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https://www.readbyqxmd.com/read/29025715/runx1-in-t-all-tumor-suppressive-or-oncogenic
#1
Takaomi Sanda
No abstract text is available yet for this article.
October 12, 2017: Blood
https://www.readbyqxmd.com/read/29023469/the-common-oncogenomic-program-of-notch1-and-notch3-signaling-in-t-cell-acute-lymphoblastic-leukemia
#2
Sung Hee Choi, Eric Severson, Warren S Pear, Xiaole S Liu, Jon C Aster, Stephen C Blacklow
Notch is a major oncogenic driver in T cell acute lymphoblastic leukemia (T-ALL), in part because it binds to an enhancer that increases expression of MYC. Here, we exploit the capacity of activated NOTCH1 and NOTCH3 to induce T-ALL, despite substantial divergence in their intracellular regions, as a means to elucidate a broad, common Notch-dependent oncogenomic program through systematic comparison of the transcriptomes and Notch-bound genomic regulatory elements of NOTCH1- and NOTCH3-dependent T-ALL cells...
2017: PloS One
https://www.readbyqxmd.com/read/28989582/patterns-of-dnmt1-promoter-methylation-in-patients-with-acute-lymphoblastic-leukemia
#3
Tirdad Rahmani, Mehdi Azad, Bahram Chahardouli, Hajar Nasiri, Mousa Vatanmakanian, Saeid Kaviani
Background: Acute lymphoblastic leukemia (ALL) is a clonal malignant disorder characterized by an uncontrolled proliferation of immature T or B lymphocytes. Extensive studies have shown that the epigenetic changes, especially modified DNA methylation patterns in the regulatory regions through the DNA methyltransferase (DNMTs), play an important role in the development of genetic disorders and abnormal growth and maturation capacity of leukemic stem cells (LSCs).The aim of this study was to evaluate the changes in DNMT1 promoter methylation and its expression pattern in patients with ALL...
July 1, 2017: International Journal of Hematology-oncology and Stem Cell Research
https://www.readbyqxmd.com/read/28979681/mir-139-acts-as-a-tumor-suppressor-in-t-cell-acute-lymphoblastic-leukemia-by-targeting-cx-chemokine-receptor-4
#4
Ling Qin, Hui-Yang Deng, Sheng-Jiang Chen, Wei Wei, Yi-Ting Zhang
MicroRNAs (miRNAs) act as tumor regulators in T-cell acute lymphoblastic leukemia (T-ALL). However, the molecular mechanisms by which miRNA-139 (miR-139) regulates T-ALL remain unclear. In this study, we found that miR-139 was lowly expressed whereas C-X-C chemokine receptor type 4 (CXCR4) was highly expressed in T-ALL cell lines and patient samples. The T-ALL patients simultaneously with high levels of CXCR4 and low expression of miR-139 possessed poor prognosis. Moreover, the introduction of miR-139 inhibited T-ALL cell proliferation and invasion in vitro and suppressed tumor growth and lung metastasis in vivo...
2017: American Journal of Translational Research
https://www.readbyqxmd.com/read/28978840/current-treatment-of-adult-acute-lymphoblastic-leukemia
#5
Shin Fujisawa
The survival outcomes for children with acute lymphoblastic leukemia (ALL) have dramatically improved over recent years, and improved outcomes in adolescents and young adults patients have been achieved by applying regimens based on pediatric protocols. The treatment strategies for adult ALL are similar to those for pediatric ALL. T-cell ALL is less common than B-cell ALL. Therefore, there are only few reports of investigations in a large group of adult T-ALL patients. In Japan, nelarabine-combined chemotherapy has been tested in a phase II study in patients with newly diagnosed T-ALL...
2017: [Rinshō Ketsueki] the Japanese Journal of Clinical Hematology
https://www.readbyqxmd.com/read/28978087/fir-haplodeficiency-promotes-splicing-to-pyruvate-kinase-m2-in-mice-thymic-lymphoma-tissues-revealed-by-six-plex-tandem-mass-tag-quantitative-proteomic-analysis
#6
Asako Kimura, Kouichi Kitamura, Guzhanuer Ailiken, Mamoru Satoh, Toshinari Minamoto, Nobuko Tanaka, Fumio Nomura, Kazuyuki Matsushita
The switch of pyruvate kinase (PK) M1 to PKM2 is pivotal for glucose metabolism in cancers. The PKM1/M2 shift is controlled by the alternative splicing of two mutually exclusive exons in the PKM gene. PKM1 is expressed in differentiated tissues, whereas PKM2 is expressed in cancer tissues. This study revealed that the haplodeficiency of FUSE-binding protein (FBP)-interacting repressor (FIR), a transcriptional repressor of the c-myc gene, contributed to the splicing of PKM1 to PKM2 in mice thymic lymphoma and/or T-cell type acute lymphoblastic leukemia (T-ALL) using six-plex tandem mass tag (TMT) quantitative proteomic analysis...
