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https://www.readbyqxmd.com/read/28720765/c-ebp%C3%AE-deregulation-as-a-paradigm-for-leukemogenesis
#1
REVIEW
J A Pulikkan, D G Tenen, G Behre
Myeloid master regulator CCAAT enhancer binding protein alpha (C/EBPα) is deregulated by multiple mechanisms in leukemia. Inhibition of C/EBPα function plays pivotal roles in leukemogenesis. While much is known about how C/EBPα orchestrates granulopoiesis, our understanding of molecular transformation events, the role(s) of cooperating mutations and clonal evolution during C/EBPα deregulation in leukemia remains elusive. In this review we will summarize the latest research addressing these topics with special emphasis on CEBPΑ mutations...
July 19, 2017: Leukemia: Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K
https://www.readbyqxmd.com/read/28718379/expression-of-embryonic-stem-cell-markers-in-acute-myeloid-leukemia
#2
Tiphanie Picot, Carmen Mariana Aanei, Amandine Fayard, Pascale Flandrin-Gresta, Sylvie Tondeur, Marina Gouttenoire, Emmanuelle Tavernier-Tardy, Eric Wattel, Denis Guyotat, Lydia Campos
Acute myeloid leukemia is driven by leukemic stem cells which can be identified by cross lineage expression or arrest of differentiation compared to normal hematopoietic stem cells. Self-renewal and lack of differentiation are also features of stem cells and have been associated with the expression of embryonic genes. The aim of our study was to evaluate the expression of embryonic antigens (OCT4, NANOG, SOX2, SSEA1, SSEA3) in hematopoietic stem cell subsets (CD34(+)CD38(-) and CD34(+)CD38(+)) from normal bone marrows and in samples from acute myeloid leukemia patients...
July 2017: Tumour Biology: the Journal of the International Society for Oncodevelopmental Biology and Medicine
https://www.readbyqxmd.com/read/28708320/monosomy-7-del-7q-in-inherited-bone-marrow-failure-syndromes-a-systematic-review
#3
REVIEW
Alex Pezeshki, Shreya Podder, Ralph Kamel, Seth J Corey
Inherited bone marrow failure syndromes (IBMFS) are rare cancer predisposition syndromes with an especially high risk of transformation to myelodysplastic syndrome (MDS) and/or acute myeloid leukemia (AML). We performed a retrospective systematic review of reported MDS/AML arising in the eight most common IBMFS to determine the frequency and outcome of chromosome 7 abnormalities. We identified 738 MDS/AML cases of 4,293 individuals. Monosomy 7 or del (7q) occurred in ∼17%. Greater understanding of the roles played by sequential acquisition of genetic and cytogenetic changes will provide insights into myeloid leukemogenesis and improve the surveillance and hopefully outcomes for individuals with IBMFS...
July 14, 2017: Pediatric Blood & Cancer
https://www.readbyqxmd.com/read/28707218/the-dna-damage-response-pathway-in-normal-hematopoiesis-and-malignancies
#4
REVIEW
Domenico Delia, Shuki Mizutani
In mammalian cells, the DNA damage response (DDR) prevents the replication and propagation of DNA errors to the next generation, thus maintaining genomic stability. At the heart of the DDR are the related signaling kinases ATM, ATR, and DNA-PK, which regulate DNA repair and associated events such as cell cycle checkpoints, chromatin remodeling, transcription, and ultimately apoptosis. Several findings highlight the occurrence of DDR in hemopoietic stem cells (HSCs), and persistence of DNA lesions in these cells promotes their functional decline and accumulation of leukemogenic mutations...
