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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/30232464/correction-myeloproliferative-leukemia-protein-activation-directly-induces-fibrocyte-differentiation-to-cause-myelofibrosis
#1
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
Owing to the insufficient specificity of the anti-myeloproliferative leukemia protein (MPL) antibody in the original version of this Article, Figure 6 and parts of Figures 2a, 4e, and 5a do not represent the correct information. The corrected version of Figure 6 is in this correction and those of Figures 2a, 4e, and 5a are shown in the supplemental information.
September 19, 2018: Leukemia: Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K
https://www.readbyqxmd.com/read/30232463/correction-mutant-jak3-phosphoproteomic-profiling-predicts-synergism-between-jak3-inhibitors-and-mek-bcl2-inhibitors-for-the-treatment-of-t-cell-acute-lymphoblastic-leukemia
#2
S Degryse, C E de Bock, S Demeyer, I Govaerts, S Bornschein, D Verbeke, K Jacobs, S Binos, D A Skerrett-Byrne, H C Murray, N M Verrills, P Van Vlierberghe, J Cools, M D Dun
Following the publication of this article the authors noted that data describing precisely where phosphorylation sites in proteins modulated following JAK1 or JAK3 inhibition in mutant T-ALL samples was not clearly annotated. Therefore an additional sheet has been added to Supplementary Table 2.
September 19, 2018: Leukemia: Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K
https://www.readbyqxmd.com/read/30218009/correction-ng2-antigen-is-involved-in-leukemia-invasiveness-and-central-nervous-system-infiltration-in-mll-rearranged-infant-b-all
#3
C Prieto, B López-Millán, H Roca-Ho, R W Stam, D Romero-Moya, F J Rodríguez-Baena, A Sanjuan-Pla, V Ayllón, M Ramírez, M Bardini, P De Lorenzo, M G Valsecchi, M Stanulla, M Iglesias, P Ballerini, Á M Carcaboso, J Mora, F Locatelli, A Bertaina, L Padilla, Juan Carlos Rodríguez-Manzaneque, C Bueno, P Menéndez
The original version of this Article contained an error in the spelling of the author Juan Carlos Rodriguez-Manzaneque, which was incorrectly given as J Carlos Rodríguez-Manzaneque. This has now been corrected in both the PDF and HTML versions of the Article.
September 14, 2018: Leukemia: Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K
https://www.readbyqxmd.com/read/30218008/correction-pomalidomide-bortezomib-and-low-dose-dexamethasone-in-lenalidomide-refractory-and-proteasome-inhibitor-exposed-myeloma
#4
P G Richardson, C C Hofmeister, N S Raje, D S Siegel, S Lonial, J Laubach, Y A Efebera, D H Vesole, A K Nooka, J Rosenblatt, D Doss, M H Zaki, A Bensmaine, J Herring, Y Li, L Watkins, M S Chen, K C Anderson
Following the publication of this article, the authors noted that the pomalidomide dose for the additional SC cohort in Fig. 1 was incorrectly listed. The correct dose for pomalidomide in the additional SC cohort should be the maximum tolerated dose of 4 mg/day, not 2 mg/day as listed in the original Fig. 1. The authors apologize for any inconvenience caused.
September 14, 2018: Leukemia: Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K
https://www.readbyqxmd.com/read/30209404/marcks-regulates-tonic-and-chronic-active-b-cell-receptor-signaling
#5
Chenguang Xu, Yan Fang, Zhiyong Yang, Yukai Jing, Yonghui Zhang, Chaohong Liu, Wanli Liu
Tonic or chronic active B-cell receptor (BCR) signaling is essential for the survival of normal or some malignant B cells, respectively. However, the molecular mechanism regulating the strength of these two types of BCR signaling remains unknown. Here, using high-speed high-resolution single-molecule tracking in live cells, we identified that PKCβ, STIM1, and IP3R1/2/3 molecules affected the lateral Brownian mobile behavior of BCRs on the plasma membrane of quiescent B cells, which was correlated to the strength of BCR signaling...
