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1.
Chinese Journal of Oncology ; (12): 436-440, 2015.
Artigo em Chinês | WPRIM | ID: wpr-248336

RESUMO

<p><b>OBJECTIVE</b>To analyze the clinicopathological characteristics of patients with anaplastic lymphoma kinase (ALK) rearrangements in lung adenocarcinoma, and the clinical therapy and prognosis of the patients.</p><p><b>METHODS</b>Clinicopathological data of 34 cases of ALK-positive patients treated in the Beijing Chest Hospital from 2005 to 2014 were reviewed. The expression of ALK proteins in the resected tumors was detected by immunohistochemistry, and EGFR mutations were examined by polymerase chain reaction and a direct DNA sequencing method.</p><p><b>RESULTS</b>Among the 34 patients, 20 were male and 14 were female, the median age was 49, and 11 were smokers and 23 were never smokers. The clinical stages of the patients were stage IA in 5 patients, IB in one patient, IIA in two patients, IIIA in 16 patients, IIIB in 5 patients, IV in 4 patients, and one patient of unknown stage. ALK-positive tumors showed strong granular staining in cell cytoplasm by immunohistochemistry. Forteen patients were solid predominant subtype with mucin production, 10 of acinar predominant subtype, 6 of papillary predominant subtype, 3 of micropapillary predominant subtype, and one was of colloid variant. There were 18 cases with mucin production, 6 cases had signet-ring cell morphology, and 10 cases showed cribriform pattern. Only one patient had coexistence of ALK rearrangement and EGFR mutation (L858R at exon 21). Of the 34 patients, 24 patients were followed up. The median follow up of the 24 patients was 11.0 months (1.7-48.7 months).</p><p><b>CONCLUSIONS</b>ALK-positive tumors as a molecular subtype of lung adenocarcinoma have distinct clinicopathological features. The histological findings of ALK-positive tumors are characterized by solid predominant subtype with mucin production, acinar predominant subtype, signet-ring cells and cribriform structures. They were rarely co-mutated with EGFR mutation.</p>


Assuntos
Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Adenocarcinoma , Patologia , Terapêutica , Éxons , Rearranjo Gênico , Genes erbB-1 , Imuno-Histoquímica , Neoplasias Pulmonares , Patologia , Terapêutica , Mucinas , Mutação , Proteínas de Neoplasias , Genética , Reação em Cadeia da Polimerase , Prognóstico , Receptores Proteína Tirosina Quinases , Genética , Análise de Sequência de DNA
2.
Cancer Research and Clinic ; (6): 145-149, 2011.
Artigo em Chinês | WPRIM | ID: wpr-413262

RESUMO

Objective To describe the development of nodules of altered hepatocytes (NAH) in chronic hepatitis B and to reveal progression of the nodules to hepatocellular carcinoma (HCC). Methods HCC, NAH and ordinary regenerative nodules (ORN) were identified and compared histologically. Expression levels of hepatitis B virus (HBV) antigens, mitoactivity and p53 accumulation in these lesions were evaluated by immunohistochemistry. Results Multiple foci of altered hepatocytes (FAH) and NAH were identified in the liver parenchyma surrounding HCC in all of the samples examined. Sequential architectural and cellular changes were observed during the progression of FAH to NAH and HCC. Expression levels of HBV surface and core antigens were found to be significantly decreased in ORN, NAH and HCC, with their positive rates being 70 % (35/50), 50 % (25/50), 10 % (5/50) and 60 % (30/50), 40 % (20/50), 6 % (3/50), respectively (P <0.05). Ki-67-1abelling indices were determined to be (0.58±0.49) %, (2.46±1.05) % and (40.36±26.27) %in these lesions, respectively (P <0.05). Nuclear p53 accumulation was found only in HCC. Its occurrence was associated to a high histological grade, with its frequencies being 13 % (1/8), 41% (11/27) and 73 % (11/15)in grade 1, 2 and 3 lesions, respectively. Conclusion NAH lesions, identified by their morphologic features and mitoactivity elevation, are detectable in resected liver samples with chronic hepatitis B and cirrhosis. They represent a common HCC precursor and can be used as a surrogate marker for the surveillance of high-risk individuals.

3.
Cancer Research and Clinic ; (6): 80-83,88, 2010.
Artigo em Chinês | WPRIM | ID: wpr-554376

RESUMO

Objective Focal nodular hyperplasia(FNH) is composed of multiple hyperplastic liver cell nodules,but its pathogenesis has not been elucidated. Foci (FAH) or nodules of altered hepatocytes (NAH) are precursors of hepatocellular adenoma (HCA) and carcinoma.This study aimed at identifying FAH and NAH from FNH and evaluating their role in FNH development.Methods 6 FNH lesions from 5 patients and 10 HCA from 9 patients were examined histologically,and expression levels of CD_(34) cytokeratin 19(CKl9) and Ki-67 antigen were demonstrated immunohistochemicailly.Proliferative activity was evaluated by Ki-67 antigen-labeling indices(Ki-67 LI).Results Multiple FAH and NAH were identified in all of the 6 FNH lesions. Whiie micmvasculatures were demonstrated by CD_(34) immunoreactivity in both HCA and FNH,their density and distribution were different in these two lesions,being diffuse in HCA and focal or nodular,mainly within NAH.CKl9 expression Was found in FNH,localized in ductal and ductular cells,but not within NAH and HCA.Average Ki.67 LI of 73 NAH(2.8%) was shown to be higher than that of the whole FNH lesions (0.6%),and had no statistieal difference comparable to that of HCA(1.8%).Conclusion Muhiple NAH are present in all classical FNH lesions.Unlike the surrounding parenchyma,NAH lesions are more proliferative and equipped with CD_(34)-positive microvasculatures as in HCA.

4.
Chinese Journal of General Surgery ; (12)2001.
Artigo em Chinês | WPRIM | ID: wpr-673792

RESUMO

Objective To investigate the relationship of c erbB2 with endocrine therapy and prognosis, to investigate the rapid and effective method to detect c erbB2 alteration in breast carcinoma(BC).Metheds Semi quantitative PCR was used to detect the amplification of c erbB2, and immunohistochemistry was used to detect the expression of protein of c erbB2. 58 cases of BC were followed up .Results There was significant relationship between c erbB2 protein overexpression and gene amplification(P

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