Results 121 to 130 of about 68,946 (284)

High‐throughput screening identifies bazedoxifene as a potential therapeutic for dysferlin‐deficient limb girdle muscular dystrophy

British Journal of Pharmacology, Volume 182, Issue 13, Page 2930-2949, July 2025.
Abstract Background and Purpose Limb‐girdle muscular dystrophy R2 (LGMD R2) is a rare genetic disorder characterised by progressive weakness and wasting of proximal muscles. LGMD R2 is caused by the loss of function of dysferlin, a transmembrane protein crucial for plasma membrane repair in skeletal muscles.
Celine Bruge, Nathalie Bourg, Emilie Pellier, Johana Tournois, Jerome Polentes, Manon Benabides, Noella Grossi, Anne Bigot, Anthony Brureau, Isabelle Richard, Xavier Nissan   +10 more
wiley   +1 more source

Long persistent bcr-abl positive transcript detected by polymerase chain reaction after marrow transplant for chronic myelogenous leukemia without clinical relapse: a study of 64 patients [PDF]

, 1993
K Miyamura, T Tahara, Masashi Tanimoto, Y Morishita, Kohei Kawashima, Y Morishima, Hajime Saito, Shinobu Tsuzuki, K. Takeyama, Y Kodera   +9 more
openalex   +3 more sources

Detection of BCR-ABL kinase domain mutations in CD34+ cells from newly diagnosed chronic phase CML patients and their association with imatinib resistance [PDF]

, 2011
BCR-ABL kinase domain (KD) mutations, the most common cause of imatinib resistance, are infrequently detected in newly diagnosed chronic-phase chronic myeloid leukemia (CP-CML) patients.
Aamer Aleem, Abdul Qayyum, Abid Jamil, Abid Taj, Ahmad Khalid, Ammara Tahir, Ijaz Shah, Mahwish Khan, Mubashar Naqvi, Mudassar Iqbal, Muhammad Abbad, Muhammad Ferhan, Muhammad Khalid, Najeeb ur-Rehman, Riaz ul-Haq, Shahid Baig, Tanveer Akhtar, Tariq Gill, Weng Qin, Zafar Iqbal   +19 more
core   +1 more source

Targeting quiescent leukemic stem cells using second generation autophagy inhibitors [PDF]

, 2019
In chronic myeloid leukemia (CML), tyrosine kinase inhibitor (TKI) treatment induces autophagy that promotes survival and TKI-resistance in leukemic stem cells (LSCs).
A Hamilton, A Kuma, AS Corbin, B Ronan, B Zhang, B Zhang, BJ Druker, C Bellodi, D Mahalingam, DJ Klionsky, DT Vogl, E Weisberg, F Liu, G Karsli-Uzunbas, JD Mancias, JY Guo, JY Guo, M Karvela, M Komatsu, M Mortensen, M Schemionek, MR Rosenfeld, MR Warr, MT Rosenfeldt, N Mizushima, P Rousselot, Q McAfee, R Bago, R Rangwala, R Rangwala, S Brenner, S Kimura, S Koschmieder, SM Graham, T Holyoake, TL Holyoake, TL Holyoake, TT Ho, V Kirkin, VW Rebecca, WE Dowdle, XH Ma, Z Tothova   +42 more
core   +2 more sources

Hypusination of eukaryotic initiation factor 5A (eIF5A): a novel therapeutic target in BCR-ABL-positive leukemias identified by a proteomics approach.

