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https://www.readbyqxmd.com/read/27903959/genome-wide-haplotype-association-study-identify-the-fgfr2-gene-as-a-risk-gene-for-acute-myeloid-leukemia
#1
Hongchao Lv, Mingming Zhang, Zhenwei Shang, Jin Li, Shanshan Zhang, Duan Lian, Ruijie Zhang
Acute myeloid leukemia (AML) is a cancer of the myeloid line of blood cells, and generally considered to be caused by environment and genetic factors. In this study, we combined a genome-wide haplotype association study (GWHAS) and gene prioritization strategy to mine AML-related genetic affect factors and understand its pathogenesis. A total of 175 AML patients were downloaded from the public GEO database (GSE32462) and 218 matched Caucasian controls were from the HapMap Project. We first identified the linkage disequilibrium (LD) blocks and performed a GWHAS to scan AML-related haplotypes...
November 26, 2016: Oncotarget
https://www.readbyqxmd.com/read/27899806/preleukemia-one-name-many-meanings
#2
REVIEW
H P Koeffler, G Leong
Definition of preleukemia has evolved. It was first used to describe the myelodysplastic syndrome (MDS) with a propensity to progress to acute myeloid leukemia (AML). Individuals with germline mutations of either RUNX1, CEBPA, or GATA2 can also be called as preleukemic because they have a markedly increased incidence of evolution into AML. Also, alkylating chemotherapy or radiation can cause MDS/preleukemia which nearly always progress to AML. More recently investigators noted that AML patients who achieved complete morphological remission after chemotherapy often have clonal hematopoiesis predominantly marked by either DNMT3A, TET2 or IDH1/2 mutations which were also present at diagnosis of AML...
November 30, 2016: Leukemia: Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K
https://www.readbyqxmd.com/read/27899515/bringing-in-fresh-blood-sox7-runx1-ap-1-and-tead4
#3
(no author information available yet)
No abstract text is available yet for this article.
December 1, 2016: Development
https://www.readbyqxmd.com/read/27895713/coexistence-of-iamp21-and-etv6-runx1-fusion-in-an-adolescent-with-b-cell-acute-lymphoblastic-leukemia-literature-review-of-six-additional-cases
#4
Jun Gu, Alexandra Reynolds, Lianghua Fang, Corrie DeGraffenreid, Kenneth Sterns, Keyur P Patel, L Jeffrey Medeiros, Pei Lin, Xinyan Lu
BACKGROUND: Intrachromosomal amplification of chromosome 21 (iAMP21) results from breakage-fusion-bridge cycles and chromothripsis is a distinct marker of a subgroup of B cell acute lymphoblastic leukemia (B-ALL) cases associated with a poor prognosis. iAMP21 accounts for 2% of pediatric B-ALL and occurs predominantly in older children or adolescents. ETV6-RUNX1 fusion, resulting from t(12;21)(p13;q22), is associated with an excellent outcome in younger children with B-ALL. Coexistence of iAMP21 with ETV6-RUNX1 fusion is extremely rare with limited clinical information available...
2016: Molecular Cytogenetics
https://www.readbyqxmd.com/read/27894958/poly-adp-ribose-polymerase-inhibitors-selectively-induce-cytotoxicity-in-tcf3-hlf-positive-leukemic-cells
#5
Jinhua Piao, Shiori Takai, Takahiro Kamiya, Takeshi Inukai, Kanji Sugita, Kazuma Ohyashiki, Domenico Delia, Mitsuko Masutani, Shuki Mizutani, Masatoshi Takagi
Poly (ADP-ribose) polymerase (PARP) is an indispensable component of the DNA repair machinery. PARP inhibitors are used as cutting-edge treatments for patients with homologous recombination repair (HRR)-defective breast cancers harboring mutations in BRCA1 or BRCA2. Other tumors defective in HRR, including some hematological malignancies, are predicted to be good candidates for treatment with PARP inhibitors. Screening of leukemia-derived cell lines revealed that lymphoid lineage-derived leukemia cell lines, except for those derived from mature B cells and KMT2A (MLL)-rearranged B-cell precursors, were relatively sensitive to PARP inhibitors...
November 25, 2016: Cancer Letters
https://www.readbyqxmd.com/read/27889575/isthmus-time-is-here-runx1-identifies-mucosal-stem-cells-in-the-gastric-corpus
#6
EDITORIAL
James R Goldenring, Jason C Mills
No abstract text is available yet for this article.
