Results 21 to 30 of about 454 (136)

Current Trends in the Diagnosis and Evidence-Based Management of Patients with Myeloproliferative Disorders [PDF]

, 2023
Myeloproliferative disorders (MPD) are clonal hematopoietic disorders characterized by abnormal clone expansion of haematological progenitor cells, which can lead to thrombosis, bleeding, and/or transformation to leukaemia. Chronic myelogenous leukaemia (
Ali, Hauwa Buhari, Bagudo, Ibrahim Aliyu, Bello, Yazid, Garba, Aliyu, Haruna, Lukman, Kasimu, Muhammad Sani, Kwaifa, Ibrahim Kalle, Ouigwe, Festus, Sani, Sani Lawal, Yakubu, Abdulrahman   +9 more
core   +2 more sources

Understanding sensitivity to BH3 mimetics: ABT-737 as a case study to foresee the complexities of personalized medicine. [PDF]

, 2012
BH3 mimetics such as ABT-737 and navitoclax bind to the BCL-2 family of proteins and induce apoptosis through the intrinsic apoptosis pathway. There is considerable variability in the sensitivity of different cells to these drugs.
Redman, CW, Richardson, A, Stamelos, VA
core   +2 more sources

Protein Kinase CK2: A Targetable BCR-ABL Partner in Philadelphia Positive Leukemias

Advances in Hematology, 2015
BCR-ABL-mediated leukemias, either Chronic Myeloid Leukemia (CML) or Philadelphia positive Acute Lymphoblastic Leukemia (ALL), are the paradigm of targeted molecular therapy of cancer due to the impressive clinical responses obtained with BCR-ABL ...
Alessandro Morotti, Giovanna Carrà, Cristina Panuzzo, Sabrina Crivellaro, Riccardo Taulli, Angelo Guerrasio, Giuseppe Saglio   +6 more
doaj   +1 more source

The burden of cystic fibrosis in North Africa. [PDF]

, 2023
Background: Over 200 pathogenic variants in the cystic fibrosis transmembrane conductance regulator (CFTR) gene are associated with cystic fibrosis (CF)-the most prevalent autosomal recessive disease globally, the p.Phe508del variant being the most ...
Abriel, Hugues, Bouguenouch, Laila, Daimi, Houria, EL Makhzen, Nada   +3 more
core   +1 more source

EHA2021 Virtual Congress Abstract Book

, 2021
HemaSphere, Volume 5, Issue S2, June 2021.
wiley   +1 more source

PF396 HISTONE DEACETYLASE INHIBITOR PANOBINOSTAT TARGETS CALCINEURIN/NFATC1 SIGNALING AND ABROGATES THE RESISTANCE OF PH+ LEUKEMIA CELLS TO DASATINIB

HemaSphere, Volume 3, Issue S1, Page 150, June 2019., 2019
Background: BCR‐ABL‐targeted tyrosine kinase inhibitors (TKI) revolutionized the outcome of patients inflicted with CML and Ph+ B‐ALL. However, TKI resistance continues to pose challenges for both CML and ALL. Aims: We hypothesized that overcoming the BM microenvironment‐mediated protection of Ph+ leukemic cells from TKI‐mediated apoptosis may further ...
K. Beider, O. Landes, A.H. Grushchenko‐Polaq, O. Ostrovsky, V. Dimenshtein, I. Danylesko, A. Shimoni, A. Peled, B. Gaugler, A. Nagler   +9 more
wiley   +1 more source

Inhibition of BCR/ABL protein expression by miR-203 sensitizes for imatinib mesylate.

PLoS ONE, 2013
Selective inhibition of BCR/ABL expression by RNA interference has been demonstrated as an effective strategy in CML treatment and a reversal to imatinib resistance.
Yajuan Li, Ying Yuan, Kun Tao, Xin Wang, Qing Xiao, Zhenglan Huang, Liang Zhong, Weixi Cao, Jianping Wen, Wenli Feng   +9 more
doaj   +1 more source

PF397 IDENTIFICATION OF PROTEIN‐PROTEIN INTERACTIONS NECESSARY FOR MAINTENANCE OF BCR‐ABL CORE COMPLEX

HemaSphere, Volume 3, Issue S1, Page 151, June 2019., 2019
Background: Approximately 50% of chronic myeloid leukemia (CML) patients in deep remission experience a return of clinical CML after withdrawal of tyrosine kinase inhibitors (TKIs), suggesting signaling of catalytically inactive BCR‐ABL. This allows for survival of cancer cells responsible for CML relapse after discontinuation of the TKI therapy ...
T. Gregor, M.K. Bosakova, J. Rynes, S.F. Trantirkova, J. Mayer, L. Trantirek, P. Krejci   +6 more
wiley   +1 more source

Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR Cascade Inhibitors: How Mutations Can Result in Therapy Resistance and How to Overcome Resistance [PDF]

