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https://www.readbyqxmd.com/read/28331056/monitoring-of-childhood-all-using-bcr-abl1-genomic-breakpoints-identifies-a-subgroup-with-cml-like-biology
#1
Lenka Hovorkova, Marketa Zaliova, Nicola C Venn, Kirsten Bleckmann, Marie Trkova, Eliska Potuckova, Martina Vaskova, Jana Linhartova, Katerina Machova Polakova, Eva Fronkova, Walter Muskovic, Jodie E Giles, Peter J Shaw, Gunnar Cario, Rosemary Sutton, Jan Stary, Jan Trka, Jan Zuna
We used the genomic breakpoint between BCR and ABL1 genes for the DNA-based monitoring of minimal residual disease (MRD) in 48 patients with childhood acute lymphoblastic leukemia (ALL). Comparing the results with standard MRD monitoring based on immunoglobulin/T-cell receptor (Ig/TCR) gene rearrangements and with quantification of IKZF1 deletion, we observed very good correlation for the methods in a majority of patients; however, over 20% of children (25% [8/32] with minor and 12.5% [1/8] with Major-BCR-ABL1 variants in the consecutive cohorts) had significantly (>1 log) higher levels of BCR-ABL1 fusion than Ig/TCR rearrangements and/or IKZF1 deletion...
March 22, 2017: Blood
https://www.readbyqxmd.com/read/28321124/combined-inhibition-of-%C3%AE-catenin-and-bcr-abl-synergistically-targets-tyrosine-kinase-inhibitor-resistant-blast-crisis-chronic-myeloid-leukemia-blasts-and-progenitors-in-vitro-and-in-vivo
#2
H Zhou, P Y Mak, H Mu, D H Mak, Z Zeng, J Cortes, Q Liu, M Andreeff, B Z Carter
Tyrosine kinase inhibitor (TKI) resistance and progression to blast crisis (BC), both related to persistent β-catenin activation remain formidable challenges for chronic myeloid leukemia (CML). We observed overexpression of β-catenin in BC-CML stem/progenitor cells, particularly in GMP progenitors, and highest among a novel CD34(+)CD38(+)CD123(hi)Tim-3(hi) subset as determined by CyTOF analysis. Co-culture with mesenchymal stromal cells (MSCs) induced the expression of β-catenin and its target CD44 in CML cells...
March 21, 2017: Leukemia: Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K
https://www.readbyqxmd.com/read/28315428/p53-modulates-the-effect-of-ribosomal-protein-s6-kinase1-s6k1-on-cisplatin-toxicity-in-chronic-myeloid-leukemia-cells
#3
Ling-Yi Xiao, Wai-Ming Kan
Chronic myeloid leukemia (CML) is characterized by the expression of the oncoprotein, BCR-ABL. BCR-ABL inhibitors revolutionized CML chemotherapy while blast crisis (BC) CML patients are less responsive. Since suppression of ribosomal protein S6 kinase1 (S6K1) phosphorylation reverses the resistance to BCR-ABL inhibitor in CML cells and S6K1 inhibitors augment cisplatin toxicity in lung cancer cells, we speculated that combination of S6K1 inhibitor and cisplatin may be beneficial for eliminating BC CML cells...
March 14, 2017: Pharmacological Research: the Official Journal of the Italian Pharmacological Society
https://www.readbyqxmd.com/read/28274536/chronic-myelomonocytic-leukemia-blast-crisis-in-a-patient-with-advanced-non-small-cell-lung-cancer-treated-with-egfr-tyrosine-kinase-inhibitors
#4
Hiroaki Ogata, Isamu Okamoto, Goichi Yoshimoto, Teppei Obara, Kayo Ijichi, Eiji Iwama, Taishi Harada, Koichi Akashi, Yoichi Nakanishi
A 59-year-old woman with epidermal growth factor receptor gene (EGFR) mutation-positive advanced lung adenocarcinoma was treated with afatinib after a diagnosis of chronic myelomonocytic leukemia (CMML). Twenty-one weeks later, she developed agranulocytosis, and CMML subsequently progressed to blast crisis. After complete remission of CMML, gefitinib was initiated; however, agranulocytosis recurred. This is the first reported case of both EGFR mutation-positive advanced non-small cell lung cancer with CMML, and of CMML blast crisis...
