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https://www.readbyqxmd.com/read/28447248/somatic-setbp1-mutations-in-myeloid-neoplasms
#1
REVIEW
Hideki Makishima
SETBP1 is a SET-binding protein regulating self-renewal potential through HOXA-protein activation. Somatic SETBP1 mutations were identified by whole exome sequencing in several phenotypes of myelodysplastic/myeloproliferative neoplasms (MDS/MPN), including atypical chronic myeloid leukemia, chronic myelomonocytic leukemia, and juvenile myelomonocytic leukemia as well as in secondary acute myeloid leukemia (sAML). Surprisingly, its recurrent somatic activated mutations are located at the identical positions of germline mutations reported in congenital Schinzel-Giedion syndrome...
April 26, 2017: International Journal of Hematology
https://www.readbyqxmd.com/read/28446316/-prognostic-value-of-recurrent-molecular-genetics-and-epigenetics-abnormity-in-t-lymphoblastic-lymphoma-leukemia-review
#2
Wei Guan, Yu Jing, Li Yu
T lymphoblastic lymphoma / leukemia is a strong invasive and has a high incidence of various molecular genetic abnormalities. The NOTCH1 / FBXW7 mutation is one of the most common mutations, and related with good prognosis in T-LBL / ALL. PTEN mutation, a poor prognostic factor, could be overcome by NOTCH1 mutations in pediatric patients to some extent. Patients with MLL gene abnormality and loss of heterozygosity 6q have worse prognosis than those with normal karyotype. The incidence of MLL gene abnormality, RUNX1 mutation and DNMT3A mutation in early precursor T-lymphoblastic leukemia was higher than that of other mature subtypes, which could be used as risk stratification factors...
April 2017: Zhongguo Shi Yan Xue Ye Xue za Zhi
https://www.readbyqxmd.com/read/28443460/augmented-expression-of-runx1-deregulates-the-global-gene-expression-of-u87-glioblastoma-multiforme-cells-and-inhibits-tumor-growth-in-mice
#3
Yoel Bogoch, Gilgi Friedlander-Malik, Lior Lupu, Ekaterina Bondar, Nitzan Zohar, Sheila Langier, Zvi Ram, Ido Nachmany, Joseph M Klausner, Niv Pencovich
Glioblastoma multiforme is the most common and aggressive primary brain tumor in adults. A mesenchymal phenotype was associated with tumor aggressiveness and poor prognosis in glioblastoma multiforme patients. Recently, the transcription factor RUNX1 was suggested as a driver of the glioblastoma multiforme mesenchymal gene expression signature; however, its independent role in this process is yet to be described. Here, we assessed the role of RUNX1 in U87 glioblastoma multiforme cells in correspondence to its mediated transcriptome and genome-wide occupancy pattern...
April 2017: Tumour Biology: the Journal of the International Society for Oncodevelopmental Biology and Medicine
https://www.readbyqxmd.com/read/28436029/wnt4-acts-downstream-of-bmp2-to-mediate-the-regulation-of-atra-signaling-on-runx1-expression-implications-for-terminal-differentiation-of-antler-chondrocytes
#4
Hong-Liang Zhang, Zhan-Qing Yang, Cui-Cui Duan, Shuang Geng, Kai Wang, Hai-Fan Yu, Zhan-Peng Yue, Bin Guo
Although ATRA is involved in regulating the proliferation and differentiation of chondrocytes, its underlying mechanism remains unknown. Here we showed that ATRA could stimulate the proliferation of antler chondrocytes and expression of COL X and MMP13 which were two well-known markers for hypertrophic chondrocytes. Silencing of CRABP2 prevented the induction of ATRA on chondrocyte terminal differentiation, while overexpression of CRABP2 exhibited the opposite effects. CYP26A1 and CYP26B1 weakened the sensitivity of antler chondrocytes to ATRA...
