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[PMID]: 29524739
[Au] Autor:Medeiros BC
[Ad] Address:Department of Medicine, Stanford University School of Medicine, 875 Blake Wilbur Dr, Stanford, CA, USA. Electronic address: brunom@stanford.edu.
[Ti] Title:Interpretation of clinical endpoints in trials of acute myeloid leukemia.
[So] Source:Leuk Res;68:32-39, 2018 Feb 07.
[Is] ISSN:1873-5835
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Treatment regimens for acute myeloid leukemia (AML) have remained largely unchanged until recently. Molecular advances have opened the door to targeted therapies, many of which are in late-phase clinical trials. As new therapeutic opportunities arise, it is appropriate to review key aspects of clinical trial design, statistical interpretation of outcomes, and methods of data reporting. Complete remission and overall survival (OS) are common primary endpoints in early-phase AML clinical trials. OS and event-free survival are frequent primary endpoints in phase 3 trials. Clinical trials are designed to address the primary endpoint using prespecified α and power levels. Interpretation of additional endpoints (eg, secondary endpoints and subgroup analyses) must be viewed in light of a trial's statistical design. Furthermore, variations in reporting of endpoints must be considered in order to understand trial outcomes. Time-to-event endpoints are typically reported using Kaplan-Meier curves, which are visually informative. Statistical data derived from these curves can be complex, and a variety of factors may impact interpretation. The purpose of this review is to discuss the nuances of common AML trial endpoints and their data presentation to better inform evaluation and understanding of clinical trial data.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

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[PMID]: 29524504
[Au] Autor:Qiu F; Dong C; Liu Y; Shao X; Huang D; Han Y; Wang B; Liu Y; Huo R; Paulo P; Zhang Z; Zhao D; Chu WF
[Ad] Address:Department of Pharmacology (the State-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education), College of Pharmacy, Harbin Medical University, Harbin, Heilongjiang 150081, PR China.
[Ti] Title:Pharmacological inhibition of SUMO-1 with ginkgolic acid alleviates cardiac fibrosis induced by myocardial infarction in mice.
[So] Source:Toxicol Appl Pharmacol;, 2018 Mar 07.
[Is] ISSN:1096-0333
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND AND PURPOSE: Protein modification by small ubiquitin-like modifier (SUMO) plays a critical role in the pathogenesis of heart diseases. The present study was designed to determine whether ginkgolic acid (GA) as a SUMO-1 inhibitor exerts an inhibitory effect on cardiac fibrosis induced by myocardial infarction (MI). EXPERIMENTAL APPROACH: GA was delivered by osmotic pumps in MI mice. Masson staining, electron microscopy (EM) and echocardiography were used to assess cardiac fibrosis, ultrastructure and function. Expression of SUMO-1, PML, TGF-ß1 and Pin1 was measured with Western blot or Real-time PCR. Collagen content, cell viability and myofibroblast transformation were measured in neonatal mouse cardiac fibroblasts (NMCFs). Promyelocytic leukemia (PML) protein was over-expressed by plasmid transfection. KEY RESULTS: GA improved cardiac fibrosis and dysfunction, and decreased SUMO-1 expression in MI mice. GA (>20 µM) inhibited NMCF viability in a dose-dependent manner. Nontoxic GA (10 µM) restrained angiotensin II (Ang II)-induced myofibroblast transformation and collagen production. GA also inhibited expression of TGF-ß1 mRNA and protein in vitro and in vivo. GA suppressed PML SUMOylation and PML nuclear body (PML-NB) organization, and disrupted expression and recruitment of Pin1 (a positive regulator of TGF-ß1 mRNA), whereas over-expression of PML reversed that. CONCLUSIONS AND IMPLICATIONS: Inhibition of SUMO-1 by GA alleviated MI-induced heart dysfunction and fibrosis, and the SUMOylated PML/Pin1/TGF-ß1 pathway is crucial for GA-inhibited cardiac fibrosis.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

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[PMID]: 29516013
[Au] Autor:Yang X; Yao R; Wang H
[Ad] Address:Department of Hematology, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, China.
[Ti] Title:Update of ALDH as a Potential Biomarker and Therapeutic Target for AML.
[So] Source:Biomed Res Int;2018:9192104, 2018.
[Is] ISSN:2314-6141
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Studies employing mouse transplantation have illustrated the role of aldehyde dehydrogenase (ALDH) defining hematopoietic stem cells (HSCs) and leukemia stem cells (LSCs). Besides being a molecular marker, ALDH mediates drug resistance in AML, which induces poor prognosis of the patients. In AML patients, either CD34 ALDH population or CD34 CD38 ALDH population was found to denote LSCs and minimal residual disease (MRD). A bunch of reagents targeting ALDH directly or indirectly have been evaluated. ATRA, disulfiram, and dimethyl ampal thiolester (DIMATE) are all shown to be potential candidates to open new perspective for AML treatment. However, inconsistent results have been shown for markers of LSCs, which makes it even more difficult to differentiate LSCs and HSCs. In this review, we elevated the role of ALDH to be a potential marker to define and distinguish HSCs and LSCs and its importance in prognosis and target therapy in AML patients. In addition to immunophenotypical markers, ALDH is also functionally active in defining and distinguishing HSCs and LSCs and offers intracellular protections against cytotoxic drugs. Targeting ALDH may be a potential strategy to improve AML treatment. Additional studies concerning specific targeting ALDH and mechanisms of its roles in LSCs are warranted.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Process
[do] DOI:10.1155/2018/9192104