September 15, 2017: Oncotarget
https://www.readbyqxmd.com/read/28977998/nkl-homeobox-gene-msx1-acts-like-a-tumor-suppressor-in-nk-cell-leukemia
#7
Stefan Nagel, Claudia Pommerenke, Corinna Meyer, Maren Kaufmann, Roderick A F MacLeod, Hans G Drexler
NKL homeobox gene MSX1 is physiologically expressed in lymphoid progenitors and subsequently downregulated in developing T- and B-cells. In contrast, elevated expression levels of MSX1 persist in mature natural killer (NK)-cells, indicating a functional role in this compartment. While T-cell acute lymphoblastic leukemia (T-ALL) subsets exhibit aberrant overexpression of MSX1, we show here that in malignant NK-cells the level of MSX1 transcripts is aberrantly downregulated. Chromosomal deletions at 4p16 hosting the MSX1 locus have been described in NK-cell leukemia patients...
September 15, 2017: Oncotarget
https://www.readbyqxmd.com/read/28974511/tox-regulates-growth-dna-repair-and-genomic-instability-in-t-cell-acute-lymphoblastic-leukemia
#8
Riadh Lobbardi, Jordan Pinder, Barbara Martinez-Pastor, Marina Theodorou, Jessica S Blackburn, Brian J Abraham, Yuka Namiki, Marc Mansour, Nouran S Abdelfattah, Aleksey Molodtsov, Gabriela Alexe, Debra Toiber, Manon de Waard, Esha Jain, Myriam Boukhali, Mattia Lion, Deepak Bhere, Khalid Shah, Alejandro Gutierrez, Kimberly Stegmaier, Lewis B Silverman, Ruslan I Sadreyev, John M Asara, Marjorie A Oettinger, Wilhelm Haas, A Thomas Look, Richard A Young, Raul Mostoslavsky, Graham Dellaire, David M Langenau
T-cell Acute Lymphoblastic Leukemia (T-ALL) is an aggressive malignancy of thymocytes. Using a transgenic screen in zebrafish, thymocyte selection-associated high mobility box protein (TOX) was uncovered as a collaborating oncogenic driver that accelerated T-ALL onset by expanding the initiating pool of transformed clones and elevating genomic instability. TOX is highly expressed in a majority of human T-ALL and is required for proliferation and continued xenograft growth in mice. Using a wide array of functional analyses, we uncovered that TOX binds directly to KU70/80 and suppresses recruitment of this complex to DNA breaks to inhibit Non-Homologous End Joining repair (NHEJ)...
October 3, 2017: Cancer Discovery
https://www.readbyqxmd.com/read/28950691/helicobacter-pylori-is-associated-with-mir-133a-expression-through-promoter-methylation-in-gastric-carcinogenesis
#9
Joo Hyun Lim, Sang Gyun Kim, Ji Min Choi, Hyo-Joon Yang, Joo Sung Kim, Hyun Chae Jung
Background/Aims: To investigate whether Helicobacter pylori eradication can reverse epigenetic silencing of microRNAs (miRNAs) which are associated with H. pylori-induced gastric carcinogenesis. Methods: We examined expression and promoter methylation of miR-34b/c, miR-133a, let-7a, and let-7i in gastric cancer cell line, before/after demethylation. Among them, epigenetically controlled miRNAs were identified. Their expression and promoter methylation was examined in human tissues of H...
September 28, 2017: Gut and Liver
https://www.readbyqxmd.com/read/28943936/nhe1-has-a-notable-role-in-metastasis-and-drug-resistance-of-t-cell-acute-lymphoblastic-leukemia
#10
Ehtisham Altaf, Xiaoxing Huang, Jie Xiong, Xiangyong Yang, Xinzhou Deng, Meng Xiong, Lu Zhou, Shan Pan, Wen Yuan, Xinran Li, Ling Hao, Kingsley Miyanda Tembo, Ruijing Xiao, Qiuping Zhang
T-cell acute lymphoblastic leukemia (T-ALL) represents a spectrum of hematological malignancies that affect human health. Metastasis and chemotherapeutic drug resistance are the primary causes of mortality in patients with T-ALL. Sodium-hydrogen antiporter 1 (NHE1) is established to serve a role in metastasis and drug resistance in numerous types of cancer; however, the function of NHE1 in T-ALL remains to be elucidated. Previously, the C-C-motif chemokine ligand 25 (CCL25) was identified to be involved in metastasis and drug resistance in the MOLT4 T-ALL cell line, as was the ezrin protein...
