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Leukemia: Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K

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https://www.readbyqxmd.com/read/28386105/measurable-residual-disease-testing-in-acute-myeloid-leukaemia
#1
REVIEW
C S Hourigan, R P Gale, N J Gormley, G J Ossenkoppele, R B Walter
There is considerable interest in developing techniques to detect and/or quantify remaining leukaemia cells termed measurable or, less precisely, minimal residual disease (MRD) in persons with acute myeloid leukaemia (AML) in complete remission defined by cytomorphological criteria. An important reason for AML MRD-testing is the possibility of estimating the likelihood (and timing) of leukaemia relapse. A perfect MRD-test would precisely quantify leukaemia cells biologically able and likely to cause leukaemia relapse within a defined interval...
April 21, 2017: Leukemia: Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K
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 granulocyte-macrophage 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...
April 18, 2017: Leukemia: Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K
https://www.readbyqxmd.com/read/28400620/tunneling-nanotubes-facilitate-autophagosome-transfer-in-the-leukemic-niche
#3
B de Rooij, R Polak, F Stalpers, R Pieters, M L den Boer
Acute lymphoblastic leukemia (ALL) cells create a leukemic niche with mesenchymal stromal cells (MSCs). Cytoskeletal structures called tunneling nanotubes (TNTs) facilitate communication between ALL cells and MSCs by transporting molecules and inducing the secretion of pro-survival cytokines. The identity of the molecules driving these malignant processes are currently unknown. Here we investigate which structures are transported from ALL cells toward MSCs by quantifying the transfer of ectopically expressed fluorescent marker proteins using flow cytometry...
April 12, 2017: Leukemia: Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K
https://www.readbyqxmd.com/read/28400619/dysfunction-of-the-wt1-meg3-signaling-promotes-aml-leukemogenesis-via-p53-dependent-and-independent-pathways
#4
Y Lyu, J Lou, Y Yang, J Feng, Y Hao, S Huang, L Yin, J Xu, D Huang, B Ma, D Zou, Y Wang, Y Zhang, B Zhang, P Chen, K Yu, Ew-F Lam, X Wang, Q Liu, J Yan, B Jin
Long non-coding RNAs (lncRNAs) play a pivotal role in tumorigenesis, exemplified by the recent finding that lncRNA MEG3 inhibits tumor growth in a p53-dependent manner. Acute myeloid leukemia (AML) is the most common malignant myeloid disorder in adults, and TP53 mutations or loss are frequently detected in patients with therapy-related AML or AML with complex karyotype. Here, we reveal that MEG3 is significantly down-regulated in AML and suppresses leukemogenesis in not only a p53-dependent, but also a p53-independent manner...
April 12, 2017: Leukemia: Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K
https://www.readbyqxmd.com/read/28400618/donor-type-in-addition-to-transplantation-in-chronic-phase-and-myeloablative-conditioning-influence-transplant-survival-for-patients-with-advanced-chronic-myeloid-leukemia-in-the-era-of-tyrosine-kinase-inhibitors
#5
P Kongtim, K Adekola, D R Milton, R Ramlal, A Jimenez, J Chen, G Rondon, S Ahmed, P Kebriaei, O Betul, C M Hosing, U Popat, I Khouri, E Jabbour, J E Cortes, H M Kantarjian, R E Champlin, S O Ciurea
Leukemia accepted article preview online, 12 April 2017. doi:10.1038/leu.2017.118.
April 12, 2017: Leukemia: Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K
https://www.readbyqxmd.com/read/28400617/nek2-induces-osteoclast-differentiation-and-bone-destruction-via-heparanase-in-multiple-myeloma
#6
M Hao, R F Machin, H Xu, J Shaughnessy, B Barlogie, D Roodman, D E Quelle, S Janz, M H Tomasson, R D Sanderson, L Qiu, I Frech, G Tricot, F Zhan
Leukemia accepted article preview online, 12 April 2017. doi:10.1038/leu.2017.115.
