نتایج جستجو برای: tki

تعداد نتایج: 3304  

2016
Yan Li Yanmei Wang Kai Niu Xiewan Chen Liqin Xia Dingxi Lu Rui Kong Zhengtang Chen Yuzhong Duan Jianguo Sun

PURPOSE Acquired resistance is a bottleneck that restricts the efficacy of epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) for lung cancer. Ginsenoside Rg3 is an antiangiogenic agent which can down-regulate the expressions of vascular endothelial growth factor (VEGF) and EGFR. Combination of EGFR-TKI and ginsenoside Rg3 may be a promising strategy to delay acquired resista...

2016
Hong-Fei Gao Jin-Ji Yang Zhi-Hong Chen Xu-Chao Zhang Hong-Hong Yan Wei-Bang Guo Qing Zhou Lou-Ying Gou Zhong-Yi Dong Yi-Long Wu

BACKGROUND The activation of c-Met has been associated with both primary and acquired resistance to EGFR-TKI therapy in NSCLC patients. Thus, c-Met status during EGFR-TKI therapy should receive much attention. RESULTS Forty-nine patients were selected as training cohort and 52 cases as validation cohort. With disease progression, IHC results showed that 37 (75.5%) of the patients were tissue ...

2016
Zhengbo Song Yiping Zhang

INTRODUCTION The aim of this study was to investigate the treatment and prognosis of advanced non-small cell lung cancer (NSCLC) patients after failure of long-term treatment with epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI). MATERIAL AND METHODS We retrospectively analyzed all NSCLC patients with EGFR-TKI (gefitinib or erlotinib) treatment at our institution between ...

2017
Cheng Zhang Xi Zhang Shi-Jie Yang Xing-Hua Chen

Human bone marrow stromal cells (hBMSCs) may contribute to the growth of tyrosine kinase inhibitor (TKI)-resistant chronic myelogenous leukemia (CML). However, there are certain differences in biology between CML and Philadelphia-positive acute lymphoblastic leukemia (Ph+ ALL). Little is known about the role and mechanism of hBMSCs on the growth of TKI-resistant Ph+ ALL. The current study co-cu...

2017
Tomasz Chojnacki Piotr Rzepecki

WHO 2016 guidelines regarding chronic myeloid leukemia (CML) do not contain groundbreaking changes [1]. Mainly criteria of acceleration phase (AP) identification were revised. Despite these changes, the guidelines are still not standardized and differ significantly, even when compared to guidelines of European Leukemia Net (ELN) [2], International Bone Marrow Transplant Registry (IBMTR) or M. D...

Journal: :Molecular cancer therapeutics 2013
Simone Filosto David S Baston Samuel Chung Cathleen R Becker Tzipora Goldkorn

The EGF receptor (EGFR) is a proto-oncogene commonly dysregulated in several cancers including non-small cell lung carcinoma (NSCLC) and, thus, is targeted for treatment using tyrosine kinase inhibitors (TKI) such as erlotinib. However, despite the efficacy observed in patients with NSCLC harboring oncogenic variants of the EGFR, general ineffectiveness of TKIs in patients with NSCLC who are cu...

2017
Roxana Alina Tudor Adrijana D'Silva Alain Tremblay Paul MacEachern Don Morris Darren Brenner Karen Kopciuk Dafydd Gwyn Bebb

PURPOSE Treatment and clinical-outcomes were described in a sub-cohort of non-small-cell lung cancer (NSCLC) patients with disease-progression (PD) after epidermal growth factor tyrosine kinase inhibitors (EGFR-TKIs) treatment. PATIENTS AND METHODS We retrospectively analyzed a single-institutional EGFR mutation positive (EGFRmut+) NSCLC cohort for post-TKI-PD management, and assessed overall...

2012
Stephanie Heon Beow Y. Yeap Neal I. Lindeman Victoria A. Joshi Mohit Butaney Gregory J. Britt Daniel B. Costa Michael S. Rabin David M. Jackman Bruce E. Johnson

Purpose: This retrospective studywas undertaken to investigate the impact of initial gefitinib or erlotinib (EGFR tyrosine kinase inhibitor, EGFR-TKI) versus chemotherapy on the risk of central nervous system (CNS) progression in advanced non–small cell lung cancer (NSCLC) with EGFR mutations. Experimental Design: Patients with stage IV or relapsed NSCLC with a sensitizing EGFR mutation initial...

2018
Yao-Chen Wang De-Wei Wu Tzu-Chin Wu Lee Wang Chih-Yi Chen Huei Lee

Resistance to tyrosine kinase inhibitors (TKIs) results in tumor relapse and poor prognosis in patients with lung adenocarcinoma. TKI resistance caused by epidermal growth factor receptor (EGFR) mutations at T790M and c-Met amplification occurs through persistent activation of the MEK/ERK and PI3K/AKT signaling pathways. We therefore expected that dual inhibitors of both signaling pathways coul...

Journal: :Blood 2015
Jamshid S Khorashad Anna M Eiring Clinton C Mason Kevin C Gantz Amber D Bowler Hannah M Redwine Fan Yu Ira L Kraft Anthony D Pomicter Kimberly R Reynolds Anthony J Iovino Matthew S Zabriskie William L Heaton Srinivas K Tantravahi Michael Kauffman Sharon Shacham Alex Chenchik Kyle Bonneau Katharine S Ullman Thomas O'Hare Michael W Deininger

The mechanisms underlying tyrosine kinase inhibitor (TKI) resistance in chronic myeloid leukemia (CML) patients lacking explanatory BCR-ABL1 kinase domain mutations are incompletely understood. To identify mechanisms of TKI resistance that are independent of BCR-ABL1 kinase activity, we introduced a lentiviral short hairpin RNA (shRNA) library targeting ∼5000 cell signaling genes into K562(R), ...

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