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https://www.readbyqxmd.com/read/27492707/the-molecular-mechanism-of-thalidomide-analogs-in-hematologic-malignancies
#1
REVIEW
Stefanie Lindner, Jan Krönke
Thalidomide was sold in the 1950s as a sedative and was also used by pregnant women to treat morning sickness. It became notorious for causing severe birth defects and was removed from the market. More than four decades later, thalidomide had a renaissance in the treatment of cancer. Thalidomide and its more potent analogs, lenalidomide and pomalidomide, are nowadays approved treatments for multiple myeloma and myelodysplastic syndrome with deletion of chromosome 5q. In addition, thalidomide and its analogs inhibit release of tumor necrosis factor-α and increase interleukin-2 (IL-2) and interferon-γ release from T cells...
August 5, 2016: Journal of Molecular Medicine: Official Organ of the "Gesellschaft Deutscher Naturforscher und Ärzte"
https://www.readbyqxmd.com/read/27453112/-association-between-ikzf3-gene-polymorphisms-and-systemic-lupus-erythematosus-in-han-ethnic-group-in-southern-china-a-case-control-study
#2
L X Ye, C W Fu, F Jiang, W Meng
OBJECTIVE: To understand the association between IKZF3 gene polymorphism and the risk of systemic lupus erythematosus(SLE)in Han ethnic group in southern China. METHODS: A case-control study was conducted among 213 SLE patients and 234 healthy controls. Venous blood samples were collected from them to measure single nucleotide polymorphism(SNP)in IKZF3 by using the method of restriction fragment length polymorphism(PCR-RFLP). Multivariate logistic analysis and generalized multifactor dimensionality reduction(GMDR)method were used under multiple genetic models(additive, dominant, recessive), to analyze the association between IKZF3 and SLE susceptibility or different clinical features and gene-gene interactions...
July 2016: Zhonghua Liu Xing Bing Xue za Zhi, Zhonghua Liuxingbingxue Zazhi
https://www.readbyqxmd.com/read/27302879/identification-of-master-regulator-genes-in-human-periodontitis
#3
A D Sawle, M Kebschull, R T Demmer, P N Papapanou
Analytic approaches confined to fold-change comparisons of gene expression patterns between states of health and disease are unable to distinguish between primary causal disease drivers and secondary noncausal events. Genome-wide reverse engineering approaches can facilitate the identification of candidate genes that may distinguish between causal and associative interactions and may account for the emergence or maintenance of pathologic phenotypes. In this work, we used the algorithm for the reconstruction of accurate cellular networks (ARACNE) to analyze a large gene expression profile data set (313 gingival tissue samples from a cross-sectional study of 120 periodontitis patients) obtained from clinically healthy (n = 70) or periodontitis-affected (n = 243) gingival sites...
August 2016: Journal of Dental Research
https://www.readbyqxmd.com/read/27080863/allelic-imbalance-of-multiple-sclerosis-susceptibility-genes-ikzf3-and-iqgap1-in-human-peripheral-blood
#4
Pankaj K Keshari, Hanne F Harbo, Kjell-Morten Myhr, Jan H Aarseth, Steffan D Bos, Tone Berge
BACKGROUND: Multiple sclerosis is a chronic inflammatory, demyelinating disease of the central nervous system. Recent genome-wide studies have revealed more than 110 single nucleotide polymorphisms as associated with susceptibility to multiple sclerosis, but their functional contribution to disease development is mostly unknown. RESULTS: Consistent allelic imbalance was observed for rs907091 in IKZF3 and rs11609 in IQGAP1, which are in strong linkage disequilibrium with the multiple sclerosis associated single nucleotide polymorphisms rs12946510 and rs8042861, respectively...
2016: BMC Genetics
https://www.readbyqxmd.com/read/27070758/risk-stratification-of-t-cell-acute-lymphoblastic-leukemia-patients-based-on-gene-expression-mutations-and-copy-number-variation
#5
Gauri Mirji, Jaydeep Bhat, Jyoti Kode, Shripad Banavali, Manju Sengar, Prashant Khadke, Osama Sait, Shubhada Chiplunkar
Gene expression, copy number variations (CNV), mutations and survival were studied to delineate TCRγδ+T-cell acute lymphoblastic leukemia (T-ALL) as a distinct subgroup from TCRαβ+T-ALL. Gene Ontology analysis showed that differential regulation of genes involved in pathways for leukemogenesis, apoptosis, cytokine-cytokine receptor interaction and antigen processing/presentation may offer a survival benefit to TCRγδ+T-ALL patients. Genes involved in disease biology and having equal expression in both the subgroups, were further analysed for mutations and CNV using droplet digital PCR...