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[PMID]: 29515676
[Au] Autor:Borssén M; Nordlund J; Haider Z; Landfors M; Larsson P; Kanerva J; Schmiegelow K; Flaegstad T; Jónsson ÓG; Frost BM; Palle J; Forestier E; Heyman M; Hultdin M; Lönnerholm G; Degerman S
[Ad] Address:1Department of Medical Biosciences, Umeå University, Blg 6M, 2nd floor, SE-90185 Umeå, Sweden.
[Ti] Title:DNA methylation holds prognostic information in relapsed precursor B-cell acute lymphoblastic leukemia.
[So] Source:Clin Epigenetics;10:31, 2018.
[Is] ISSN:1868-7083
[Cp] Country of publication:Germany
[La] Language:eng
[Ab] Abstract:Background: Few biological markers are associated with survival after relapse of B-cell precursor acute lymphoblastic leukemia (BCP-ALL). In pediatric T-cell ALL, we have identified promoter-associated methylation alterations that correlate with prognosis. Here, the prognostic relevance of CpG island methylation phenotype (CIMP) classification was investigated in pediatric BCP-ALL patients. Methods: Six hundred and one BCP-ALL samples from Nordic pediatric patients (age 1-18) were CIMP classified at initial diagnosis and analyzed in relation to clinical data. Results: Among the 137 patients that later relapsed, patients with a CIMP- profile ( = 42) at initial diagnosis had an inferior overall survival (pOS 33%) compared to CIMP+ patients ( = 95, pOS 65%) ( = 0.001), which remained significant in a Cox proportional hazards model including previously defined risk factors. Conclusion: CIMP classification is a strong candidate for improved risk stratification of relapsed BCP-ALL.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1186/s13148-018-0466-3

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[PMID]: 29514461
[Au] Autor:Moore IMK; Koerner KM; Gundy PM; Montgomery DW; Insel KC; Harris LL; Taylor OA; Hockenberry MJ
[Ad] Address:1 College of Nursing, The University of Arizona, Tucson, AZ, USA.
[Ti] Title:Changes in Oxidant Defense, Apoptosis, and Cognitive Abilities During Treatment for Childhood Leukemia.
[So] Source:Biol Res Nurs;:1099800418763124, 2018 Jan 01.
[Is] ISSN:1552-4175
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Aggressive central nervous system (CNS)-directed treatment for acute lymphoblastic leukemia (ALL), the most prevalent cancer among children and adolescents, prevents metastasis of leukemia cells into the brain. Up to 60% of survivors experience cognitive problems, but knowledge about risk factors for and mechanisms of neurologic injury is lacking. Objectives of the present study were to (1) quantify changes in oxidant defense and apoptosis over the course of ALL therapy and (2) elucidate risk factors for long-term cognitive problems. The sample included 71 children with ALL. Cerebrospinal fluid (CSF) samples were collected at diagnosis and during intrathecal chemotherapy administration. Oxidant defense was measured by reduced glutathione (GSH), oxidized glutathione (GSSG), and the ratio of GSH:GSSG. Apoptosis was measured by activity of several cysteine-dependent aspartate-specific protease (abbreviated as caspase) enzymes that initiate (caspases 8 and 9) or execute (caspases 3/7) apoptosis. Cognitive abilities were assessed by standardized measures of short-term memory, visual-motor integration, and attention 3 years after ALL diagnosis. GSH and GSSG concentration increased significantly during ALL therapy, and a low GSH:GSSG ratio was indicative of an oxidized extracellular environment. Caspase enzyme activity increased significantly, and caspases 3/7 activity was significantly and negatively associated with performance on measures of cognitive abilities. Younger age at time of ALL diagnosis was associated with some measures of attention. Efflux of glutathione into CSF maintains oxidant defense by scavenging free radicals and other reactive oxygen species and is an early event in apoptosis. These mechanisms may be involved in neurologic injury associated with CNS-directed treatment and subsequent cognitive problems.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:Publisher
[do] DOI:10.1177/1099800418763124