, 2012
The Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR cascades are often activated by genetic alterations in upstream signaling molecules such as receptor tyrosine kinases (RTK).
Abell, Abken, Abken, Acquas, Ahn, Alessi DR, Amaravadi, Ambrosetti, Amler, Andre, Andreeff, Antoch, Arteaga, Atasoy, Auberger, Auberger, Auernhammer, Awada, Ayral-Kaloustian, Bakkenist, Ball, Bartek, Baselga, Basilico, Batist, Belvin, Belvin, Belvin, Bendell, Bendtzen, Benjamin, Berberich, Bernhardt, Bierer, Birnbaum, Bissell, Blagosklonny, Blagosklonny, Blagosklonny, Blagosklonny, Bonati, Bouscary, Bouscary, Bouscary, Brown, Brown, Calvo, Campbell, Caro, Cervello, Cervello, Cervello, Chang, Chapman, Chen, Chen, Cheng, Cheng, Choi, Citrin, Cloos, Cocco, Coin, Conejo-Garcia, Cook, Cook, Croasdell, Cross, D'Ambrosio, D'Orazi, Damia, Dammacco, Dang, Darnell, Darzynkiewicz, Davey, Davis, De Pover, Del Sal, Demetri, Dennis, Di Cristofano, Ding, Direnzo, Dong, Duronio, Eckhardt, Engelman, Engelman, Escudier, Evers, Falchook, Felip, Festuccia, Feun, Figlin, Finkel, Flachook, Flaherty, Flaherty, Fotedar, Foà, Friedman, Furman, Furman, Gadgeel, Gaither, Galle, Garcia-Echeverria, Garraway, Geissler, Gibbons, Giese, Gilmer, Glazer, Glynn, Gordon, Goutopoulos, Grant, Gray, Grever, Guan, Guan, Guichard, Ha, Haas-Kogan, Hall, Hallahan, Hammond, Hedley, Hedley, Heinemann, Heitman, Helin, Herlyn, Herlyn, Hollander, Hong, Horwitz, Houghton, Howell, Huang, Iozzo, James, Jang, Jendrossek, Jiang, Johnsen, Jongstra, Kaelin, Kaina, Kane, Kaufmann, Kaufmann, Kaufmann, Kelley, Khanna, Khwaja, Kimmelman, Knudsen, Koh, Konopleva, Kopelovich, Korn, Koromilas, Kotani, Kovalchuk, Kraft, Kraft, Kraft, Kramer, Kroemer, Kroemer, Kroemer, Lain, Landberg, Lannutti, Lawrence, Leber, Lee, Lin, Lippincott-Schwartz, Lisanti, Lisanti, Lisanti, Lisanti, Lisanti, Lisanti, Lisanti, Liu, Lo, Lo, Lo, Longo, Lopez, Lu, Lu, Luedde, Macewan, Maestro, Maffucci, Maguire, Major, Marais, Marais, Marais, Marimuthu, Marks, Martelli, Martelli, Martelli, Martelli, Martelli, Martelli, Martelli, Martelli, Martelli, Mayer, Mayeux, McCann, McCubrey, McCubrey, McCubrey, McCubrey, McCubrey, McCubrey, McDaid, McDonald, Menendez, Menendez, Menendez, Merchant, Mercuri, Mijatovic, Milella, Mohammad, Montalto, Montalto, Munshi, Murata, Musgrove, Myers, Naing, Nakashima, Namchuk, Nathanson, Nawrocki, Nawrocki, Nicoletti, Nicoletti, Nijman, Nilsson, Nilsson, Noda, Noguchi, O'Dwyer, O'Dwyer, Oktay, Ouellet, Pachter, Padera, Padera, Panayotou, Pandolfi, Pandolfi, Pani, Park, Patel, Platanias, Platanias, Poli, Polman, Poroshina, Powis, Prives, Quart, Ramalingam, Reck, Ribas, Ribas, Ricart, Rieber, Roberts, Robertson, Rommel, Rosen, Rosen, Rosen, Rosen, Rosen, Roy, Roy, Ruggero, Rupprecht, Salmeron, Samuels, Sanchez, Sanders, Santoro, Sarkar, Sarkaria, Scaglioni, Schadendorf, Schellens, Schmidmaier, Schmidmaier, Schmidt, Schmidt, Schoffski, Schwartz, Scott, Sebolt-Leopold, Sebti, Selivanova, Sellers, Sellers, Sellers, Settleman, Sharan, Shaw, Shaw, Shellooe, Shields, Simeone, Simon, Sitzmann, Siu, Slingluff, Smalley, Smalley, Smalley, Smalley, Smalley, Smalley, Smith, Solary, Solit, Soria, Sotgia, Spratlin, Springer, Stathopoulos, Stegmeier, Stern, Stoeltzing, Stromblad, Stromblad, Su, Suh, Sun, Sutherland, Syed, Syljuasen, Tafuri, Tang, Theurkauf, Thompson, Thompson, Tran, Tse, Turhan, Valerie, van den Bent, van Montfort, van Montfort, Varticovski, Vassilev, Vazquez-Martin, Vidal, Vogt, Wacheck, Wang, Wang, Wang, Warmuth, Waterfield, Weinberg, Weiss, Weiss, Weissgerber, Weissman, Wessels, Wicha, Williams, Williams, Williamson, Winquist, Workman, Wrana, Xing, Yahalom, Yonezawa, Yu, Yung, Zacksenhaus, Zhang, Zhang, Zhang, Zhang, Zheng, Zhou, Zhou, Zopf   +402 more
core   +2 more sources

PF398 KNOCKDOWN OF LASP1 IN CXCR4 EXPRESSING CML CELLS PROMOTES CELL PERSISTENCE, PROLIFERATION AND TKI RESISTANCE

HemaSphere, Volume 3, Issue S1, Page 151, June 2019., 2019
Background: Chronic myeloid leukemia (CML) is a hematopoietic stem cell disorder characterized by a fusion protein, the constitutively active BCR–ABL tyrosine kinase, leading to expansion of differentiated granulocytes. Although tyrosine kinase inhibitors (TKI) have significantly improved patient care, minimal residual disease (MRD) remains a clinical ...
A.B. Herrmann, M.‐L. Müller, M.F. Orth, J.P. Müller, A. Zernecke, A. Hochhaus, T. Ernst, E. Butt, J.J. Frietsch   +8 more
wiley   +1 more source