Adenocarcinoma/genética
Adenocarcinoma/metabolismo
Adenocarcinoma/patologia
Adenocarcinoma Bronquíolo-Alveolar/genética
Adenocarcinoma Bronquíolo-Alveolar/metabolismo
Adenocarcinoma Bronquíolo-Alveolar/patologia
Adenomatose Pulmonar/genética
Adenomatose Pulmonar/metabolismo
Adenomatose Pulmonar/patologia
Adulto
Idoso
Idoso de 80 Anos ou mais
Progressão da Doença
Feminino
Seres Humanos
Técnicas Imunoenzimáticas
Neoplasias Pulmonares/patologia
Masculino
Meia-Idade
Invasividade Neoplásica
Estadiamento de Neoplasias
Reação em Cadeia da Polimerase
Lesões Pré-Cancerosas/genética
Lesões Pré-Cancerosas/metabolismo
Lesões Pré-Cancerosas/patologia
Prognóstico
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (TP53 protein, human); 0 (Tumor Suppressor Protein p53); EC 2.7.10.1 (EGFR protein, human); EC 2.7.10.1 (Receptor, Epidermal Growth Factor)
[Em] Mês de entrada:1010
[Cu] Atualização por classe:100628
[Lr] Data última revisão:
100628
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:100601
[St] Status:MEDLINE
[do] DOI:10.1097/JTO.0b013e3181dd15c0


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[PMID]:18379350
[Au] Autor:Soh J; Toyooka S; Ichihara S; Asano H; Kobayashi N; Suehisa H; Otani H; Yamamoto H; Ichimura K; Kiura K; Gazdar AF; Date H
[Ad] Endereço:Department of Cancer and Thoracic Surgery, Okayama University Graduate School of Medicine and Dentistry, 2-5-1 Shikata-cho, Okayama 700-8558, Japan.
[Ti] Título:Sequential molecular changes during multistage pathogenesis of small peripheral adenocarcinomas of the lung.
[So] Source:J Thorac Oncol;3(4):340-7, 2008 Apr.
[Is] ISSN:1556-1380
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: We investigated EGFR and KRAS alterations among atypical adenomatous hyperplasia and small lung adenocarcinomas with bronchioloalveolar features to understand their role during multistage pathogenesis. METHODS: Sixty lesions measuring 2 cm or less were studied, including 38 noninvasive lesions (4 atypical adenomatous hyperplasias, 19 Noguchi type A and 15 type B) and 22 invasive lesions (type C) based on the World Health Organization classification and Noguchi's criteria. EGFR and KRAS mutations were examined using PCR-based assays. EGFR copy number was evaluated using fluorescence in situ hybridization. RESULTS: EGFR and KRAS mutations were found in 26 (43.3%) and 5 (8.3%) lesions, respectively. Increased EGFR copy number status was identified in 10 lesions (16.7%), both mutant and wild type. EGFR or KRAS mutations were present in 39.5% and 7.9% (respectively) of noninvasive lesions and 50% or 9.1% (respectively) of invasive lesions. EGFR copy number was increased in 7.9% and 31.8% of noninvasive and invasive lesions (P = 0.029). Multivariate analysis revealed that increased EGFR copy number was the only significant factor to associate with invasive lesions (P = 0.035). CONCLUSIONS: EGFR and KRAS mutations occur early during the multistage pathogenesis of peripheral lung adenocarcinomas. By contrast, increased EGFR copy number is a late event during tumor development and plays a role in the progression of lung adenocarcinoma independent of the initiating molecular events.
[Mh] Termos MeSH primário: Adenocarcinoma Bronquíolo-Alveolar/genética
Neoplasias Pulmonares/genética
Neoplasias Primárias Múltiplas/genética
Proteínas Proto-Oncogênicas/genética
Receptor do Fator de Crescimento Epidérmico/genética
Proteínas ras/genética
[Mh] Termos MeSH secundário: Adenomatose Pulmonar/genética
Adulto
Idoso
Idoso de 80 Anos ou mais
Análise Mutacional de DNA
Feminino
Dosagem de Genes
Seres Humanos
Hiperplasia/genética
Hibridização in Situ Fluorescente
Masculino
Meia-Idade
Lesões Pré-Cancerosas/genética
Proteínas Proto-Oncogênicas p21(ras)
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Reação em Cadeia da Polimerase Via Transcriptase Reversa
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (KRAS protein, human); 0 (Proto-Oncogene Proteins); 0 (RNA, Messenger); EC 2.7.10.1 (Receptor, Epidermal Growth Factor); EC 3.6.5.2 (Proto-Oncogene Proteins p21(ras)); EC 3.6.5.2 (ras Proteins)
[Em] Mês de entrada:0805
[Cu] Atualização por classe:161124
[Lr] Data última revisão:
161124
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:080402
[St] Status:MEDLINE
[do] DOI:10.1097/JTO.0b013e318168d20a


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[PMID]:18299280
[Au] Autor:Kohno T; Kunitoh H; Suzuki K; Yamamoto S; Kuchiba A; Matsuno Y; Yanagitani N; Yokota J
[Ad] Endereço:Biology Division, National Cancer Center Research Institute, Tokyo 1040045, Japan.