April 24, 2017: Journal of Cellular Physiology
https://www.readbyqxmd.com/read/28432293/quiescence-of-adult-oligodendrocyte-precursor-cells-requires%C3%A2-thyroid-hormone-and-hypoxia-to-activate-runx1
#5
Yasuhito Tokumoto, Shinpei Tamaki, Yasuaki Kabe, Keiyo Takubo, Makoto Suematsu
The adult mammalian central nervous system (CNS) contains a population of slowly dividing oligodendrocyte precursor cells (OPCs), i.e., adult OPCs, which supply new oligodendrocytes throughout the life of animal. While adult OPCs develop from rapidly dividing perinatal OPCs, the mechanisms underlying their quiescence remain unknown. Here, we show that perinatal rodent OPCs cultured with thyroid hormone (TH) under hypoxia become quiescent and acquire adult OPCs-like characteristics. The cyclin-dependent kinase inhibitor p15/INK4b plays crucial roles in the TH-dependent cell cycle deceleration in OPCs under hypoxia...
April 21, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28431504/erratum-to-runx1-induces-dna-replication-independent-active-dna-demethylation-at-spi1-regulatory-regions
#6
Shubham Goyal, Takahiro Suzuki, Jing-Ru Li, Shiori Maeda, Mami Kishima, Hajime Nishimura, Yuri Shimizu, Harukazu Suzuki
No abstract text is available yet for this article.
April 21, 2017: BMC Molecular Biology
https://www.readbyqxmd.com/read/28424161/response-and-progression-on-midostaurin-in-advanced-systemic-mastocytosis-kit-d816v-and-other-molecular-markers
#7
Mohamad Jawhar, Juliana Schwaab, Nicole Naumann, Hans-Peter Horny, Karl Sotlar, Torsten Haferlach, Georgia Metzgeroth, Alice Fabarius, Peter Valent, Wolf-Karsten Hofmann, Nicholas C P Cross, Manja Meggendorfer, Andreas Reiter
In advanced systemic mastocytosis (advSM), disease evolution is often triggered by activating KIT mutations (D816V in >80% of cases) and by additional mutations, e.g. in SRSF2, ASXL1 and/or RUNX1 (S/A/R(pos), >60% of cases). In a recently reported phase-II-study, midostaurin, a multikinase/KIT inhibitor, demonstrated an overall response rate (ORR) of 60% in advSM but biomarkers predictive of response are lacking. We evaluated the impact of molecular markers (KIT D816V, S/A/R(pos)) at baseline and during follow-up in 38 midostaurin-treated advSM patients...
April 19, 2017: Blood
https://www.readbyqxmd.com/read/28418909/pathogenesis-of-etv6-runx1-positive-childhood-acute-lymphoblastic-leukemia-and-mechanisms-underlying-its-relapse
#8
REVIEW
Congcong Sun, Lixian Chang, Xiaofan Zhu
ETV6/RUNX1 (E/R) is the most common fusion gene in childhood acute lymphoblastic leukemia (ALL). Multiple lines of evidence imply a "two-hit" model for the molecular pathogenesis of E/R-positive ALL, whereby E/R rearrangement is followed by a series of secondary mutations that trigger overt leukemia. The cellular framework in which E/R arises and the maintenance of a pre-leukemic condition by E/R are fundamental to the mechanism that underlies leukemogenesis. Accordingly, a variety of studies have focused on the relationship between the clones giving rise to the primary and recurrent E/R-positive ALL...
March 18, 2017: Oncotarget
https://www.readbyqxmd.com/read/28416505/hematopoietic-transcription-factors-mutations-important-players-in-inherited-platelet-defects
#9
Natthapol Songdej, A Koneti Rao
Transcription factors (TF) are proteins that bind to specific DNA sequences and regulate expression of genes. The molecular and genetic mechanisms in most patients with inherited platelet defects are unknown. There is now increasing evidence that mutations in hematopoietic TFs are an important underlying cause for defects in platelet production, morphology, and function. The hematopoietic TFs implicated in patients with impaired platelet function and number include runt related transcription factor 1 (RUNX1), Fli-1 proto-oncogene, ETS transcription factor (FLI1), GATA-binding protein 1 (GATA1), growth factor independent 1B transcriptional repressor (GFI1B), ETS variant 6 (ETV6), ecotropic viral integration site 1 (EVI1), and homeobox A11 (HOXA11)...