April 12, 2017: Leukemia: Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K
https://www.readbyqxmd.com/read/28397868/cobll1-is-linked-to-drug-resistance-and-blastic-transformation-in-chronic-myeloid-leukemia
#7
S H Han, S-H Kim, H-J Kim, Y Lee, S-Y Choi, G Park, D-H Kim, A Lee, J Kim, J-M Choi, Y Kim, K Myung, H Kim, D-W Kim
No abstract text is available yet for this article.
April 11, 2017: Leukemia: Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K
https://www.readbyqxmd.com/read/28321121/dnmt3a-regulates-t-cell-development-and-suppresses-t-all-transformation
#8
A C Kramer, A Kothari, W C Wilson, H Celik, J Nikitas, C Mallaney, E L Ostrander, E Eultgen, A Martens, M C Valentine, A L Young, T E Druley, M E Figueroa, B Zhang, G A Challen
T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematopoietic neoplasm resulting from the malignant transformation of T-cell progenitors, and comprises ~15% and 25% of pediatric and adult ALL cases, respectively. It is well-established that activating NOTCH1 mutations are the major genetic lesions driving T-ALL in most patients, but efforts to develop targeted therapies against this pathway have produced limited success in decreasing leukemic burden and come with significant clinical side effects...
April 11, 2017: Leukemia: Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K
https://www.readbyqxmd.com/read/28386122/epistasis-between-tifab-and-mir-146a-neighboring-genes-in-del-5q-myelodysplastic-syndrome
#9
M E Varney, K Choi, L Bolanos, S Christie, J Fang, H L Grimes, J P Maciejewski, J-I Inoue, D T Starczynowski
No abstract text is available yet for this article.
April 7, 2017: Leukemia: Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K
https://www.readbyqxmd.com/read/28386107/constitutively-active-abl-family-kinases-tel-abl-and-tel-arg-harbor-distinct-leukemogenic-activities-in-vivo
#10
A Yokota, H Hirai, T Shoji, T Maekawa, K Okuda
ABL (ABL1) and ARG (ABL2) are highly homologous to each other in overall domain structure and amino acid sequence, with the exception of their C-termini. As with ABL, translocations that fuse ARG to ETV6/TEL have been identified in patients with leukemia. To assess the in vivo leukemogenic activity of constitutively active ABL and ARG, we generated a bone marrow (BM) transplantation model using the chimeric forms TEL/ABL and TEL/ARG, which have comparable kinase activities. TEL/ABL rapidly induced fatal myeloid leukemia in recipient mice, whereas recipients of TEL/ARG-transduced cells did not develop myeloid leukemia; instead, they succumbed to a long-latency infiltrative mastocytosis that could be adoptively transferred to secondary recipients...
April 7, 2017: Leukemia: Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K
https://www.readbyqxmd.com/read/28386106/mpl-activation-directly-induces-fibrocyte-differentiation-to-cause-myelofibrosis
#11
T Maekawa, Y Osawa, T Izumi, S Nagao, K Takano, Y Okada, N Tachi, M Teramoto, T Kawamura, T Horiuchi, R Saga, S Kato, T Yamamura, J Watanabe, A Kobayashi, S Kobayashi, K Sato, M Hashimoto, S Suzu, F Kimura
Myelofibrosis (MF) may be caused by various pathogenic mechanisms such as elevation in circulating cytokine levels, cellular interactions, and genetic mutations. However, the underlying mechanism of MF still remains unknown. Recent studies have revealed that fibrocytes, the spindle-shaped fibroblast-like hematopoietic cells, and the thrombopoietin (TPO)/myeloproliferative leukemia protein (MPL; TPO receptor) signaling pathway play a certain role in the development of MF. In the present study, we aimed to investigate the relationship between fibrocytes and MPL activation...
April 7, 2017: Leukemia: Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K
https://www.readbyqxmd.com/read/28373701/benefit-of-continuous-treatment-for-responders-with-newly-diagnosed-multiple-myeloma-in-the-randomized-first-trial
#12
N J Bahlis, A Corso, L-O Mugge, Z-X Shen, P Desjardins, A-M Stoppax, O Decaux, T de Revel, M Granell, G Marit, H Nahi, H Demuynck, S-Y Huang, S Basu, T H Guthrie, A Ervin-Haynes, J Marek, G Chen, T Facon
The phase 3, randomized FIRST trial investigating lenalidomide plus low-dose dexamethasone until disease progression (Rd continuous) vs melphalan, prednisone, and thalidomide for 12 cycles (MPT) and Rd for 18 cycles (Rd18) in transplant-ineligible patients with newly diagnosed multiple myeloma (NDMM) showed that Rd continuous prolonged progression-free survival and overall survival compared with MPT. A subanalysis of the FIRST trial was conducted to determine the benefits of Rd continuous in patients with NDMM based on depth of response...
