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Chronic Myeloid disease ph -

Ying Li, Kevin Zhao, Chenjiao Yao, Samir Kahwash, Yan Tang, Guojiuan Zhang, Kara Patterson, Qi-En Wang, Weiqiang Zhao
Unlike chronic myeloid leukemia, patients with acute lymphoblastic leukemia (ALL) with Philadelphia chromosome (Ph+) do not respond well to Imatinib or tyrosine kinase inhibitors (TKI). In addition, TKI might induce resistant mutations in kinase domain (KD) of ABL in patients with relapsed diseases. Of the histone deacetylase (HDAC) inhibitors, suberoylanilide hydroxamic acid (SAHA) has shown to induce potent cytotoxicity on acute myeloid leukemia cell lines but Givinostat effect on acute lymphoblastic leukemia (ALL) has not been reported...
September 2016: Genes & Cancer
Nira Varda-Bloom, Ivetta Danylesko, Roni Shouval, Shiran Eldror, Atar Lev, Jacqueline Davidson, Esther Rosenthal, Yulia Volchek, Noga Shem-Tov, Ronit Yerushalmi, Avichai Shimoni, Raz Somech, Arnon Nagler
Allogeneic stem cell transplantation remains the standard treatment for resistant advanced chronic myeloid leukemia and Philadelphia chromosome-positive acute lymphoblastic leukemia. Relapse is the major cause of treatment failure in both diseases. Post-allo-SCT administration of TKIs could potentially reduce relapse rates, but concerns regarding their effect on immune reconstitution have been raised. We aimed to assess immune functions of 12 advanced CML and Ph+ ALL patients who received post-allo-SCT nilotinib...
January 3, 2017: Oncotarget
Yiguo Hu
Chronic myeloid leukemia (CML) is a myeloproliferative disorder with a high number of well-differentiated neutrophils in peripheral blood and myeloid cells in bone marrow (BM). CML is derived from the hematopoietic stem cells (HSCs) with the Philadelphia chromosome (Ph(+), t(9;22)-(q34;q11)), resulting in generating a fusion oncogene, BCR/ABL1. HSCs with Ph(+) are defined as leukemia stem cells (LSCs), a subpopulation cell at the apex of hierarchies in leukemia cells and responsible for the disease continuous propagation...
2016: Methods in Molecular Biology
Haojian Zhang, Shaoguang Li
Chronic myeloid leukemia (CML) is a myeloproliferative disorder derived from a hematopoietic stem cell (HSC), harboring Philadelphia chromosome (Ph chromosome). Formation of the Ph chromosome is caused by a reciprocal translocation between the chromosomes 9 and 22 t(9;22)(q34;q11), resulting in a fusion protein known as BCR-ABL which has constitutive tyrosine kinase activity and promotes the proliferation of leukemia cells via multiple mechanisms. Studies on CML have led to the identification of the first cancer-associated chromosomal abnormality and the subsequent development of tyrosine kinase inhibitors (TKIs) that inhibit BCR-ABL kinase activity in CML...
2016: Methods in Molecular Biology
Javier Pinilla-Ibarz, Kendra L Sweet, Gabriela M Corrales-Yepez, Rami S Komrokji
An important pathogenetic distinction in the classification of myeloproliferative neoplasms (MPNs) is the presence or absence of the BCR-ABL fusion gene, which encodes a unique oncogenic tyrosine kinase. The BCR-ABL fusion, caused by the formation of the Philadelphia chromosome (Ph) through translocation, constitutes the disease-initiating event in chronic myeloid leukemia. The development of successive BCR-ABL-targeted tyrosine-kinase inhibitors has led to greatly improved outcomes in patients with chronic myeloid leukemia, including high rates of complete hematologic, cytogenetic, and molecular responses...