September 12, 2018: Leukemia: Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K
https://www.readbyqxmd.com/read/30209403/molecular-pathogenesis-of-disease-progression-in-mll-rearranged-aml
#6
Shinichi Kotani, Akinori Yoda, Ayana Kon, Keisuke Kataoka, Yotaro Ochi, Yusuke Shiozawa, Cassandra Hirsch, June Takeda, Hiroo Ueno, Tetsuichi Yoshizato, Kenichi Yoshida, Masahiro M Nakagawa, Yasuhito Nannya, Nobuyuki Kakiuchi, Takuji Yamauchi, Kosuke Aoki, Yuichi Shiraishi, Satoru Miyano, Takahiro Maeda, Jaroslaw P Maciejewski, Akifumi Takaori-Kondo, Seishi Ogawa, Hideki Makishima
Leukemic relapse is frequently accompanied by progressively aggressive clinical course. To understand the molecular mechanism of leukemic relapse, MLL/AF9-transformed mouse leukemia cells were serially transplanted in C57BL/6 mice (N = 96) by mimicking repeated recurrences, where mutations were monitored by exome sequencing (N = 42). The onset of leukemia was progressively promoted with advanced transplants, during which increasing numbers of somatic mutations were acquired (P < 0.005). Among these, mutations in Ptpn11 (p...
September 12, 2018: Leukemia: Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K
https://www.readbyqxmd.com/read/30209402/cll-cells-cumulate-genetic-aberrations-prior-to-the-first-therapy-even-in-outwardly-inactive-disease-phase
#7
María Hernández-Sánchez, Jana Kotaskova, Ana E Rodríguez, Lenka Radova, David Tamborero, María Abáigar, Karla Plevova, Rocío Benito, Nikola Tom, Miguel Quijada-Álamo, Vasileos Bikos, Ana África Martín, Karol Pal, Alfonso García de Coca, Michael Doubek, Nuria López-Bigas, Jesús-María Hernández-Rivas, Sarka Pospisilova
No abstract text is available yet for this article.
September 12, 2018: Leukemia: Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K
https://www.readbyqxmd.com/read/30206308/downregulating-notch-counteracts-kras-g12d-induced-erk-activation-and-oxidative-phosphorylation-in-myeloproliferative-neoplasm
#8
Guangyao Kong, Xiaona You, Zhi Wen, Yuan-I Chang, Shuiming Qian, Erik A Ranheim, Christopher Letson, Xinmin Zhang, Yun Zhou, Yangang Liu, Adhithi Rajagopalan, Jingfang Zhang, Elliot Stieglitz, Mignon Loh, Inga Hofmann, David Yang, Xuehua Zhong, Eric Padron, Lan Zhou, Warren S Pear, Jing Zhang
The Notch signaling pathway contributes to the pathogenesis of a wide spectrum of human cancers, including hematopoietic malignancies. Its functions are highly dependent on the specific cellular context. Gain-of-function NOTCH1 mutations are prevalent in human T-cell leukemia, while loss of Notch signaling is reported in myeloid leukemias. Here, we report a novel oncogenic function of Notch signaling in oncogenic Kras-induced myeloproliferative neoplasm (MPN). We find that downregulation of Notch signaling in hematopoietic cells via DNMAML expression or Pofut1 deletion significantly blocks MPN development in KrasG12D mice in a cell-autonomous manner...
September 11, 2018: Leukemia: Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K
https://www.readbyqxmd.com/read/30206307/transmissible-er-stress-reconfigures-the-aml-bone-marrow-compartment
#9
Ben Doron, Sherif Abdelhamed, John T Butler, Saman K Hashmi, Terzah M Horton, Peter Kurre
Successive adaptation of the bone marrow (BM) from homeostatic hematopoietic microenvironment to a self-reinforcing niche is an integral aspect of leukemogenesis. Yet, the cellular mechanisms underlying these functional alterations remain to be defined. Here, we found that AML incursion precipitates compartmental endoplasmic reticulum (ER) stress and an unfolded protein response (UPR) in both leukemia and stromal cells. We observed that extracellular vesicles (EV) transmit ER stress in vivo from the AML xenograft to BM stroma, whereby the upregulation of core UPR components drives subsequent osteolineage differentiation of mesenchymal stem cells (MSC)...