April 17, 2017: Blood
https://www.readbyqxmd.com/read/28416284/distinct-roles-for-matrix-metalloproteinases-2-and-9-in-embryonic-hematopoietic-stem-cell-emergence-migration-and-niche-colonization
#10
Lindsay N Theodore, Elliott J Hagedorn, Mauricio Cortes, Kelsey Natsuhara, Sarah Y Liu, Julie R Perlin, Song Yang, Madeleine L Daily, Leonard I Zon, Trista E North
Hematopoietic stem/progenitor cells (HSPCs) are formed during ontogeny from hemogenic endothelium in the ventral wall of the dorsal aorta (VDA). Critically, the cellular mechanism(s) allowing HSPC egress and migration to secondary niches are incompletely understood. Matrix metalloproteinases (MMPs) are inflammation-responsive proteins that regulate extracellular matrix (ECM) remodeling, cellular interactions, and signaling. Here, inhibition of vascular-associated Mmp2 function caused accumulation of fibronectin-rich ECM, retention of runx1/cmyb(+) HSPCs in the VDA, and delayed caudal hematopoietic tissue (CHT) colonization; these defects were absent in fibronectin mutants, indicating that Mmp2 facilitates endothelial-to-hematopoietic transition via ECM remodeling...
April 12, 2017: Stem Cell Reports
https://www.readbyqxmd.com/read/28415763/low-numbers-of-pre-leukemic-fusion-genes-are-frequently-present-in-umbilical-cord-blood-without-affecting-dna-damage-response
#11
Pavol Kosik, Milan Skorvaga, Matus Durdik, Lukas Jakl, Ekaterina Nikitina, Eva Markova, Katarina Kozics, Eva Horvathova, Igor Belyaev
Despite widely accepted notion that many childhood leukemias are likely developed from hematopoietic stem/progenitor cells (HSPC) with pre-leukemic fusion genes (PFG) formed in embryonic/fetal development, the data on PFG incidence in newborns are contradictive. To provide a better understanding of a prenatal origin of leukemia, umbilical cord blood from 500 newborns was screened for the presence of the most frequent PFG associated with pediatric B-cell acute lymphoblastic leukemia. This screening revealed relatively high incidence of ETV6-RUNX1, BCR-ABL1 (p190) and MLL-AF4 at very low frequencies, averaging ~14 copies per 100,000 cells...
March 15, 2017: Oncotarget
https://www.readbyqxmd.com/read/28411256/epigenetically-induced-ectopic-expression-of-uncx-impairs-the-proliferation-and-differentiation-of-myeloid-cells
#12
Giulia Daniele, Giogia Simonetti, Caterina Fusilli, Ilaria Iacobucci, Angelo Lonoce, Antonio Palazzo, Mariana Lomiento, Fabiana Mammoli, Rene' Massimiliano Marsano, Elena Marasco, Vilma Mantovani, Hilmar Quentmeier, Hans G Drexler, Jie Ding, Orazio Palumbo, Massimo Carella, Niroshan Nadarajah, Margherita Perricone, Emanuela Ottaviani, Carmen Baldazzi, Nicoletta Testoni, Cristina Papayannidis, Sergio Ferrari, Tommaso Mazza, Giovanni Martinelli, Clelia Tiziana Storlazzi
We here describe a leukemogenic role of the homeobox gene UNCX, activated by epigenetic modifications in acute myeloid leukemia. We found the ectopic activation of UNCX in a leukemia patient harboring a t(7;10)(p22;p14) translocation, in 22/61 of additional cases [a total of 23 positive patients out of 62 (37.1%)], and in 6/75 (8%) of acute myeloid leukemia cell lines. UNCX is embedded within a low-methylation region (canyon) and encodes for a transcription factor involved in somitogenesis and neurogenesis, with specific expression in the eye, brain, and kidney...