April 4, 2017: Leukemia: Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K
https://www.readbyqxmd.com/read/28366935/plcg2-c2-domain-mutations-co-occur-with-btk-and-plcg2-resistance-mutations-in-chronic-lymphocytic-leukemia-undergoing-ibrutinib-treatment
#13
D Jones, J A Woyach, W Zhao, S Caruthers, H Tu, J Coleman, J C Byrd, A J Johnson, G Lozanski
Leukemia accepted article preview online, 03 April 2017. doi:10.1038/leu.2017.110.
April 3, 2017: Leukemia: Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K
https://www.readbyqxmd.com/read/28366934/acute-myeloid-leukemia-in-the-elderly-is-characterized-by-a-distinct-genetic-and-epigenetic-landscape
#14
P Silva, M Neumann, M P Schroeder, S Vosberg, C Schlee, K Isaakidis, J O Tánchez, L R Fransecky, T Hartung, S Türkmen, A Graf, S Krebs, H Blum, C Müller-Tidow, C Thiede, G Ehninger, H Serve, J Hecht, W E Berdel, P A Greif, C Röllig, C D Baldus
Leukemia accepted article preview online, 03 April 2017. doi:10.1038/leu.2017.109.
April 3, 2017: Leukemia: Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K
https://www.readbyqxmd.com/read/28366933/a-novel-ahi-1-bcr-abl-dnm2-complex-regulates-leukemic-properties-of-primitive-cml-cells-through-enhanced-cellular-endocytosis-and-ros-mediated-autophagy
#15
X Liu, K Rothe, R Yen, C Fruhstorfer, T Maetzig, M Chen, D L Forrest, K Humphries, X Jiang
Tyrosine kinase inhibitor (TKI) therapies induce clinical remission with remarkable effects on chronic myeloid leukemia (CML). However, very few TKIs completely eradicate the leukemic clone and persistence of leukemic stem cells (LSCs) remains challenging, warranting new, distinct targets for improved treatments. We demonstrated that the scaffold protein AHI-1 is highly deregulated in LSCs and interacts with multiple proteins, including Dynamin-2 (DNM2), to mediate TKI-resistance of LSCs. We have now demonstrated that the SH3 domain of AHI-1 and the proline rich domain of DNM2 are mainly responsible for this interaction...
April 3, 2017: Leukemia: Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K
https://www.readbyqxmd.com/read/28360416/heterodimerization-of-aml1-eto-with-cbf%C3%AE-is-required-for-leukemogenesis-but-not-for-myeloproliferation
#16
V Thiel, B D Giaimo, P Schwarz, K Soller, V Vas, M Bartkuhn, T J Blätte, K Döhner, L Bullinger, T Borggrefe, H Geiger, F Oswald
The AML1/Runx1 transcription factor and its heterodimerization partner CBFβ are essential regulators of myeloid differentiation. The chromosomal translocation t(8;21), fusing the DNA binding domain of AML1 to the corepressor eight-twenty-one (ETO), is frequently associated with acute myeloid leukemia (AML) and generates the AML1/ETO (AE) fusion protein. AE represses target genes usually activated by AML1 and also affects the endogenous repressive function of ETO at Notch target genes. In order to analyze the contribution of CBFβ in AE-mediated leukemogenesis and deregulation of Notch target genes, we introduced two point mutations in a leukemia initiating version of AE in mice, called AE9a, that disrupt the AML1/CBFβ interaction (AE9aNT)...