[Ti] Título:Association of KRAS polymorphisms with risk for lung adenocarcinoma accompanied by atypical adenomatous hyperplasias.
[So] Source:Carcinogenesis;29(5):957-63, 2008 May.
[Is] ISSN:1460-2180
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The pulmonary adenoma susceptibility 1 (Pas1) gene affects susceptibility to the development of lung adenomas in mice with a subset of the adenomas progressing to adenocarcinoma (ADC). In this study, genotype distributions for 10 polymorphisms in the human counterparts for three mouse candidate Pas1 genes, KRAS, CASC1/LAS1 and LRMP, were examined in a hospital-based case-control study consisting of 364 lung ADC cases and 253 controls. All the ADC cases were subjected to lobectomy and subsequent pathological investigation of atypical adenomatous hyperplasia (AAH), a putative precursor for peripheral lung ADC, including bronchioloalveolar carcinoma, in the resected lobes. Eighty-one (22%) of the ADC cases carried at least one AAH lesion in addition to the primary ADC and 34 (9%) of them carried multiple AAH lesions. None of the 10 polymorphisms examined showed significant associations with overall lung ADC risk (P > 0.05). However, minor allele carriers for two polymorphisms in the KRAS gene, KRAS-1 and -6, showed significantly increased odds ratios (ORs) for ADC accompanied by multiple AAHs [OR = 3.0; 95% confidence interval (CI) = 1.4-6.2, P = 0.004 and OR = 2.4; 95% CI = 1.1-4.7, P = 0.02, respectively]. Minor haplotypes including the minor allele for the KRAS-6 polymorphism showed increased ORs for ADC accompanied by multiple AAHs, and KRAS transcripts from the minor allele for this polymorphism were more abundantly detected in lung tissues than those from the major allele. Thus, KRAS polymorphisms were indicated to be involved in risk for the development of AAHs that progress to ADC by causing differential KRAS oncogene expression in the lungs.
[Mh] Termos MeSH primário: Adenocarcinoma/genética
Neoplasias Pulmonares/genética
Polimorfismo Genético
Polimorfismo de Nucleotídeo Único
Proteínas Proto-Oncogênicas/genética
Proteínas ras/genética
[Mh] Termos MeSH secundário: Adenocarcinoma/epidemiologia
Adenocarcinoma/patologia
Adenomatose Pulmonar/epidemiologia
Adenomatose Pulmonar/genética
Idoso
Antígenos de Neoplasias/genética
Antígenos Nucleares/genética
DNA de Neoplasias/sangue
DNA de Neoplasias/genética
DNA de Neoplasias/isolamento & purificação
Feminino
Seres Humanos
Hiperplasia/complicações
Hiperplasia/epidemiologia
Hiperplasia/genética
Japão/epidemiologia
Neoplasias Pulmonares/epidemiologia
Neoplasias Pulmonares/patologia
Masculino
Meia-Idade
Proteínas Proto-Oncogênicas p21(ras)
Fatores de Risco
Fumar/epidemiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antigens, Neoplasm); 0 (Antigens, Nuclear); 0 (DNA, Neoplasm); 0 (KRAS protein, human); 0 (PASD1 protein, human); 0 (Proto-Oncogene Proteins); EC 3.6.5.2 (Proto-Oncogene Proteins p21(ras)); EC 3.6.5.2 (ras Proteins)
[Em] Mês de entrada:0808
[Cu] Atualização por classe:161124
[Lr] Data última revisão:
161124
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:080227
[St] Status:MEDLINE
[do] DOI:10.1093/carcin/bgn048


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[PMID]:18208799
[Au] Autor:Sartori G; Cavazza A; Bertolini F; Longo L; Marchioni A; Costantini M; Barbieri F; Migaldi M; Rossi G
[Ad] Endereço:Section of Pathologic Anatomy, Azienda Policlinico, Modena, Italy.
