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Journal articles on the topic 'ACML'

Author: Grafiati

Published: 9 March 2023

Last updated: 31 July 2025

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1

Piazza, Rocco, Sara Redaelli, Simona Valletta, et al. "SETBP1 and CSF3R Mutations In Atypical Chronic Myeloid Leukemia." Blood 122, no. 21 (2013): 2598. http://dx.doi.org/10.1182/blood.v122.21.2598.2598.

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Abstract Atypical Chronic Myeloid Leukemia (aCML) is a clonal disorder belonging to the group of myelodysplastic/myeloproliferative (MDS/MPN) syndromes. In aCML many clinical features suggest the diagnosis of CML, however the lack of the BCR-ABL1 fusion point to a different pathogenetic process. Recently, we identified the presence of clonal somatic mutations occurring in the SETBP1 gene in approximately 25% of aCML samples (Piazza R. et al., Nat Genet. 2013 Jan;45(1):18-24). A subsequent study (Maxson J. et al., N Engl J Med. 2013 May 9;368(19):1781-90) demonstrated the presence of somatic mu

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Crisà, Elena, Maura Nicolosi, Valentina Ferri, Chiara Favini, Gianluca Gaidano, and Andrea Patriarca. "Atypical Chronic Myeloid Leukemia: Where Are We Now?" International Journal of Molecular Sciences 21, no. 18 (2020): 6862. http://dx.doi.org/10.3390/ijms21186862.

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Atypical chronic myeloid leukemia, BCR-ABL1 negative (aCML) is a rare myelodysplastic syndrome (MDS)/myeloproliferative neoplasm (MPN) with a high rate of transformation to acute myeloid leukemia, and poor survival. Until now, the diagnosis has been based on morphological grounds only, possibly making the real frequency of the disease underestimated. Only recently, new insights in the molecular biology of MDS/MPN syndromes have deepened our knowledge of aCML, enabling us to have a better molecular profile of the disease. The knowledge gleaned from next generation sequencing has complemented mo

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3

Dao, Kim-Hien T., and Jeffrey W. Tyner. "What's different about atypical CML and chronic neutrophilic leukemia?" Hematology 2015, no. 1 (2015): 264–71. http://dx.doi.org/10.1182/asheducation-2015.1.264.

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Abstract Atypical chronic myeloid leukemia (aCML) and chronic neutrophilic leukemia (CNL) are rare myeloid neoplasms defined largely by morphologic criteria. The discovery of CSF3R mutations in aCML and CNL have prompted a more comprehensive genetic profiling of these disorders. These studies have revealed aCML to be a genetically more heterogeneous disease than CNL, however, several groups have reported that SETBP1 and ASXL1 mutations occur at a high frequency and carry prognostic value in both diseases. We also report a novel finding—our study reveals a high frequency of U2AF1 mutations at c

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Gambacorti-Passerini, Carlo, Simona Valletta, Nils Winkelmann, et al. "Recurrent SETBP1 Mutations in Atypical Chronic Myeloid Leukemia Abrogate an Ubiquitination Site and Dysregulate SETBP1 Protein Levels." Blood 120, no. 21 (2012): LBA—2—LBA—2. http://dx.doi.org/10.1182/blood.v120.21.lba-2.lba-2.

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Abstract Abstract LBA-2 The SETBP1 gene codes for a predominantly nuclear protein with a predicted MW of 170 kD. Germline mutations of SETBP1 were described in patients affected by the Schinzel-Giedion syndrome (SGS), a rare disease characterized by bone, muscle and cardiac abnormalities, and presenting neuroepithelial neoplasms. In an effort to investigate the molecular pathogenesis of myeloid malignancies we applied a HTS strategy, including both exome sequencing and RNA-SEQ, to atypical Chronic Myeloid Leukemia (aCML), as defined by WHO criteria, with the aim of identifying novel recurrent

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5

Raizada, N., T. Sagar, and S. Ramanan. "Comparative study of safety and efficacy of imatinib mesylate therapy in pediatric and adult chronic myeloid leukemia." Journal of Clinical Oncology 25, no. 18_suppl (2007): 20016. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.20016.

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20016 Background: Chronic Myeloid Leukemia (CML) is one of the rare pediatric cancers. Imatinib is now the standard of care in adult CML (ACML) with newer compounds being investigated to overcome the burden of Imatinib resistance. Pediatric CML (PCML) has been an area little explored and effective strategies are not yet defined. Although, allogenic hematopoietic stem cell transplantation (HSCT) still remains the gold-standard treatment, the choice of drug in the subset in which HSCT is not a suitable option remains to be determined. Methods: This was a single-institution prospective study cond

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Kahleifeh, Zachary, and Himanshu Thapliyal. "EE-ACML: Energy-Efficient Adiabatic CMOS/MTJ Logic for CPA-Resistant IoT Devices." Sensors 21, no. 22 (2021): 7651. http://dx.doi.org/10.3390/s21227651.

