CD22 Exon 12 Deletion as an Independent Predictor of Poor Treatment Outcomes in B-ALL
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[1] R. Wilson,et al. Acute lymphoblastic leukemia displays a distinct highly methylated genome , 2022, Nature Cancer.
[2] A. Christoffels,et al. Upregulation of FHL1, SPNS3, and MPZL2 predicts poor prognosis in pediatric acute myeloid leukemia patients with FLT3-ITD mutation , 2022, Leukemia & lymphoma.
[3] L. Silverman,et al. Whole-transcriptome analysis in acute lymphoblastic leukemia: a report from the DFCI ALL Consortium Protocol 16-001 , 2021, Blood advances.
[4] O. Abdel-Wahab,et al. Splicing-Mediated Antigen Escape from Immunotherapy for B-cell Malignancies. , 2021, Blood cancer discovery.
[5] Deanne M. Taylor,et al. Modulation of CD22 Protein Expression in Childhood Leukemia by Pervasive Splicing Aberrations: Implications for CD22-Directed Immunotherapies , 2021, Blood cancer discovery.
[6] M. Loh,et al. Outcomes in adolescent and young adult patients (16 to 30 years) compared to younger patients treated for high-risk B-lymphoblastic leukemia: report from Children’s Oncology Group Study AALL0232 , 2021, Leukemia.
[7] M. Loh,et al. Favorable Trisomies and ETV6-RUNX1 Predict Cure in Low-Risk B-Cell Acute Lymphoblastic Leukemia: Results From Children's Oncology Group Trial AALL0331 , 2021, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[8] M. D. Den Boer,et al. A Phase I study of inotuzumab ozogamicin in pediatric relapsed/refractory acute lymphoblastic leukemia (ITCC-059 study). , 2020, Blood.
[9] M. Loh,et al. Outcome in Children With Standard-Risk B-Cell Acute Lymphoblastic Leukemia: Results of Children's Oncology Group Trial AALL0331. , 2019, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[10] Gennady Korotkevich,et al. Fast gene set enrichment analysis , 2019, bioRxiv.
[11] T. Tsubata. Inhibitory B cell co-receptors and autoimmune diseases , 2019, Immunological medicine.
[12] Matthew R. Gazzara,et al. Aberrant splicing in B-cell acute lymphoblastic leukemia , 2018, Nucleic acids research.
[13] F. Uckun,et al. Identification and targeting of CD22ΔE12 as a molecular RNAi target to overcome drug resistance in high-risk B-lineage leukemias and lymphomas , 2018, Cancer drug resistance.
[14] Yang Feng,et al. CD22-CAR T Cells Induce Remissions in CD19-CAR Naïve and Resistant B-ALL , 2017, Nature Medicine.
[15] M. Loh,et al. Dexamethasone and High-Dose Methotrexate Improve Outcome for Children and Young Adults With High-Risk B-Acute Lymphoblastic Leukemia: A Report From Children's Oncology Group Study AALL0232. , 2016, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[16] M. Liedtke,et al. Inotuzumab Ozogamicin versus Standard Therapy for Acute Lymphoblastic Leukemia. , 2016, The New England journal of medicine.
[17] M. Loh,et al. Prognostic significance of minimal residual disease in high risk B-ALL: a report from Children's Oncology Group study AALL0232. , 2015, Blood.
[18] F. Uckun,et al. CD22ΔE12 as a molecular target for RNAi therapy , 2015, British journal of haematology.
[19] L. Mitchell,et al. Development of Polypeptide-based Nanoparticles for Non-viral Delivery of CD22 RNA Trans-splicing Molecule as a New Precision Medicine Candidate Against B-lineage ALL , 2015, EBioMedicine.
[20] L. Mitchell,et al. CD22ΔE12 as a molecular target for corrective repair using RNA trans-splicing: anti-leukemic activity of a rationally designed RNA trans-splicing molecule. , 2015, Integrative biology : quantitative biosciences from nano to macro.
[21] W. Huber,et al. Moderated estimation of fold change and dispersion for RNA-seq data with DESeq2 , 2014, Genome Biology.
[22] F. Uckun,et al. A rationally designed nanoparticle for RNA interference therapy in B-lineage lymphoid malignancies , 2014, EBioMedicine.
[23] G. Reaman,et al. CD22 Exon 12 deletion is a characteristic genetic defect of therapy‐refractory clones in paediatric acute lymphoblastic leukaemia , 2012, British journal of haematology.
[24] J. Shuster,et al. Augmented therapy improves outcome for pediatric high risk acute lymphocytic leukemia: Results of Children's Oncology Group trial P9906 , 2011, Pediatric blood & cancer.
[25] F. Uckun,et al. CD22 EXON 12 deletion as a pathogenic mechanism of human B-precursor leukemia , 2010, Proceedings of the National Academy of Sciences.
[26] Joseph K. Pickrell,et al. Understanding mechanisms underlying human gene expression variation with RNA sequencing , 2010, Nature.
[27] P. Crocker,et al. Siglecs as positive and negative regulators of the immune system. , 2008, Biochemical Society transactions.
[28] Karine Tremblay,et al. Proteins Targets for the Major Human Hnrnp Multiple and Specific Mrna Processing Supplemental Material , 2008 .
[29] V. Beneš,et al. Diverse roles of hnRNP L in mammalian mRNA processing: a combined microarray and RNAi analysis. , 2007, RNA.
[30] L. Nitschke. The role of CD22 and other inhibitory co-receptors in B-cell activation. , 2005, Current opinion in immunology.
[31] Monika Heiner,et al. Intronic CA‐repeat and CA‐rich elements: a new class of regulators of mammalian alternative splicing , 2005, The EMBO journal.
[32] K. Haas,et al. CD22: a multifunctional receptor that regulates B lymphocyte survival and signal transduction. , 2005, Advances in immunology.
[33] J. Venables. Aberrant and Alternative Splicing in Cancer , 2004, Cancer Research.
[34] Martin Vingron,et al. Variance stabilization applied to microarray data calibration and to the quantification of differential expression , 2002, ISMB.
[35] S. Paust,et al. Definition of the Sites of Interaction between the Protein Tyrosine Phosphatase SHP-1 and CD22* , 1999, The Journal of Biological Chemistry.
[36] J. Cyster,et al. Polygenic autoimmune traits: Lyn, CD22, and SHP-1 are limiting elements of a biochemical pathway regulating BCR signaling and selection. , 1998, Immunity.