[Ti] Título:A subset of lung adenocarcinomas and atypical adenomatous hyperplasia-associated foci are genotypically related: an EGFR, HER2, and K-ras mutational analysis.
[So] Source:Am J Clin Pathol;129(2):202-10, 2008 Feb.
[Is] ISSN:0002-9173
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Atypical adenomatous hyperplasia (AAH) is considered the preinvasive lesion of pulmonary adenocarcinoma, and mutations of EGFR, HER2, and K-ras are involved in the early stage of lung adenocarcinoma carcinogenesis, also predicting clinical response to anti-EGFR small molecule inhibitors. We analyzed 18 cases of primary lung adenocarcinoma with concomitant AAH foci from 13 patients for mutations of EGFR (exons 18-21), HER2 (exons 19-20), and K-ras (exon 2) by direct sequencing polymerase chain reaction. Among mutated cases, concordant mutations of EGFR or K-ras in adenocarcinoma and related AAH were observed in 5 (63%) of 8 cases. In particular, 3 of 4 adenocarcinomas with EGFR mutations (all L858R point mutations in women, never or former smokers) had a concomitant and identical mutation in AAH, and 2 of 4 adenocarcinomas with K-ras mutations (both at codon 12 in women, a never and a current smoker) showed the same mutation in concomitant AAH. All cases were wild-type for HER2. Mutations of EGFR and K-ras genes represent an early event in lung adenocarcinomagenesis, and AAH convincingly seems to be a precursor lesion in a subset of cases of adenocarcinoma.
[Mh] Termos MeSH primário: Adenocarcinoma/genética
Genes erbB-2
Genes ras
Hiperplasia/genética
Neoplasias Pulmonares/genética
Lesões Pré-Cancerosas/genética
Receptor do Fator de Crescimento Epidérmico/genética
[Mh] Termos MeSH secundário: Adenomatose Pulmonar/genética
Adulto
Idoso
Sequência de Bases
Análise Mutacional de DNA
Feminino
Seres Humanos
Masculino
Meia-Idade
Dados de Sequência Molecular
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
EC 2.7.10.1 (Receptor, Epidermal Growth Factor)
[Em] Mês de entrada:0803
[Cu] Atualização por classe:091119
[Lr] Data última revisão:
091119
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:080123
[St] Status:MEDLINE
[do] DOI:10.1309/THU13F3JRJVWLM30


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[PMID]:17706134
[Au] Autor:Huo Z; Liu HR; Wan JW
[Ad] Endereço:Department of Pathology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Beijing 100730, China.
[Ti] Título:[Atypical adenomatous hyperplasia of lung: clinicopathologic study of 8 cases and review of literature].
[So] Source:Zhonghua Bing Li Xue Za Zhi;36(5):292-6, 2007 May.
[Is] ISSN:0529-5807
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:OBJECTIVE: To study the clinicopathologic and immunohistochemical features of atypical adenomatous hyperplasia (AAH) of lung. METHODS: Eight cases of AAH of lung were studied by light microscopy and immunohistochemical staining for p16, thyroid transcription factor-1 (TTF-1), Ki-67, p53, epidermal growth factor receptor (EGFR) and c-erbB-2. RESULTS: The mean age of the patients was 52 years. The male-to-female ratio was 1:3. Two patients were chronic smokers. The clinical symptoms were relatively non-specific. Three patients had past history of non-pulmonary tumors, while 4 patients had lung adenocarcinoma. CT scan revealed solitary or multifocal hyperdense opacities. Histologically, the lesions ranged from 1 mm to 6 mm in size. Two cases were solitary and 6 cases were multifocal. All were of high-grade lesions. Associated low-grade component was noted in 3 cases. There was no evidence of local recurrence or disease progression in the 7 patients with post-operative follow-up information available (mean duration of follow up = 23 months). Four patients had received chemotherapy as well. Immunohistochemical study showed variable positivity for p16 (5/8), TTF-1 (5/8), Ki-67 (with proliferation index ranging from 1% to 10%), p53 (1/8) and EGFR (1/8). The staining for c-erbB-2 was negative (0/8). Four cases of AAH were associated with pulmonary adenocarcinoma. The adenocarcinoma cells were diffusely positive for TTF-1 (4/4), variably positive for p16 (2/4), Ki-67 (with proliferation index ranging from 2% to 40%), p53 (1/4) and EGFR (3/4), and negative for c-erbB-2 (0/4). CONCLUSIONS: AAH of lung is associated with pulmonary adenocarcinoma. Diagnosis of AAH requires correlation with CT findings and pathologic examination.
