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1.
Siglo cero (Madr.) ; 52(1): 79-99, ene.-mar. 2021. tab
Artigo em Espanhol | IBECS (Espanha) | ID: ibc-201650

RESUMO

En los últimos años, ha habido un incremento exponencial en el número de guías, materiales e informes que se encuentran a disposición de los centros escolares para orientar su camino hacia la inclusión. Partiendo de esta realidad, se ha llevado a cabo un estudio de naturaleza cualitativa cuyo objetivo principal ha consistido en una selección de guías sobre inclusión que resultan de utilidad para iniciar procesos de re­flexión-acción en la comunidad educativa. El análisis documental de contenido (de un total de 13 guías) ha permitido identificar los facilitadores/limitadores que posibilitan/ dificultan el avance de la inclusión. Asimismo, se han especificado los recursos/instru­mentos que ofrecen las guías para acompañar a los centros en el camino hacia una edu­cación más inclusiva. Los resultados recogen la importancia que tiene la formación del profesorado en la atención a la diversidad, la puesta en marcha de redes de colaboración y la reformulación de barreras en facilitadores. Las conclusiones apuntan a la necesidad de iniciar/sostener procesos de mejora para una mayor inclusión dentro y fuera de las aulas y de dar a conocer este corpus de guías a los profesionales que están en la práctica


In recent years, a growing number of guides and reports have become available for schools to guide them on their paths towards inclusion. A qualitative study has been carried out, whose main aim was to select guides on inclusion that are useful for initiating reflection-action processes within educational community. The documentary analysis (of 13 guides in all) led to the identification of the facilitators/barriers that fa­vor/hinder the advance of inclusion. Likewise, the resources/instruments offered by the guides have been specified in order to support schools on their journeys towards a more inclusive education. The results reflect the importance of teacher training in dealing with diversity, the implementation of collaborative networks and the reformulation of barri­ers into facilitators. The conclusions point to the need to initiate/sustain improvement processes for greater inclusion within and outside the classroom, and to make this cor­pus of guidance known to practitioners


Assuntos
Humanos , Guias como Assunto/normas , Inclusão Escolar/normas , Capacitação de Professores/normas , Instituições Acadêmicas/normas , Pesquisa Qualitativa , Inclusão Escolar/métodos , Modelos Educacionais , Capacitação de Professores/métodos
2.
J Thorac Oncol ; 3(11): 1224-35, 2008 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-18978556

RESUMO

BACKGROUND: Detection of epidermal growth factor receptor (EGFR) mutations in advanced non-small cell lung cancer (NSCLC) patients has relied on DNA purification from biopsies, amplification, and sequencing. However, the number of tumor cells in a sample is often insufficient for EGFR assessment. METHODS: We prospectively screened 1380 NSCLC patients for EGFR mutations but found that 268 were not evaluable because of insufficient tumor tissue. We therefore developed and validated a method of detecting EGFR mutations in these samples. Tumor cells were microdissected into polymerase chain reaction buffer and amplified. EGFR mutations were detected by length analysis of fluorescently labeled polymerase chain reaction products and TaqMan assay. RESULTS: We determined EGFR status in 217 (81%) of the 268 primary NSCLC samples not evaluable in our original study-fresh and paraffin-embedded with less than 150 cells. Exon 19 deletions were detected in 11.5% of patients and exon 21 L858R mutations in 5.5%. In addition, the exon 20 T790M mutation was detected in 6 of 15 (40%) patients at the time of progression to erlotinib. The primary, sensitive mutation was present in all tumor cells, whereas the T790M mutation was absent in some groups. CONCLUSIONS: The method presented here eliminates the need for DNA purification and allows for detection of EGFR mutations in samples containing as few as eight cancer cells.


Assuntos
Carcinoma Pulmonar de Células não Pequenas/genética , Receptores ErbB/genética , Neoplasias Pulmonares/genética , Mutação/genética , Reação em Cadeia da Polimerase/métodos , Adenocarcinoma/tratamento farmacológico , Adenocarcinoma/genética , Adenocarcinoma/patologia , Adulto , Idoso , Idoso de 80 Anos ou mais , Carcinoma Pulmonar de Células não Pequenas/tratamento farmacológico , Carcinoma Pulmonar de Células não Pequenas/patologia , DNA de Neoplasias/genética , Receptores ErbB/antagonistas & inibidores , Cloridrato de Erlotinib , Éxons , Feminino , Humanos , Neoplasias Pulmonares/tratamento farmacológico , Neoplasias Pulmonares/patologia , Masculino , Pessoa de Meia-Idade , Estadiamento de Neoplasias , Prognóstico , Estudos Prospectivos , Inibidores de Proteínas Quinases/uso terapêutico , Quinazolinas/uso terapêutico , Sensibilidade e Especificidade , Taxa de Sobrevida
3.
Transl Oncogenomics ; 1: 11-8, 2006.
Artigo em Inglês | MEDLINE | ID: mdl-23662036

RESUMO

BACKGROUND: c-Met mutations play a critical role in the development and progression of primary tumors and metastases. Activation of the HGF/SF-c-Met pathway determines a poor prognosis in non-small-cell and small-cell lung cancer (SCLC) patients. Missense mutations of c-Met have been identified in SCLC patients located in the juxtamembrane (JM) and in the Sema domain. To determine the role of the c-Met pathway in SCLC, we have investigated the presence of c-Met mutations in SCLC patients. PATIENTS AND METHODS: Forty-four tumor tissue samples from SCLC patients were obtained with bronchoscopy before beginning treatment. Analysis of c-Met mutations was performed in exon 2 and exon 14. RESULTS: Of the 44 patients included in this study, 23 were classified as limited disease and were treated with sequential or concurrent chemotherapy and thoracic radiotherapy. Twenty-one patients with extensive disease received chemotherapy alone, the majority with cisplatin or carboplatin plus etoposide. The median survival was 14 months (95% CI: 9.4 to 18.5 months) and the 2- and 5-year survival rates were 24% and 15%, respectively. Previously identified missense mutations E168D, R988C and T1010I in c-Met were not found in our study. However, novel mutations were identified, including T995I in the juxtamembrane domain (T995I) and a mutation which does not change amino acid in codon 178 in the Sema domain. CONCLUSION: In SCLC patients, the presence of mutations in c-Met gene is a rare event. Other genetic alterations involved in the HGF/SF-c-Met pathway should be assessed to define the role of this signaling pathway in SCLC.

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