April 14, 2017: Haematologica
https://www.readbyqxmd.com/read/28408464/targetable-kinase-gene-fusions-in-high-risk-b-all-a-study-from-the-children-s-oncology-group
#13
Shalini C Reshmi, Richard C Harvey, Kathryn G Roberts, Eileen Stonerock, Amy Smith, Heather Jenkins, I-Ming Chen, Marc Valentine, Yu Liu, Yongjin Li, Ying Shao, John Easton, Debbie Payne-Turner, Zhaohui Gu, Thai Hoa Tran, Jonathan V Nguyen, Meenakshi Devidas, Yunfeng Dai, Nyla A Heerema, Andrew J Carroll, Elizabeth A Raetz, Michael J Borowitz, Brent L Wood, Anne L Angiolillo, Michael J Burke, Wanda L Salzer, Patrick A Zweidler-McKay, Karen R Rabin, William L Carroll, Jinghui Zhang, Mignon L Loh, Charles G Mullighan, Cheryl L Willman, Julie M Gastier-Foster, Stephen P Hunger
Philadelphia chromosome-like acute lymphoblastic leukemia (Ph-like ALL) is a high-risk subtype characterized by genomic alterations that activate cytokine receptor and kinase signaling. We examined the frequency and spectrum of targetable genetic lesions in a retrospective cohort of 1389 consecutively diagnosed childhood B-ALL patients with high-risk clinical features and/or elevated minimal residual disease at the end of remission induction therapy. The Ph-like gene expression profile was identified in 341 of 1389 patients, 57 of which were excluded from additional analysis because of the presence of BCR-ABL1 (n=46) or ETV6-RUNX1 (n=11)...
April 13, 2017: Blood
https://www.readbyqxmd.com/read/28407696/runx1-a-new-regulator-of-emt-in-breast-cancer
#14
Saleh Khawaled, Rami I Aqeilan
No abstract text is available yet for this article.
March 14, 2017: Oncotarget
https://www.readbyqxmd.com/read/28407681/runx1-stabilizes-the-mammary-epithelial-cell-phenotype-and-prevents-epithelial-to-mesenchymal-transition
#15
Deli Hong, Terri L Messier, Coralee E Tye, Jason R Dobson, Andrew J Fritz, Kenneth R Sikora, Gillian Browne, Janet L Stein, Jane B Lian, Gary S Stein
Runx1 is a well characterized transcription factor essential for hematopoietic differentiation and Runx1 mutations are the cause of leukemias. Runx1 is highly expressed in normal epithelium of most glands and recently has been associated with solid tumors. Notably, the function of Runx1 in the mammary gland and how it is involved in initiation and progression of breast cancer is still unclear. Here we demonstrate the consequences of Runx1 loss in normal mammary epithelial and breast cancer cells. We first observed that Runx1 is decreased in tumorigenic and metastatic breast cancer cells...
March 14, 2017: Oncotarget
https://www.readbyqxmd.com/read/28400392/identification-of-runx1-as-a-mediator-of-aberrant-retinal-angiogenesis
#16
Jonathan D Lam, Daniel J Oh, Lindsay L Wong, Dhanesh Amarnani, Cindy Park-Windhol, Angie V Sanchez, Jonathan Cardona-Velez, Declan McGuone, Anat O Stemmer-Rachamimov, Dean Eliott, Diane R Bielenberg, Tave van Zyl, Lishuang Shen, Xiaowu Gai, Patricia A D'Amore, Leo A Kim, Joseph F Arboleda-Velasquez
Proliferative diabetic retinopathy (PDR) is a common cause of blindness in the developed world's working adult population, and affects those with type 1 and type 2 diabetes mellitus. We identified Runt-related transcription factor 1 (RUNX1) as a gene upregulated in CD31+ vascular endothelial cells obtained from human PDR fibrovascular membranes (FVM) via transcriptomic analysis. In vitro studies using human retinal microvascular endothelial cells (HRMECs) showed increased RUNX1 RNA and protein expression in response to high glucose whereas RUNX1 inhibition reduced HRMEC migration, proliferation, and tube formation...