  6 / 386808 MEDLINE  
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[PMID]: 29511686
[Au] Autor:Carlberg M; Koppel T; Ahonen M; Hardell L
[Ad] Address:Department of Oncology, Faculty of Medicine and Health, Örebro University, 701 82 Örebro, Sweden.
[Ti] Title:Case-Control Study on Occupational Exposure to Extremely Low-Frequency Electromagnetic Fields and the Association with Meningioma.
[So] Source:Biomed Res Int;2018:5912394, 2018.
[Is] ISSN:2314-6141
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Objective: Exposure to extremely low-frequency electromagnetic fields (ELF-EMF) was in 2002 classified as a possible human carcinogen, Group 2B, by the International Agency for Research on Cancer at WHO based on an increased risk for childhood leukemia. In case-control studies on brain tumors during 1997-2003 and 2007-2009 we assessed lifetime occupations in addition to exposure to different agents. The INTEROCC ELF-EMF Job-Exposure Matrix was used for associating occupations with ELF-EMF exposure ( T) with meningioma. Cumulative exposure ( T-years), average exposure ( T), and maximum exposed job ( T) were calculated. Results: No increased risk for meningioma was found in any category. For cumulative exposure in the highest exposure category 8.52+ T years odds ratio (OR) = 0.9, 95% confidence interval (CI) = 0.7-1.2, and linear trend = 0.45 were calculated. No statistically significant risks were found in different time windows. Conclusion: In conclusion occupational ELF-EMF was not associated with an increased risk for meningioma.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Process
[do] DOI:10.1155/2018/5912394

  7 / 386808 MEDLINE  
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[PMID]: 29510661
[Au] Autor:Wang L; Jiang Z; Huang D; Duan J; Huang C; Sullivan S; Vali K; Yin Y; Zhang M; Wegrzyn J; Tian XC; Tang Y
[Ad] Address:Department of Animal Science, Institute for Systems Genomics, University of Connecticut, Storrs, CT, USA.
[Ti] Title:JAK/STAT3 regulated global gene expression dynamics during late-stage reprogramming process.
[So] Source:BMC Genomics;19(1):183, 2018 Mar 06.
[Is] ISSN:1471-2164
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: The generation of induced pluripotent stem cells (iPSCs) has underdefined mechanisms. In addition, leukemia inhibitory factor (LIF) activated Janus kinase/signal transducer and activator of transcription 3 (JAK/STAT3) pathway is the master regulator for naïve-state pluripotency achievement and maintenance. However, the regulatory process to attain naïve pluripotent iPSCs is not well understood. RESULTS: We performed transcriptome analysis to dissect the genomic expression during mouse iPSC induction, with or without blocking the JAK/STAT3 activity. We describe JAK/STAT3 signaling-specific biological events such as gametogenesis, meiotic/mitotic cell cycle, and DNA repair, and JAK/STAT3-dependent expression of key transcription factors such as the naïve pluripotency-specific genes, developmental pluripotency associated (Dppa) family, along with histone modifiers and non-coding RNAs in reprogramming. We discover that JAK/STAT3 activity does not affect early phase mesenchymal to epithelial transition (MET) but is necessary for proper imprinting of the Dlk1-Dio3 region, an essential event for pluripotency achievement at late-reprogramming stage. This correlates with the JAK/STAT3-dependent stimulation of Dppa3 and Polycomb repressive complex 2 (PRC2) genes. We further demonstrate that JAK/STAT3 activity is essential for DNA demethylation of pluripotent loci including Oct4, Nanog, and the Dlk1-Dio3 regions. These findings correlate well with the previously identified STAT3 direct targets. We further propose a model of pluripotency achievement regulated by JAK/STAT3 signaling during the reprogramming process. CONCLUSIONS: Our study illustrates novel insights for JAK/STAT3 promoted pluripotency establishment, which are valuable for further improving the naïve-pluripotent iPSC generation across different species including humans.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1186/s12864-018-4507-2