June 2016: Leukemia Research
https://www.readbyqxmd.com/read/26939566/genetic-variants-associated-with-rheumatoid-arthritis-patients-and-serotypes-in-european-populations
#6
Otsanda Ruiz-Larrañaga, Maria Uribarri, Maria C Alcaro, Sergio Escorza-Treviño, Jokin Del Amo, Mikel Iriondo, Carmen Manzano, Paola Migliorini, Veronika Lóránd, Andone Estonba
OBJECTIVES: To replicate the association of rheumatoid arthritis (RA) susceptibility loci in an independent European sample and to assess their specificity with anti-citrullinated protein antibodies (ACPA) status. METHODS: A selection of 64 SNP previously associated with RA have been typed in a cohort of 267 RA patients (169 ACPA-positive and 98 ACPA-negative) and 152 controls from the Rheumatology Units of the University Hospital of Pisa (Italy) and the University of Pécs Medical Center (Hungary)...
March 2016: Clinical and Experimental Rheumatology
https://www.readbyqxmd.com/read/26914976/pomalidomide-in-combination-with-dexamethasone-results-in-synergistic-anti-tumour-responses-in-pre-clinical-models-of-lenalidomide-resistant-multiple-myeloma
#7
Emily Rychak, Derek Mendy, Tao Shi, Yuhong Ning, Jim Leisten, Ling Lu, Karen Miller, Rama K Narla, Robert Z Orlowski, Heather K Raymon, Chad C Bjorklund, Anjan Thakurta, Anita K Gandhi, Brian E Cathers, Rajesh Chopra, Thomas O Daniel, Antonia Lopez-Girona
Pomalidomide is an IMiD(®) immunomodulatory agent, which has shown clinically significant benefits in relapsed and/or refractory multiple myeloma (rrMM) patients when combined with dexamethasone, regardless of refractory status to lenalidomide or bortezomib. (Schey et al, ; San Miguel et al, 2013; Richardson et al, 2014; Scott, ) In this work, we present preclinical data showing that the combination of pomalidomide with dexamethasone (PomDex) demonstrates potent anti-proliferative and pro-apoptotic activity in both lenalidomide-sensitive and lenalidomide-resistant MM cell lines...
March 2016: British Journal of Haematology
https://www.readbyqxmd.com/read/26909574/structural-basis-of-lenalidomide-induced-ck1%C3%AE-degradation-by-the-crl4-crbn-ubiquitin-ligase
#8
Georg Petzold, Eric S Fischer, Nicolas H Thomä
Thalidomide and its derivatives, lenalidomide and pomalidomide, are immune modulatory drugs (IMiDs) used in the treatment of haematologic malignancies. IMiDs bind CRBN, the substrate receptor of the CUL4-RBX1-DDB1-CRBN (also known as CRL4(CRBN)) E3 ubiquitin ligase, and inhibit ubiquitination of endogenous CRL4(CRBN) substrates. Unexpectedly, IMiDs also repurpose the ligase to target new proteins for degradation. Lenalidomide induces degradation of the lymphoid transcription factors Ikaros and Aiolos (also known as IKZF1 and IKZF3), and casein kinase 1α (CK1α), which contributes to its clinical efficacy in the treatment of multiple myeloma and 5q-deletion associated myelodysplastic syndrome (del(5q) MDS), respectively...
April 7, 2016: Nature
https://www.readbyqxmd.com/read/26657848/immunomodulatory-drugs-act-as-inhibitors-of-dna-methyltransferases-and-induce-pu-1-up-regulation-in-myeloma-cells
#9
Shinya Endo, Masayuki Amano, Nao Nishimura, Niina Ueno, Shikiko Ueno, Hiromichi Yuki, Shiho Fujiwara, Naoko Wada, Shinya Hirata, Hiroyuki Hata, Hiroaki Mitsuya, Yutaka Okuno
Immunomodulatory drugs (IMiDs) such as thalidomide, lenalidomide, and pomalidomide are efficacious in the treatment of multiple myeloma and significantly prolong their survival. However, the mechanisms of such effects of IMiDs have not been fully elucidated. Recently, cereblon has been identified as a target binding protein of thalidomide. Lenalidomide-resistant myeloma cell lines often lose the expression of cereblon, suggesting that IMiDs act as an anti-myeloma agent through interacting with cereblon. Cereblon binds to damaged DNA-binding protein and functions as a ubiquitin ligase, inducing degradation of IKZF1 and IKZF3 that are essential transcription factors for B and T cell development...