2016: OncoTargets and Therapy
Jorge E Cortes, Hanna J Khoury, Hagop M Kantarjian, Jeff H Lipton, Dong-Wook Kim, Philippe Schafhausen, Ewa Matczak, Eric Leip, Kay Noonan, Tim H Brümmendorf, Carlo Gambacorti-Passerini
Bosutinib is an Src/Abl tyrosine kinase inhibitor (TKI) indicated for adults with Ph+ chronic myeloid leukemia (CML) resistant/intolerant to prior TKIs. This long-term update of an ongoing phase 1/2 study evaluated the efficacy and safety of third-/fourth-line bosutinib in adults with chronic phase (CP) CML. Median durations of treatment and follow-up were 8.6 (range, 0.2-87.7) months and 32.7 (0.3-93.3) months, respectively. Cumulative confirmed complete hematologic response (cCHR) and major cytogenetic response (MCyR) rates were 74% (95% CI, 65-81%) and 40% (31-50%), respectively; Kaplan-Meier (K-M) probability of maintaining cCHR or MCyR at 4 years was 63% (95% CI, 50-73%) and 69% (52-81%)...
December 2016: American Journal of Hematology
Jorge Luis Ángeles-Velázquez, Rafael Hurtado-Monroy, Pablo Vargas-Viveros, Silvia Carrillo-Muñoz, Myrna Candelaria-Hernández
BACKGROUND: Over the past years, the survival of patients with Philadelphia-positive chronic myeloid leukemia (CML Ph(+)) has increased as a result of therapy with tyrosin kinase inhibitors (TKIs). Intolerance to TKIs has been described in approximately 20% of patients receiving treatment. We studied the incidence of imatinib intolerance in patients with CML Ph(+) and their outcome in our CML reference site, as there is no information about the evolution of patients intolerant to TKIs...
August 2016: Clinical Lymphoma, Myeloma & Leukemia
Krupa Shah, Sonia Parikh, Rakesh Rawal
Chronic myeloid leukaemia (CML) is a clonal myeloproliferative hematopoietic stem cell disorder. Deregulated BCRABL fusion tyrosine kinase activity is the main cause of CML disease pathogenesis, making BCRABL an ideal target for inhibition. Current tyrosine kinase inhibitors (TKIs) designed to inhibit BCRABL oncoprotein activity, have completely transformed the prognosis of CML. Interruption of TKI treatment leads to minimal residual disease reside (MRD), thought to reside in TKIinsensitive leukaemia stem cells which remain a potential reservoir for disease relapse...
2016: Asian Pacific Journal of Cancer Prevention: APJCP
Anthony A Oyekunle, Muheez A Durosinmi, Ramoni A Bolarinwa, Temilola Owojuyigbe, Lateef Salawu, Norah O Akinola
OBJECTIVES: The advent of the tyrosine kinase inhibitors has markedly changed the prognostic outlook for patients with Ph(+) and/or BCR-ABL1 (+) chronic myeloid leukemia (CML). This study was designed to assess the overall survival (OS) of Nigerian patients with CML receiving imatinib therapy and to identify the significant predictors of OS. METHODS: All patients with CML receiving imatinib from July 2003 to June 2013 were studied. The clinical and hematological parameters were studied...
2016: Clinical Medicine Insights. Blood Disorders
Ibrahim Aldoss, Karl Gaal, Monzr M Al Malki, Haris Ali, Ryotaro Nakamura, Stephen J Forman, Vinod Pullarkat
The tyrosine kinase inhibitor dasatinib is often used after allogeneic hematopoietic cell transplantation to treat minimal residual disease in Philadelphia chromosome-positive (Ph+) acute lymphoblastic leukemia (ALL). Colitis, sometimes hemorrhagic, has occasionally been described with the use of dasatinib for both chronic myeloid leukemia and Ph+ ALL. The pathogenesis of dasatinib-induced colitis is unclear but may be related to effects of dasatinib on immune function. We describe a series of 5 patients who had 7 episodes of colitis during dasatinib use...