September 11, 2018: Leukemia: Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K
https://www.readbyqxmd.com/read/30206306/cova4231-a-potent-cd3-cd33-bispecific-fynomab-with-igg-like-pharmacokinetics-for-the-treatment-of-acute-myeloid-leukemia
#10
Kristina Klupsch, Vanessa Baeriswyl, Roland Scholz, Joana Dannenberg, Roger Santimaria, David Senn, Elena Kage, Adrian Zumsteg, Isabella Attinger-Toller, Ulrike von der Bey, Susann König-Friedrich, Fanny Dupuy, Wibke Lembke, Clara Albani, Severin Wendelspiess, Lucijana Dinkel, Dorina Saro, Robert W Hepler, George S Laszlo, Chelsea J Gudgeon, Julian Bertschinger, Simon Brack, Roland B Walter
No abstract text is available yet for this article.
September 11, 2018: Leukemia: Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K
https://www.readbyqxmd.com/read/30214012/combining-bh3-mimetics-to-target-both-bcl-2-and-mcl1-has-potent-activity-in-pre-clinical-models-of-acute-myeloid-leukemia
#11
Donia M Moujalled, Giovanna Pomilio, Corina Ghiurau, Adam Ivey, Jessica Salmon, Sewa Rijal, Sarah Macraild, Lan Zhang, Tse-Chieh Teh, Ing-Soo Tiong, Ping Lan, Maia Chanrion, Audrey Claperon, Francesca Rocchetti, Adrien Zichi, Laurence Kraus-Berthier, Youzhen Wang, Ensar Halilovic, Erick Morris, Frédéric Colland, David Segal, David Huang, Andrew W Roberts, Ana Leticia Maragno, Guillaume Lessene, Olivier Geneste, Andrew H Wei
Improving outcomes in acute myeloid leukemia (AML) remains a major clinical challenge. Overexpression of pro-survival BCL-2 family members rendering transformed cells resistant to cytotoxic drugs is a common theme in cancer. Targeting BCL-2 with the BH3-mimetic venetoclax is active in AML when combined with low-dose chemotherapy or hypomethylating agents. We now report the pre-clinical anti-leukemic efficacy of a novel BCL-2 inhibitor S55746, which demonstrates synergistic pro-apoptotic activity in combination with the MCL1 inhibitor S63845...
September 10, 2018: Leukemia: Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K
https://www.readbyqxmd.com/read/30201985/risk-of-mgus-in-relatives-of-multiple-myeloma-cases-by-clinical-and-tumor-characteristics
#12
Alyssa I Clay-Gilmour, Shaji Kumar, S Vincent Rajkumar, Abdul Rishi, Robert A Kyle, Jerry A Katzmann, David L Murray, Aaron D Norman, Alexandra J Greenberg, Dirk R Larson, Megan M O'Byrne, Susan L Slager, Celine M Vachon
We and others have shown increased risk of monoclonal gammopathy of undetermined significance (MGUS) in first-degree relatives of patients with multiple myeloma (MM). Whether familial risk of MGUS differs by the MM proband's age at onset, tumor or clinical characteristics is unknown. MM and smoldering MM (SMM) cases (N = 430) were recruited from the Mayo Clinic in Rochester, Minnesota between 2005-2015. First-degree relatives over age 40 provided serum samples for evaluation of MGUS (N = 1179). Age and sex specific rates of MGUS among first-degree relatives were compared to a population-based sample...
September 10, 2018: Leukemia: Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K
https://www.readbyqxmd.com/read/30201984/cardiovascular-events-in-chronic-myeloid-leukemia-clinical-trials-is-it-time-to-reassess-and-report-the-events-according-to-cardiology-guidelines
#13
REVIEW
Nazanin Aghel, Diego Hernan Delgado, Jeffrey Howard Lipton
Tyrosine kinase inhibitors (TKIs) have revolutionized the treatment of chronic myeloid leukemia (CML). Although these treatments have changed the natural course of CML and many other cancers, they may cause cardiovascular and/or metabolic complications. In this review, we discuss how overlooking the main drivers of cardiovascular events (CVEs) and lack of standard definitions for cardiovascular adverse events might have affected these event rates in CML trials. Methodological limitations that affect the available data are discussed, with an emphasis on the future direction of cardiovascular safety research in trials of investigational drugs in cancer treatment...