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[PMID]: 29505034
[Au] Autor:Zhang B; Nguyen LXT; Li L; Zhao D; Kumar B; Wu H; Lin A; Pellicano F; Hopcroft L; Su YL; Copland M; Holyoake TL; Kuo CJ; Bhatia R; Snyder DS; Ali H; Stein AS; Brewer C; Wang H; McDonald T; Swiderski P; Troadec E; Chen CC; Dorrance A; Pullarkat V; Yuan YC; Perrotti D; Carlesso N; Forman SJ; Kortylewski M; Kuo YH; Marcucci G
[Ad] Address:Gehr Family Center for Leukemia Research, Hematology Malignancies and Stem Cell Transplantation Institute, City of Hope Medical Center, Duarte, California, USA.
[Ti] Title:Bone marrow niche trafficking of miR-126 controls the self-renewal of leukemia stem cells in chronic myelogenous leukemia.
[So] Source:Nat Med;, 2018 Mar 05.
[Is] ISSN:1546-170X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Leukemia stem cells (LSCs) in individuals with chronic myelogenous leukemia (CML) (hereafter referred to as CML LSCs) are responsible for initiating and maintaining clonal hematopoiesis. These cells persist in the bone marrow (BM) despite effective inhibition of BCR-ABL kinase activity by tyrosine kinase inhibitors (TKIs). Here we show that although the microRNA (miRNA) miR-126 supported the quiescence, self-renewal and engraftment capacity of CML LSCs, miR-126 levels were lower in CML LSCs than in long-term hematopoietic stem cells (LT-HSCs) from healthy individuals. Downregulation of miR-126 levels in CML LSCs was due to phosphorylation of Sprouty-related EVH1-domain-containing 1 (SPRED1) by BCR-ABL, which led to inhibition of the RAN-exportin-5-RCC1 complex that mediates miRNA maturation. Endothelial cells (ECs) in the BM supply miR-126 to CML LSCs to support quiescence and leukemia growth, as shown using mouse models of CML in which Mir126a (encoding miR-126) was conditionally knocked out in ECs and/or LSCs. Inhibition of BCR-ABL by TKI treatment caused an undesired increase in endogenous miR-126 levels, which enhanced LSC quiescence and persistence. Mir126a knockout in LSCs and/or ECs, or treatment with a miR-126 inhibitor that targets miR-126 expression in both LSCs and ECs, enhanced the in vivo anti-leukemic effects of TKI treatment and strongly diminished LSC leukemia-initiating capacity, providing a new strategy for the elimination of LSCs in individuals with CML.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:Publisher
[do] DOI:10.1038/nm.4499

  9 / 386808 MEDLINE  
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Clinical Trials Registry
Clinical Trials Registry
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[PMID]: 29477379
[Au] Autor:Vela M; Corral D; Carrasco P; Fernández L; Valentín J; González B; Escudero A; Balas A; de Paz R; Torres J; Leivas A; Martinez-Lopez J; Pérez-Martínez A
[Ad] Address:Translational Research in Pediatric Oncology, Hematopoietic Transplantation & Cell Therapy, Hospital La Paz Institute for Health Research (IdiPAZ), Madrid, Spain. Electronic address: maria.vela@idipaz.es.
[Ti] Title:Haploidentical IL-15/41BBL activated and expanded natural killer cell infusion therapy after salvage chemotherapy in children with relapsed and refractory leukemia.
[So] Source:Cancer Lett;422:107-117, 2018 Feb 23.
[Is] ISSN:1872-7980
[Cp] Country of publication:Ireland
[La] Language:eng
[Ab] Abstract:Primary refractory or relapsed pediatric leukemia yield significant morbidity and mortality, with long-term survival rates <40%. Here we present a post-hoc analysis assessing safety and efficacy of infusing activated and expanded Natural Killer cells (NKAE) from haploidentical donors in patients from 2 clinical trials. In total, 18 children, adolescents and young adults with relapse or refractory acute leukemia were treated with two cycles of rescue chemotherapy followed by fresh NKAE cells infusions and low doses of IL-2. The overall response rate, complete remission achievement at the end of the study, was 72% (13 of 18). We infused 52 NKAE cell products containing a median of 6.76 × 10 NK cells/kg (0.7-34.16) and 0.49 × 10 T cells/kg (0-11). All infusions were well tolerated with no graft versus host disease nor other serious adverse events. Among the 14 patients who completed treatment, 4 of them are alive and leukemia-free more than 750 days post-transplant. We conclude that infusion of fresh NKAE cell therapy is feasible and safe in heavily pretreated pediatric population, and should be further investigated in advanced-phase clinical trials as well as a consolidation therapy to decrease relapse in patients with high-risk leukemia. TRIALS REGISTRATION: Registered at www.clinicaltrials.gov as NCT01944982 and NCT02074657.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[Cl] Clinical Trial:ClinicalTrial
[St] Status:Publisher

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[PMID]: 29474869
[Au] Autor:Wieduwilt MJ
[Ad] Address:Moores Cancer Center, University of California, San Diego, La Jolla, California. Electronic address: mwieduwilt@ucsd.edu.
[Ti] Title:In the Era of BCR-ABL1 Inhibitors, Are We Closing the Survival Gap Between Allogeneic Hematopoietic Cell Transplantation and Chemotherapy for Philadelphia Chromosome-Positive Acute Lymphoblastic Leukemia in First Complete Remission?
[So] Source:Biol Blood Marrow Transplant;, 2018 Feb 21.
[Is] ISSN:1523-6536
[Cp] Country of publication:United States
[La] Language:eng
[Pt] Publication type:EDITORIAL
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher


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