[Mh] Termos MeSH primário: Adenocarcinoma/patologia
Adenomatose Pulmonar/patologia
Neoplasias Pulmonares/patologia
Neoplasias Primárias Múltiplas/patologia
[Mh] Termos MeSH secundário: Adenocarcinoma/metabolismo
Adenocarcinoma/cirurgia
Adenomatose Pulmonar/metabolismo
Adenomatose Pulmonar/cirurgia
Adulto
Inibidor p16 de Quinase Dependente de Ciclina
Proteínas de Ligação a DNA/metabolismo
Feminino
Seguimentos
Seres Humanos
Hiperplasia/metabolismo
Hiperplasia/patologia
Hiperplasia/cirurgia
Antígeno Ki-67/metabolismo
Neoplasias Pulmonares/metabolismo
Neoplasias Pulmonares/cirurgia
Masculino
Meia-Idade
Proteínas de Neoplasias/metabolismo
Neoplasias Primárias Múltiplas/metabolismo
Neoplasias Primárias Múltiplas/cirurgia
Lesões Pré-Cancerosas/metabolismo
Lesões Pré-Cancerosas/patologia
Lesões Pré-Cancerosas/cirurgia
Fatores de Transcrição
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Cyclin-Dependent Kinase Inhibitor p16); 0 (DNA-Binding Proteins); 0 (Ki-67 Antigen); 0 (Neoplasm Proteins); 0 (P16 protein, human); 0 (TTF1 protein, human); 0 (Transcription Factors)
[Em] Mês de entrada:1006
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:070821
[St] Status:MEDLINE


  9 / 47 MEDLINE  
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[PMID]:17618248
[Au] Autor:Sakuma Y; Matsukuma S; Yoshihara M; Nakamura Y; Nakayama H; Kameda Y; Tsuchiya E; Miyagi Y
[Ad] Endereço:Molecular Pathology and Genetics Division, Kanagawa Cancer Center Research Institute, Kanagawa Cancer Center Hospital, Asahi-ku, Yokohama, Japan.
[Ti] Título:Epidermal growth factor receptor gene mutations in atypical adenomatous hyperplasias of the lung.
[So] Source:Mod Pathol;20(9):967-73, 2007 Sep.
[Is] ISSN:0893-3952
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Activating epidermal growth factor receptor (EGFR) gene mutations are frequently detected in lung adenocarcinomas, especially adenocarcinomas with a nonmucinous bronchioloalveolar carcinoma component. EGFR-mutated lung adenocarcinomas respond well to EGFR tyrosine kinase inhibitors. We previously found that most (88%) pure nonmucinous bronchioloalveolar carcinomas (adenocarcinoma in situ) already harbor EGFR mutations, indicating that the mutations are an early genetic event in the pathogenesis. We examined 54 atypical adenomatous hyperplasias, precursor lesions of lung adenocarcinomas, obtained from 28 Japanese patients for the hotspot mutations of EGFR exons 19 and 21 and K-ras codon 12. EGFR mutations were observed in 17 of the 54 (32%) atypical adenomatous hyperplasias examined: Ten and seven atypical adenomatous hyperplasias had deletion mutations at exon 19 or point mutations (L858R) at exon 21, respectively. We did not observe apparent histological differences between atypical adenomatous hyperplasias with and without EGFR mutations. K-ras mutation (G12S) was detected in only one atypical adenomatous hyperplasia. As EGFR mutational frequency of atypical adenomatous hyperplasias was much lower than that of nonmucinous bronchioloalveolar carcinomas, we surmise that EGFR-mutated atypical adenomatous hyperplasias, but not atypical adenomatous hyperplasias with wild-type EGFR, are likely to progress to nonmucinous bronchioloalveolar carcinomas.