September 10, 2018: Leukemia: Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K
https://www.readbyqxmd.com/read/30201983/nt5c2-germline-variants-alter-thiopurine-metabolism-and-are-associated-with-acquired-nt5c2-relapse-mutations-in-childhood-acute-lymphoblastic-leukaemia
#14
Morten Tulstrup, Marie Grosjean, Stine Nygaard Nielsen, Kathrine Grell, Benjamin Ole Wolthers, Peder Skov Wegener, Olafur Gisli Jonsson, Bendik Lund, Arja Harila-Saari, Jonas Abrahamsson, Goda Vaitkeviciene, Kaie Pruunsild, Nina Toft, Mette Holm, Erik Hulegårdh, Sigurd Liestøl, Laimonas Griskevicius, Mari Punab, Jinhua Wang, William L Carroll, Zeyu Zhang, Marlene D Dalgaard, Ramneek Gupta, Jacob Nersting, Kjeld Schmiegelow
The antileukaemic drug 6-mercaptopurine is converted into thioguanine nucleotides (TGN) and incorporated into DNA (DNA-TG), the active end metabolite. In a series of genome-wide association studies, we analysed time-weighted means (wm ) of erythrocyte concentrations of TGN (Ery-TGN) and DNA-TG in 1009 patients undergoing maintenance therapy for acute lymphoblastic leukaemia (ALL). In discovery analyses (454 patients), the propensity for DNA-TG incorporation (wm DNA-TG/wm Ery-TGN ratio) was significantly associated with three intronic SNPs in NT5C2 (top hit: rs72846714; P = 2...
September 10, 2018: Leukemia: Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K
https://www.readbyqxmd.com/read/30185935/characterization-of-an-x-chromosome-linked-telomere-biology-disorder-in-females-with-dkc1-mutation
#15
Elina A M Hirvonen, Saara Peuhkuri, Anna Norberg, Sofie Degerman, Katariina Hannula-Jouppi, Hannamari Välimaa, Outi Kilpivaara, Ulla Wartiovaara-Kautto
No abstract text is available yet for this article.
September 5, 2018: Leukemia: Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K
https://www.readbyqxmd.com/read/30185934/targeting-quiescent-leukemic-stem-cells-using-second-generation-autophagy-inhibitors
#16
Pablo Baquero, Amy Dawson, Arunima Mukhopadhyay, Elodie M Kuntz, Rebecca Mitchell, Orianne Olivares, Angela Ianniciello, Mary T Scott, Karen Dunn, Michael C Nicastri, Jeffrey D Winkler, Alison M Michie, Kevin M Ryan, Christina Halsey, Eyal Gottlieb, Erin P Keaney, Leon O Murphy, Ravi K Amaravadi, Tessa L Holyoake, G Vignir Helgason
In chronic myeloid leukemia (CML), tyrosine kinase inhibitor (TKI) treatment induces autophagy that promotes survival and TKI-resistance in leukemic stem cells (LSCs). In clinical studies hydroxychloroquine (HCQ), the only clinically approved autophagy inhibitor, does not consistently inhibit autophagy in cancer patients, so more potent autophagy inhibitors are needed. We generated a murine model of CML in which autophagic flux can be measured in bone marrow-located LSCs. In parallel, we use cell division tracing, phenotyping of primary CML cells, and a robust xenotransplantation model of human CML, to investigate the effect of Lys05, a highly potent lysosomotropic agent, and PIK-III, a selective inhibitor of VPS34, on the survival and function of LSCs...
September 5, 2018: Leukemia: Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K
https://www.readbyqxmd.com/read/30135465/april-signaling-via-taci-mediates-immunosuppression-by-t-regulatory-cells-in-multiple-myeloma-therapeutic-implications
#17
Yu-Tzu Tai, Liang Lin, Lijie Xing, Shih-Feng Cho, Tengteng Yu, Chirag Acharya, Kenneth Wen, Phillip A Hsieh, John Dulos, Andrea van Elsas, Nikhil Munshi, Paul Richardson, Kenneth C Anderson
We investigate here how APRIL impacts immune regulatory T cells and directly contributes to the immunosuppressive multiple myeloma (MM) bone marrow (BM) microenvironment. First, APRIL receptor TACI expression is significantly higher in regulatory T cells (Tregs) than conventional T cells (Tcons) from the same patient, confirmed by upregulated Treg markers, i.e., Foxp3, CTLA-4. APRIL significantly stimulates proliferation and survival of Tregs, whereas neutralizing anti-APRIL monoclonal antibodies (mAbs) inhibit these effects...