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Internet of Things (IoT) devices have strict energy constraints as they often operate on a battery supply. The cryptographic operations within IoT devices consume substantial energy and are vulnerable to a class of hardware attacks known as side-channel attacks. To reduce the energy consumption and defend against side-channel attacks, we propose combining adiabatic logic and Magnetic Tunnel Junctions to form our novel Energy Efficient-Adiabatic CMOS/MTJ Logic (EE-ACML). EE-ACML is shown to be both low energy and secure when compared to existing CMOS/MTJ architectures. EE-ACML reduces dynamic e

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7

Redaelli, Sara, Rocco Piazza, Alessandra Pirola, et al. "Recurrent KIT D816V Mutation in Atypical Chronic Myeloid Leukemia." Blood 124, no. 21 (2014): 3576. http://dx.doi.org/10.1182/blood.v124.21.3576.3576.

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Abstract INTRODUCTION: Atypical Chronic Myeloid Leukemia (aCML) is a heterogeneous disorder belonging to the group of myelodysplastic/myeloproliferative syndromes, characterized by a poor prognosis with a median survival time of 37 months. In 2013, by applying Next Generation Sequencing (NGS) technologies on 8 aCML cases, we demonstrated the presence of a recurrent somatic mutations in the SETBP1 gene (Piazza et al, Nat Gen 2013). SETBP1 mutations were identified in approximately 30% of aCML cases. AIM: To further characterize the molecular pathogenesis of aCML and to possibly identify other r

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8

Nam, Myung-Hyun, Ju-Yeon Kim, Soo-Young Yoon, et al. "JAK2 V617F Mutation In Atypical Chronic Myeloid Leukemia." Blood 116, no. 21 (2010): 5069. http://dx.doi.org/10.1182/blood.v116.21.5069.5069.

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Abstract Abstract 5069 Atypical chronic myeloid leukemia (aCML) is a rare leukemic disorder which shows myelodysplastic and myeloproliferative features simultaneously. Some cases of JAK2 V617F mutation in aCML were reported before WHO criteria introduced (Jelinek J et al. Blood 2005; Jones AV et al. Blood 2005; Levine RL et al. Blood 2005). However, Fend F et al observed no JAK2 V617F mutation in aCML as defined by WHO classification (Fend F et al. Leuk Res 2008), which result was refuted by a case report (Campiotti L et al. Leuk Res 2009). Here we analyzed JAK2 V617F mutation with amplificati

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9

Huard, Carine, Guy Miranda, Yulia Redko, Franï¿½oise Wessner, Simon J. Foster, and Marie-Pierre Chapot-Chartier. "Analysis of the Peptidoglycan Hydrolase Complement of Lactococcus lactis: Identification of a Third N-Acetylglucosaminidase, AcmC." Applied and Environmental Microbiology 70, no. 6 (2004): 3493–99. http://dx.doi.org/10.1128/aem.70.6.3493-3499.2004.

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ABSTRACT The peptidoglycan hydrolase (PGH) complement of Lactococcus lactis was identified by amino acid sequence similarity searching of the L. lactis IL-1403 complete genome sequence. Five PGHs that are not encoded by prophages were detected, including the previously characterized AcmA and AcmB proteins. Four of these PGHs, AcmA to AcmD, contain a catalytic domain homologous to that of enterococcal muramidase, but they have different domain structures. The fifth one (YjgB) has sequence similarity with the active-site domain of peptidoglycan-specific endopeptidases. The three new PGH-encoding

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Ma, Yan, Xiaoping Xu, Xiaoqin Wang, Bobin Chen, and Guowei Lin. "Atypical Chronic Myeloid Leukemia: An Analysis of 9 Cases." Blood 112, no. 11 (2008): 4285. http://dx.doi.org/10.1182/blood.v112.11.4285.4285.

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Abstract Objective FTo investigate the clinical characteristics of atypical chronic myeloid leukemia (aCML) and characterize the aCML. Methods FFrom 2003 to 2007, the consecutive samples of 54 MDS/MPD patients in Sino-US Shanghai Leukemia Cooperative Group were collected by prospective methods and diagnosed with WHO classification. We identified 9 aCML cases and analyzed the clinical and laboratory data of these cases. Results FThe median age of 9 cases was 66 years old(range 38~78y). The ratio of male and female is 1:1.25. Median hemoglobin concentration was 76.5g/L(range 43.3~116), median wh

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Carreño-Tarragona, Gonzalo, Alberto Álvarez-Larrán, Claire Harrison, et al. "CNL and aCML should be considered as a single entity based on molecular profiles and outcomes." Blood Advances 7, no. 9 (2023): 1672–81. http://dx.doi.org/10.1182/bloodadvances.2022008204.