March 31, 2017: Leukemia: Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K
https://www.readbyqxmd.com/read/28360415/hiv-tat-induces-a-prolonged-myc-relocalization-next-to-igh-in-circulating-b-cells
#17
D Germini, T Tsfasman, M Klibi, R El-Amine, A Pichugin, O Iarovaia, C Bilhou-Nabera, F Subra, Y B Saada, A Sukhanova, D Boutboul, M Raphaël, J Wiels, S Razin, S Bury-Moné, E Oksenhendler, M Lipinski, Y Vassetzky
With combined antiretroviral therapy (cART), the risk for HIV-infected individuals to develop a non-Hodgkin lymphoma is diminished. However, the incidence of Burkitt lymphoma (BL) remains strikingly elevated. Most BL present a t(8;14) chromosomal translocation which must take place at a time of spatial proximity between the translocation partners. The two partner genes, MYC and IGH, were found colocalized only very rarely in the nuclei of normal peripheral blood B-cells examined using 3D-FISH while circulating B-cells from HIV-infected individuals whose exhibited consistently elevated levels of MYC-IGH colocalization...
March 31, 2017: Leukemia: Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K
https://www.readbyqxmd.com/read/28348390/donor-cell-leukemia-evidence-for-multiple-pre-leukemic-clones-and-parallel-long-term-clonal-evolution-in-donor-and-recipient
#18
S Herold, M Kuhn, M V Bonin, T Stange, U Platzbecker, J Radke, T Lange, K Sockel, K Gutsche, J Schetelig, C Röllig, C Schuster, I Roeder, A Dahl, B Mohr, H Serve, C Brandts, G Ehninger, M Bornhäuser, C Thiede
Leukemia accepted article preview online, 28 March 2017. doi:10.1038/leu.2017.104.
March 28, 2017: Leukemia: Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K
https://www.readbyqxmd.com/read/28280276/regulation-of-pi3k-signaling-in-t-cell-acute-lymphoblastic-leukemia-a-novel-pten-ikaros-mir-26b-mechanism-reveals-a-critical-targetable-role-for-pik3cd
#19
T Yuan, Y Yang, J Chen, W Li, W Li, Q Zhang, Y Mi, R S Goswami, J Q You, D Lin, M D Qian, S Calin, Y Liang, R N Miranda, G A Calin, X Zhou, L Ma, P A Zweidler-McKay, B Liu, A P Weng, L J Medeiros, Y Zhang, M J You
T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematologic malignancy, and T-ALL patients are prone to early disease relapse and suffer from poor outcomes. The PTEN, PI3K/AKT and Notch pathways are frequently altered in T-ALL. PTEN is a tumor suppressor that inactivates the PI3K pathway. We profiled miRNAs in Pten-deficient mouse T-ALL and identified miR-26b as a potentially dysregulated gene. We validated decreased expression levels of miR-26b in mouse and human T-ALL cells. In addition, expression of exogenous miR-26b reduced proliferation and promoted apoptosis of T-ALL cells in vitro, and hindered progression of T-ALL in vivo...
March 28, 2017: Leukemia: Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K
https://www.readbyqxmd.com/read/28280275/high-mtorc1-activity-drives-glycolysis-addiction-and-sensitivity-to-g6pd-inhibition-in-acute-myeloid-leukemia-cells
#20
L Poulain, P Sujobert, F Zylbersztejn, S Barreau, L Stuani, M Lambert, T L Palama, V Chesnais, R Birsen, F Vergez, T Farge, C Chenevier-Gobeaux, M Fraisse, F Bouillaud, C Debeissat, O Herault, C Récher, C Lacombe, M Fontenay, P Mayeux, T T Maciel, J-C Portais, J-E Sarry, J Tamburini, D Bouscary, N Chapuis
Alterations in metabolic activities are cancer hallmarks that offer a wide range of new therapeutic opportunities. Here we decipher the interplay between mTORC1 activity and glucose metabolism in acute myeloid leukemia (AML). We show that mTORC1 signaling that is constantly overactivated in AML cells promotes glycolysis and leads to glucose addiction. The level of mTORC1 activity determines the sensitivity of AML cells to glycolysis inhibition as switch-off mTORC1 activity leads to glucose-independent cell survival that is sustained by an increase in mitochondrial oxidative phosphorylation...
March 28, 2017: Leukemia: Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K
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