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Journal articles on the topic 'Points aberrants'

Author: Grafiati

Published: 4 June 2021

Last updated: 12 February 2022

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1

Huot, Guy. "L’effet des points aberrants dans la désaisonnalisation." Articles 57, no. 3 (January 21, 2009): 407–22. http://dx.doi.org/10.7202/600992ar.

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ABSTRACT This article is devoted to an improved estimation of the seasonal factors in the X-11-ARIMA method given the presence of outliers in the unadjusted series. The series are modelled by an ARIMA process and the outliers are identified relative to the fitted values of the model. They are then replaced by their corresponding function values. A good replacement of the outliers improves both the performance of the ARIMA model fitted to the modified series and the revisions to the seasonal factors, especially the latter.

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2

Ye Qingwei, Wang Dandan, and Zhou Yu. "Aberrant Point Clustering and Elimination of Vibration Signal." INTERNATIONAL JOURNAL ON Advances in Information Sciences and Service Sciences 5, no. 6 (March 31, 2013): 110–18. http://dx.doi.org/10.4156/aiss.vol5.issue6.14.

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3

Shao, Hai-peng, Juan Yin, Wen-hao Yu, and Qiu-ling Wang. "Aberrant Driving Behaviours on Risk Involvement among Drivers in China." Journal of Advanced Transportation 2020 (June 29, 2020): 1–8. http://dx.doi.org/10.1155/2020/8878711.

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The purpose of this study is to validate the version of Driver Behaviour Questionnaire (DBQ) by considering distractions, fatigue, and drunk driving, the main reasons for accidents in China, as independent parts of violations and errors and further explore the effects of demographic/driving variables and all factors on risk involvement (accident involvement and penalized points). 241 drivers filled in a self-completion questionnaire with 28 items conducted in Xi’an in August 2018. Exploratory factor analysis confirmed a five-factor structure, including violations, distracted driving, errors, drunk driving, and fatigued driving. The frequency of aberrant driving behaviours indicated that distractions were the most prevalent behaviours followed by fatigue. The results showed that drivers with lower education and longer annual mileages were positive with accident involvement while there was no significance in penalized points. Violations and distractions were important factors causing both accidents and penalized points. Therefore, it is effective to reduce accident involvement by establishing educational training and related laws or installing intelligent monitor vehicle equipment to warn drivers to improve safety.

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4

Theofani, Efthymia, Spyridon Alexis, Paul Costeas, Christos Andriopoulos, Georgia Feleskoura, Panagiotis Zikos, Anthi Aktypi, Alexandros Spyridonidis, and Konstantina Nika. "Ectopic Lck expression in CLL demarcates intratumoral subpopulations with aberrant B-cell receptor signaling." Blood Advances 2, no. 8 (April 18, 2018): 877–82. http://dx.doi.org/10.1182/bloodadvances.2017015321.

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5

Hawke, Lindsey, Mackenzie L. Bowman, Man-Chiu Poon, Mary-Frances Scully, Georges-Etienne Rivard, and Paula D. James. "Characterization of aberrant splicing of von Willebrand factor in von Willebrand disease: an underrecognized mechanism." Blood 128, no. 4 (July 28, 2016): 584–93. http://dx.doi.org/10.1182/blood-2015-10-678052.

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6

Siwaponanan, Panjaree, Jurre Ynze Siegers, Razi Ghazali, Thian Ng, Bradley McColl, Garrett Zhen-Wei Ng, Philip Sutton, et al. "Reduced PU.1 expression underlies aberrant neutrophil maturation and function in β-thalassemia mice and patients." Blood 129, no. 23 (June 8, 2017): 3087–99. http://dx.doi.org/10.1182/blood-2016-07-730135.

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7

Manara, Elena, Emma Baron, Claudia Tregnago, Sanja Aveic, Valeria Bisio, Silvia Bresolin, Riccardo Masetti, Franco Locatelli, Giuseppe Basso, and Martina Pigazzi. "MLL-AF6 fusion oncogene sequesters AF6 into the nucleus to trigger RAS activation in myeloid leukemia." Blood 124, no. 2 (July 10, 2014): 263–72. http://dx.doi.org/10.1182/blood-2013-09-525741.

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8

Pellagatti, Andrea, Richard N. Armstrong, Violetta Steeples, Eshita Sharma, Emmanouela Repapi, Shalini Singh, Andrea Sanchi, et al. "Impact of spliceosome mutations on RNA splicing in myelodysplasia: dysregulated genes/pathways and clinical associations." Blood 132, no. 12 (September 20, 2018): 1225–40. http://dx.doi.org/10.1182/blood-2018-04-843771.

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Key Points RNA-seq analysis of CD34+ cells identifies novel aberrantly spliced genes and dysregulated pathways in splicing factor mutant MDS. Aberrantly spliced isoforms predict MDS survival and implicate dysregulation of focal adhesion and exosomes as drivers of poor survival.

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9

Kamijo, Hiroaki, Tomomitsu Miyagaki, Naomi Shishido-Takahashi, Rina Nakajima, Tomonori Oka, Hiraku Suga, Makoto Sugaya, and Shinichi Sato. "Aberrant CD137 ligand expression induced by GATA6 overexpression promotes tumor progression in cutaneous T-cell lymphoma." Blood 132, no. 18 (November 1, 2018): 1922–35. http://dx.doi.org/10.1182/blood-2018-04-845834.

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Key Points Overexpression of GATA6 induces aberrant CD137L expression on tumor cells of CTCL. CD137-CD137L interactions promote cell proliferation and migration in CTCL cells, representing potential therapeutic targets.

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10

Hilcenko, Christine, Paul J. Simpson, Andrew J. Finch, Frank R. Bowler, Mark J. Churcher, Li Jin, Len C. Packman, et al. "Aberrant 3′ oligoadenylation of spliceosomal U6 small nuclear RNA in poikiloderma with neutropenia." Blood 121, no. 6 (February 7, 2013): 1028–38. http://dx.doi.org/10.1182/blood-2012-10-461491.

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Key Points Crystal structure of human USB1 identifies it as a member of the LigT-like superfamily of 2H phosphoesterases. USB1 protects spliceosomal U6 small nuclear RNA from aberrant 3′ oligoadenylation.