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Abstract Chronic neutrophilic leukemia (CNL) and atypical chronic myeloid leukemia (aCML) are rare myeloid disorders that are challenging with regard to diagnosis and clinical management. To study the similarities and differences between these disorders, we undertook a multicenter international study of one of the largest case series (CNL, n = 24; aCML, n = 37 cases, respectively), focusing on the clinical and mutational profiles (n = 53 with molecular data) of these diseases. We found no differences in clinical presentations or outcomes of both entities. As previously described, both CNL and

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Meggendorfer, Manja, Tamara Alpermann, Torsten Haferlach, et al. "Mutational Screening Of CSF3R, ASXL1, SETBP1, and SRSF2 In Chronic Neutrophilic Leukemia (CNL), Atypical CML and CMML Cases." Blood 122, no. 21 (2013): 105. http://dx.doi.org/10.1182/blood.v122.21.105.105.

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Abstract Introduction Chronic neutrophilic leukemia (CNL) and atypical chronic myeloid leukemia (aCML) are rare myeloproliferative and myelodysplastic/myeloproliferative neoplasms. So far, the diagnosis of CNL and aCML has been based on cytomorphology and the absence of JAK2V617F and PDGFR rearrangements. Recently, mutations in CSF3R and SETBP1 were identified and associated with CNL and aCML, respectively. Chronic myelomonocytic leukemia (CMML) and aCML also share several characteristics and need to be discriminated especially by the absolute number of monocytes in the peripheral blood. Aim T

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13

Gao, Tianqi, Changhui Yu, Si Xia, Ting Liang, Xuekui Gu, and Zenghui Liu. "A rare atypical chronic myeloid leukemia BCR-ABL1 negative with concomitant JAK2 V617F and SETBP1 mutations: a case report and literature review." Therapeutic Advances in Hematology 11 (January 2020): 204062072092710. http://dx.doi.org/10.1177/2040620720927105.

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Atypical chronic myeloid leukemia (aCML) BCR-ABL1 negative is a rare myelodysplastic syndromes/myeloproliferative neoplasm (MDS/MPN) for which no standard treatment currently exists. The advent of next-generation sequencing has allowed our understanding of the molecular pathogenesis of aCML to be expanded and has made it possible for clinicians to more accurately differentiate aCML from similar MDS/MPN overlap syndrome and MPN counterparts, as MPN-associated driver mutations in JAK2, CALR, or MPL are typically absent in aCML. A 55-year old male with main complaints of weight loss and fatigue f

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14

Schauwecker, Florian, Frank Pfennig, Werner Schröder, and Ullrich Keller. "Molecular Cloning of the Actinomycin Synthetase Gene Cluster from Streptomyces chrysomallus and Functional Heterologous Expression of the Gene Encoding Actinomycin Synthetase II." Journal of Bacteriology 180, no. 9 (1998): 2468–74. http://dx.doi.org/10.1128/jb.180.9.2468-2474.1998.

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ABSTRACT The actinomycin synthetases ACMS I, II, and III catalyze the assembly of the acyl peptide lactone precursor of actinomycin by a nonribosomal mechanism. We have cloned the genes of ACMS I (acmA) and ACMS II (acmB) by hybridization screening of a cosmid library of Streptomyces chrysomallusDNA with synthetic oligonucleotides derived from peptide sequences of the two enzymes. Their genes were found to be closely linked and are arranged in opposite orientations. Hybridization mapping and partial sequence analyses indicate that the gene of an additional peptide synthetase, most likely the g

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15

Donadoni, Carla, Rocco Piazza, Diletta Fontana, et al. "Evidence of ETNK1 Somatic Variants in Atypical Chronic Myeloid Leukemia." Blood 124, no. 21 (2014): 2212. http://dx.doi.org/10.1182/blood.v124.21.2212.2212.

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Abstract Atypical Chronic Myeloid Leukemia (aCML) is a clonal disorder belonging to the Myeloproliferative/Myelodysplastic (MPN/MDS) group. The molecular lesions responsible for the onset of aCML remained unknown until 2013 when recurrent somatic mutations of SETBP1 were identified. However, the frequency of SETBP1 mutations in aCML does not exceed 25-30%, which suggests that other lesions may play a role in the remaining cases. To gain further insight into the somatic variants responsible for the onset of aCML, we generated whole-exome and transcriptome sequencing data on 15 matched case/cont

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16

Grand, Francis H., Claire E. Hidalgo-Curtis, Thomas Ernst, et al. "Frequent CBL mutations associated with 11q acquired uniparental disomy in myeloproliferative neoplasms." Blood 113, no. 24 (2009): 6182–92. http://dx.doi.org/10.1182/blood-2008-12-194548.