October 2017: Oncology Letters
https://www.readbyqxmd.com/read/28905428/cost-effective-screening-of-dnmt3a-coding-sequence-identifies-somatic-mutation-in-pediatric-t-cell-acute-lymphoblastic-leukemia
#11
Bronisława Szarzyńska-Zawadzka, Maria Kosmalska, Łukasz Sędek, Alicja Sonsala, Magdalena Twardoch, Jerzy R Kowalczyk, Tomasz Szczepański, Michał Witt, Małgorzata Dawidowska
BACKGROUND AND OBJECTIVES: In pediatric T-cell acute lymphoblastic leukemia (T-ALL) risk assignment schemes preclude reliable prediction of outcome and thus new prognostic factors are needed. Mutations in DNMT3A are candidate prognostic and classification markers in adults with acute myeloid leukemia (AML) and T-ALL and thus were considered as candidates prognostic markers in pediatric T-ALL. PATIENTS AND METHODS: DNMT3A mutational status was investigated in 74 pediatric T-ALL samples collected at diagnosis...
September 14, 2017: European Journal of Haematology
https://www.readbyqxmd.com/read/28891074/nelarabine-toxicity-in-children-and-adolescents-with-relapsed-refractory-t-all-t-lbl-can-we-avoid-throwing-the-baby-out-with-the-bathwater
#12
EDITORIAL
Andrea Malone, Owen P Smith
No abstract text is available yet for this article.
October 2017: British Journal of Haematology
https://www.readbyqxmd.com/read/28888074/early-recovery-of-circulating-immature-b-cells-in-b-lymphoblastic-leukemia-patients-after-cd19-targeted-car-t-cell-therapy-a-pitfall-for-minimal-residual-disease-detection
#13
Wenbin Xiao, Dalia Salem, Catherine McCoy, Daniel Lee, Nirali N Shah, Maryalice Stetler-Stevenson, Constance M Yuan
BACKGROUND: CD19-targeted chimeric-antigen receptor-modified T-cells (CAR-T) are promising in the treatment of refractory B-lymphoblastic leukemia (B-ALL). Minimal residual disease (MRD) detection by multicolor flow cytometry (FCM) is critical to distinguish B-ALL MRD from regenerating, non-neoplastic B-cell populations. METHODS: FCM was performed on samples from 9 patients with B-ALL treated with CAR-T. RESULTS: All 9 patients showed response to CAR-T...
September 9, 2017: Cytometry. Part B, Clinical Cytometry
https://www.readbyqxmd.com/read/28885610/in-silico-and-preclinical-drug-screening-identifies-dasatinib-as-a-targeted-therapy-for-t-all
#14
S Laukkanen, T Grönroos, P Pölönen, H Kuusanmäki, J Mehtonen, J Cloos, G Ossenkoppele, B Gjertsen, B Øystein, C Heckman, M Heinäniemi, M Kontro, O Lohi
No abstract text is available yet for this article.
September 8, 2017: Blood Cancer Journal
https://www.readbyqxmd.com/read/28884915/severe-mucha-habermann-like-ulceronecrotic-skin-disease-in-t-cell-acute-lymphoblastic-leukemia-responsive-to-basiliximab-and-stem-cell-transplant
#15
Lauren A V Orenstein, Carrie C Coughlin, Andrea T Flynn, Vinodh Pillai, Markus D Boos, Gerald B Wertheim, James R Treat, David T Teachey
A 5-year-old girl with T-cell acute lymphoblastic leukemia (T-ALL) developed a progressive eruption of crusted papules and ulcerative plaques involving 80% of her body surface area with histopathology consistent with febrile ulceronecrotic Mucha-Habermann disease (FUMHD), although multiple specimens also contained clonal leukemic cells. Her skin disease was refractory to many classic treatments for FUMHD, including methotrexate, and became so severe that concern about superinfection prevented intensification of chemotherapy for her malignancy...