March 2017: Respiratory Investigation
https://www.readbyqxmd.com/read/28259737/medication-adherence-molecular-monitoring-and-clinical-outcomes-in-patients-with-chronic-myelogenous-leukemia-in-a-large-hmo
#5
Reina Haque, Jiaxiao Shi, Joanie Chung, Xiaoqing Xu, Chantal Avila, Christopher Campbell, Syed A Ahmed, Lei Chen, Joanne E Schottinger
OBJECTIVE: Our objective was to examine the association between adherence to tyrosine kinase inhibitors (TKIs) and molecular monitoring and the risk of disease progression or mortality among patients with chronic phase chronic myeloid leukemia (CML). DESIGN: We assembled a retrospective cohort of patients with CML (chronic phase, no prior cancer history, and confirmed to be Philadelphia chromosome positive) using data from electronic health records and chart reviews...
March 1, 2017: Journal of the American Pharmacists Association: JAPhA
https://www.readbyqxmd.com/read/28191543/the-third-time-chronic-myeloid-leukemia-in-lymphoblastic-crisis-with-abl1-kinase-mutation-induced-by-decitabine-dexamethason-combined-with-nilotinib-and-dasatinib
#6
Suli Wang, Chun Qiao, Yu Zhu, Wenyi Shen, Guangsheng He, Jianyong Li
Blast crisis (BC) is the major remaining challenge in the management of chronic myeloid leukemia (CML). The prognosis of the BC patient who carries ABL kinase mutation is very poor. One patient, with lymphoid CML-BC third time, was detected with T315A/F359I/M244V compound mutation by direct sequencing after treatment with tyrosine kinase inhibitions three years. The patient was treated with decitabine, dexamethasone, in combination with nilotinib and dasatinib. Then this patient received a complete hematologic response and cytogenetic response after two cycles of treatment...
December 1, 2016: Journal of Translational Internal Medicine
https://www.readbyqxmd.com/read/28186602/-analysis-of-isodicentric-ph-chromosomes-in-chronic-myeloid-leukemia-blast-crisis
#7
Qian Li, Xiaoji Lin, Ying Lin, Rongxin Yao, Wu Huang, Handong Mei, Jian Gong, Hui Chen, Ningyan Teng
OBJECTIVE: To explore the genetic and clinical characteristics of isodicentric Ph chromosomes [idic(Ph)] in lymphoid blast crisis of chronic myeloid leukemia (CML-BLC). METHODS: Bone marrow aspirates of 2 patients with CML-BLC were analyzed by R banding after 24 hours of culturing. Genomic copy number variations (CNV) were analyzed by single nucleotide polymorphism array (SNP array) in case 1. The results were confirmed with fluorescence in situ hybridization (FISH)...
February 10, 2017: Zhonghua Yi Xue Yi Chuan Xue za Zhi, Zhonghua Yixue Yichuanxue Zazhi, Chinese Journal of Medical Genetics
https://www.readbyqxmd.com/read/28179280/gata-factor-mutations-in-hematologic-disease
#8
John D Crispino, Marshall S Horwitz
GATA family proteins play essential roles in development of many cell types, including hematopoietic, cardiac, and endodermal lineages. The first three factors, GATAs 1,2 and 3, are essential for normal hematopoiesis, and their mutations are responsible for a variety of blood disorders. Acquired and inherited GATA1 mutations contribute to Diamond Blackfan anemia, acute megakaryoblastic leukemia, transient myeloproliferative disorder and a group of related congenital dyserythropoietic anemias with thrombocytopenia...