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11

Fan, Hong-Bo, Yi-Jie Liu, Lei Wang, Ting-Ting Du, Mei Dong, Li Gao, Zhao-Zheng Meng, et al. "miR-142-3p acts as an essential modulator of neutrophil development in zebrafish." Blood 124, no. 8 (August 21, 2014): 1320–30. http://dx.doi.org/10.1182/blood-2013-12-545012.

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Key Points The miR-142-3p double mutant zebrafish displayed aberrant neutrophil hypermaturation and homeostasis in myelopoiesis. Abnormal activation of IFN-γ signaling mediated the impaired neutrophil development in miR-142-3p–deficient zebrafish.

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12

van Keimpema, Martine, Leonie J. Grüneberg, Michal Mokry, Ruben van Boxtel, Menno C. van Zelm, Paul Coffer, Steven T. Pals, and Marcel Spaargaren. "The forkhead transcription factor FOXP1 represses human plasma cell differentiation." Blood 126, no. 18 (October 29, 2015): 2098–109. http://dx.doi.org/10.1182/blood-2015-02-626176.

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Key Points Aberrant expression of FOXP1 in human MBCs represses their ability to differentiate into PCs. Human IgG+ MBCs combine lower FOXP1 expression with a higher propensity to differentiate as compared with IgM+ MBCs.

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13

Beguelin, Wendy, Alisa Chalmers, Lucas Tsikitas, Wayne Tam, Govind Bhagat, and Rita Shaknovich. "IL10 Receptor a Is a Novel Therapeutic Target That Is Epigenetically Disregulated in Low Grade Lymphomas with Plasmacytic Differentiation." Blood 120, no. 21 (November 16, 2012): 2383. http://dx.doi.org/10.1182/blood.v120.21.2383.2383.

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Abstract Abstract 2383 Waldenstrom's Macroglobulinemia (WM) is the clinical manifestation of lymphoproliferative disorders characterized by a clonal lymphoplasmacytic proliferation, excessive IgM secretion and elevated serum viscosity. Most common B-cell non-Hodgkin lymphomas associated with WM are Lymphoplasmacytic Lymphomas (LPL) and Marginal Zone Lymphomas (MZL), especially those displaying plasmacytic differentiation (MZL-P). In order to elucidate common pathogenetic mechanisms that result in WM across lymphoma types, we profiled the methylome of 6 LPLs, 10 MZL-Ps, as well as normal B-cell subsets purified from human tonsillar tissue –germinal center B-cell controls (GCB, n=3) and plasma cell (PC, n=3) controls, using HELP assay and high-density oligonucleotide microarray from RocheNImblegen that queries DNA methylation level of 50,000 cytosine residues distributed among 14,000 gene promoters. Unsupervised hierarchical clustering approach using Ward's method and Eucledian distances separated normal GCB and PC from the lymphoma cases and identified bi-directional changes in gene methylation: with aberrant gain or loss of methylation at specific genomic locations. We further utilized a t-test and identified 208 probesets that were differentially methylated between controls and lymphomas at p<0.01 and mean log-ratio difference between 2 groups >1.5 corresponding to 30% methylation difference. Ingenuity pathway analysis revealed CDKN1A and TGFb networks as the most aberrantly methylated in lymphomas. Remarkably, we observed that Interleukin 10 Receptor a (IL10RA), was aberrantly hypomethylated in both lymphoma subtypes, resulting in its aberrant overexpression. IL10RA is a subunit of the IL10 cytokine receptor that is known to be a key factor in terminating the inflammatory responses via signaling through the JAK/STAT pathway resulting in STAT3 activation, which also plays an integral part in GCB differentiation and commitment to the plasma cell lineage. We thus hypothesized that aberrant epigenetic upregulation of IL10RA might promote survival and expansion of lymphoma cells. We predicted that stimulating IL10RA with IL10 ligand may lead to increased cell growth, while the blockade of IL10RA would inhibit cell growth. We selected 2 anti-IL10RA antibodies, which have previously been reported to have receptor blocking properties in vivo in mice. We tested 1ug/ml, 5ug/ml and 10ug/ml of each antibody and 10 ng/ml of the stimulatory IL10 ligand and observed that ligand provided stimulatory effect on the growth rate of a panel of B-cell lymphoma, including LPL cell line, while both anti-IL10RA antibodies had marked growth inhibitory effects. We further determined that growth inhibition resulted from dramatic induction of apoptosis in cells treated with the blocking anti-IL10RA antibodies. Further studies revealed that induction of apoptosis followed specific inhibition of signaling through JAK1/2 and phosphorylation of STAT3Y705 immediately after treatment and inhibition of signaling through MAPK and phosphorylation of STAT3S727 at later treatment time points. In conclusion, we determined that IL10RA is aberrantly methylated and overexpressed in subtypes of low grade lymphomas exhibiting plasmacytic differentiation and manifesting as WM. Hence, strategies targeting this pathway should be explored as potential therapy for WM (irrespective of the underlying type of lymphoma). Disclosures: No relevant conflicts of interest to declare.

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14

Shaham, Lital, Elena Vendramini, Yubin Ge, Yaron Goren, Yehudit Birger, Marloes R. Tijssen, Maureen McNulty, et al. "MicroRNA-486-5p is an erythroid oncomiR of the myeloid leukemias of Down syndrome." Blood 125, no. 8 (February 19, 2015): 1292–301. http://dx.doi.org/10.1182/blood-2014-06-581892.

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Key Points miR-486-5p, a GATA1 regulated miR, is expressed in ML-DS and enhances their aberrant erythroid phenotype. miR-486-5p cooperates with GATA1s to promote the survival of pre-leukemic and leukemic cells.

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15

Jiang, Wenxia, Brian J. Lee, Chen Li, Richard L. Dubois, Monica Gostissa, Frederick W. Alt, and Shan Zha. "Aberrant TCRδ rearrangement underlies the T-cell lymphocytopenia and t(12;14) translocation associated with ATM deficiency." Blood 125, no. 17 (April 23, 2015): 2665–68. http://dx.doi.org/10.1182/blood-2015-01-622621.