July 13, 2017: International Journal of Hematology
https://www.readbyqxmd.com/read/28697759/the-distinct-biological-implications-of-asxl1-mutation-and-its-roles-in-leukemogenesis-revealed-by-a-knock-in-mouse-model
#5
Yueh-Chwen Hsu, Yu-Chiao Chiu, Chien-Chin Lin, Yuan-Yeh Kuo, Hsin-An Hou, Yi-Shiuan Tzeng, Chein-Jun Kao, Po-Han Chuang, Mei-Hsuan Tseng, Tzu-Hung Hsiao, Wen-Chien Chou, Hwei-Fang Tien
BACKGROUND: Additional sex combs-like 1 (ASXL1) is frequently mutated in myeloid malignancies. Recent studies showed that hematopoietic-specific deletion of Asxl1 or overexpression of mutant ASXL1 resulted in myelodysplasia-like disease in mice. However, actual effects of a "physiological" dose of mutant ASXL1 remain unexplored. METHODS: We established a knock-in mouse model bearing the most frequent Asxl1 mutation and studied its pathophysiological effects on mouse hematopoietic system...
July 11, 2017: Journal of Hematology & Oncology
https://www.readbyqxmd.com/read/28693523/inhibition-of-lin28b-impairs-leukemia-cell-growth-and-metabolism-in-acute-myeloid-leukemia
#6
Jianbiao Zhou, Chonglei Bi, Ying Qing Ching, Jing-Yuan Chooi, Xiao Lu, Jessie Yiying Quah, Sabrina Hui-Min Toh, Zit-Liang Chan, Tuan Zea Tan, Phyllis Sy Chong, Wee-Joo Chng
BACKGROUND: Current conventional chemotherapy for acute myeloid leukemia (AML) can achieve remission in over 70% of patients, but a majority of them will relapse within 5 years despite continued treatment. The relapse is postulated to be due to leukemia stem cells (LSCs), which are different from normal hematopoietic stem cells (HSCs). LIN28B is microRNA regulator and stem cell reprogramming factor. Overexpression of LIN28B has been associated with advance human malignancies and cancer stem cells (CSCs), including AML...
July 11, 2017: Journal of Hematology & Oncology
https://www.readbyqxmd.com/read/28693140/acute-myeloid-leukemia-with-t-3-21-q26-2-q22-developing-following-low-dose-methotrexate-therapy-for-rheumatoid-arthritis-and-expressing-two-aml1-mds1-evi1-fusion-proteins-a-case-report
#7
Keisuke Tanaka, Gaku Oshikawa, Hiroki Akiyama, Shinya Ishida, Toshikage Nagao, Masahide Yamamoto, Osamu Miura
The t(3;21)(q26.2;q22) translocation is a rare chromosomal abnormality exhibited almost exclusively in therapy-related myelodysplastic syndrome/acute myeloid leukemia (t-MDS/AML) or in the blastic crisis phase of chronic myelogenous leukemia, which results in the fusion of the runt related transcription factor 1 (RUNX1, also called AML1) gene at 21q22 to the myelodysplasia syndrome 1 (MDS1)-ecotropic virus integration site 1 (EVI1) complex locus (MECOM) at 3q26.2, generating various fusion transcripts, including AML1/MDS1/EVI1 (AME)...
July 2017: Oncology Letters
https://www.readbyqxmd.com/read/28684528/wnt-%C3%A3-catenin-activation-by-epigenetically-aberrant-stroma-drives-myelodysplastic-syndrome
#8
Tushar Bhagat, Si Chen, Matthias Bartenstein, Trevor S Barlowe, Dagny von Ahrens, Gaurav S Choudhary, Patrick Tivnan, Elianna Amin, A Mario Marcondes, Mathijs A Sanders, Remco M Hoogenboezem, Suman Kambhampati, Nandini Ramachandra, Ioannis Mantzaris, Vineeth Sukrithan, Remi Laurence, Robert Lopez, Prafulla Bhagat, Orsi Giricz, Davendra Sohal, Amittha Wickrema, Cecilia Cs Yeung, Kira Gritsman, Peter D Aplan, Konrad Hochedlinger, Yiting Yu, Kith Pradhan, Jinghang Zhang, John Greally, Siddhartha Mukherjee, Andrea Pellagatti, Jacqueline Boultwood, Britta Will, Ulrich Steidl, Marc Hgp Raaijmakers, H J Deeg, Michael G Kharas, Amit Verma
The bone marrow microenvironment influences malignant hematopoiesis but how it promotes leukemogenesis has not been elucidated. Additionally, the role of the bone marrow stroma in regulating clinical responses to DNA methyltransferase inhibitors (DNMTi) is also poorly understood. In this study, we conducted a DNA methylome analysis of bone marrow-derived stromal cells from myelodysplastic syndrome (MDS) patients and observed widespread aberrant cytosine hypermethylation occurring preferentially outside CpG islands...
