TY - JOUR. T1 - Prognostic value of AML 1/ETO fusion transcripts in patients with acute myelogenous leukemia.. AU - Cho, Eun Kyung. AU - Bang, Soo Mee. AU - Ahn, Jeong Yeal. AU - Yoo, Seung Min. AU - Park, Pil Whan. AU - Seo, Yieh Hea. AU - Shin, Dong Bok. AU - Lee, Jae Hoon. PY - 2003/1/1. Y1 - 2003/1/1. N2 - BACKGROUND: The t (8;21) (q22;q22), which produces the fusion gene AML1/ETO, is associated with relatively good prognosis and, in particular, with a good response to cytosine arabinoside. Analysis of t (8;21) positive leukemic blasts has shown characteristic morphological and immunological features. We performed this study to investigate the incidence of AML1/ETO rearrangement in adult acute myelogenous leukemia (AML), especially in M2 subtype, to make a comparison of clinical, morphological and immunophenotypic characteristics between AML1/ETO rearrangement positive and negative group in patients with AML and to analyze the correlation with other biological parameters. METHODS: From May ...
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. While expression of AML1-ETO in myeloid differentiated induced pluripotent stem cells (iPSCs) induces leukemic characteristics, overexpression increases cell death. We find that expression of wild-type transcription factors RUNX1 and ERG in AML is required to prevent this oncogene overexpression. Together our results show that the interplay ...
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Loss of RUNX1/ETO Triggers C/EBPα-Driven Reorganization of the Leukemic Transcriptional Network(A) RUNX1/ETO and CEBPA mRNA expression levels in Kasumi-1 cells
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Chromosome changes in the bone marrow (BM) of patients with persistent cytopenia are often considered diagnostic for a myelodysplastic syndrome (MDS). Comprehensive cytogenetic evaluations may give evidence of the real pathogenetic role of these changes in cases with cytopenia without morphological signs of MDS. Chromosome anomalies were found in the BM of three patients, without any morphological evidence of MDS: 1) an acquired complex rearrangement of chromosome 21 in a boy with severe aplastic anaemia (SAA); the rearrangement caused the loss of exons 2-8 of the RUNX1 gene with subsequent hypoexpression. 2) a constitutional complex rearrangement of chromosome 21 in a girl with congenital thrombocytopenia; the rearrangement led to RUNX1 disruption and hypoexpression. 3) an acquired paracentric inversion of chromosome 1, in which two regions at the breakpoints were shown to be lost, in a boy with aplastic anaemia; the MPL gene, localized in chromosome 1 short arms was not mutated neither disrupted, but
The TEL-AML1 fusion not only characterizes the most frequent genetic rearrangement in initial childhood ALL (20-25%) but its presence has also been associated with a favorable prognosis (9, 10, 11 , 28 , 32) . In clinical studies on initial ALL, probability of event-free survival (EFS) at 4 years was as high as 90-100% for TEL-AML1+ patients (9 , 10 , 32) . These results certainly do not represent final outcome considering that, regardless of the different prevalence of TEL-AML1 positivity at relapse of BCP-ALL (range, 3- 28%), TEL-AML1+ leukemia is biologically characterized by a long duration of first CR and that the majority of relapses (80%) occur off-therapy (median, 46 months; range, 13-125 months; Refs. 18, 19, 20, 21, 22, 23 , 33 ). The prevalence of TEL-AML1 positivity in our ongoing prospective study on first relapse of BCP-ALL is ∼17% (31 of 178 children; 33 ).. Obviously, the predictive value of TEL-AML1 positivity alone is insufficient to stratify patients to appropriate treatment ...
Further we asked if VLA-4 and VLA-5 integrin upregulation is maintained by RUNX1/ETO in the transformed human leukemia cell line Kasumi-1, derived from a t(8;21)+ AML patient. Kasumi-1 cells, which express RUNX1/ETO and to a lesser extent RUNX1/ETOtr,4 bear high levels of VLA-4 whereas the integrin αL subunit is absent in these cells. We specifically down-regulated RUNX1/ETO via lentivirally delivered shRNA targeting the RUNX1/ETO breakpoint sequences (shRE), which are present in both full length and truncated forms (Online Supplementary Figure S3). At Day 4 after transduction with vectors co-expressing shRE and eGFP, α4, α5 and β1 expression levels were significantly reduced as assessed using flow cytometry, while CXCR4 levels remained unaltered (Figure 1I). Similar results were obtained with NHR2 competitive peptides (N89) (Figure 1J), which also interfere with both RUNX1/ETO forms by disrupting RUNX1/ETO tetramer formation.6 These results suggest that integrin subunit expression remains ...
