PMID- 19176054 OWN - NLM STAT- MEDLINE DCOM- 20100527 LR - 20211203 IS - 0253-2727 (Print) IS - 0253-2727 (Linking) VI - 29 IP - 10 DP - 2008 Oct TI - [Study on activation of AKT/mTOR pathway in anaplastic large cell lymphoma]. PG - 649-53 AB - OBJECTIVE: To study the expression of anaplastic lymphoma kinase (ALK) and the phosphorylation status of AKT, mammalian target of rapamycin (mTOR), 4E-binding protein 1 (4E-BP1) and ribosomal protein S6 kinase (p70S6K) and their interrelationships and clinical pathological significance in anaplastic large cell lymphoma (ALCL) patients. METHODS: Immunohistochemical and EnVision methods were used to detect the expression of ALK, p-AKT, p-mTOR, p-4E-BP1 and p-p70S6K. RESULTS: Among the 81 ALCL patients, 51 (63.0%) expressed ALK, whereas the other 30 (37.0%) did not. Patients with ALK(+) ALCL had a better prognosis than those with ALK-ALCL (P < 0.05). Out of the 71 ALCL samples studied, p-AKT was detected in 54 (76.1%) samples and its phosphorylation was correlated with ALK expression (P < 0.05); p-mTOR was detected in 57 (80.3%) samples and its expression was correlated with both ALK and p-AKT (P < 0.05); p-4E-BP1 and p-p70S6K were detected in 64 (90.1%) and 66 (93.0%) samples respectively, and their expressions were related with p-mTOR (P < 0.05), but not with ALK or p-AKT (P > 0.05). COX Proportional Hazard Model analysis showed that both the expression of ALK and the B symptoms affected the prognosis (P < 0.05), moreover, the former had greater impact than the later. CONCLUSION: Expressions of p-AKT, p-mTOR, p-4E-BP1 and p-p70S6K are detected in ALCL, while ALK(+) cases have higher incidence than those with ALK(-) cases. Phosphorylation of AKT and mTOR is correlated with ALK expression, suggesting that there is an activated pathway of AKT/mTOR in patients with ALK(+) ALCL, but the activation have no obvious prognostic significance. FAU - Li, Jin-Fan AU - Li JF AD - Department of Pathology, West China Hospital, Sichuan University, Chengdu 610041, China. FAU - Li, Gan-di AU - Li GD FAU - Gu, Ling AU - Gu L FAU - Liu, Wei-Ping AU - Liu WP FAU - Li, Feng-Yuan AU - Li FY FAU - Liao, Dian-Ying AU - Liao DY FAU - Ma, Zhi-Gui AU - Ma ZG LA - chi PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - China TA - Zhonghua Xue Ye Xue Za Zhi JT - Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi JID - 8212398 RN - 0 (Adaptor Proteins, Signal Transducing) RN - 0 (Cell Cycle Proteins) RN - 0 (EIF4EBP1 protein, human) RN - 0 (Intracellular Signaling Peptides and Proteins) RN - 0 (Phosphoproteins) RN - EC 2.7.1.1 (MTOR protein, human) RN - EC 2.7.10.1 (ALK protein, human) RN - EC 2.7.10.1 (Anaplastic Lymphoma Kinase) RN - EC 2.7.10.1 (Protein-Tyrosine Kinases) RN - EC 2.7.10.1 (Receptor Protein-Tyrosine Kinases) RN - EC 2.7.11.1 (Protein Serine-Threonine Kinases) RN - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt) RN - EC 2.7.11.1 (Ribosomal Protein S6 Kinases, 70-kDa) RN - EC 2.7.11.1 (TOR Serine-Threonine Kinases) SB - IM MH - Adaptor Proteins, Signal Transducing/metabolism MH - Adolescent MH - Adult MH - Aged MH - Anaplastic Lymphoma Kinase MH - Cell Cycle Proteins MH - Child MH - Child, Preschool MH - Female MH - Humans MH - Intracellular Signaling Peptides and Proteins/*metabolism MH - Lymphoma, Large-Cell, Anaplastic/*metabolism MH - Male MH - Middle Aged MH - Phosphoproteins/metabolism MH - Phosphorylation MH - Protein Serine-Threonine Kinases/*metabolism MH - Protein-Tyrosine Kinases/*metabolism MH - Proto-Oncogene Proteins c-akt/*metabolism MH - Receptor Protein-Tyrosine Kinases MH - Ribosomal Protein S6 Kinases, 70-kDa/metabolism MH - Signal Transduction MH - TOR Serine-Threonine Kinases MH - Young Adult EDAT- 2009/01/30 09:00 MHDA- 2010/05/28 06:00 CRDT- 2009/01/30 09:00 PHST- 2009/01/30 09:00 [entrez] PHST- 2009/01/30 09:00 [pubmed] PHST- 2010/05/28 06:00 [medline] PST - ppublish SO - Zhonghua Xue Ye Xue Za Zhi. 2008 Oct;29(10):649-53.