July 6, 2017: Cancer Research
https://www.readbyqxmd.com/read/28680740/haploinsufficient-tumor-suppressor-genes
#9
Kazushi Inoue, Elizabeth A Fry
Haploinsufficiency of tumor suppressor genes (TSGs) indicates that the reduced levels of proteins in cells that lack one allele of the genomic locus results in the inability of the cell to execute normal cellular functions contributing to tumor development. Representative cases of haploinsufficient TSGs are p27(Kip1), p53, DMP1, NF1, and PTEN. Tumor development is significantly accelerated in both mice with homozygous and heterozygous gene deletion, with expression of the wild type allele in the latter. Newly characterized TSGs such as AML1, EGR1, TGFβR1/2, and SMAD4 have also shown haploid insufficiency for tumor suppression...
2017: Advances in Medicine and Biology
https://www.readbyqxmd.com/read/28679949/aml-induced-osteogenic-differentiation-in-mesenchymal-stromal-cells-supports-leukemia-growth
#10
V Lokesh Battula, Phuong M Le, Jeffrey C Sun, Khoa Nguyen, Bin Yuan, Ximin Zhou, Sonali Sonnylal, Teresa McQueen, Vivian Ruvolo, Keith A Michel, Xiaoyang Ling, Rodrigo Jacamo, Elizabeth Shpall, Zhiqiang Wang, Arvind Rao, Gheath Al-Atrash, Marina Konopleva, R Eric Davis, Melvyn A Harrington, Catherine W Cahill, Carlos Bueso-Ramos, Michael Andreeff
Genotypic and phenotypic alterations in the bone marrow (BM) microenvironment, in particular in osteoprogenitor cells, have been shown to support leukemogenesis. However, it is unclear how leukemia cells alter the BM microenvironment to create a hospitable niche. Here, we report that acute myeloid leukemia (AML) cells, but not normal CD34+ or CD33+ cells, induce osteogenic differentiation in mesenchymal stromal cells (MSCs). In addition, AML cells inhibited adipogenic differentiation of MSCs. Mechanistic studies identified that AML-derived BMPs activate Smad1/5 signaling to induce osteogenic differentiation in MSCs...
July 6, 2017: JCI Insight
https://www.readbyqxmd.com/read/28679293/sh3bgrl-as-a-novel-prognostic-biomarker-is-down-regulated-in-acute-myeloid-leukemia
#11
Limei Xu, Mingming Zhang, Hui Li, Wen Guan, Bin Liu, Fengqi Liu, Hehua Wang, Juan Li, Shulan Yang, Xiuzhen Tong, Haihe Wang
Phosphatase PRL-3 expression is positively associated to acute myeloid leukemia (AML) progression and drug resistance. SH3-domain-binding glutamic acid-rich protein-like protein (SH3BGRL), a downstream effector of PRL-3, plays a tumor suppressive role in solid tumors, but it remains elusive in AML. Here, we followed up and validated the relevance of SH3BGRL expression to AML progression in 116 cases. Results showed that SH3BGRL is down-regulated in 62.37% AML cases with poor prognosis. Cases with positive response to therapy accompanies with SH3GRL expression restoration...