November 23, 2016: Gastroenterology
https://www.readbyqxmd.com/read/27887572/maternal-smoking-impacts-key-biological-pathways-in-newborns-through-epigenetic-modification-in-utero
#7
Daniel M Rotroff, Bonnie R Joubert, Skylar W Marvel, Siri E Håberg, Michael C Wu, Roy M Nilsen, Per M Ueland, Wenche Nystad, Stephanie J London, Alison Motsinger-Reif
BACKGROUND: Children exposed to maternal smoking during pregnancy exhibit increased risk for many adverse health effects. Maternal smoking influences methylation in newborns at specific CpG sites (CpGs). Here, we extend evaluation of individual CpGs to gene-level and pathway-level analyses among 1062 participants in the Norwegian Mother and Child Cohort Study (MoBa) using the Illumina 450 K platform to measure methylation in newborn DNA and maternal smoking in pregnancy, assessed using the biomarker, plasma cotinine...
November 25, 2016: BMC Genomics
https://www.readbyqxmd.com/read/27884971/progression-in-patients-with-low-and-intermediate1-risk-del-5q-myelodysplastic-syndromes-is-predicted-by-a-limited-subset-of-mutations
#8
Christian Scharenberg, Valentina Giai, Andrea Pellagatti, Leonie Saft, Marios Dimitriou, Monica Jansson, Martin Jädersten, Alf Grandien, Iyadh Douagi, Donna S Neuberg, Katarina LeBlanc, Jacqueline Boultwood, Mohsen Karimi, Sten Eirik W Jacobsen, Petter S Woll, Eva Hellström-Lindberg
A high proportion of patients with lower-risk del(5q) myelodysplastic syndromes (MDS) will respond to treatment with lenalidomide. Median duration of transfusion-independence is 2 years with some long-lasting responses, but almost 40% of patients progress to acute leukemia by 5 years after start of treatment. Mechanisms underlying disease progression other than the well-established finding of small TP53-mutated subclones at diagnosis remain unclear. We studied a longitudinal cohort of 35 low- and intermediate-1-risk del(5q) patients treated with lenalidomide (n=22) or not (n=13) by flow cytometric surveillance of hematopoietic stem and progenitor cells (HSPC) subsets, targeted sequencing of mutational patterns, and changes in the bone marrow microenvironment...
November 24, 2016: Haematologica
https://www.readbyqxmd.com/read/27881874/acute-myeloid-leukemia-derived-from-lympho-myeloid-clonal-hematopoiesis
#9
F Thol, S Klesse, L Köhler, R Gabdoulline, A Kloos, A Liebich, M Wichman, A Chaturvedi, J Fabisch, V I Gaidzik, P Paschka, L Bullinger, G Bug, H Serve, G Göhring, B Schlegelberger, M Lübbert, H Kirchner, M Wattad, D Kraemer, B Hertenstein, G Heil, W Fiedler, J Krauter, R Schlenk, K Döhner, H Döhner, A Ganser, M Heuser
We studied acute myeloid leukemia (AML) patients with lympho-myeloid clonal hematopoiesis (LM-CH), defined by the presence of DNA methyltransferase 3A (DNMT3A) mutations in both the myeloid and lymphoid T-cell compartment. Diagnostic, CR and relapse samples were sequenced for 34 leukemia-related genes in 171 DNMT3A mutated adult AML patients. AML with LM-CH was found in 40 patients (23%) and was associated with clonal haematopoiesis of indeterminate potential (CHIP) years prior to AML, older age, secondary AML, and more frequent MDS-type co-mutations (TET2, RUNX1 and EZH2)...
November 24, 2016: Leukemia: Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K
https://www.readbyqxmd.com/read/27879203/fetal-and-neonatal-hematopoietic-progenitors-are-functionally-and-transcriptionally-resistant-to-flt3-itd-mutations
#10
Shaina N Porter, Andrew S Cluster, Wei Yang, Kelsey A Busken, Riddhi M Patel, Jiyeon A Ryoo, Jeffrey A Magee
The FLT3 Internal Tandem Duplication (FLT3(ITD)) mutation is common in adult acute myeloid leukemia (AML) but rare in early childhood AML. It is not clear why this difference occurs. Here we show that Flt3(ITD) and cooperating Flt3(ITD)/Runx1 mutations cause hematopoietic stem cell depletion and myeloid progenitor expansion during adult but not fetal stages of murine development. In adult progenitors, FLT3(ITD) simultaneously induces self-renewal and myeloid commitment programs via STAT5-dependent and STAT5-independent mechanisms, respectively...