October 2016: Biology of Blood and Marrow Transplantation
Zachariah DeFilipp, Amelia A Langston, Zhengjia Chen, Chao Zhang, Martha L Arellano, Fuad El Rassi, Christopher R Flowers, Vamsi K Kota, Zaid Al-Kadhimi, Rachel Veldman, Anand P Jillella, Sagar Lonial, Edmund K Waller, Hanna J Khoury
INTRODUCTION: The effect of post-transplant maintenance tyrosine kinase inhibitors (TKIs) on the outcomes of allogeneic hematopoietic stem cell transplantation in high-risk Philadelphia chromosome-positive (Ph(+)) leukemia remains unknown. PATIENTS AND METHODS: A retrospective analysis that included allograft recipients with accelerated phase and blast phase chronic myeloid leukemia or Ph(+) acute lymphoblastic leukemia who had received post-transplant maintenance TKI therapy from 2004 to 2014...
August 2016: Clinical Lymphoma, Myeloma & Leukemia
Taghrid Mohamed Gaafar, Inas Ismail Raafat, Azza Ahmed Aly, Nagwa Abd El-Ghaffar Mohamed, Reem Jan Farid, Neveen Ezzat Saad, Rabab El-Hawary, Naglaa Mostafaa, Mirhan Mohamed Ahmed
BACKGROUND: Chronic myeloid leukemia (CML) is a clonal myeloproliferative disorder of hematopoietic stem cells. It is characterized at the cytogenetic level by Philadelphia (ph) chromosome and at the molecular level by the BCR/ABL gene rearrangement. Bone marrow derived mesenchymal stem cells (MSCs) are pluripotent stem cells that can differentiate into several mesenchymal tissues. AIM: To observe the biological characteristics of MSCS from CML patients and to determine whether MSCs harbor the abnormal BCR/ABL translocation similar to CML bone marrow cells...
June 15, 2015: Open Access Macedonian Journal of Medical Sciences
Adisak Tantiworawit, Supanat Kongjarern, Ekarat Rattarittamrong, Suree Lekawanvijit, Kanokkan Bumroongkit, Nonglak Boonma, Thanawat Rattanathammethee, Sasinee Hantrakool, Chatree Chai-Adisaksopha, Lalita Norasetthada
BACKGROUND: A diagnosis of chronic myeloid leukemia (CML) is made on discovery of the presence of a Philadelphia (Ph) chromosome. The success of the treatment of this form of leukemia with tyrosine kinase inhibitor (TKI) is monitored by reduction of the Ph chromosome. OBJECTIVE: To compare the role of conventional cytogenetic (CC) methods with a real time quantitative polymerase chain reaction (RQ-PCR) and fluorescence in situ hybridization (FISH) for diagnosis and treatment monitoring of CML patients...
2016: Asian Pacific Journal of Cancer Prevention: APJCP
L Charaf, F-X Mahon, I Lamrissi-Garcia, I Moranvillier, F Beliveau, B Cardinaud, S Dabernat, H de Verneuil, F Moreau-Gaudry, A Bedel
Although tyrosine kinase inhibitors (TKIs) efficiently cure chronic myeloid leukemia (CML), they can fail to eradicate CML stem cells (CML-SCs). The mechanisms responsible for CML-SC survival need to be understood for designing therapies. Several previous studies suggest that TKIs could modulate CML-SC quiescence. Unfortunately, CML-SCs are insufficiently available. Induced pluripotent stem cells (iPSCs) offer a promising alternative. In this work, we used iPSCs derived from CML patients (Ph+). Ph+ iPSC clones expressed lower levels of stemness markers than normal iPSCs...
January 2017: Leukemia: Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K
David Gómez-Almaguer, Olga G Cantú-Rodríguez, Cesar H Gutiérrez-Aguirre, Guillermo J Ruiz-Argüelles
OBJECTIVES: This article reviews clinical experiences in the treatment of chronic myeloid leukemia (CML) in an environment of limited resources. METHODS: We reviewed recent publications on Pub med and abstracts from mayor congresses relevant to the disease. RESULTS: CML is a hematological neoplasm observed more frequently in adults, regardless of their socioeconomic status. Until recently, available treatments improved patients' quality of life but did not modify survival...