July 6, 2017: Leukemia & Lymphoma
https://www.readbyqxmd.com/read/28676638/cbl-mediated-k63-linked-ubiquitination-of-jak2-enhances-jak2-phosphorylation-and-signal-transduction
#12
Chun-Shan Liu, Hsin-Fang Yang-Yen, Ching-Shu Suen, Ming-Jing Hwang, Jeffrey Jong-Young Yen
JAK2 activation is crucial for cytokine receptor signal transduction and leukemogenesis. However, the underlying processes that lead to full activation of JAK2 are unclear. Here, we report a positive role for ubiquitination of JAK2 during GM-CSF-induced activation. Upon GM-CSF stimulation, JAK2 ubiquitination is significantly enhanced through K63-linked poly-ubiquitination. Studies employing both knockout and overexpression of Cbl, an E3 ubiquitin ligase, led to the conclusion that Cbl specifically promotes JAK2 ubiquitination, and this was further confirmed in vitro using a Cbl ubiquitination assay...
July 4, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28675638/azacitidine-successfully-maintained-the-second-remission-in-an-infant-with-kmt2a-rearranged-acute-lymphoblastic-leukemia-who-relapsed-after-unrelated-cord-blood-transplantation
#13
Ikue Chijimatsu, Yusuke Imanaka, Daisuke Tomizawa, Mariko Eguchi, Shiho Nishimura, Shuhei Karakawa, Mizuka Miki, Kazuko Hamamoto, Naoto Fujita
The outcome for infants with KMT2A (MLL)-rearranged acute lymphoblastic leukemia (MLL-r ALL) is dismal despite intensive therapy, including hematopoietic stem cell transplantation (HSCT). Epigenetic dysregulation is considered a key driver of MLL-r leukemogenesis, which theoretically supports the use of epigenetic modifiers as a treatment option. We report an infant MLL-r ALL case with post-HSCT relapse. After achieving a second remission, which was maintained for 10 months using only the DNA methyltransferase inhibitor, azacitidine, the patient successfully received the second HSCT...
July 4, 2017: Pediatric Blood & Cancer
https://www.readbyqxmd.com/read/28669733/bcl11b-is-frequently-downregulated-in-htlv-1-infected-t-cells-through-tax-mediated-proteasomal-degradation
#14
Happy Kurnia Permatasari, Shingo Nakahata, Tomonaga Ichikawa, Kazuhiro Morishita
Human T-cell leukemia virus type 1 (HTLV-1) is a causative agent of adult T-cell leukemia-lymphoma (ATLL). The HTLV-1-encoded protein Tax plays important roles in the proliferation of HTLV-1-infected T-cells by affecting cellular proteins. In this study, we showed that Tax transcriptionally and post-transcriptionally downregulates the expression of the tumor suppressor gene B-cell leukemia/lymphoma 11B (BCL11B), which encodes a lymphoid-related transcription factor. BCL11B expression was downregulated in HTLV-1-infected T-cell lines at the mRNA and protein levels, and forced expression of BCL11B suppressed the proliferation of these cells...
June 29, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/28661409/cytogenetic-characterization-of-myeloid-neoplasms-with-t-2-3-p13-25-q25-29-an-analysis-of-60-cases
#15
Alexis V Dowiak, Carlos A Tirado
Chromosomal translocations involving the short arm of chromosome 2 (p13-25) and the distal part of the long arm of chromosome 3 (q25-29) are rare and still poorly studied to date. These abnormalities are common in myeloid neoplasms and are associated with a poor prognosis. Chromosomal abnormalities within the involved range of bands may contribute to the ectopic expression or formation of fusion genes involving the EVI1 gene, but the exact mechanism by which EVI1 affects leukemogenesis remains unclear. Herein, we report an analysis of 60 patient cases presenting various myeloid malignancies with t(2;3)(p13-25;q25-29) compiled from the Mitelman Database of Chromosome Aberrations and Gene Fusions in Cancer...