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Abstract Recent evidence has demonstrated that acquired uniparental disomy (aUPD) is a novel mechanism by which pathogenetic mutations in cancer may be reduced to homozygosity. To help identify novel mutations in myeloproliferative neoplasms (MPNs), we performed a genome-wide single nucleotide polymorphism (SNP) screen to identify aUPD in 58 patients with atypical chronic myeloid leukemia (aCML; n = 30), JAK2 mutation–negative myelofibrosis (MF; n = 18), or JAK2 mutation–negative polycythemia vera (PV; n = 10). Stretches of homozygous, copy neutral SNP calls greater than 20Mb were seen in 10 (

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17

Ashangari, Chandralekha, and Praveen K. Tumula. "Atypical Chronic Myeloid Leukemia." Blood 132, Supplement 1 (2018): 5455. http://dx.doi.org/10.1182/blood-2018-99-110189.

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Abstract Introduction: Atypical chronic myeloid leukemia (aCML), BCR-ABL1 negative is a rare myelodysplastic syndromes (MDS)/myeloproliferative neoplasm (MPN) for which no current standard of care exists. We present one of the rare presentations of aCML in an elderly patient. Case: A 76 year old male presented to the Hematology clinic for consultation after discharge from local hospital for elevated WBC count. Past medical history was significant for COPD, acid reflux, peripheral arterial disease and hypertension. Physical exam was unremarkable. Initial labs were significant for leukocytosis o

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Dao, Kim-Hien T., Jason Gotlib, Michael M. N. Deininger, et al. "Efficacy of Ruxolitinib in Patients With Chronic Neutrophilic Leukemia and Atypical Chronic Myeloid Leukemia." Journal of Clinical Oncology 38, no. 10 (2020): 1006–18. http://dx.doi.org/10.1200/jco.19.00895.

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PURPOSE Colony-stimulating factor-3 receptor ( CSF3R)-T618I is a recurrent activating mutation in chronic neutrophilic leukemia (CNL) and to a lesser extent in atypical chronic myeloid leukemia (aCML) resulting in constitutive JAK-STAT signaling. We sought to evaluate safety and efficacy of the JAK1/2 inhibitor ruxolitinib in patients with CNL and aCML, irrespective of CSF3R mutation status. METHODS We conducted a phase II study of ruxolitinib in 44 patients (21 CNL and 23 aCML). The primary end point was overall hematologic response rate (ORR) by the end of 6 continuous 28-day cycles for the

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Meggendorfer, Manja, Wencke Walter, Stephan Hutter, Wolfgang Kern, Claudia Haferlach, and Torsten Haferlach. "FOS Expression Distinguishes Two Groups of Atypical CML (aCML) Allowing Targeted Therapy." Blood 132, Supplement 1 (2018): 3893. http://dx.doi.org/10.1182/blood-2018-99-111832.

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Abstract BCR-ABL1 negative myeloproliferative neoplasms not only include atypical chronic myeloid leukemia (aCML), but also chronic myelomonocytic leukemia (CMML), chronic neutrophilic leukemia (CNL), and myelodysplastic/myeloproliferative neoplasm, unclassifiable (MDS/MPN, U). Despite the recent advances in characterizing aCML more specifically, based on next generation sequencing data, the differential diagnosis and subsequent treatment decisions remain difficult. Therefore, we analyzed the transcriptome and performed whole genome sequencing (WGS) in a cohort of morphologically defined 231 p

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Meggendorfer, Manja, Torsten Haferlach, Sabine Jeromin, Claudia Haferlach, Wolfgang Kern, and Susanne Schnittger. "Molecular Analyses of MDS/MPN Overlap Entities According to WHO Classification Reveal a Distinct Molecular Pattern for MDS/MPN, Unclassifiable." Blood 124, no. 21 (2014): 4618. http://dx.doi.org/10.1182/blood.v124.21.4618.4618.

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Abstract Introduction: The World Health Organization (WHO) classification defines myelodysplastic/myeloproliferative neoplasms (MDS/MPN) based on clinical, morphologic, and laboratory findings that show features of MDS and characteristics more consistent with MPN. This category includes atypical chronic myeloid leukemia (aCML), chronic myelomonocytic leukemia (CMML), MDS/MPN, unclassifiable (MDS/MPN, U), and refractory anemia with ring sideroblasts associated with marked thrombocytosis (RARS-T). In recent years RARS-T, CMML, and also aCML were deciphered by several molecular studies, while MDS

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Braun, Thorsten, Aziza Debache, Hervé Roudot, et al. "Therapeutic Strategies in Patients with Atypical CML (aCML) and Unclassified MDS/MPN (MDS/MPN-U). a Single Center Report." Blood 124, no. 21 (2014): 5610. http://dx.doi.org/10.1182/blood.v124.21.5610.5610.

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Abstract Introduction: The WHO defined overlapping MDS/MPN group includes two rare entities: BCR-ABL negative aCML and MDS/MPN-U, defined by at least 3 months persistent WBC >13G/l or platelets >450G/l with at least 1 cytopenia, significant dysplasia (>10%) in at least 1 lineage, no circulating monocytosis (<1G/l or less <10% WBC) and <20% peripheral and/or BM blasts (Wang et al. Blood 2014). aCML is distinguished from MDS/MPN-U by >10% immature circulating precursors. Median overall survival (OS) in aCML and MDS/MPN-U ranges from 12 to 22 months, without any standard trea

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Kloos, Arnold, Felicitas Thol, Sabrina Klesse, et al. "Patient Derived Xenotransplantation Model of Atypical Chronic Myeloid Leukemia (aCML)." Blood 126, no. 23 (2015): 2836. http://dx.doi.org/10.1182/blood.v126.23.2836.2836.