February 8, 2017: Blood
https://www.readbyqxmd.com/read/28129457/tumor-suppressor-gene-methylation-on-the-short-arm-of-chromosome-1-in-chronic-myelogenous-leukemia
#9
Naoki Mori, Mari Ohwashi-Miyazaki, Kentaro Yoshinaga, Michiko Okada, Masayuki Shiseki, Toshiko Motoji, Junji Tanaka
OBJECTIVES: We previously reported loss of heterozygosity on 1p in chronic myelogenous leukemia (CML). We analyzed promoter methylation and mutation of tumor suppressor genes on 1p36 in CML. METHODS: We performed methylation specific PCR (MS-PCR) analysis of the PRDM2, RUNX3, and TP73 genes in 61 patients with CML (43 chronic phase, CP; 2 accelerated phase; and 16 blast crisis, BC). Oxidative MS-PCR, PCR-single strand conformation polymorphism, and real time reverse transcriptase-PCR were also analyzed...
January 27, 2017: European Journal of Haematology
https://www.readbyqxmd.com/read/28107692/rna-binding-protein-msi2-positively-regulates-flt3-expression-in-myeloid-leukemia
#10
Ayuna Hattori, Daniel McSkimming, Natarajan Kannan, Takahiro Ito
FLT3 is frequently mutated and overexpressed in acute myelogenous leukemia (AML) and other hematologic malignancies. Although signaling events downstream of FLT3 receptor tyrosine kinase have been studied in depth, molecular mechanisms of how FLT3 expression is regulated at the post-transcriptional level in particular remain elusive. In this study, we investigated the roles of an RNA binding protein MSI2 as a regulator of FLT3 expression. MSI2 and FLT3 are significantly co-regulated in human AML and chronic myelogenous leukemia in blast crisis (BC-CML)...
January 11, 2017: Leukemia Research
https://www.readbyqxmd.com/read/28101208/effect-of-bovine-dialyzable-leukocyte-extract-on-induction-of-cell-differentiation-and-death-in-k562-human-chronic-myelogenous-leukemia-cells
#11
Crystel A Sierra-Rivera, Moisés A Franco-Molina, Edgar Mendoza-Gamboa, Pablo Zapata-Benavides, Jesús Santaolalla-Tapia, Erika E Coronado-Cerda, Reyes S Tamez-Guerra, Cristina Rodríguez-Padilla
Differentiation induction therapy is an attractive approach in leukemia treatment due to the fact that in blast crisis stage, leukemic cells lose their differentiation capacity. Therefore, it has been proposed as a therapeutic strategy to induce terminal differentiation of leukemic blast cells into a specific lineage, leading to prevention of high proliferation rates. The aim of the present study was to demonstrate the potential of cell differentiation and death induced by bovine dialyzable leukocyte extract (bDLE) in the K562 cell line...
December 2016: Oncology Letters
https://www.readbyqxmd.com/read/28079885/mirna182-regulates-percentage-of-myeloid-and-erythroid-cells-in-chronic-myeloid-leukemia
#12
Deepak Arya, Sasikala P Sachithanandan, Cecil Ross, Dasaradhi Palakodeti, Shang Li, Sudhir Krishna
The deregulation of lineage control programs is often associated with the progression of haematological malignancies. The molecular regulators of lineage choices in the context of tyrosine kinase inhibitor (TKI) resistance remain poorly understood in chronic myeloid leukemia (CML). To find a potential molecular regulator contributing to lineage distribution and TKI resistance, we undertook an RNA-sequencing approach for identifying microRNAs (miRNAs). Following an unbiased screen, elevated miRNA182-5p levels were detected in Bcr-Abl-inhibited K562 cells (CML blast crisis cell line) and in a panel of CML patients...