November 23, 2016: ELife
https://www.readbyqxmd.com/read/27869314/runx1-orchestrates-sphingolipid-metabolism-and-glucocorticoid-resistance-in-lymphomagenesis
#11
A Kilbey, A Terry, S Wotton, G Borland, Q Zhang, N Mackay, A McDonald, M Bell, M J O Wakelam, E R Cameron, J C Neil
The three-membered RUNX gene family includes RUNX1, a major mutational target in human leukemias, and displays hallmarks of both tumour suppressors and oncogenes. In mouse models the Runx genes appear to act as conditional oncogenes, as ectopic expression is growth suppressive in normal cells but drives lymphoma development potently when combined with over-expressed Myc or loss of p53. Clues to underlying mechanisms emerged previously from murine fibroblasts where ectopic expression of any of the Runx genes promotes survival through direct and indirect regulation of key enzymes in sphingolipid metabolism associated with a shift in the 'sphingolipid rheostat' from ceramide to sphingosine-1-phosphate (S1P)...
November 21, 2016: Journal of Cellular Biochemistry
https://www.readbyqxmd.com/read/27869129/reprogramming-mouse-fibroblasts-into-engraftable-myeloerythroid-and-lymphoid-progenitors
#12
Hui Cheng, Heather Yin-Kuan Ang, Chadi A El Farran, Pin Li, Hai Tong Fang, Tong Ming Liu, Say Li Kong, Michael Lingzi Chin, Wei Yin Ling, Edwin Kok Hao Lim, Hu Li, Tara Huber, Kyle M Loh, Yuin-Han Loh, Bing Lim
Recent efforts have attempted to convert non-blood cells into hematopoietic stem cells (HSCs) with the goal of generating blood lineages de novo. Here we show that hematopoietic transcription factors Scl, Lmo2, Runx1 and Bmi1 can convert a developmentally distant lineage (fibroblasts) into 'induced hematopoietic progenitors' (iHPs). Functionally, iHPs generate acetylcholinesterase(+) megakaryocytes and phagocytic myeloid cells in vitro and can also engraft immunodeficient mice, generating myeloerythoid and B-lymphoid cells for up to 4 months in vivo...
November 21, 2016: Nature Communications
https://www.readbyqxmd.com/read/27851970/the-hematopoietic-transcription-factors-runx1-and-erg-prevent-aml1-eto-oncogene-overexpression-and-onset-of-the-apoptosis-program-in-t-8-21-amls
#13
Amit Mandoli, Abhishek A Singh, Koen H M Prange, Esther Tijchon, Marjolein Oerlemans, Rene Dirks, Menno Ter Huurne, Albertus T J Wierenga, Eva M Janssen-Megens, Kim Berentsen, Nilofar Sharifi, Bowon Kim, Filomena Matarese, Luan N Nguyen, Nina C Hubner, Nagesha A Rao, Emile van den Akker, Lucia Altucci, Edo Vellenga, Hendrik G Stunnenberg, Joost H A Martens
The t(8;21) acute myeloid leukemia (AML)-associated oncoprotein AML1-ETO disrupts normal hematopoietic differentiation. Here, we have investigated its effects on the transcriptome and epigenome in t(8,21) patient cells. AML1-ETO binding was found at promoter regions of active genes with high levels of histone acetylation but also at distal elements characterized by low acetylation levels and binding of the hematopoietic transcription factors LYL1 and LMO2. In contrast, ERG, FLI1, TAL1, and RUNX1 bind at all AML1-ETO-occupied regulatory regions, including those of the AML1-ETO gene itself, suggesting their involvement in regulating AML1-ETO expression levels...
November 15, 2016: Cell Reports
https://www.readbyqxmd.com/read/27843138/mutations-in-the-ccnd1-and-ccnd2-genes-are-frequent-events-in-adult-patients-with-t-8-21-q22-q22-acute-myeloid-leukemia
#14
A-K Eisfeld, J Kohlschmidt, S Schwind, D Nicolet, J S Blachly, S Orwick, C Shah, M Bainazar, K W Kroll, C J Walker, A J Carroll, B L Powell, R M Stone, J E Kolitz, M R Baer, A de la Chapelle, K Mrózek, J C Byrd, C D Bloomfield
Core-binding factor acute myeloid leukemia (CBF-AML) is defined by the presence of either t(8;21)(q22;q22)/RUNX1-RUNX1T1 or inv(16)(p13.1q22)/t(16;16)(p13.1;q22)/CBFB-MYH11. The resulting fusion genes require a 'second hit' to initiate leukemogenesis. Mutation assessment of 177 adults with CBF-AML, including 68 with t(8;21) and 109 with inv(16)/t(16;16), identified not only mutations well-known in CBF-AML, but also mutations in the CCND1 and CCND2 genes, which represent novel frequent molecular alterations in AML with t(8;21)...