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Abstract Background: Atypical chronic myeloid leukemia (aCML) is a rare disorder classified as one of the MPN/MDS overlap syndromes. aCML usually presents like CML but lacks the pathognomonic BCR-ABL fusion found in CML. Most patients progress to acute myeloid leukemia (AML) with a median time to AML of 11.2 months and have a median overall survival of only 12.4 months (Wang et al. Blood 2014). Recurrently mutated genes found in aCML patients include SETBP1 , CSF3R, NRAS, EZH2, ASXL1, ETNK1, and U2AF1. The pathogenesis of aCML is poorly understood and neither specific nor effective treatments

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Leung, Chi Sing. "Special issue on ACML 2015." Neurocomputing 258 (October 2017): 1–2. http://dx.doi.org/10.1016/j.neucom.2017.02.076.

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Gotlib, Jason. "How I treat atypical chronic myeloid leukemia." Blood 129, no. 7 (2017): 838–45. http://dx.doi.org/10.1182/blood-2016-08-693630.

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Abstract Atypical chronic myeloid leukemia, BCR-ABL1 negative (aCML) is a rare myelodysplastic syndrome (MDS)/myeloproliferative neoplasm (MPN) for which no current standard of care exists. The challenges of aCML relate to its heterogeneous clinical and genetic features, high rate of transformation to acute myeloid leukemia, and historically poor survival. Therefore, allogeneic hematopoietic stem cell transplantation should always be an initial consideration for eligible patients with a suitable donor. Nontransplant approaches for treating aCML have otherwise largely relied on adopting treatme

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Choi, Hyun-Woo, Hye-Ran Kim, Hwan-Young Kim, et al. "Prevalence and Clinical Impacts Of SETBP1 Mutation In East Asian Patients With MDS/MPN." Blood 122, no. 21 (2013): 2629. http://dx.doi.org/10.1182/blood.v122.21.2629.2629.

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Abstract Introduction Recently, recurrent somatic SET-binding protein 1 (SETBP1) mutations were found in atypical chronic myeloid leukemia (aCML) and other related myeloid neoplasms. According to reports so far, SETBP1 mutations occur in 9% of myelodysplastic/myeloproliferative neoplasms (MDS/MPN), especially in high frequency (24∼30%) of aCML. SETBP1 mutations were associated with worse prognosis and higher white blood cell (WBC) counts. Most of the reports came from western countries and there was a need to further study its clinicopathological impacts in East Asian patients because of pauci

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Fontana, Diletta, Daniele Ramazzotti, Andrea Aroldi, et al. "Integrated Genomic, Functional and Prognostic Characterization of Atypical Chronic Myeloid Leukemia (aCML) in a Cohort of 43 Patients." Blood 134, Supplement_1 (2019): 1714. http://dx.doi.org/10.1182/blood-2019-126467.

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Atypical chronic myeloid leukemia (aCML) is a rare BCR-ABL1 negative clonal disorder, which belongs to the myelodysplastic/myeloproliferative group. This disease is characterized by recurrent somatic mutations in several genes including SETBP1, ASXL1 and ETNK1, as well as high genetic heterogeneity, thus posing a great therapeutic challenge. The clinical prognosis for aCML is poor, with a median overall survival of 18 months after diagnosis, and no established standards of care exist for its treatment. The dissection of the molecular processes underlying aCML leukemogenesis could therefore res

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Jihane, Oussaga, Et-Tahouri Zineddine, mouhsine Hamam, et al. "ATYPICAL CHRONIC MYELOID LEUKEMIA BCR-ABL 1 NEGATIVE: A CASE REPORT AND LITERATURE REVIEW." International Journal of Advanced Research and Review 7, no. 2 (2022): 01–04. https://doi.org/10.5281/zenodo.6405892.

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Atypical chronic myeloid leukemia BCR-ABL negative is rare myelodysplastic syndrome/myeloproliferative neoplasm for which there is no current standard of therapy. Patients with aCML had pronounced immature granulocytosis and granulocytotic dysplasia in their blood smears. We admitted a 60-year-old man with splenomegaly, hyperleukocytosis, anemia, and thrombocytopenia; after cytology, cytogenetic, and molecular biology analyses of bone marrow, we diagnosed aCML using 2016 World Health Organization classification. Chemotherapy was used to treat the patient at first, but the patient’s anemi

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Khanna, Vishesh, Christopher A. Eide, Cristina E. Tognon, et al. "Recurrent Pathogenic Cyclin D2 Mutations in Myeloid Malignancies." Blood 128, no. 22 (2016): 2734. http://dx.doi.org/10.1182/blood.v128.22.2734.2734.