2017: Journal of the Association of Genetic Technologists
https://www.readbyqxmd.com/read/28654205/driving-toward-precision-medicine-for-acute-leukemias-are-we-there-yet
#16
Clement Chung, Hilary Ma
Despite recent progress in the understanding of the molecular basis of acute leukemias, treatment options for these diseases have not shown significant changes over the last few decades. In this review, we present a nonexhaustive key summary of the current cytogenetic and molecular changes associated with acute leukemias in disease prognostication and potential targeted therapies. An emerging paradigm is that many genetic or molecular alterations target similar signal transduction, transcriptional, and epigenetic pathways...
June 27, 2017: Pharmacotherapy
https://www.readbyqxmd.com/read/28652130/tal1-as-a-master-oncogenic-transcription-factor-in-t-cell-acute-lymphoblastic-leukemia
#17
REVIEW
Takaomi Sanda, Wei Zhong Leong
In hematopoietic cell development, the transcriptional program is strictly regulated in a lineage- and stage-specific manner that requires a number of transcription factors to work in a cascade or in a loop, in addition to interactions with nonhematopoietic cells in the microenvironment. Disruption of the transcriptional program alters the cellular state and may predispose cells to the acquisition of genetic abnormalities. Early studies have shown that proteins that promote cell differentiation often serve as tumor suppressors, whereas inhibitors of those proteins act as oncogenes in the context of acute leukemia...
June 24, 2017: Experimental Hematology
https://www.readbyqxmd.com/read/28651627/induction-of-endoplasmic-reticulum-calcium-pump-expression-during-early-leukemic-b-cell-differentiation
#18
Lamia Aït Ghezali, Atousa Arbabian, Hervé Roudot, Jean-Philippe Brouland, Fanny Baran-Marszak, Evelyn Salvaris, Andrew Boyd, Hans G Drexler, Agnes Enyedi, Remi Letestu, Nadine Varin-Blank, Bela Papp
BACKGROUND: Endoplasmic reticulum (ER) calcium storage and release play important roles in B lymphocyte maturation, survival, antigen-dependent cell activation and immunoglobulin synthesis. Calcium is accumulated in the endoplasmic reticulum (ER) by Sarco/Endoplasmic Reticulum Calcium ATPases (SERCA enzymes). Because lymphocyte function is critically dependent on SERCA activity, it is important to understand qualitative and quantitative changes of SERCA protein expression that occur during B lymphoid differentiation and leukemogenesis...
June 26, 2017: Journal of Experimental & Clinical Cancer Research: CR
https://www.readbyqxmd.com/read/28637661/the-full-transforming-capacity-of-mll-af4-is-interlinked-with-lymphoid-lineage-commitment
#19
Shan Lin, Roger T Luo, Mahesh Shrestha, Michael J Thirman, James C Mulloy
Chromosome rearrangements involving mixed-lineage leukemia gene (MLL) create MLL-fusion proteins, which could drive both acute lymphoblastic and myeloid leukemia (ALL and AML). The lineage decision of MLL-fusion leukemia is influenced by the fusion partner and microenvironment. To investigate the interplay of fusion proteins and microenvironment in lineage choice, we transplanted human hematopoietic stem and progenitor cells (HSPC) expressing MLL-AF9 or MLL-Af4 into immunodeficient NSGS mice, which strongly promote myeloid development...
June 21, 2017: Blood
https://www.readbyqxmd.com/read/28637624/etv6-in-hematopoiesis-and-leukemia-predisposition
#20
REVIEW
Hanno Hock, Akiko Shimamura
The ETV6 (also known as TEL) gene encodes a transcriptional repressor that plays a critical role in hematopoiesis and in embryonic development. While somatic ETV6 translocations and missense mutations are frequently observed in human cancers, the role of ETV6 in malignant transformation was unclear. Recently, autosomal dominant germline ETV6 mutations were discovered in families with inherited thrombocytopenia and a propensity to develop hematological malignancy, unequivocally demonstrating a role for ETV6 in leukemogenesis...
April 2017: Seminars in Hematology
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