November 15, 2016: Leukemia: Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K
https://www.readbyqxmd.com/read/27836890/core-binding-factor-amls-have-distinct-genomic-landscapes
#15
(no author information available yet)
RUNX1-RUNX1T1 AML has an enrichment of mutations in epigenetic regulators compared with CBFB-MYH11 AML.
November 11, 2016: Cancer Discovery
https://www.readbyqxmd.com/read/27819671/protease-activated-receptor-1-inhibits-proliferation-but-enhances-leukemia-stem-cell-activity-in-acute-myeloid-leukemia
#16
S Goyama, M Shrestha, J Schibler, L Rosenfeldt, W Miller, E O'Brien, B Mizukawa, T Kitamura, J S Palumbo, J C Mulloy
Eradication of leukemia stem cells (LSCs) is the ultimate goal of treating acute myeloid leukemia (AML). We recently showed that the combined loss of Runx1/Cbfb inhibited the development of MLL-AF9-induced AML. However, c-Kit(+)/Gr-1(-) cells remained viable in Runx1/Cbfb-deleted cells, indicating that suppressing RUNX activity may not eradicate the most immature LSCs. In this study, we found upregulation of several hemostasis-related genes, including the thrombin-activatable receptor PAR-1 (protease-activated receptor-1), in Runx1/Cbfb-deleted MLL-AF9 cells...
November 7, 2016: Oncogene
https://www.readbyqxmd.com/read/27819178/myelodysplastic-syndromes-and-acute-leukemia-with-genetic-predispositions-a-new-challenge-for-hematologists
#17
Nicolas Duployez, Sophie Lejeune, Aline Renneville, Claude Preudhomme
The determination of an underlying genetic predisposition is not automatically part of the diagnosis of hematological malignancies (HM) in routine practice. However, it is assumed that genetic predispositions to HM are currently underestimated due to great variations in disease phenotype, variable latency and incomplete penetrance. Most of patients do not display any biological or clinical signs besides the overt hematological disease and many of them have a lack of personal or family history of malignancies...
December 2016: Expert Review of Hematology
https://www.readbyqxmd.com/read/27811935/integrated-computational-approach-to-the-analysis-of-rna-seq-data-reveals-new-transcriptional-regulators-of-psoriasis
#18
Alena Zolotarenko, Evgeny Chekalin, Alexandre Mesentsev, Ludmila Kiseleva, Elena Gribanova, Rohini Mehta, Ancha Baranova, Tatiana V Tatarinova, Eleonora S Piruzian, Sergey Bruskin
Psoriasis is a common inflammatory skin disease with complex etiology and chronic progression. To provide novel insights into the regulatory molecular mechanisms of the disease, we performed RNA sequencing analysis of 14 pairs of skin samples collected from patients with psoriasis. Subsequent pathway analysis and extraction of the transcriptional regulators governing psoriasis-associated pathways was executed using a combination of the MetaCore Interactome enrichment tool and the cisExpress algorithm, followed by comparison to a set of previously described psoriasis response elements...
November 4, 2016: Experimental & Molecular Medicine
https://www.readbyqxmd.com/read/27804971/runx1-mutations-in-acute-myeloid-leukemia-are-associated-with-distinct-clinico-pathologic-and-genetic-features
#19
V I Gaidzik, V Teleanu, E Papaemmanuil, D Weber, P Paschka, J Hahn, T Wallrabenstein, B Kolbinger, C H Köhne, H A Horst, P Brossart, G Held, A Kündgen, M Ringhoffer, K Götze, M Rummel, M Gerstung, P Campbell, J M Kraus, H A Kestler, F Thol, M Heuser, B Schlegelberger, A Ganser, L Bullinger, R F Schlenk, K Döhner, H Döhner
No abstract text is available yet for this article.
November 2016: Leukemia: Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K
https://www.readbyqxmd.com/read/27802191/molecular-combing-a-new-tool-in-diagnosing-leukemia
#20
Antoine Ittel, Hélène Zattara, Charlène Chaix, Gérard Michel, Nicolas Levy
BACKGROUND: According to the World Health Organization (WHO), recurrent cytogenetic abnormalities define many specific groups of hematopoietic tumors of acute myeloid and lymphoblastic leukemia, and these abnormalities are often strongly associated with prognosis and sometimes require specific treatments. These rearrangements are commonly detected by conventional and molecular cytogenetic techniques. OBJECTIVE: Using an alternative method, we sought to highlight the presence of chromosomal rearrangements...
September 30, 2016: Cancer Biomarkers: Section A of Disease Markers
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