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Abstract Introduction: Atypical chronic myeloid leukemia (aCML) and chronic neutrophilic leukemia (CNL) are rare hematologic neoplasms characterized by leukocytosis, a hypercellular bone marrow with granulocytic predominance, absence of the Philadelphia chromosome (t(9;22); BCR-ABL1), and absence of PDGFRA/B or FGFR1 gene rearrangements. While oncogenic mutations in colony stimulating factor 3 receptor (CSF3R) are commonly reported in CNL and, to a lesser extent, in aCML, a significant percentage of aCML and CNL cases lack well-defined pathogenetic lesions. In this study, we utilized whole exo

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Castellino, Alessia, Elisa Santambrogio, Davide Rapezzi, and Massimo Massaia. "Atypical Chronic Myeloid Leukemia: New Developments from Molecular Diagnosis to Treatment." Medicina 57, no. 10 (2021): 1104. http://dx.doi.org/10.3390/medicina57101104.

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Atypical Chronic Myeloid Leukemia, BCR-ABL1 negative (aCML) is a rare hematological entity, included in the group of myelodysplastic (MDS)/myeloproliferative (MPN) overlap syndromes. It is characterized by an aggressive course, a high rate of acute myeloid leukemia (AML) transformation, and a dismal outcome. The clinical presentation includes splenomegaly and leukocytosis with neutrophilia and left-shifted granulocytosis accompanied by granulocytic dysplasia and sometimes multilineage dysplasia. In past years, the disease incidence was likely underestimated, as diagnosis was only based on morp

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Kesarwani, Meenu, Zachary Kincaid, and Mohammad Azam. "MEK/ERK addiction in CNL/aCML." Oncotarget 8, no. 59 (2017): 99215–16. http://dx.doi.org/10.18632/oncotarget.22283.

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Niro, Antonio, Rocco Piazza, Gabriele Merati, et al. "ETNK1 Is an Early Event and SETBP1 a Late Event in Atypical Chronic Myeloid Leukemia." Blood 126, no. 23 (2015): 3652. http://dx.doi.org/10.1182/blood.v126.23.3652.3652.

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Abstract Atypical Chronic Myeloid Leukemia (aCML) is a clonal disorder belonging to the myelodisplastic-myeloproliferative neoplasms, according to the WHO-2008 classification. From a clinical point of view it closely resembles the classical Chronic Myeloid Leukemia (CML), however it lacks the presence of the Philadelphia chromosome and of the BCR-ABL1 fusion gene. In recent works, we and others characterized the somatic lesions present in the aCML genome, mainly by using Next Generation Sequencing (NGS) technologies, demonstrating the presence of a large set of recurrent somatic mutations invo

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Shuvaev, Vasily, Karina Krutikova, Svetlana Menshakova, et al. "Atypical Chronic Myeloid Leukemia Challenge in Russian Hematology Practice." Blood 132, Supplement 1 (2018): 5483. http://dx.doi.org/10.1182/blood-2018-99-114885.

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Abstract Background. The Atypical Chronic Myeloid Leukemia (aCML) and Chronic Neutrophilic Leukemia (CNL) had put in separate sections of myeloid neoplasms classification but have common entity and bone marrow changes. aCML and CNL hard to differentiate from each other. The main differential criterion is the proportion of immature white blood cells in blood, but it is not strong due to its instability. The achievement of recent years is discovering of aCML and CNL molecular factors: mutations in SETBP1 and CSFR3R genes gave the basis for the diagnosis confirmation in part of patients but could

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Chen, Lihan, Victoria Savalei, and Mijke Rhemtulla. "Two-stage maximum likelihood approach for item-level missing data in regression." Behavior Research Methods 52, no. 6 (2020): 2306–23. http://dx.doi.org/10.3758/s13428-020-01355-x.

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AbstractPsychologists use scales comprised of multiple items to measure underlying constructs. Missing data on such scales often occur at the item level, whereas the model of interest to the researcher is at the composite (scale score) level. Existing analytic approaches cannot easily accommodate item-level missing data when models involve composites. A very common practice in psychology is to average all available items to produce scale scores. This approach, referred to as available-case maximum likelihood (ACML), may produce biased parameter estimates. Another approach researchers use to de

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Wu, Wubin, Jingchao Wang, Tianyong Zhang, et al. "Controllable synthesis of Ag/AgCl@MIL-88A via in situ growth method for morphology-dependent photocatalytic performance." Journal of Materials Chemistry C 7, no. 18 (2019): 5451–60. http://dx.doi.org/10.1039/c9tc00398c.

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Kosmider, Olivier. "Mutations of ETNK1 in aCML and CMML." Blood 125, no. 3 (2015): 422–23. http://dx.doi.org/10.1182/blood-2014-11-609057.