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Key Points ATM-deficient T-cell lymphocytopenia is in part caused by defects in TCRδ rearrangements. Aberrant TCRδ arrangement is required for the recurrent t(12;14) translocations, but not chromosome 14 amplification, in ATM-deficient thymic lymphomas.

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16

Maude, Shannon L., Sibasish Dolai, Cristina Delgado-Martin, Tiffaney Vincent, Alissa Robbins, Arthavan Selvanathan, Theresa Ryan, et al. "Efficacy of JAK/STAT pathway inhibition in murine xenograft models of early T-cell precursor (ETP) acute lymphoblastic leukemia." Blood 125, no. 11 (March 12, 2015): 1759–67. http://dx.doi.org/10.1182/blood-2014-06-580480.

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Key Points ETP-ALL, a high-risk subtype of T-ALL, is characterized by aberrant activation of the JAK/STAT signaling pathway. The JAK1/2 inhibitor ruxolitinib demonstrates robust activity in patient-derived xenograft models of ETP-ALL.

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17

Jahn, Lorenz, Pleun Hombrink, Chopie Hassan, Michel G. D. Kester, Dirk M. van der Steen, Renate S. Hagedoorn, J. H. Frederik Falkenburg, Peter A. van Veelen, and Mirjam H. M. Heemskerk. "Therapeutic targeting of the BCR-associated protein CD79b in a TCR-based approach is hampered by aberrant expression of CD79b." Blood 125, no. 6 (February 5, 2015): 949–58. http://dx.doi.org/10.1182/blood-2014-07-587840.

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Key Points B-cell malignancies were efficiently recognized by T cells expressing high-affinity alloHLA-restricted TCRs specific for CD79b. Aberrant expression of CD79b in non–B cells caused unwanted reactivity, rendering CD79b unsuitable for TCR-based immunotherapies.

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18

Cai, Qi, Robin Jeannet, Wei-Kai Hua, Guerry J. Cook, Bin Zhang, Jing Qi, Hongjun Liu, et al. "CBFβ-SMMHC creates aberrant megakaryocyte-erythroid progenitors prone to leukemia initiation in mice." Blood 128, no. 11 (September 15, 2016): 1503–15. http://dx.doi.org/10.1182/blood-2016-01-693119.

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19

Carll, Timothy, Anand Patel, Benjamin Derman, Elizabeth Hyjek, Angela Lager, Pankhuri Wanjari, Jeremy Segal, Olatoyosi Odenike, Shiraz Fidai, and Daniel Arber. "Diagnosis and treatment of mixed phenotype (T-myeloid/lymphoid) acute leukemia with novel ETV6-FGFR2 rearrangement." Blood Advances 4, no. 19 (October 13, 2020): 4924–28. http://dx.doi.org/10.1182/bloodadvances.2019001282.

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Key Points Myeloid/lymphoid neoplasms with eosinophilia are driven by aberrant tyrosine kinases in pluripotent cells and display variable phenotypes. FGFR-driven hematolymphoid neoplasms are targetable by TKI inhibitors such as ponatinib; studies of specific FGFR inhibitors are ongoing.

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20

Scarfò, Irene, Elisa Pellegrino, Elisabetta Mereu, Ivo Kwee, Luca Agnelli, Elisa Bergaggio, Giulia Garaffo, et al. "Identification of a new subclass of ALK-negative ALCL expressing aberrant levels of ERBB4 transcripts." Blood 127, no. 2 (January 14, 2016): 221–32. http://dx.doi.org/10.1182/blood-2014-12-614503.

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Key Points Endogenous intronic long terminal repeats promote the ectopic expression of truncated ERBB4 transcripts in 24% of ALK-negative ALCL. The expression of ERBB4-aberrant transcripts defines a new subclass of ALK-negative ALCL and may contribute to ALCL transformation.

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21

Luo, Huacheng, Fei Wang, Jie Zha, Haoli Li, Bowen Yan, Qinghua Du, Fengchun Yang, et al. "CTCF boundary remodels chromatin domain and drives aberrant HOX gene transcription in acute myeloid leukemia." Blood 132, no. 8 (August 23, 2018): 837–48. http://dx.doi.org/10.1182/blood-2017-11-814319.

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Key Points CRISPR-Cas9 library screening identifies CBS7/9 boundary that defines an aberrant HOXA chromatin domain and HOX gene transcription in AML. Attenuation of CBS7/9 boundary impairs the leukemic transcription program and attenuates leukemic progressions in AML mouse models.

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22

Ono, Ryoichi, Masahiro Masuya, Hideaki Nakajima, Yutaka Enomoto, Eri Miyata, Akihide Nakamura, Satomi Ishii, et al. "Plzf drives MLL-fusion–mediated leukemogenesis specifically in long-term hematopoietic stem cells." Blood 122, no. 7 (August 15, 2013): 1271–83. http://dx.doi.org/10.1182/blood-2012-09-456665.

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Key Points MLL-ENL targets long-term HSCs exclusively to develop leukemia in a novel conditional transgenic mouse through upregulation of Plzf. Plzf is critically involved in the aberrant self-renewal program in HSCs induced by the MLL fusion gene.

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23

Agrawal, Anant A., Michael Seiler, Lindsey T. Brinton, Rose Mantel, Rosa Lapalombella, Jennifer A. Woyach, Amy J. Johnson, et al. "Novel SF3B1 in-frame deletions result in aberrant RNA splicing in CLL patients." Blood Advances 1, no. 15 (June 14, 2017): 995–1000. http://dx.doi.org/10.1182/bloodadvances.2017007062.

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Key Points We identify and characterize novel SF3B1 in-frame deletions in chronic lymphocytic leukemia. These deletions are functionally similar to well-known SF3B1 hotspot mutations and are sensitive to splicing modulation.

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24

Poe, Jonathan C., Wei Jia, Hsuan Su, Sarah Anand, Jeremy J. Rose, Prasanthi V. Tata, Amy N. Suthers, et al. "An aberrant NOTCH2-BCR signaling axis in B cells from patients with chronic GVHD." Blood 130, no. 19 (November 9, 2017): 2131–45. http://dx.doi.org/10.1182/blood-2017-05-782466.