MGA is an incompletely studied gene with a high mutation frequency in MLL-PTD AML (9%) and in core bind factor AML (8%). This gene encodes a MAX-interacting protein and is believed to act as a transcription factor that suppresses MYC binding to its target. By in silico analysis, we found that MGA is expressed in normal myeloid hematopoietic cells and AML, and the expression level is comparable with TET2 or DNMT3A. Further data mining of TCGA revealed a high frequency of inactivating mutations of the MGA gene in a variety of cancers such as various adenocarcinomas. To interrogate functionally its role in leukemogenesis, lentiviral constructs containing either shRNA or CRISPR-sgRNA targeted to different regions of the MGA gene were generated. MGA expressing AML cell line EOL-1 was silenced by shRNA or CRISPER system. Silencing was confirmed by western blot (shRNA) and Sanger Sequencing (sgRNA). An increase of methylcellulose colony number (~30%) was observed in MGA silenced cell lines. Control ...
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The mechanism underlying the lineage decision made by CD4(+)CD8(+) double-positive (DP) thymocytes that give rise to two T lymphocyte subset with distinct functionalities, that is, helper and cytotoxic T cells, remains a major issue in immunology. The lineage decision process involves several phases and terminates when cells loose their developmental plasticity to become the alternate lineage. A detailed picture of the transcription factor network governing helper versus cytotoxic-lineage decision has recently emerged. Studies published only past year provided new insights into how the expression of ThPOK, a central transcription factor for helper T cell development, is regulated. It has now become evident that an antagonistic interplay between ThPOK and Runx transcription factor complexes plays an essential role in thwarting an alternate fate during the commitment process.
Scientists from the Cancer Science Institute of Singapore (CSI Singapore) at the National University of Singapore (NUS) have discovered that modifications to a protein called RUNX3 may promote cancer progression. The results of the study were published in the prestigious journal Proceedings of the National Academy of Sciences (PNAS) in June 2016. The research team, led by Professor Yoshiaki Ito, Senior Principal Investigator at CSI Singapore, found that a modification called phosphorylation made to RUNX3 promotes cancer progression by allowing cell division. Uncontrolled cell division in the body is a process by which tumours form and hence is a hallmark of cancer. RUNX3 is a tumour suppressor gene that prevents the formation of tumours by binding to DNA. The phosphorylation, or the addition of a phosphate group to a molecule, is carried out by an enzyme called Aurora Kinase, which has been observed to be present in unusually high levels in some cancers. Phosphorylation prevents the binding of ...
Study hypothesis: Treatment with dasatinib 100 mg QD is safe and efficacious when given to patients with Ph+ ALL in the post SCT setting.
The inherited platelet disorders are an uncommon cause of symptomatic bleeding. They may be difficult to diagnose (and are likely to be under-diagnosed) and pose problems in management. This review discusses the inherited platelet disorders summarising the current state of the art with respect to in …
If you have a platelet disorder, you may not be able to form clots as easily. That means you could be at risk for excessive bleeding.
RUNX1 antibody (runt-related transcription factor 1) for WB. Anti-RUNX1 pAb (GTX11903) is tested in Human, Mouse samples. 100% Ab-Assurance.
RUNX1 antibody (runt-related transcription factor 1) for ICC/IF, WB. Anti-RUNX1 pAb (GTX129100) is tested in Human, Mouse, Rat samples. 100% Ab-Assurance.
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AML-2 (Acute myeloid leukemia 2 or Runx3) antibody against the runt transcription factor 3 for use in supershift (EMSA) and Western blotting.