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Wang, John S., Omar Elghawy, Brett R. Kurpiel, and Michael G. Douvas. "Diagnosis and Management of Atypical Chronic Myeloid Leukemia with a t(2;13)(q33;q12) Translocation." Case Reports in Hematology 2022 (May 4, 2022): 1–5. http://dx.doi.org/10.1155/2022/4628183.

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Atypical chronic myeloid leukemia (aCML) is a rare myeloproliferative disorder that shares clinical features with chronic myeloid leukemia but lacks the classic t(9;22) BCR-ABL1 translocation and features prominent dysgranulopoiesis and granulocytic dysplasia. Challenges of this diagnosis include clinical and biologic heterogeneity, the high risk of transformation to acute myeloid leukemia, and the lack of standard treatment options. Allogeneic hematopoietic stem cell transplant is likely the preferred treatment, but this can be limited by patient psychosocial support, age, concomitant medical

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Morita, Junya. "Research work in the Applied Cognitive Modelling Lab." Impact 2020, no. 7 (2020): 9–11. http://dx.doi.org/10.21820/23987073.2020.7.9.

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Dr Junya Morita is based at the Applied Cognitive Modelling Laboratory (ACML) within the Department of Behavior Informatics at Shizuoka University in Japan. His team is conducting investigations that use computational models in an effort to improve our understanding of human minds and their inner workings. There are currently two directions of study underway at ACML. The first is concerned with theoretical studies of cognitive modelling, where the team try to construct models that explain human minds as computational and algorithmic levels. The second direction of study is the application of c

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Piazza, Rocco, Simona Valletta, Alessandra Pirola, et al. "Whole-Exome Sequencing of 8 Atypical Chronic Myeloid Leukaemia Patients,." Blood 118, no. 21 (2011): 3853. http://dx.doi.org/10.1182/blood.v118.21.3853.3853.

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Abstract Abstract 3853 INTRODUCTION According to the WHO-2008 classification, atypical chronic myeloid leukemia (aCML) is a myelodysplastic/myeloproliferative disorder clinically resembling the Philadelphia positive CML but lacking the BCR-ABL fusion. In aCML, the molecular lesions underlying the onset of the disease are unknown. To investigate the somatic events occurring in the genome of the aCML leukemic cells, we carried out whole-exome high-throughput sequencing analyses of 8 aCML patients. The results are described here. METHODS Peripheral blood (PB) or bone marrow cells were obtained af

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Tyner, Jeffrey W., Christopher A. Eide, Eric P. Stoffregen, et al. "Identification of Tyrosine Kinase Mutations by Large-Scale DNA Sequencing in Patients with Chronic Myelomonocytic Leukemia/Atypical Chronic Myeloid Leukemia." Blood 108, no. 11 (2006): 3606. http://dx.doi.org/10.1182/blood.v108.11.3606.3606.

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Abstract Chronic myeloid leukemia (CML) is caused by Bcr-Abl, a constitutively active tyrosine kinase. Chronic myelomonocytic leukemia (CMML) and atypical chronic myeloid leukemia (aCML) both represent diseases with clinical features resembling CML, suggesting that their pathogenesis may be similar. Consistent with this, activating mutations of the platelet-derived growth factor receptor (PDGFR) and other tyrosine kinases are found in isolated patients, but the pathogenesis remains unclear in the majority. Elucidation of mechanistically important targets in the pathogenesis of CMML/aCML would

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Di Savino, Augusta, Cristina Panuzzo, Stefania Rocca, et al. "Morgana acts as an oncosuppressor in chronic myeloid leukemia." Blood 125, no. 14 (2015): 2245–53. http://dx.doi.org/10.1182/blood-2014-05-575001.

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Key Points Morgana haploinsufficiency in mice causes a lethal and transplantable CML-like myeloid neoplasm. Morgana is underexpressed in aCML and in a subgroup of CMLs, where it predicts a worse response to imatinib but sensitivity to ROCK inhibitors.

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Borate, Uma, Stephen Medearis, and Kim-Hien Dao. "Primer on CNL and aCML Diagnosis and Therapy." Clinical Lymphoma Myeloma and Leukemia 19 (September 2019): S34—S35. http://dx.doi.org/10.1016/j.clml.2019.07.410.

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Wang, Sa A., Robert P. Hasserjian, Patricia S. Fox, et al. "Atypical chronic myeloid leukemia is clinically distinct from unclassifiable myelodysplastic/myeloproliferative neoplasms." Blood 123, no. 17 (2014): 2645–51. http://dx.doi.org/10.1182/blood-2014-02-553800.

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Key Points Within MDS/MPN, the WHO 2008 criteria for aCML identify a subgroup of patients with aggressive clinical features distinct from MDS/MPN-U. The MDS/MPN-U category is heterogeneous, and patient risk can be further stratified by a number of clinicopathological parameters.