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Key Points NOTCH2 activation confers a marked increase in BCR responsiveness by cGVHD patient B cells that associates with increased BLNK. ATRA increases the IRF4-to-IRF8 ratio and blocks aberrant NOTCH2-BCR activation without affecting cGVHD patient B-cell viability/function.

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25

Ray, Debleena, So Yeon Kwon, Hiromi Tagoh, Olaf Heidenreich, Anetta Ptasinska, and Constanze Bonifer. "Lineage-inappropriate PAX5 expression in t(8;21) acute myeloid leukemia requires signaling-mediated abrogation of polycomb repression." Blood 122, no. 5 (August 1, 2013): 759–69. http://dx.doi.org/10.1182/blood-2013-02-482497.

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Key Points Lineage-inappropriate expression of the B-cell master regulator PAX5 in t(8;21) AML depends on aberrant MAP kinase signaling. MAP kinase signaling by a mutated growth factor receptor leads to the dissociation of polycomb-repressive complexes from PAX5 chromatin.

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26

Arikan, Sevtap, Pınar Yurdakul, and Gulsen Hascelik. "Comparison of Two Methods and Three End Points in Determination of In Vitro Activity of Micafungin against Aspergillus spp." Antimicrobial Agents and Chemotherapy 47, no. 8 (August 2003): 2640–43. http://dx.doi.org/10.1128/aac.47.8.2640-2643.2003.

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ABSTRACT We investigated the in vitro activity of micafungin against clinical Aspergillus isolates (n = 37) (Aspergillusfumigatus [n = 21], Aspergillusflavus [n = 14], and Aspergillus niger [n = 2]) by using NCCLS M38A microdilution and an investigational disk diffusion assay. Microdilution assay results were evaluated by using the end points of a MIC-2 (measured in micrograms per milliliter) and minimum effective concentration (MEC, measured in micrograms per milliliter; the lowest concentration of micafungin that produces short and aberrant hyphal branchings microscopically). Disk diffusion results were interpreted by measuring the zone(s) of inhibition (ZOI, measured in millimeters). Micafungin proved to be similarly active against all Aspergillus species tested. At 24 h, MIC-2s and MECs were identical. At 48 h, however, MIC-2s increased unpredictably, leading to the loss of a consistent correlation between the two end points. MECs and ZOI remained consistent and correlated at both reading times, suggesting their use as relevant end points in susceptibility testing of micafungin against Aspergillus. All Aspergillus isolates yielded intrazonal growth on disk diffusion agar plates. The intrazonal colonies contained short, aberrant hyphal branchings microscopically. The in vivo significance of these findings remains to be further investigated.

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27

Deshpande, Aniruddha J., Liying Chen, Maurizio Fazio, Amit U. Sinha, Kathrin M. Bernt, Deepti Banka, Stuart Dias, et al. "Leukemic transformation by the MLL-AF6 fusion oncogene requires the H3K79 methyltransferase Dot1l." Blood 121, no. 13 (March 28, 2013): 2533–41. http://dx.doi.org/10.1182/blood-2012-11-465120.

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Key Points Our study demonstrates aberrant genome-wide deposition of histone 3 lysine 79 dimethylation on MLL-target genes in MLL-AF6–driven leukemia cells. We provide evidence that leukemia cells bearing the MLL-AF6 fusion are sensitive to genetic and pharmacologic DOT1L inhibition.

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28

Wang, Jinyong, Guangyao Kong, Yangang Liu, Juan Du, Yuan-I. Chang, Sin Ruow Tey, Xinmin Zhang, et al. "NrasG12D/+ promotes leukemogenesis by aberrantly regulating hematopoietic stem cell functions." Blood 121, no. 26 (June 27, 2013): 5203–7. http://dx.doi.org/10.1182/blood-2012-12-475863.

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Key Points NrasG12D/+ induces proliferation and increases self-renewal and myeloid differentiation bias in HSCs. ERK1/2 is constitutively hyperactivated in NrasG12D/+ HSCs and downregulation of the MEK/ERK signaling attenuates NrasG12D/+ HSC phenotypes.

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Kern, Wolfgang, Richard Schabath, Tamara Alpermann, Claudia Haferlach, Susanne Schnittger, and Torsten Haferlach. "Use Of Flow Cytometry To Identify Myelodysplasia In Peripheral Blood." Blood 122, no. 21 (November 15, 2013): 2774. http://dx.doi.org/10.1182/blood.v122.21.2774.2774.