January 8, 2016: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/26544893/genetic-and-epigenetic-characterization-of-hypodiploid-acute-lymphoblastic-leukemia
#10
Setareh Safavi, Linda Olsson, Andrea Biloglav, Srinivas Veerla, Molly Blendberg, Johnbosco Tayebwa, Mikael Behrendtz, Anders Castor, Markus Hansson, Bertil Johansson, Kajsa Paulsson
PURPOSE: To investigate the genetic and epigenetic landscape of hypodiploid (<45 chromosomes) acute lymphoblastic leukemia (ALL). METHODS: Single nucleotide polymorphism array, whole exome sequencing, RNA sequencing, and methylation array analyses were performed on eleven hypodiploid ALL cases. RESULTS: In line with previous studies, mutations in IKZF3 and FLT3 were detected in near-haploid (25-30 chromosomes) cases. Low hypodiploidy (31-39 chromosomes) was associated with somatic TP53 mutations...
December 15, 2015: Oncotarget
https://www.readbyqxmd.com/read/26542096/meta-analysis-identifies-seven-susceptibility-loci-involved-in-the-atopic-march
#11
Ingo Marenholz, Jorge Esparza-Gordillo, Franz Rüschendorf, Anja Bauerfeind, David P Strachan, Ben D Spycher, Hansjörg Baurecht, Patricia Margaritte-Jeannin, Annika Sääf, Marjan Kerkhof, Markus Ege, Svetlana Baltic, Melanie C Matheson, Jin Li, Sven Michel, Wei Q Ang, Wendy McArdle, Andreas Arnold, Georg Homuth, Florence Demenais, Emmanuelle Bouzigon, Cilla Söderhäll, Göran Pershagen, Johan C de Jongste, Dirkje S Postma, Charlotte Braun-Fahrländer, Elisabeth Horak, Ludmila M Ogorodova, Valery P Puzyrev, Elena Yu Bragina, Thomas J Hudson, Charles Morin, David L Duffy, Guy B Marks, Colin F Robertson, Grant W Montgomery, Bill Musk, Philip J Thompson, Nicholas G Martin, Alan James, Patrick Sleiman, Elina Toskala, Elke Rodriguez, Regina Fölster-Holst, Andre Franke, Wolfgang Lieb, Christian Gieger, Andrea Heinzmann, Ernst Rietschel, Thomas Keil, Sven Cichon, Markus M Nöthen, Craig E Pennell, Peter D Sly, Carsten O Schmidt, Anja Matanovic, Valentin Schneider, Matthias Heinig, Norbert Hübner, Patrick G Holt, Susanne Lau, Michael Kabesch, Stefan Weidinger, Hakon Hakonarson, Manuel A R Ferreira, Catherine Laprise, Maxim B Freidin, Jon Genuneit, Gerard H Koppelman, Erik Melén, Marie-Hélène Dizier, A John Henderson, Young Ae Lee
Eczema often precedes the development of asthma in a disease course called the 'atopic march'. To unravel the genes underlying this characteristic pattern of allergic disease, we conduct a multi-stage genome-wide association study on infantile eczema followed by childhood asthma in 12 populations including 2,428 cases and 17,034 controls. Here we report two novel loci specific for the combined eczema plus asthma phenotype, which are associated with allergic disease for the first time; rs9357733 located in EFHC1 on chromosome 6p12...
November 6, 2015: Nature Communications
https://www.readbyqxmd.com/read/26512454/lenalidomide-deciphering-mechanisms-of-action-in-myeloma-myelodysplastic-syndrome-and-beyond
#12
REVIEW
Andrew A Guirguis, Benjamin L Ebert
Lenalidomide and its related 'analogues' modulate the substrate specificity of the CRL4(CRBN) E3 ubiquitin ligase complex. Polyubiquitination and subsequent proteasomal degradation of IKZF1 and IKZF3 in multiple myeloma and CK1α in del(5q) MDS has recently been linked to therapeutic efficacy of this class of compounds. Harnessing ubiquitin ligase substrate specificity, may in time facilitate the degradation of other 'undruggable' proteins and allow for separation of detrimental side effects of IMiD compounds from those associated with therapeutic efficacy...