Blood, 2007
Inhibition of BCR-ABL tyrosine kinase with imatinib represents a major breakthrough in the treatment of patients with chronic myeloid leukemia (CML). However, resistance to imatinib develops frequently, particularly in late-stage disease. To identify new
S. Balabanov, A. Gontarewicz, P. Ziegler, U. Hartmann, W. Kammer, M. Copland, U. Brassat, M. Priemer, I. Hauber, T. Wilhelm, Gerold Schwarz, L. Kanz, C. Bokemeyer, J. Hauber, T. Holyoake, A. Nordheim, T. Brümmendorf   +16 more
semanticscholar   +1 more source

GANT61 Modulates Autophagy and Lipid Metabolism in Ovarian Cancer

Cell Proliferation, Volume 58, Issue 7, July 2025.
GANT61 induced autophagy via the AKT pathway and promoted the accumulation of lipid droplets in both cell lines. The molecular mechanism behind this lipid accumulation appears to involve the mediation of SREBP1. Furthermore, the combination of GANT61 with CQ/Fatostatin significantly inhibited the proliferation and clonogenicity of SKOV3 and SKOV3PTX ...
Yibin Pan, Lingfeng Chen, Jinlu Shen, Shihao Hong, Xiaojing Guan, Xudong Ma, Rongrong Tang, Meifei Lu, Fangying Sun, Shanliang Shang, Yongdong Dai, Zhaokai Zhou, Songying Zhang, Jianhua Yang   +13 more
wiley   +1 more source

Expression of p190 BCR-ABL fusion gene in a patient with chronic myeloid leukemia Expressão do rearranjo gênico BCR-ABL com ponto de quebra na região menor do gene BCR em um paciente com leucemia mielóide crônica

Revista Brasileira de Hematologia e Hemoterapia, 2003
A minority of chronic myeloid leukemia cases have breakpoints in the minor cluster region (m-bcr) of the BCR-ABL gene. We report on a patient with Ph-positive and m-bcr breakpoint at diagnosis. She was treated with hydroxyurea and interferon-alpha.
P. V. B. Carvalho, Gustavo J. Lourenço, Maristela Zocca, K. B. B. Pagnano, Irene Lorand-Metze, Carmino A. De Souza, Carmen S. P. Lima   +6 more
doaj   +1 more source

Celecoxib inhibits proliferation and survival of chronic myelogeous leukemia (CML) cells via AMPK-dependent regulation of β-catenin and mTORC1/2. [PDF]

, 2016
CML is effectively treated with tyrosine kinase inhibitors (TKIs). However, the efficacy of these drugs is confined to the chronic phase of the disease and development of resistance to TKIs remains a pressing issue.
Calabretta, Bruno, Canonico, Pier Luigi, Condorelli, Fabrizio, De Dominici, Marco, Genazzani, Armando A, Gnemmi, Ilaria, Mariani, Samanta A., Minassi, Alberto, Minieri, Valentina, Riva, Beatrice, Salomoni, Paolo   +10 more
core   +2 more sources

A novel mechanism for imatinib mesylate-induced cell death of BCR-ABL-positive human leukemic cells: caspase-independent, necrosis-like programmed cell death mediated by serine protease activity.

Blood, 2004
Caspase-independent programmed cell death can exhibit either an apoptosis-like or a necrosis-like morphology. The ABL kinase inhibitor, imatinib mesylate, has been reported to induce apoptosis of BCR-ABL-positive cells in a caspase-dependent fashion.
Masayuki Okada, S. Adachi, T. Imai, Kenichiro Watanabe, S. Toyokuni, M. Ueno, A. Zervos, G. Kroemer, T. Nakahata   +8 more
semanticscholar   +1 more source

Phosphorylation of BECLIN-1 by BCR-ABL suppresses autophagy in chronic myeloid leukemia

Haematologica, 2020
Autophagy is a genetically regulated process of adaptation to metabolic stress and was recently shown to be involved in the treatment response of chronic myeloid leukemia (CML).
Chuanjiang Yu, Sivahari P. Gorantla, Alina Müller-Rudorf, Tony A. Müller, Stefanie Kreutmair, Corinna Albers, Lena Jakob, Lena J. Lippert, Zhenyu Yue, Monika Engelhardt, Marie Follo, Robert Zeiser, Tobias B. Huber, Justus Duyster, Anna L. Illert   +14 more
doaj   +1 more source