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Abstract Background Flow cytometry (FC) is increasingly used in diagnostic work-up of bone marrow (BM) from patients with suspected or proven myelodysplastic syndrome (MDS). Data on FC in peripheral blood (PB) is scarce. Aims Evaluate the use of FC for PB in suspected or proven MDS by comparison to BM analyzed during follow-up. Methods PB of 157 patients (pts) with suspected MDS was analyzed by FC applying ELN criteria defined recently for diagnosis of MDS in BM (Westers et al., Leukemia 2012). For all pts during follow-up at least one BM sample was evaluable by morphology, cytogenetics, and FC in parallel to confirm or exclude MDS (according to WHO 2008 criteria). Pts were then grouped according to results obtained from BM analysis during follow-up time points into 1) proven MDS (n=96), 2) no MDS (n=32), and 3) MPN, MDS/MPN, or “MDS possible” (presence of dysplastic features by morphology but not sufficient to diagnose MDS) (n=29) (median time to MDS confirmation, 0.9 months, range, 0.1-53.0; median time to last BM assessment without confirmation of MDS; 0.8 months, range, 0.2-23.0). Results First, results of FC on PB were compared between pts with finally proven MDS (n=96) by BM vs. those with no MDS by BM as diagnosed during follow-up. All 34 pts with myeloid progenitor cells (MPC) by FC in PB had finally proven MDS. However, in addition 62/94 (66.0%) of those without MPC (p<0.0001) also had proven MDS. Thus, the presence of MPC in PB was at least strongly indicative of MDS while there were also cases with MDS without MPC in PB. Moreover, besides the presence of MPC in PB, 17 of these 34 cases in addition displayed an aberrant antigen expression on MPC. Focusing on granulocytes we first analyzed side-scatter (SSC) signals in granulocytes as ratio of mean SSC signals granulocytes/lymphocytes (G/L). While for BM samples a reduced SSC ratio G/L had been described which reflects hypogranulation, we indeed found similar data for PB with a significantly lower SSC ratio G/L in pts with proven MDS as compared to those without (mean±SD 5.7±1.1 vs. 6.3±1.0, p=0.015). More strict, a mean SSC ratio G/L of 3.9 was found to most specifically identify pts with MDS: all 6 cases with a ratio <3.9 had MDS. Regarding aberrant antigen expression in granulocytes, MDS was more frequently diagnosed among cases with vs. without the following features: aberrant CD11b/CD16 expression pattern (43/46 investigated, 93.5% vs. 53/82, 64.6%; p=0.0002), lack of CD10 expression (37/43, 86.0% vs. 59/85, 69.4%; p=0.052), CD56 expression (19/21, 90.5% vs. 77/107, 72.0%; p=0.098). Cumulating this data, ≥2 aberrantly expressed antigens on granulocytes were found indicative of MDS: 42/45 (93.3%) of pts with aberrant expression of ≥2 antigens had MDS while only 54/83 (65.1%) of those with 0 or 1 aberrantly expressed antigen had finally proven MDS (p=0.0003). Regarding aberrant antigen expression in monocytes, pts with the following features more frequently had MDS as compared to those without: reduced expression of HLA-DR, CD13, CD11b, or CD15, aberrant expression of CD2 or CD34 (as single makers all n.s.). However, cumulating this data also resulted in a significant relation to a diagnosis of MDS during follow-up: 31/36 (86.1%) of pts with aberrant expression of ≥2 antigens on monocytes were diagnosed MDS vs. 65/92 (70.7%) of those without (p=0.052). Integrating the data for the different cell compartments, pts were separated according to the presence of the following 4 criteria: 1) presence of MPC in PB by FC, 2) aberrant expression of ≥1 antigen in MPC in PB, 3) aberrant expression of ≥2 antigens in granulocytes in PB, and 4) aberrant expression of ≥2 antigens in monocytes in PB: 68/76 (89.5%) of pts with ≥1 of these criteria had MDS, which was the case in 28/52 (53.8%) of cases fulfilling none of these criteria (p<0.0001). Strengthening the selection to presence of ≥2 of the criteria, all such 36 cases had MDS which was true for 60/92 (65.2%) of those with ≤1 criterion (p<0.0001). Applying these criteria to the set of remaining 29 pts with MPN, MDS/MPN, or possible MDS, 17 (58.6%) of them fulfilled ≥1 criterion which was true for 8/32 (25.0%) of pts not diagnosed MDS (p=0.010). Conclusions FC reveals MDS-related findings in PB samples using a specific panel targeting 10 antigens and may be used to identify pts with a high probability of MDS. Further studies with direct comparison of PB and BM should clarify the role of PB analysis by FC in the diagnostic work-up of pts with suspected MDS. Disclosures: Kern: MLL Munich Leukemia Laboratory: Employment, Equity Ownership. Schabath:MLL Munich Leukemia Laboratory: Employment. Alpermann:MLL Munich Leukemia Laboratory: Employment. Haferlach:MLL Munich Leukemia Laboratory: Employment, Equity Ownership. Schnittger:MLL Munich Leukemia Laboratory: Employment, Equity Ownership. Haferlach:MLL Munich Leukemia Laboratory: Employment, Equity Ownership.

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Stelling, Anna, Hind Hashwah, Katrin Bertram, Markus G. Manz, Alexandar Tzankov, and Anne Müller. "The tumor suppressive TGF-β/SMAD1/S1PR2 signaling axis is recurrently inactivated in diffuse large B-cell lymphoma." Blood 131, no. 20 (May 17, 2018): 2235–46. http://dx.doi.org/10.1182/blood-2017-10-810630.

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Key Points The sphingosine-1-phosphate receptor 2 is a bona fide tumor suppressor and transcriptionally regulated by the TGF-β/TGF-βR2/SMAD1 axis. The aberrant loss of SMAD1 expression is very common in DLBCL and provides a proliferative advantage to B cells in vitro and in vivo.

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31

Rutherford, Sarah C., Angela A. Fachel, Sheng Li, Seema Sawh, Ashlesha Muley, Jennifer Ishii, Ashish Saxena, et al. "Extracellular vesicles in DLBCL provide abundant clues to aberrant transcriptional programming and genomic alterations." Blood 132, no. 7 (August 16, 2018): e13-e23. http://dx.doi.org/10.1182/blood-2017-12-821843.

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Key Points EVs derived from DLBCL cells can be traced from and provide insight into cell of origin. Mutated RNAs may be preferentially packaged into EVs, and this could enable disease monitoring through liquid biopsy.

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32

Huang, Yuanshen, Ming-Wan Su, Xiaoyan Jiang, and Youwen Zhou. "Evidence of an oncogenic role of aberrant TOX activation in cutaneous T-cell lymphoma." Blood 125, no. 9 (February 26, 2015): 1435–43. http://dx.doi.org/10.1182/blood-2014-05-571778.

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Key Points TOX is aberrantly expressed in primary Sézary cells and its levels correlate with increased risk of disease-specific mortality. TOX knockdown promotes apoptosis and reduces cell proliferation in CTCL cells, partially through inducing p27 and p57.

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Kim, Wun-Jae, Eun-Jung Kim, Pildu Jeong, Changyi Quan, Jiyeon Kim, Qing-Lin Li, Jeong-Ook Yang, Yoshiaki Ito, and Suk-Chul Bae. "RUNX3 Inactivation by Point Mutations and Aberrant DNA Methylation in Bladder Tumors." Cancer Research 65, no. 20 (October 15, 2005): 9347–54. http://dx.doi.org/10.1158/0008-5472.can-05-1647.

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34

Ito, Mitsugu, Kazuaki Teshima, Sho Ikeda, Akihiro Kitadate, Atsushi Watanabe, Miho Nara, Junsuke Yamashita, Koichi Ohshima, Kenichi Sawada, and Hiroyuki Tagawa. "MicroRNA-150 inhibits tumor invasion and metastasis by targeting the chemokine receptor CCR6, in advanced cutaneous T-cell lymphoma." Blood 123, no. 10 (March 6, 2014): 1499–511. http://dx.doi.org/10.1182/blood-2013-09-527739.