January 12, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/27999193/the-novel-anticancer-agent-jnj-26854165-is-active-in-chronic-myeloid-leukemic-cells-with-unmutated-bcr-abl-and-t315i-mutant-bcr-abl-through-promoting-proteosomal-degradation-of-bcr-abl-proteins
#13
Liangshun You, Hui Liu, Jian Huang, Wanzhuo Xie, Jueying Wei, Xiujin Ye, Wenbin Qian
Chronic myeloid leukemia (CML) is a clonal malignant disease caused by the expression of BCR/ABL. MDM2 (human homolog of the murine double minute-2) inhibitors such as Nutlin-3 have been shown to induce apoptosis in a p53-dependent manner in CML cells and sensitize cells to Imatinib. Here, we demonstrate that JNJ-26854165, an inhibitor of MDM2, inhibits proliferation and triggers cell death in a p53-independent manner in various BCR/ABL-expressing cells, which include primary leukemic cells from patients with CML blast crisis and cells expressing the Imatinib-resistant T315I BCR/ABL mutant...
January 31, 2017: Oncotarget
https://www.readbyqxmd.com/read/27967290/ecotropic-viral-integration-site-i-regulates-alpha1-6-fucosyl-transferase-expression-and-blocks-erythropoiesis-in-chronic-myeloid-leukemia
#14
Nivedita Kuila, Kasturi Bala Nayak, Arundhati Halder, Subramaniam Agatheeswaran, Ghanashyam Biswas, Sutapa Biswas, Naresh Chandra Pattnayak, Soumen Chakraborty
Although BCR-ABL is the hallmark genetic abnormality of chronic myeloid leukemia (CML), secondary molecular events responsible for the evolution of the disease to blast crisis are yet to be deciphered. Taking into account the significant association of ecotropic viral integration site I (EVI1) in CML drug resistance, it is necessary to decipher the other roles played by EVI1 in CML disease progression. In this regard, we cross-hybridized three microarray datasets and deduced a set of 11 genes that seems to be regulated by EVI1 in CML...
August 2017: Leukemia & Lymphoma
https://www.readbyqxmd.com/read/27908728/activation-of-evi1-transcription-by-the-lef1-%C3%AE-catenin-complex-with-p53-alteration-in-myeloid-blast-crisis-of-chronic-myeloid-leukemia
#15
Nawin Manachai, Yusuke Saito, Shingo Nakahata, Avinash Govind Bahirvani, Motomi Osato, Kazuhiro Morishita
The presence of a BCR-ABL1 fusion gene is necessary for the pathogenesis of chronic myeloid leukemia (CML) through t(9;22)(q34;q11) translocation. Imatinib, an ABL tyrosine kinase inhibitor, is dramatically effective in CML patients; however, 30% of CML patients will need further treatment due to progression of CML to blast crisis (BC). Aberrant high expression of ecotropic viral integration site 1 (EVI1) is frequently observed in CML during myeloid-BC as a potent driver with a CML stem cell signature; however, the precise molecular mechanism of EVI1 transcriptional regulation during CML progression is poorly defined...
January 22, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/27890073/switching-to-nilotinib-versus-imatinib-dose-escalation-in-patients-with-chronic-myeloid-leukaemia-in-chronic-phase-with-suboptimal-response-to-imatinib-lasor-a-randomised-open-label-trial
#16
Jorge E Cortes, Carmino Antonio De Souza, Manuel Ayala, Jose Luis Lopez, Eduardo Bullorsky, Sandip Shah, Xiaojun Huang, K Govind Babu, Kudrat Abdulkadyrov, José Salvador Rodrigues de Oliveira, Zhi-Xiang Shen, Tomasz Sacha, Israel Bendit, Zhizhou Liang, Tina Owugah, Tomasz Szczudlo, Sadhvi Khanna, Rafik Fellague-Chebra, Philipp D le Coutre
BACKGROUND: Optimal management of patients with chronic myeloid leukaemia in chronic phase with suboptimal cytogenetic response remains undetermined. This study aimed to investigate the safety and efficacy of switching to nilotinib vs imatinib dose escalation for patients with suboptimal cytogenetic response on imatinib. METHODS: We did a phase 3, open-label, randomised trial in patients with chronic myeloid leukaemia in chronic phase with suboptimal cytogenetic response to imatinib according to the 2009 European LeukemiaNet criteria, in Latin America, Europe, and Asia (59 hospitals and care centres in 12 countries)...