December 2015: Current Opinion in Cell Biology
https://www.readbyqxmd.com/read/26484354/gene-expression-genotype-analysis-implicates-gsdma-gsdmb-and-lrrc3c-as-contributors-to-inflammatory-bowel-disease-susceptibility
#13
Jan Söderman, Linda Berglind, Sven Almer
To investigate the biological foundation of the inflammatory bowel disease (IBD), ulcerative colitis and Crohn's disease, susceptibility locus rs2872507, we have investigated the expression of 13 genes using ileal and colonic biopsies from patients with IBD (inflamed and noninflamed mucosa) or from individuals without IBD (noninflamed mucosa). The susceptibility allele was consistently associated with reduced expression of GSDMB (P = 4.1 × 10(-3)-7.2 × 10(-10)). The susceptibility allele was also associated with the increased expression of GSDMA (P = 1...
2015: BioMed Research International
https://www.readbyqxmd.com/read/26466571/mutations-driving-cll-and-their-evolution-in-progression-and-relapse
#14
Dan A Landau, Eugen Tausch, Amaro N Taylor-Weiner, Chip Stewart, Johannes G Reiter, Jasmin Bahlo, Sandra Kluth, Ivana Bozic, Mike Lawrence, Sebastian Böttcher, Scott L Carter, Kristian Cibulskis, Daniel Mertens, Carrie L Sougnez, Mara Rosenberg, Julian M Hess, Jennifer Edelmann, Sabrina Kless, Michael Kneba, Matthias Ritgen, Anna Fink, Kirsten Fischer, Stacey Gabriel, Eric S Lander, Martin A Nowak, Hartmut Döhner, Michael Hallek, Donna Neuberg, Gad Getz, Stephan Stilgenbauer, Catherine J Wu
Which genetic alterations drive tumorigenesis and how they evolve over the course of disease and therapy are central questions in cancer biology. Here we identify 44 recurrently mutated genes and 11 recurrent somatic copy number variations through whole-exome sequencing of 538 chronic lymphocytic leukaemia (CLL) and matched germline DNA samples, 278 of which were collected in a prospective clinical trial. These include previously unrecognized putative cancer drivers (RPS15, IKZF3), and collectively identify RNA processing and export, MYC activity, and MAPK signalling as central pathways involved in CLL...
October 22, 2015: Nature
https://www.readbyqxmd.com/read/26438514/the-novel-mechanism-of-lenalidomide-activity
#15
REVIEW
Emma C Fink, Benjamin L Ebert
Lenalidomide acts by a novel drug mechanism-modulation of the substrate specificity of the CRL4(CRBN) E3 ubiquitin ligase. In multiple myeloma, lenalidomide induces the ubiquitination of IKZF1 and IKZF3 by CRL4(CRBN). Subsequent proteasomal degradation of these transcription factors kills multiple myeloma cells. In del(5q) myelodysplastic syndrome, lenalidomide induces the degradation of CK1α, which preferentially affects del(5q) cells because they express this gene at haploinsufficient levels. In the future, modulation of ubiquitin ligase function may enable us to target previously "undruggable" proteins...
November 19, 2015: Blood
https://www.readbyqxmd.com/read/26344709/distinct-and-overlapping-functions-of-the-cullin-e3-ligase-scaffolding-proteins-cul4a-and-cul4b
#16
REVIEW
Jeffrey Hannah, Pengbo Zhou
The cullin 4 subfamily of genes includes CUL4A and CUL4B, which share a mostly identical amino acid sequence aside from the elongated N-terminal region in CUL4B. Both act as scaffolding proteins for modular cullin RING ligase 4 (CRL4) complexes which promote the ubiquitination of a variety of substrates. CRL4 function is vital to cells as loss of both genes or their shared substrate adaptor protein DDB1 halts proliferation and eventually leads to cell death. Due to their high structural similarity, CUL4A and CUL4B share a substantial overlap in function...