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Key Points Aberrantly diminished expression of miR-150 allows advanced CTCL to invade multiple organs with upregulation of CCR6. MiR-150 inhibits IL-22-CCL20-CCR6 autocrine signaling in advanced CTCL.

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35

Adamia, Sophia, Michal Bar-Natan, Benjamin Haibe-Kains, Patrick M. Pilarski, Christian Bach, Samuel Pevzner, Teresa Calimeri, et al. "NOTCH2 and FLT3 gene mis-splicings are common events in patients with acute myeloid leukemia (AML): new potential targets in AML." Blood 123, no. 18 (May 1, 2014): 2816–25. http://dx.doi.org/10.1182/blood-2013-02-481507.

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Key Points Overall, our results suggest that NOTCH2 and FLT3 aberrant splicing is a common event in AML that correlates with disease status and may correlate with disease outcomes. Selected variants of NOTCH2 and FLT3 transcripts were detected in a significant number of AML patients and could be useful as disease markers.

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36

Qu, Ying, Lee Siggens, Lina Cordeddu, Verena I. Gaidzik, Kasper Karlsson, Lars Bullinger, Konstanze Döhner, Karl Ekwall, Sören Lehmann, and Andreas Lennartsson. "Cancer-specific changes in DNA methylation reveal aberrant silencing and activation of enhancers in leukemia." Blood 129, no. 7 (February 16, 2017): e13-e25. http://dx.doi.org/10.1182/blood-2016-07-726877.

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Key Points DNA demethylation activates new and poised enhancers in AML that cause a leukemic transcriptome. Only a subset of DNA demethylated enhancers becomes activated. A specific additional activation step is required for enhancer activation.

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37

Dietrich, Philipp A., Chen Yang, Halina H. L. Leung, Jennifer R. Lynch, Estrella Gonzales, Bing Liu, Michelle Haber, Murray D. Norris, Jianlong Wang, and Jenny Yingzi Wang. "GPR84 sustains aberrant β-catenin signaling in leukemic stem cells for maintenance of MLL leukemogenesis." Blood 124, no. 22 (November 20, 2014): 3284–94. http://dx.doi.org/10.1182/blood-2013-10-532523.

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Key Points GPR84 simultaneously augments β-catenin signaling and an oncogenic transcription program essential for establishment of MLL. Our study demonstrates a strong dependence of hematopoietic stem cell–derived MLL leukemic cells on GPR84 for disease maintenance in vivo.

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Qingwei, Ye, Wang Dandan, and Zhou Yu. "Mode Parameters Estimation of Vibration Signal Based on Aberrant Point Clustering and Elimination." Research Journal of Applied Sciences, Engineering and Technology 6, no. 5 (June 25, 2013): 802–6. http://dx.doi.org/10.19026/rjaset.6.4123.

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39

Liu, Suiyang, Li Yin, Dina Stroopinsky, Hasan Rajabi, Alexandre Puissant, Kimberly Stegmaier, David Avigan, Surender Kharbanda, Donald Kufe, and Richard Stone. "MUC1-C oncoprotein promotes FLT3 receptor activation in acute myeloid leukemia cells." Blood 123, no. 5 (January 30, 2014): 734–42. http://dx.doi.org/10.1182/blood-2013-04-493858.

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Key Points The MUC1-C oncoprotein is aberrantly expressed in AML cells and contributes to activation of the mutant FLT3 receptor. Targeting MUC1-C thus inhibits FLT3 signaling and represents a potential approach for AML cells resistant to FLT3 inhibitors.

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40

Kon, Ayana, Satoshi Yamazaki, Yasuhito Nannya, Keisuke Kataoka, Yasunori Ota, Masahiro Marshall Nakagawa, Kenichi Yoshida, et al. "Physiological Srsf2 P95H expression causes impaired hematopoietic stem cell functions and aberrant RNA splicing in mice." Blood 131, no. 6 (February 8, 2018): 621–35. http://dx.doi.org/10.1182/blood-2017-01-762393.

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Key Points Blood-specific expression of the Srsf2 P95H mutant results in decreased stem/progenitor cell numbers and a reduced repopulation capacity. Srsf2 P95H mutation by itself is not sufficient to develop MDS but contributes to the MDS phenotype in transplantation settings.

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41

Linger, Rachel M. A., Alisa B. Lee-Sherick, Deborah DeRyckere, Rebecca A. Cohen, Kristen M. Jacobsen, Amy McGranahan, Luis N. Brandão, et al. "Mer receptor tyrosine kinase is a therapeutic target in pre–B-cell acute lymphoblastic leukemia." Blood 122, no. 9 (August 29, 2013): 1599–609. http://dx.doi.org/10.1182/blood-2013-01-478156.

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Key Points Mer tyrosine kinase is aberrantly expressed in ∼30% of pediatric pre–B-ALL patients, including most patients with an E2A-PBX1 translocation. Mer inhibition decreased B-ALL cell survival signal transduction, caused chemosensitization, and prolonged survival in a xenograft model.

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42

Narayanan, Sathiya Pandi, Smriti Singh, and Sanjeev Shukla. "A saga of cancer epigenetics: linking epigenetics to alternative splicing." Biochemical Journal 474, no. 6 (March 7, 2017): 885–96. http://dx.doi.org/10.1042/bcj20161047.

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The discovery of an increasing number of alternative splicing events in the human genome highlighted that ∼94% of genes generate alternatively spliced transcripts that may produce different protein isoforms with diverse functions. It is now well known that several diseases are a direct and indirect consequence of aberrant splicing events in humans. In addition to the conventional mode of alternative splicing regulation by ‘cis’ RNA-binding sites and ‘trans’ RNA-binding proteins, recent literature provides enormous evidence for epigenetic regulation of alternative splicing. The epigenetic modifications may regulate alternative splicing by either influencing the transcription elongation rate of RNA polymerase II or by recruiting a specific splicing regulator via different chromatin adaptors. The epigenetic alterations and aberrant alternative splicing are known to be associated with various diseases individually, but this review discusses/highlights the latest literature on the role of epigenetic alterations in the regulation of alternative splicing and thereby cancer progression. This review also points out the need for further studies to understand the interplay between epigenetic modifications and aberrant alternative splicing in cancer progression.