December 2016: Lancet Haematology
https://www.readbyqxmd.com/read/27784881/bilineal-extramedullary-blast-crisis-as-an-initial-presentation-of-chronic-myeloid-leukemia-a-case-report-and-literature-review
#17
REVIEW
Xiaoning Gao, Jie Li, Lili Wang, Ji Lin, Hongshi Jin, Yihan Xu, Nan Wang, Yu Zhao, Daihong Liu, Li Yu, Quanshun Wang
BACKGROUND Chronic myeloid leukemia (CML) is a clonal myeloproliferative disorder characterized by the Philadelphia chromosome generated by the reciprocal translocation t(9: 22)(q34;q11). CML is usually diagnosed in the chronic phase. Blast crisis represents an advanced phase of CML. Extramedullary blast crisis as the initial presentation of CML with bone marrow remaining in chronic phase is an unusual event. Further, extramedullary blast crisis with T lymphoid/myeloid bilineal phenotype as an initial presentation for CML is extremely unusual...
October 27, 2016: American Journal of Case Reports
https://www.readbyqxmd.com/read/27736287/high-expression-of-interleukin-2-receptor-%C3%AE-chain-cd25-in-myelodysplastic-syndrome-preceding-acute-myeloid-leukemia-and-chronic-myeloid-leukemia-in-myeloid-blast-crisis
#18
Kazunori Nakase, Kenkichi Kita, Taiichi Kyo, Naoyuki Katayama
No abstract text is available yet for this article.
October 13, 2016: Leukemia & Lymphoma
https://www.readbyqxmd.com/read/27721761/an-atypical-initial-presentation-of-chronic-myeloid-leukemia-with-central-nervous-system-and-lymph-node-blast-crises
#19
Khadega A Abuelgasim, Saeed Alshieban, Nada A Almubayi, Ayman Alhejazi, Abdulrahman R Jazieh
We describe the case of a young man with therapy-naive chronic myeloid leukemia who did not initially have any peripheral blood or bone marrow excess blasts but presented with extramedullary myeloid blast crises involving the central nervous system and multiple lymph nodes. Conventional cytogenetic tests were positive for t(9;22)(q34:q11) as well as for trisomy 8, 14 and 21 and del(16q). The patient's peripheral blood and bone marrow were positive for the BCR-ABL oncogene when analyzed by fluorescence in situ hybridization and polymerase chain reaction...
May 2016: Case Reports in Oncology
https://www.readbyqxmd.com/read/27628325/the-new-clinicopathologic-and-molecular-findings-in-myeloid-neoplasms-with-inv-3-q21q26-t-3-3-q21-q26-2
#20
REVIEW
Huan-You Wang, Hooman H Rashidi
CONTEXT: - Inv(3)(q21q26)/t(3;3)(q21;q26.2) is the most common form of genetic abnormality of the so-called 3q21q26 syndrome. Myeloid neoplasms with 3q21q26 aberrancies include acute myeloid leukemia (AML), myelodysplastic syndrome (MDS), and blast crisis of myeloproliferative neoplasms. Recent advances on myeloid neoplasms with inv(3)/t(3;3) with regard to clinicopathologic features and novel molecular or genomic findings warrant a comprehensive review on this topic. OBJECTIVE: - To review the clinicopathologic features and molecular as well as genomic alterations in myeloid neoplasms with inv(3)/t(3;3)...
December 2016: Archives of Pathology & Laboratory Medicine
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