PHF2라는 단백질이 뼈를 만드는 세포(조골세포)를 활성화시킨다는 사실을 처음으로 규명했다. 조골세포는 Runx2라는 단백질에 의해 분화가 조절된다. 반면, SUV39HI1라는 효소는 Runx2에 메틸기(CH3)를 붙임으로써 Runx2가 기능을 하지 못하게 하는 장식으로 분화를 방해한다. 성장이 끝난 성인들이 더 이상 키가 크지 않는 것도 SUV39HI1 효소 때문이다. 이에 착안해 Runx2에 붙어 있는 메틸기를 제거하는 방안을 연구한 결과, PHF2 단백질이 조골세포 분화를 유도함으로써, 소아의 뼈 발달 과정이나 골절 후 뼈가 새로 형성되는 과정에 작용한다는 것을 증명했다.. PHF2 단백질은 Runx2에 붙어 있는 메틸기를 제거했으며, 이후 본연의 기능을 회복한 Runx2는 조골세포의 분화를 촉진하여 다시 뼈를 만들기 시작했다. 실제 유전자 조작으로 PHF2 단백질이 과발현된 쥐를 만들어 ...
Accountants have been warned to expect an increase in AML compliance work in the wake of a new report criticising bodies for a widespread lack of ML
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Runt-related transcription factor 1 (RUNX1) is generally considered to function as a tumor suppressor in the development of leukemia, but a growing body of evidence suggests that it has pro-oncogenic properties in acute myeloid leukemia (AML). Here we have demonstrated that the antileukemic effect mediated by RUNX1 depletion is highly dependent on a functional p53-mediated cell death pathway. Increased expression of other RUNX family members, including RUNX2 and RUNX3, compensated for the antitumor effect elicited by RUNX1 silencing, and simultaneous attenuation of all RUNX family members as a cluster led to a much stronger antitumor effect relative to suppression of individual RUNX members. Switching off the RUNX cluster using alkylating agent-conjugated pyrrole-imidazole (PI) polyamides, which were designed to specifically bind to consensus RUNX-binding sequences, was highly effective against AML cells and against several poor-prognosis solid tumors in a xenograft mouse model of AML without ...
TY - JOUR. T1 - Loss of runt-related transcription factor 3 induces gemcitabine resistance in pancreatic cancer. AU - Horiguchi, Shigeru. AU - Shiraha, Hidenori. AU - Nagahara, Teruya. AU - Kataoka, Jyunnro. AU - Iwamuro, Masaya. AU - Matsubara, Minoru. AU - Nishina, Shinichi. AU - Kato, Hironari. AU - Takaki, Akinobu. AU - Nouso, Kazuhiro. AU - Tanaka, Takehiro. AU - Ichimura, Koichi. AU - Yagi, Takahito. AU - Yamamoto, Kazuhide. PY - 2013/8. Y1 - 2013/8. N2 - Background & Aim: Runt-related transcription factor 3 (RUNX3) is a tumor suppressor gene that is expressed in gastric and other cancers including pancreatic cancer. However, the precise function of RUNX3 in pancreatic cancer has not been fully elucidated. In this study, we aimed to determine the effect of decreased RUNX3 expression in pancreatic cancer. Methods: This study included 36 patients with primary pancreatic cancer, who had undergone pancreaticoduodenectomy. All patients were treated with 1000mg/m2 gemcitabine after the surgery. ...
Runt-related transcription factor 1 (RUNX1) is a heterodimeric transcription factor that binds to the core element of many enhancers and promoters and can accelerate apoptosis in various tumors. However, the regulatory mechanisms underlying RUNX1 expression in neuroblastoma (NB), a highly malignant tumor in childhood, remain largely unclear. In this study, we aimed to assess the role of RUNX1 in NB and to reveal the underlying mechanisms that may contribute to finding a potential therapeutics strategy against NB. Growth, invasion, metastasis and angiogenesis were assessed using Cell Counting Kit-8 (CCK-8) immunocytochemistry, and studies involving soft agar, cell invasion, tube formation and whole animals. The levels of expression were measured using real-time quantitative PCR for RNA, Western blot and immunostaining analyses for proteins. Luciferase reporter and chromatin immunoprecipitation assays indicated that RUNX1 directly binds within the BIRC5, CSF2RB and NFKBIA promoter regions to facilitate
Hematopoietic stem cells (HSCs) are self-renewing multipotent stem cells that generate mature blood lineages throughout life. They, together with hematopoietic progenitor cells (collectively known as HSPCs), emerge from hemogenic endothelium in the floor of the embryonic dorsal aorta by an endothelial-to-hematopoietic transition (EHT). Here we demonstrate that transforming growth factor β (TGFβ) is required for HSPC specification and that it regulates the expression of the Notch ligand Jagged1a in endothelial cells prior to EHT, in a striking parallel with the epithelial-to-mesenchymal transition (EMT). The requirement for TGFβ is two fold and sequential: autocrine via Tgfβ1a and Tgfβ1b produced in the endothelial cells themselves, followed by a paracrine input of Tgfβ3 from the notochord, suggesting that the former programs the hemogenic endothelium and the latter drives EHT. Our findings have important implications for the generation of HSPCs from pluripotent cells in vitro.