December 2016: Hematology (Amsterdam, Netherlands)
Y Dong, F Liu, C Wu, S Li, X Zhao, P Zhang, J Jiao, X Yu, Y Ji, M Zhang
Breakpoint cluster region-Abelson murine leukaemia viral oncogene homologue 1 (BCR-ABL1), encoded by the Philadelphia (Ph) chromosome, is the characteristic of chronic myeloid leukaemia (CML) and a subset of acute lymphoblastic leukaemia (ALL). We demonstrated that expression of the Ik6 transcript, which lacked exons 3-6, was observed exclusively in BCR-ABL1(+) B ALL and lymphoid blast crisis CML (BC-CML) patients harbouring the IKZF1 Δ3-6 deletion. To confirm the hypothesis that illegitimate recombination activating gene protein (RAG)-mediated recombination events are involved in IKZF1 Δ3-6 deletion in BCR-ABL1 lymphoblastic leukaemia, we first demonstrated that the expression rates of RAG1 and RAG2, collectively called RAG, were higher in ALL and BC-CML (lymphoid)...
September 2016: Clinical and Experimental Immunology
Andrew L Sochacki, Melissa A Fischer, Michael R Savona
The discovery of JAK2 (V617F) a decade ago led to optimism for a rapidly developing treatment revolution in Ph(-) myeloproliferative neoplasms. Unlike BCR-ABL, however, JAK2 was found to have a more heterogeneous role in carcinogenesis. Therefore, for years, development of new therapies was slow, despite standard treatment options that did not address the overwhelming symptom burden in patients with primary myelofibrosis (MF), post-essential thrombocythemia MF, post-polycythemia vera MF, and myelodysplastic syndrome (MDS)/myeloproliferative neoplasm (MPN) syndromes...
2016: OncoTargets and Therapy
Juan Wang, Yanli Zhang, Yingling Zu, Zhen Li, Mengjuan Li, Yongping Song
OBJECTIVE: To investigate the characteristics and clinical outcome of T315I mutation in Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph(+) ALL) and chronic myeloid leukemia (CML). METHODS: The clinical data of 118 tyrosine kinase inhibitors (TKIs) resistant Ph(+) ALL and CML cases who were detected ABL kinase domain mutation in Affiliated Tumor Hospital of Zhengzhou University from March 2014 to June 2015 were collected. Karyotypes and BCR-ABL fusion gene were analyzed respectively by R-banding, real-time quantitative polymerase chain reaction (PCR)...
February 2016: Zhonghua Xue Ye Xue za Zhi, Zhonghua Xueyexue Zazhi
Noortje Thielen, Johan Richter, Matthias Baldauf, Gisela Barbany, Thoas Fioretos, Francis Giles, Bjørn-Tore Gjertsen, Andreas Hochhaus, Gerrit Jan Schuurhuis, Sieghart Sopper, Leif Stenke, Sarah Thunberg, Dominik Wolf, Gert Ossenkoppele, Kimmo Porkka, Jeroen Janssen, Satu Mustjoki
PURPOSE: Leukemic stem cells (LSCs) may harbor important resistance to tyrosine kinase inhibitors in chronic myelogenous leukemia (CML). We identified Philadelphia chromosome (Ph)-positive CD34(+)CD38(-) bone marrow cells (here denoted LSCs) and addressed their response-predictive value in patients with CML (n = 48) subjected to nilotinib in the ENEST1st trial (NCT01061177). EXPERIMENTAL DESIGN: Two flow cytometry-based cell sorting methods were used with multiparameter-directed CD45- (MPFC) and BCR-ABL1 probe-linked (FISH) identification of Ph-positive cells, respectively...
August 15, 2016: Clinical Cancer Research: An Official Journal of the American Association for Cancer Research
Priyanka A Pophali, Mrinal M Patnaik
Imatinib mesylate was the first tyrosine kinase inhibitor (TKI) approved for the management of chronic myeloid leukemia. Imatinib produces acceptable responses in approximately 60% of patients, with approximately 20% discontinuing therapy because of intolerance and approximately 20% developing drug resistance. The advent of newer TKIs, such as nilotinib, dasatinib, bosutinib, and ponatinib, has provided multiple options for patients. These agents are more potent, have unique adverse effect profiles, and are more likely to achieve relevant milestones, such as early molecular responses (3-6 months) and optimal molecular responses (12 months)...
January 2016: Cancer Journal
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