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Abdul-Rahman, Shuzlina, Mohamad Soffi Abd Razak, Aliya Hasanah Binti Mohd Mushin, Raseeda Hamzah, Nordin Abu Bakar, and Zalilah Abd Aziz. "Simulation of simultaneous localization and mapping using 3D point cloud data." Indonesian Journal of Electrical Engineering and Computer Science 16, no. 2 (2019): 941. http://dx.doi.org/10.11591/ijeecs.v16.i2.pp941-949.

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<span>Abstract—This paper presents a simulation study of Simultaneous Localization and Mapping (SLAM) using 3D point cloud data from Light Detection and Ranging (LiDAR) technology. Methods like simulation is useful to simplify the process of learning algorithms particularly when collecting and annotating large volumes of real data is impractical and expensive. In this study, a map of a given environment was constructed in Robotic Operating System platform with Gazebo Simulator. The paper begins by presenting the most currently popular algorithm that are widely used in SLAM namely Extende

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Coltro, Giacomo, Guadalupe Belen Antelo, Terra Lasho, et al. "Phenotypic Correlates and Prognostic Outcomes of TET2 Mutations in Myelodysplastic Syndrome/Myeloproliferative Neoplasm Overlap Syndromes: A Comprehensive Study of 504 Patients." Blood 134, Supplement_1 (2019): 3005. http://dx.doi.org/10.1182/blood-2019-124115.

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Introduction: Myelodysplastic syndrome/myeloproliferative neoplasm (MDS/MPN) overlap syndromes consist of 5 distinct WHO-defined entities; namely chronic myelomonocytic leukemia (CMML), atypical chronic myeloid leukemia, BCR/ABL1- (aCML), juvenile myelomonocytic leukemia (JMML), MDS/MPN with ring sideroblasts and thrombocytosis (MDS/MPN-RS-T), and MDS/MPN, unclassifiable (MDS/MPN-U) (Arber et al., Blood 2016). With the notable exception of JMML, a bona fide RASopathy, the other entities are characterized by clinical heterogeneity and molecular diversity. Loss of function TET2 mutations (TET2MT

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Breccia, Massimo. "Atypical CML: diagnosis and treatment." Hematology 2023, no. 1 (2023): 476–82. http://dx.doi.org/10.1182/hematology.2023000448.

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Abstract Atypical chronic myeloid leukemia (aCML) is included in the group of myelodysplastic/myeloproliferative neoplasms by the International Consensus Classification and has been renamed as MDS/MPN with neutrophilia by the fifth edition of World Health Organization classification. It is always characterized by morphologic identification of granulocytic dysplasia with &gt;10% circulating immature myeloid cells, 2 distinguished features that differentiate this disease among the others. Somatic mutations may help to diagnose but are not specifically pathognomonic of the disease, with the m

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Zhou, Zhi-Hua, Wee Sun Lee, Steven C. H. Hoi, Wray Buntine, and Hiroshi Motoda. "Introduction: special issue of selected papers of ACML 2012." Machine Learning 92, no. 2-3 (2013): 221–23. http://dx.doi.org/10.1007/s10994-013-5384-1.

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Ong, Cheng Soon, Wray Buntine, Tu-Bao Ho, Masashi Sugiyama, and Geoffrey I. Webb. "Introduction: special issue of selected papers of ACML 2013." Machine Learning 99, no. 2 (2015): 165–67. http://dx.doi.org/10.1007/s10994-015-5492-1.

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Li, Hang, Dinh Phung, Tru Cao, Tu-Bao Ho, and Zhi-Hua Zhou. "Introduction: special issue of selected papers from ACML 2014." Machine Learning 103, no. 2 (2016): 137–39. http://dx.doi.org/10.1007/s10994-016-5549-9.

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Holmes, Geoffrey, Tie-Yan Liu, Hang Li, Irwin King, Masashi Sugiyama, and Zhi-Hua Zhou. "Introduction: special issue of selected papers from ACML 2015." Machine Learning 106, no. 4 (2017): 459–61. http://dx.doi.org/10.1007/s10994-017-5636-6.

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Nor, N. S. M., Mohamad Deraman, N. H. Basri, et al. "Supercapacitor Activated Carbon Electrode from Composite of Green Monoliths of KOH-Treated Pre-Carbonized Oil Palm Empty Fruit Bunches and HNO₃-Treated Graphite." Advanced Materials Research 1112 (July 2015): 303–7. http://dx.doi.org/10.4028/www.scientific.net/amr.1112.303.

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Supercapacitor electrodes in the form of activated carbon monoliths (ACMs) were prepared by carbonization and activation of three different composite of green monoliths (GMs) consisting of (a) self-adhesive carbon grains (SACG) derived from pre-carbonized oil palm empty fruit bunches, KOH and graphite additive, (b) KOH-treated SACG and HNO3-treated graphite additive, and (c) SACG and HNO3-treated graphite additive. The ACM1, ACM2 and ACM3 electrodes produced from their respective GMs were characterized using nitrogen adsorption-desorption technique and the supercapacitor cell fabricated using

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