BACKGROUND: Runx transcription factors play critical roles in the developmental control of cell fate and contribute variously as oncoproteins and tumor suppressors to leukemia and other cancers. To discover fundamental Runx functions in the cell biology of animal development, we have employed morpholino antisense-mediated knockdown of the sea urchin Runx protein SpRunt-1. Previously we showed that embryos depleted of SpRunt-1 arrest development at early gastrula stage and underexpress the conventional protein kinase C SpPKC1. RESULTS: We report here that SpRunt-1 deficiency leads to ectopic cell proliferation and extensive apoptosis. Suppression of the apoptosis by pharmacological inhibition of caspase-3 prevents the ectopic proliferation and rescues gastrulation, indicating that many of the overt defects obtained by knockdown of SpRunt-1 are secondary to the apoptosis. Inhibition or knockdown of SpPKC1 also causes apoptosis, while cell survival is rescued in SpRunt-1 morphant embryos coinjected with
The Runt related transcription factors (RUNX) are recognized as key players in suppressing or promoting tumor growth. RUNX3, a member of this family, is known as a tumor suppressor in many types of cancers, although such a paradigm was challenged by some researchers. The TGF-β pathway governs major upstream signals to activate RUNX3. RUNX3 protein consists of several regions and domains. The Runt domain is a conserved DNA binding domain and is considered as the main part of RUNX proteins since. Herein, we compared the effects of Runt domains and full-Runx3 in cell viability by designing two constructs of Runx3, including N-terminal region and Runt domain. We investigated the effect of full-Runx3, N-t, and RD on growth inhibition in AGS, MCF-7, A549, and HEK293 cell lines which are different in TGF-β sensitivity, in the absence and presence of TGF-β. The full length RUNX3 did not notably inhibit growth of these cell lines while, the N-t and RD truncates showed different trends in these cell lines.
TY - JOUR. T1 - Fusion AML1 transcript in a radiation-associated leukemia results in a truncated inhibitory AML1 protein. AU - Hromas, Robert. AU - Busse, Tracey. AU - Carroll, Audra. AU - Mack, David. AU - Shopnick, Rinah. AU - Zhang, Dong Er. AU - Nakshatri, Harikrishna. AU - Richkind, Kathleen. PY - 2001/4/1. Y1 - 2001/4/1. N2 - AML1 is a transcription factor that is essential for normal hematopoietic development. It is the most frequent target for translocations in acute leukemia. Recently, fluorescence in situ hybridization was used to identify a novel syndrome of radiation-associated secondary acute myelogenous leukemia that had AML1 translocations. Using polymerase chain reaction, the AML1 fusion transcript was isolated from the patient who had a t(19;21) radiation-associated leukemia. The AML1 gene is fused out of frame to chromosome 19 sequences, resulting in a truncated AML protein bearing the DNA binding domain but not the transcriptional activation domain. This fusion AML1 protein ...
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The Runx1-CBFbeta transcription factor is required for the emergence of all definitive hematopoietic cells. It is the earliest specific marker of sites from whi...
Cancer researchers at the University of Cincinnati College of Medicine have found an obesity-associated proteins role in leukemia development and drug response which could lead to more effective therapies for the illness.
t(8;21) is one of the most frequent chromosomal abnormalities observed in acute myeloid leukemia (AML). However, expression of AML1-ETO is not sufficient to induce transformation in vivo. Consistent with this observation, patients with this translocation harbor additional genetic abnormalities, sugg …
This resource is intended for patients with acute myeloid leukemia (AML). You will find expert advice about AML to help you discuss key issues with your healthcare provider and make important decisions related to management and treatment. Easy-to-understand animations with audio narration, expert video explanations, illustrated slide shows, and educational downloads are available to you.
This information is intended for physicians and related personnel, who understand that medical information is often imperfect, and must be interpreted in the context of a patients clinical data using reasonable medical judgment. This website should not be used as a substitute for the advice of a licensed physician ...
The algorithm predicts the chance of the achievement of a complete remission and the risk for an early death for elderly patients (60 years and older) with newly diagnosed AML.