September 2017: Pediatric Dermatology
https://www.readbyqxmd.com/read/28872614/aberrant-signaling-pathways-in-t-cell-acute-lymphoblastic-leukemia
#16
REVIEW
Deborah Bongiovanni, Valentina Saccomani, Erich Piovan
T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive disease caused by the malignant transformation of immature progenitors primed towards T-cell development. Clinically, T-ALL patients present with diffuse infiltration of the bone marrow by immature T-cell blasts high blood cell counts, mediastinal involvement, and diffusion to the central nervous system. In the past decade, the genomic landscape of T-ALL has been the target of intense research. The identification of specific genomic alterations has contributed to identify strong oncogenic drivers and signaling pathways regulating leukemia growth...
September 5, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/28870926/hedgehog-stimulation-suppresses-clonogenicity-and-activates-notch-signalling-in-t-lymphoblastic-leukaemia-jurkat-cells
#17
Yuki Okuhashi, Mai Itoh, Shuji Tohda
BACKGROUND/AIM: Hedgehog (HH) and NOTCH pathways are involved in the regulation of cancer stem cells and haematopoietic malignancies. However, the effects of HH stimulation on cell growth and NOTCH signalling in acute T-lymphoblastic leukaemia (T-ALL) cells have not been elucidated. MATERIALS AND METHODS: Two T-ALL cell lines, Jurkat and KOPT-K1 harbouring activating NOTCH1 mutations, were cultured with recombinant Sonic (S) HH and analysed for proliferation, colony formation, and expression of NOTCH-regulated genes and proteins...
September 2017: Anticancer Research
https://www.readbyqxmd.com/read/28869817/dna-hypermethylation-of-tumor-suppressor-genes-rassf6-and-rassf10-as-independent-prognostic-factors-in-adult-acute-lymphoblastic-leukemia
#18
Samareh Younesian, Sepideh Shahkarami, Parisa Ghaffari, Shaban Alizadeh, Roya Mehrasa, Ardeshir Ghavamzadeh, Seyed H Ghaffari
BACKGROUND: The Hypermethylation of Ras association domain family (RASSF) often plays a key role in malignant progression of solid tumors; however, their impact on the prognosis and survival of adult ALL patients remain elusive. METHODS: The frequency of the promoter methylation pattern of RASSF6 and RASSF10 were analyzed in the peripheral blood (PB) samples taken at the time of diagnosis of 45 ALL patients. The methylation-specific PCR (MSP) assay was used to detect the DNA methylation patterns...
August 30, 2017: Leukemia Research
https://www.readbyqxmd.com/read/28854983/identification-of-cis-regulatory-mutations-generating-de-novo-edges-in-personalized-cancer-gene-regulatory-networks
#19
Zeynep Kalender Atak, Hana Imrichova, Dmitry Svetlichnyy, Gert Hulselmans, Valerie Christiaens, Joke Reumers, Hugo Ceulemans, Stein Aerts
The identification of functional non-coding mutations is a key challenge in the field of genomics. Here we introduce μ-cisTarget to filter, annotate and prioritize cis-regulatory mutations based on their putative effect on the underlying "personal" gene regulatory network. We validated μ-cisTarget by re-analyzing the TAL1 and LMO1 enhancer mutations in T-ALL, and the TERT promoter mutation in melanoma. Next, we re-sequenced the full genomes of ten cancer cell lines and used matched transcriptome data and motif discovery to identify master regulators with de novo binding sites that result in the up-regulation of nearby oncogenic drivers...
August 30, 2017: Genome Medicine
https://www.readbyqxmd.com/read/28852199/mutant-jak3-phosphoproteomic-profiling-predicts-synergism-between-jak3-inhibitors-and-mek-bcl2-inhibitors-for-the-treatment-of-t-cell-acute-lymphoblastic-leukemia
#20
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
Mutations in the interleukin-7 receptor (IL7R) or the JAK3 kinase occur frequently in T-cell acute lymphoblastic leukemia (T-ALL) and both are able to drive cellular transformation and the development of T-ALL in mouse models. However, the signal transduction pathways downstream of JAK3 mutations remain poorly characterized. Here, we describe the phosphoproteome downstream of the JAK3(L857Q)/(M511I) activating mutations in transformed Ba/F3 lymphocyte cells. Signaling pathways regulated by JAK3 mutants were assessed following acute inhibition of JAK1/JAK3 using the JAK kinase inhibitors ruxolitinib or tofacitinib...
August 30, 2017: Leukemia: Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K
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