August 22, 2018: Leukemia: Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K
https://www.readbyqxmd.com/read/30131584/dependency-on-the-tyk2-stat1-mcl1-axis-in-anaplastic-large-cell-lymphoma
#18
Nicole Prutsch, Elisabeth Gurnhofer, Tobias Suske, Huan Chang Liang, Michaela Schlederer, Simone Roos, Lawren C Wu, Ingrid Simonitsch-Klupp, Andrea Alvarez-Hernandez, Christoph Kornauth, Dario A Leone, Jasmin Svinka, Robert Eferl, Tanja Limberger, Astrid Aufinger, Nitesh Shirsath, Peter Wolf, Thomas Hielscher, Fritz Aberger, Johannes Schmoellerl, Dagmar Stoiber, Birgit Strobl, Ulrich Jäger, Philipp B Staber, Florian Grebien, Richard Moriggl, Mathias Müller, Giorgio G Inghirami, Takaomi Sanda, A Thomas Look, Suzanne D Turner, Lukas Kenner, Olaf Merkel
TYK2 is a member of the JAK family of tyrosine kinases that is involved in chromosomal translocation-induced fusion proteins found in anaplastic large cell lymphomas (ALCL) that lack rearrangements activating the anaplastic lymphoma kinase (ALK). Here we demonstrate that TYK2 is highly expressed in all cases of human ALCL, and that in a mouse model of NPM-ALK-induced lymphoma, genetic disruption of Tyk2 delays the onset of tumors and prolongs survival of the mice. Lymphomas in this model lacking Tyk2 have reduced STAT1 and STAT3 phosphorylation and reduced expression of Mcl1, a pro-survival member of the BCL2 family...
August 21, 2018: Leukemia: Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K
https://www.readbyqxmd.com/read/30131583/symptomatic-osteonecrosis-as-a-treatment-complication-in-hodgkin-lymphoma-an-analysis-of-the-german-hodgkin-study-group-ghsg
#19
Sven Borchmann, Horst Müller, Heinz Haverkamp, Christian Baues, Jana Marková, Andreas Hüttmann, Axel Glunz, Michael Fuchs, Peter Borchmann, Andreas Engert
The majority of patients with Hodgkin Lymphoma (HL) can be cured with stage and risk adapted treatment today. Therefore, current research focuses on reducing long-term sequelae of treatment. Osteonecrosis (ON) is a severe long-term complication of HL treatment which has so far not been systematically evaluated. Hence, we investigated incidence, risk factors and timing of symptomatic ON in HL patients. Further endpoints included localization, intervention and outcome of ON. We included all qualified HL patients of the randomized German Hodgkin Study Group trials HD10-15 and HD18, recruited between 05/1998 and 07/2014 and aged from 16 to 60 years...
August 21, 2018: Leukemia: Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K
https://www.readbyqxmd.com/read/30120376/mir-22-suppresses-dna-ligase-iii-addiction-in-multiple-myeloma
#20
Daniele Caracciolo, Maria Teresa Di Martino, Nicola Amodio, Eugenio Morelli, Martina Montesano, Cirino Botta, Francesca Scionti, Daniela Talarico, Emanuela Altomare, Maria Eugenia Gallo Cantafio, Valeria Zuccalà, Lorenza Maltese, Katia Todoerti, Marco Rossi, Mariamena Arbitrio, Antonino Neri, Pierosandro Tagliaferri, Pierfrancesco Tassone
Multiple myeloma (MM) is a hematologic malignancy characterized by high genomic instability. Here we provide evidence that hyper-activation of DNA ligase III (LIG3) is crucial for genomic instability and survival of MM cells. LIG3 mRNA expression in MM patients correlates with shorter survival and even increases with more advanced stage of disease. Knockdown of LIG3 impairs MM cells viability in vitro and in vivo, suggesting that neoplastic plasmacells are dependent on LIG3-driven repair. To investigate the mechanisms involved in LIG3 expression, we investigated the post-transcriptional regulation...
August 17, 2018: Leukemia: Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K
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