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43

Keerthivasan, Ganesan, Yang Mei, Baobing Zhao, Ling Zhang, Chad E. Harris, Juehua Gao, Ashley A. Basiorka, et al. "Aberrant overexpression of CD14 on granulocytes sensitizes the innate immune response in mDia1 heterozygous del(5q) MDS." Blood 124, no. 5 (July 31, 2014): 780–90. http://dx.doi.org/10.1182/blood-2014-01-552463.

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Key Points mDia1 deficiency led to a cell-autonomous overexpression of CD14 on granulocytes and a hypersensitive innate immune response. mDia1 heterozygous and knockout mice developed age-dependent MDS that was accelerated by chronic stimulation of the innate immunity.

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44

Teoh, Phaik Ju, Omer An, Tae-Hoon Chung, Jing Yuan Chooi, Sabrina H. M. Toh, Shuangyi Fan, Wilson Wang, et al. "Aberrant hyperediting of the myeloma transcriptome by ADAR1 confers oncogenicity and is a marker of poor prognosis." Blood 132, no. 12 (September 20, 2018): 1304–17. http://dx.doi.org/10.1182/blood-2018-02-832576.

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Key Points The integrity of the MM transcriptome is compromised by ADAR1 overexpression, conferring oncogenic events in an editing-dependent manner. NEIL1 is an important ADAR1 editing target, and its recoded protein has a defective functional capacity and gain-of-function properties.

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45

Patrikelis, Panayiotis, Giuliana Lucci, Athanasia Alexoudi, Stefanos Korfias, Lambros Messinis, Grigorios Nasios, Themistoklis Papasilekas, Damianos Sakas, and Stylianos Gatzonis. "Addressing Evidence Linking Secondary Alexithymia to Aberrant Humor Processing." Behavioural Neurology 2019 (July 18, 2019): 1–13. http://dx.doi.org/10.1155/2019/1803624.

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In this review, we explore current literature and assess evidence linking secondary (acquired) alexithymia to aberrant humor processing, in terms of their neurobiological underpinnings. In addition, we suggest a possible common neuropathological substrate between secondary alexithymia and deficits in humor appreciation, by drawing on neurophysiologic and neuroradiological evidence, as well as on a recent and unique single-case study showing the cooccurrence of secondary alexithymia and deficit in humor appreciation. In summary, what emerges from the literature is that the cortical midline structures, in particular the medial prefrontal cortex (mPFC), the anterior cingulate cortex (ACC), and the insular cortex, seem to play a crucial role in the expression of both alexithymia and defective humor processing, while though to a lesser extent, a right hemisphere and bilateral frontoparietal contribution becomes evident. Neurobiological evidence of secondary alexithymia and aberrant humor processing points to the putative role of ACC/mPFC and the insular cortex in representing crucial processing nodes whose damage may produce both the above clinical conditions. We believe that the association of secondary alexithymia and aberrant humor processing, especially humor appreciation deficit, and their correlation with specific brain regions, mainly ACG/mPFC, as emerged from the literature, may be of some heuristic importance. Increased awareness on this topic may be of aid for neurosurgeons when accessing emotion-relevant structures, as well as for neuropsychologists to intensify their efforts to plan evidence-based neurorehabilitative interventions to alleviate the deleterious effects of such interpersonal communication deficits.

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46

M. "Detection of Aberrant Data Points for an effective Effort Estimation using an Enhanced Algorithm with Adaptive Features." Journal of Computer Science 8, no. 2 (October 1, 2012): 195–99. http://dx.doi.org/10.3844/jcssp.2012.195.199.

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47

Venkataraman, Girish, Joo Y. Song, Alexandar Tzankov, Stephan Dirnhofer, Georg Heinze, Maria Kohl, Alexandra Traverse-Glehen, et al. "Aberrant T-cell antigen expression in classical Hodgkin lymphoma is associated with decreased event-free survival and overall survival." Blood 121, no. 10 (March 7, 2013): 1795–804. http://dx.doi.org/10.1182/blood-2012-06-439455.

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48

Kameoka, Yoshihiro, Hiroyuki Tagawa, Shinobu Tsuzuki, Akinobu Ota, Ritsuro Suzuki, and Masao Seto. "Contig Array CGH at 3p14.2 Points to the FHIT Gene as the Deleted Gene in Diffuse Large B Cell Lymphoma." Blood 104, no. 11 (November 16, 2004): 1543. http://dx.doi.org/10.1182/blood.v104.11.1543.1543.

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Abstract Diffuse large B-cell lymphoma (DLBCL) is the most common type of non-Hodgkin’s lymphoma (NHL), accounting for 30 – 40% of adult NHL. Genomic alterations in DLBCL have been investigated by various methods and many regions of amplifications and losses have been detected. Genomic deletions of the 3p arm have been reported in many solid tumors and leukemias, but no study published to date has reported genomic deletions of this region in DLBCL. Recently we demonstrated that 3p14.2 was deleted in approximately 30% of DLBCL patients and cell lines by use of a genome-wide array-comparative genomic hybridization (array-CGH) (Tagawa et al., 2004). For a more detailed examination of the genomic losses at 3p14.2, here we made use of contig BAC array for 3p14.2, and found that 12 of 27 DLBCL samples displayed losses. All of the deleted regions were located within the Fragile Histidine Triad (FHIT) gene, and the most frequently region of loss was mapped to 0.4 Mbp of the region encompassing the introns 4 and 5 and exon 5 of the FHIT gene. Genomic deletions of the FHIT gene have been observed in most common forms of cancer and it is therefore conceivable that the FHIT gene is the target one of the genomic deletion at 3p in DLBCL. To investigate the relationship between genomic deletions and transcript alterations, we performed nested reverse transcriptase-polymerase chain reaction (RT-PCR) analysis. Aberrant transcripts or loss of expression was detected in 33% (19 of 57) of the DLBCL samples, and the lost exons of the aberrant transcripts were correlated with genomic deletions detected by array CGH. We also investigated the CpG island methylation status of the promotor of the FHIT gene by means of methylation specific PCR (MSP). One case with genomic loss of the FHIT gene, and three cases without genomic loss showed methylated allele. These findings indicate that 1) Loss of genomic material at 3q14.2 is responsible for exon losses of the FHIT gene, and 2) Genomic loss of the FHIT gene is one of the causes of the generation of aberrant transcripts. 3) Both genomic deletions and methylations are involved in the causes of inactivation of the FHIT gene.