November 15, 2015: Gene
https://www.readbyqxmd.com/read/26278503/characterization-of-genetic-loci-that-affect-susceptibility-to-inflammatory-bowel-diseases-in-african-americans
#17
MULTICENTER STUDY
Chengrui Huang, Talin Haritunians, David T Okou, David J Cutler, Michael E Zwick, Kent D Taylor, Lisa W Datta, Joseph C Maranville, Zhenqiu Liu, Shannon Ellis, Pankaj Chopra, Jonathan S Alexander, Robert N Baldassano, Raymond K Cross, Themistocles Dassopoulos, Tanvi A Dhere, Richard H Duerr, John S Hanson, Jason K Hou, Sunny Z Hussain, Kim L Isaacs, Kelly E Kachelries, Howard Kader, Michael D Kappelman, Jeffrey Katz, Richard Kellermayer, Barbara S Kirschner, John F Kuemmerle, Archana Kumar, John H Kwon, Mark Lazarev, Peter Mannon, Dedrick E Moulton, Bankole O Osuntokun, Ashish Patel, John D Rioux, Jerome I Rotter, Shehzad Saeed, Ellen J Scherl, Mark S Silverberg, Ann Silverman, Stephan R Targan, John F Valentine, Ming-Hsi Wang, Claire L Simpson, S Louis Bridges, Robert P Kimberly, Stephen S Rich, Judy H Cho, Anna Di Rienzo, Linda W H Kao, Dermot P B McGovern, Steven R Brant, Subra Kugathasan
BACKGROUND & AIMS: Inflammatory bowel disease (IBD) has familial aggregation in African Americans (AAs), but little is known about the molecular genetic susceptibility. Mapping studies using the Immunochip genotyping array expand the number of susceptibility loci for IBD in Caucasians to 163, but the contribution of the 163 loci and European admixture to IBD risk in AAs is unclear. We performed a genetic mapping study using the Immunochip to determine whether IBD susceptibility loci in Caucasians also affect risk in AAs and identify new associated loci...
November 2015: Gastroenterology
https://www.readbyqxmd.com/read/26269456/the-imids-targets-ikzf-1-3-and-irf4-as-novel-negative-regulators-of-nk-cell-activating-ligands-expression-in-multiple-myeloma
#18
Cinzia Fionda, Maria Pia Abruzzese, Alessandra Zingoni, Francesca Cecere, Elisabetta Vulpis, Giovanna Peruzzi, Alessandra Soriani, Rosa Molfetta, Rossella Paolini, Maria Rosaria Ricciardi, Maria Teresa Petrucci, Angela Santoni, Marco Cippitelli
Immunomodulatory drugs (IMiDs) have potent anti-tumor activities in multiple myeloma (MM) and are able to enhance the cytotoxic function of natural killer (NK) cells, important effectors of the immune response against MM. Here, we show that these drugs can enhance the expression of the NKG2D and DNAM-1 activating receptor ligands MICA and PVR/CD155 in human MM cell lines and primary malignant plasma cells. Depletion of cereblon (CRBN) by shRNA interference strongly impaired upregulation of these ligands and, more interestingly, IMiDs/CRBN-mediated downregulation of the transcription factors Ikaros (IKZF1), Aiolos (IKZF3) and IRF4 was critical for these regulatory mechanisms...
September 15, 2015: Oncotarget
https://www.readbyqxmd.com/read/26226092/integrated-genomic-characterization-of-a-pineal-parenchymal-tumor-of-intermediate-differentiation
#19
REVIEW
Yun Jee Kang, Wenya Linda Bi, Adrian M Dubuc, Louine Martineau, Azra H Ligon, Aaron L Berkowitz, Ayal A Aizer, Eudocia Q Lee, Keith L Ligon, Shakti H Ramkissoon, Ian F Dunn
BACKGROUND: Pineal parenchymal tumors of intermediate differentiation (PPTIDs) are rare lesions. The differential diagnosis and management strategy for PPTIDs can be challenging because of the variable prognostic and pathologic characteristics of these tumors. METHODS: A 24-year-old man presented with progressive headaches, gait abnormalities, and abulia. Magnetic resonance imaging revealed a large T1-hypointense, T2-isointense, contrast-enhancing, partially cystic mass of the pineal and tectal region...
January 2016: World Neurosurgery
https://www.readbyqxmd.com/read/26185311/adult-low-hypodiploid-acute-b-lymphoblastic-leukemia-with-ikzf3-deletion-and-tp53-mutation-comparison-with-pediatric-patients
#20
COMPARATIVE STUDY
Min Fang, Pamela S Becker, Michael Linenberger, Keith D Eaton, Frederick R Appelbaum, ZoAnn Dreyer, Gladstone Airewele, Michele Redell, Dolores Lopez-Terrada, Ankita Patel, Karen R Rabin, Xinyan Lu
OBJECTIVES: Chromosomal ploidy is a major risk stratification tool for acute B-cell lymphoblastic leukemia (B-ALL). Low hypodiploidy and near-haploidy are thought to be confined to pediatric B-ALL and associated with a poor prognosis. Doubling of either a low-hypodiploid or a near-haploid clone results in an apparently high-hyperdiploid karyotype, which is often misclassified for risk. METHODS: We studied four patients with B-ALL who had chromosome genomic array testing (CGAT), along with fluorescence in situ hybridization and mutation testing...
August 2015: American Journal of Clinical Pathology
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