Results 91 to 100 of about 128,389 (322)

Genomic variant profiling in blast‐phase paediatric chronic myeloid leukaemia: Predisposing and driving alterations

British Journal of Haematology, EarlyView.
To identify pathogenic somatic and germline gene variants associated with blast‐phase transformation and cancer predisposition in paediatric chronic myeloid leukaemia (CML), n = 19 patients with blast‐phase paediatric CML were analysed with whole genome and targeted panel sequencing and compared to n = 19 patients with chronic phase paediatric CML.
Yvonne Lisa Behrens, Thea Reinkens, Winfried Hofmann, Amelie Gumann, Alisa Förster, Laura Gaschler, Tabita Ghete, Renate Strasser, Jennifer Espenkötter, Bernd Haermeyer, Michaela Losch, Stephanie Sembill, Zofia Wotschofsky, Stephan von Hörsten, Wolfgang Schuh, Nataliya Di Donato, Meinolf Suttorp, Manuela Krumbholz, Tim Ripperger, Brigitte Schlegelberger, Gudrun Göhring, Markus Metzler, Axel Karow   +22 more
wiley   +1 more source

BCR-ABL induces the expression of Skp2 through the PI3K pathway to promote p27Kip1 degradation and proliferation of chronic myelogenous leukemia cells [PDF]

, 2005
Chronic myelogenous leukemia (CML) is characterized by the expression of the BCR-ABL tyrosine kinase, which results in increased cell proliferation and inhibition of apoptosis.
Albero, M.P. (M. Pilar), Andreu, E.J. (Enrique José), Arbona, C. (C.), Ivorra, C. (Carmen), Lledo, E. (Elisa), Martinez-Climent, J.A. (José Ángel), Montiel-Duarte, C. (Cristina), Perez-Calvo, J. (Javier), Perez-Roger, I. (Ignacio), Poch, E. (Enric), Prosper, F. (Felipe), Rifon, J. (Jose)   +11 more
core  

Dasatinib overcomes AML cells resistant to BCL2 inhibition by degrading MCL1

British Journal of Haematology, EarlyView.
Summary Acute myeloid leukaemia (AML) is a severe disease occurring mainly in the elderly population. Venetoclax (VEN) combined with azacitidine has changed the paradigm of treatment of AML. Nevertheless, approximately 30% of patients are primary refractory to VEN (VEN‐R), with no current therapeutic option.
Sylvain Garciaz, Camille Montersino, Maxence Bourgoin, Arnaud Jacquel, Rémy Castellano, Arnaud Guille, Max Chaffanet, François Bertucci, Marie‐Anne Hospital, José Adélaïde, Patrick Auberger, Norbert Vey, Yves Collette   +12 more
wiley   +1 more source

Contribution of BCR-ABL kinase domain mutations to imatinib mesylate resistance in Philadelphia chromosome positive Malaysian chronic myeloid leukemia patients

Hematology Reports, 2012
Development of resistance to imatinib mesylate (IM) in chronic myeloid leukemia (CML) patients is mediated by different mechanisms that can be classified as BCR-ABL dependent or BCR-ABL independent pathways.
Marjanu Hikmah Elias, Abdul Aziz Baba, Azlan Husin, Abu Dzarr Abdullah, Rosline Hassan, Goh Ai Sim, S. Fadilah Abdul Wahid, Ravindran Ankathil   +7 more
doaj   +1 more source

α-bisabolol is an effective proapoptotic agent against BCR-ABL(+) cells in synergism with Imatinib and Nilotinib. [PDF]

PLoS ONE, 2012
We showed that α-bisabolol is active against primary acute leukemia cells, including BCR-ABL(+) acute lymphoblastic leukemias (ALL). Here we studied the activity of α-bisabolol against BCR-ABL(+) cells using 3 cell lines (K562, LAMA-84, CML-T1) and 10 ...
Massimiliano Bonifacio, Antonella Rigo, Emanuele Guardalben, Christian Bergamini, Elisabetta Cavalieri, Romana Fato, Giovanni Pizzolo, Hisanori Suzuki, Fabrizio Vinante   +8 more
doaj   +1 more source

Donor chimerism and bcr-abl gene status following non-myeloablative peripheral blood stem cell transplantation in chronic myeloid leukaemia patients in HUKM [PDF]

, 2008
Objective: This study was done to determine the relationship between donor chimerism and the presence of bcr-abl gene in chronic myeloid leukaemia (CML) patients post-transplantation.
Cheong, Soon Keng, Hussin, Noor Hamidah, Leong, Chooi Fun, Othman, Ainoon, Seman, Zainina   +4 more
core  

BCR-ABL rearrangement is not detectable in essential thrombocythemia [PDF]

Blood, 2001
Essential thrombocythemia (ET) is a chronic myeloproliferative disorder (MPD) characterized by an elevated thrombocytosis, an increased number of megakaryocytes with dismegakaryopoiesis in the bone marrow, and no identifiable underlying primary causes. The disease can evolve into myelofibrosis and,
EMILIA G., MARASCA, Roberto, ZUCCHINI, Patrizia, TEMPERANI, Paola, LUPPI, Mario, TORELLI, Giuseppe, LANZA F., DE ANGELIS C., GANDINI D., CASTOLDI G., VALLISA D., CAVANNA L., del Senno L.   +12 more
openaire   +5 more sources

GANT61 Modulates Autophagy and Lipid Metabolism in Ovarian Cancer

Cell Proliferation, EarlyView.
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

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

Inhibition of interleukin-1 signaling enhances elimination of tyrosine kinase inhibitor treated CML stem cells [PDF]

, 2016
Treatment of chronic myelogenous leukemia (CML) with BCR-ABL tyrosine kinase inhibitors (TKI) fails to eliminate leukemia stem cells (LSC). Patients remain at risk for relapse, and additional approaches to deplete CML LSC are needed to enhance the ...
Agarwal, Puneet, Bhatia, Ravi, Campbell, Victoria L., Chu, Su, Gaal, Karl, Holyoake, Tessa L., Hopcroft, Lisa, Jørgensen, Heather G., Lin, Allen, Zhang, Bin   +9 more
core   +1 more source