[Mh] Termos MeSH primário: Adenocarcinoma Bronquíolo-Alveolar/genética
Adenomatose Pulmonar/genética
Regulação Neoplásica da Expressão Gênica
Neoplasias Pulmonares/genética
Mutação
Receptor do Fator de Crescimento Epidérmico/genética
[Mh] Termos MeSH secundário: Adenocarcinoma Bronquíolo-Alveolar/patologia
Adenomatose Pulmonar/patologia
Adulto
Idoso
Grupo com Ancestrais do Continente Asiático/genética
Códon
Análise Mutacional de DNA
Progressão da Doença
Éxons
Feminino
Genes ras
Seres Humanos
Hiperplasia
Japão
Neoplasias Pulmonares/patologia
Masculino
Meia-Idade
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Codon); EC 2.7.10.1 (EGFR protein, human); EC 2.7.10.1 (Receptor, Epidermal Growth Factor)
[Em] Mês de entrada:0710
[Cu] Atualização por classe:091119
[Lr] Data última revisão:
091119
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:070710
[St] Status:MEDLINE


  10 / 47 MEDLINE  
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[PMID]:17561305
[Au] Autor:Kozuki T; Hisamoto A; Tabata M; Takigawa N; Kiura K; Segawa Y; Nakata M; Mandai K; Eguchi K; Ueoka H; Tanimoto M
[Ad] Endereço:Department of Hematology, Oncology, and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, 2-5-1 Shikata-cho, Okayama 700-8558, Japan.
[Ti] Título:Mutation of the epidermal growth factor receptor gene in the development of adenocarcinoma of the lung.
[So] Source:Lung Cancer;58(1):30-5, 2007 Oct.
[Is] ISSN:0169-5002
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Recently, a mutation of the epidermal growth factor receptor (EGFR) gene has been reported to be implicated in the development of pulmonary adenocarcinoma. However, the involvement of the mutation in atypical adenomatous hyperplasia (AAH) and multiple adenocarcinomas still remains unclear. We herein examined the EGFR mutations in 9 AAH and 31 adenocarcinoma lesions obtained from 30 Japanese patients. Nine patients had synchronous or metachronous multiple adenocarcinomas and/or AAH. Mutations in exons 18-21 of EGFR gene were analysed using polymerase chain reaction and direct sequence methods. EGFR mutations were detected in 4 (44%) of 9 AAH and in 7 (23%) of 31 adenocarcinomas. A gefitinib-resistant point mutation (T790M) in exon 20 without gefitinib treatment was detected in 1 AAH and 1 adenocarcinoma. The patient with T790M mutated AAH, which also had an exon 19 mutation of D761Y, had synchronous adenocarcinoma, which had only an exon 19 mutation of D761Y. The other exon 19 mutations were all in-frame deletions. In the two patients with synchronous AAH and adenocarcinoma, AAH had mutations at exon 19 although adenocarcinoma did not have any mutations. In the patient with synchronous 2 adenocarcinomas, each had different mutations (exons 19 and 21). In two patients with double adenocarcinomas, 1 adenocarcinoma harbored exon 21 mutations, while the other demonstrated no mutations. Although EGFR mutations appeared to be partially associated with the early steps of adenocarcinoma development, such mutations may possibly occur randomly even in multiple lesions in a single patient.
[Mh] Termos MeSH primário: Adenocarcinoma/genética
Adenomatose Pulmonar/genética
Genes erbB-1
Neoplasias Pulmonares/genética
Mutação
Neoplasias Primárias Múltiplas/genética
Receptor do Fator de Crescimento Epidérmico/genética
[Mh] Termos MeSH secundário: Adenocarcinoma/tratamento farmacológico
Adenomatose Pulmonar/tratamento farmacológico
Antineoplásicos/uso terapêutico
Resistência a Medicamentos Antineoplásicos
Éxons
Feminino
Predisposição Genética para Doença
Seres Humanos
Neoplasias Pulmonares/tratamento farmacológico
Masculino
Neoplasias Primárias Múltiplas/tratamento farmacológico
Quinazolinas/uso terapêutico
Receptor do Fator de Crescimento Epidérmico/antagonistas & inibidores
Estudos Retrospectivos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Quinazolines); EC 2.7.10.1 (Receptor, Epidermal Growth Factor); S65743JHBS (gefitinib)
[Em] Mês de entrada:0804
[Cu] Atualização por classe:130603
[Lr] Data última revisão:
130603
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:070615
[St] Status:MEDLINE



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