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49

Chu, Sung-Chao, Tso-Fu Wang, Yu-Chieh Su, Ruey-Ho Kao, Yi-Fung Wu, Dian-Kun Li, Szu-Chin Li, Chi-Cheng Li, and Michael R. Loken. "Post-Induction-BM Status Combining Minimal Residual Disease, Return to MDS and Hematogones in Predicting Prognosis in Adult AML,." Blood 118, no. 21 (November 18, 2011): 3532. http://dx.doi.org/10.1182/blood.v118.21.3532.3532.

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Abstract Abstract 3532 Introduction: The study is to analyze the prognostic impact of post-induction-BM status combining minimal residual disease (MRD), neutrophil/monocyte maturation return to MDS and quantitation of hematogones in adult AML achieving first morphologic complete remission (mCR). The hypothesis is that the detection of aberrant myeloid progenitor cells, aberrant neutrophil/monocyte maturation and hematogones in post-induction BM by flow cytometry may predict the outcome of AML in mCR even without diagnostic specimen. The positive MRD and the aberrant neutrophil/monocyte maturation will predict worse prognosis. In contrast, positive hematogones will predict better prognosis. Methods: Multidimensional flow cytometry was performed on bone marrow specimens from 47 consecutive non-M3 AML patients who had achieved mCR after standard 3+7 induction treatment. The in-remission immunophenotypic evaluation of BM was done before first consolidation treatment. The aberrant myeloid progenitor cells and aberrant neutrophil/monocyte maturation were defined by the flow cytometric scoring system (FCSS)1. Two investigators were blinded to corresponding pathologic, clinical or diagnostic flow cytometric data during initial analysis phase. After reaching agreement of the three parameters: aberrant myeloid progenitor cells (MRD ≥ 0.2% or not), aberrant neutrophil/monocyte maturation (FCSS ≥ 2 points or not) and hematogones (stages I / II B lymphoid progenitor cells ≥ 0.02% or not), those prognostic impacts on leukemia free survival (LFS) and overall survival (OS) were analyzed retrospectively. Results: Table 1 summarizes the clinical characteristics of patients according to the status of MRD and hematogones. Nine (19%) patients who had MRD ≥0.2% had a significantly worse median LFS (9.0 months vs not reached; P =.006) and worse OS (24.0 months vs not reached; P =.059). Fourteen (30%) patients who had hematogone levels ≥ 0.02% had a significantly better median LFS (not reached vs 13.5 months; P =.045) and a trend of better OS (not reached vs 24.0 months; P =.070). Six (13%) patients who had FCSS ≥ 2 points had a worse median LFS (8.0 vs 48.0 months; P =.052) but not significantly worse OS (17.0 vs 28.0 months; P =.804). A Spearman coefficient for MRD ≥0.2% and hematogone levels ≥ 0.02% was -0.317 (P <.029), indicating a mildly negative correlation. However, MRD ≥0.2% and hematogones ≥ 0.02% were almost mutually exclusive. For clinical convenience, a MRD/Hematogone score was proposed that patient with MRD ≥0.2% was defined as 1 point and hematogone ≥ 0.02% was defined as -1 point. All patients could be categorized into three subgroups: 14(30%) patients with -1 point, 24(51%) patients with 0 point and 9(19%) with 1 point. Patients were stratified based on MRD/Hematogone score to assess survival using the Kaplan-Meier method and the Log-rank test. The median LFS were not reached, 48 months and 9 months for patients with -1 point, 0 point and 1 point, respectively (P =.015; Fig. 1). The median OS were not reached (-1 point), not reached (0 point) and 24 months (1 point) (P =.088). Multivariate analyses using Cox proportional hazard model demonstrated MRD/Hematogone score was an independent predictor of LFS (HR = 2.5, 95% CI, 1.2–5.1, P =.016; Table 2) after adjusting for MRC cytogenetic classification, WBC count (above or below 50000/uL) and whether undergoing allogenetic hematopoietic stem cell transplant before 1st relapse or not. Conclusion: Even without a diagnostic specimen, flow cytometry can assess and quantify aberrant myeloid progenitor cells, aberrant neutrophil/monocyte maturation and hematogones in post-induction marrow. MRD ≥0.2% or neutrophil/monocyte abnormalities (FCSS ≥ 2) predicts shorter LFS. Hematogones ≥ 0.02% predicts longer LFS and correlates negatively with MRD ≥0.2%. Proposed MRD/Hematogone score for post-induction adult AML in mCR maybe offer a simple and practical risk assessment. And the score is worthy to be validated by prospective and larger scale study. Disclosures: No relevant conflicts of interest to declare.

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50

Russo, Giusi, Alfonso Tramontano, Ilaria Iodice, Lorenzo Chiariotti, and Antonio Pezone. "Epigenome Chaos: Stochastic and Deterministic DNA Methylation Events Drive Cancer Evolution." Cancers 13, no. 8 (April 9, 2021): 1800. http://dx.doi.org/10.3390/cancers13081800.

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Cancer evolution is associated with genomic instability and epigenetic alterations, which contribute to the inter and intra tumor heterogeneity, making genetic markers not accurate to monitor tumor evolution. Epigenetic changes, aberrant DNA methylation and modifications of chromatin proteins, determine the “epigenome chaos”, which means that the changes of epigenetic traits are randomly generated, but strongly selected by deterministic events. Disordered changes of DNA methylation profiles are the hallmarks of all cancer types, but it is not clear if aberrant methylation is the cause or the consequence of cancer evolution. Critical points to address are the profound epigenetic intra- and inter-tumor heterogeneity and the nature of the heterogeneity of the methylation patterns in each single cell in the tumor population. To analyze the methylation heterogeneity of tumors, new technological and informatic tools have been developed. This review discusses the state of the art of DNA methylation analysis and new approaches to reduce or solve the complexity of methylated alleles in DNA or cell populations.

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