April 11, 2017: Diabetes
https://www.readbyqxmd.com/read/28395444/-prognostic-value-of-dynamic-monitoring-of-runx1-runx1t1-transcript-in-pediatric-acute-myeloid-leukemia
#17
H T Gao, Y Zhang, K Sun, J M Guo, Y Q Chen, X L Chen, J Shi, X N Niu, F Wang, L Huo
Objective: To investigate the prognostic value of dynamic monitoring of RUNX1-RUNX1T1 transcript in pediatric patients with t (8;21) acute myeloid leukemia (AML) . Methods: The clinical features and RUNX1-RUNX1T1 transcript levels of 55 pediatric t (8;21) AML patients, newly diagnosed from Jan. 2010 to Apr. 2016, were analyzed retrospectively. The relationship between the minimal residual disease (MRD) and prognosis was analysed by dynamic monitoring of RUNX1-RUNX1T1 transcript levels using real-time quantitative PCR (RQ-PCR) technology...
March 14, 2017: Zhonghua Xue Ye Xue za Zhi, Zhonghua Xueyexue Zazhi
https://www.readbyqxmd.com/read/28395118/etv6-runx1-like-acute-lymphoblastic-leukemia-a-novel-b-cell-precursor-leukemia-subtype-associated-with-the-cd27-cd44-immunophenotype
#18
Marketa Zaliova, Michaela Kotrova, Silvia Bresolin, Jan Stuchly, Jan Stary, Ondrej Hrusak, Geertruy Te Kronnie, Jan Trka, Jan Zuna, Martina Vaskova
We have shown previously that ETV6/RUNX1-positive acute lymphoblastic leukemia (ALL) is distinguishable from other ALL subtypes by CD27(p) °(s) /CD44(l) °(w-neg) immunophenotype. During diagnostic immunophenotyping of 573 childhood B-cell precursor ALL (BCP-ALL), we identified eight cases with this immunophenotype among "B-other ALL" (BCP-ALL cases negative for routinely tested chromosomal/genetic aberrations). We aimed to elucidate whether these cases belong to the recently described ETV6/RUNX1-like ALL defined by the ETV6/RUNX1-specific gene expression profile, harboring concurrent ETV6 and IKZF1 lesions...
April 10, 2017: Genes, Chromosomes & Cancer
https://www.readbyqxmd.com/read/28394181/a-novel-recurrent-copy-number-loss-region-on-6q23-3-in-mds-related-myeloid-malignancy-patients-with-stable-survival-conditions
#19
Kun Chi, Yang Li, Lan Xu, Xuefeng Wang
Metaphase cytogenetics (MC) karyotyping is a fundamental way to approach cytogenetic pathogenesis of MDS-related myeloid malignancies. However, in some patients, the results are normal while the patients often show discrepancies in survival conditions. To explain this question, we analyzed CytoScan™ HD array results of 20 MC-normal/failure patients who were followed up for three years. Exon sequencing was performed in genes RUNX1, TP53, ASXL1, and TET2. The array enabled the detection of additional aberrations in 16 (80%) patients...
April 10, 2017: Leukemia & Lymphoma
https://www.readbyqxmd.com/read/28391050/the-mds-and-evi1-complex-locus-mecom-isoforms-regulate-their-own-transcription-and-have-different-roles-in-the-transformation-of-hematopoietic-stem-and-progenitor-cells
#20
Miren Maicas, Iria Vázquez, Rafael Alis, Nerea Marcotegui, Leire Urquiza, Xabier Cortés-Lavaud, Ion Cristóbal, María A García-Sánchez, María D Odero
Transcriptional activation of the EVI1 oncogene (3q26) leads to aggressive forms of human acute myeloid leukemia (AML). However, the mechanism of EVI1-mediated leukemogenesis has not been fully elucidated. Previously, by characterizing the EVI1 promoter, we have shown that RUNX1 and ELK1 directly regulate EVI1 transcription. Intriguingly, bioinformatic analysis of the EVI1 promoter region identified the presence of several EVI1 potential binding sites. Thus, we hypothesized that EVI1 could bind to these sites regulating its own transcription...
April 6, 2017: Biochimica et Biophysica Acta
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