Matthew J. Walter
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View article: Sensitivity to ATR–CHK1 pathway inhibition in AML/MDS is enhanced by <i>SRSF2</i> mutations and reduced by RUNX1 loss
Sensitivity to ATR–CHK1 pathway inhibition in AML/MDS is enhanced by <i>SRSF2</i> mutations and reduced by RUNX1 loss Open
SRSF2 mutations occur in up to 25% of acute myeloid leukemia (AML) and 17% of myelodysplastic syndrome (MDS) cases and are associated with poor prognosis, yet no mutation-directed therapy exists. Here, we aimed to identify therapeutically …
View article: Evaluation of Long-Read Genome Sequencing for Genomic Profiling of Myeloid Cancers
Evaluation of Long-Read Genome Sequencing for Genomic Profiling of Myeloid Cancers Open
Whole-genome sequencing (WGS) is a comprehensive approach for the genomic evaluation of acute myeloid leukemia (AML) and myelodysplastic syndromes (MDS). We recently described a streamlined tumor-only WGS assay (ChromoSeq) that uses Illumi…
View article: Germline genetic variation impacts clonal hematopoiesis landscape and progression to malignancy
Germline genetic variation impacts clonal hematopoiesis landscape and progression to malignancy Open
With age, clonal expansions occur pervasively across normal tissues yet only in rare instances lead to cancer, despite being driven by well-established cancer drivers. Characterization of the factors that influence clonal progression is ne…
View article: U2af1S34F and U2af1Q157R myeloid neoplasm-associated hotspot mutations induce distinct hematopoietic phenotypes in mice
U2af1S34F and U2af1Q157R myeloid neoplasm-associated hotspot mutations induce distinct hematopoietic phenotypes in mice Open
Recurrent somatic mutations in the spliceosome genes SF3B1, SRSF2, and U2AF1 are frequently identified in patients with myeloid neoplasms, such as myelodysplastic syndromes. We characterized the in vivo consequences of expressing two hotsp…
View article: Epidemiology of bone metastasis in France between 2009 and 2018
Epidemiology of bone metastasis in France between 2009 and 2018 Open
Bone is the third most frequent metastatic site, and bone metastases (BM) are responsible for severe skeletal complications requiring dedicated care. There is no recent BM epidemiology data. This study aimed to describe incident BM patient…
View article: Supplementary Figure S10 from Plasma Proteomic Signature Predicts Myeloid Neoplasm Risk
Supplementary Figure S10 from Plasma Proteomic Signature Predicts Myeloid Neoplasm Risk Open
Two-sample Mendelian randomization (MR) analyses of the causal effect of plasma protein levels on myeloid neoplasm (MN) risk in the UKBB (N=381,485).
View article: Supp_Tables_S1-S13 from The DNA Methyltransferase Inhibitor 5-Aza-4′-thio-2′-Deoxycytidine Induces C>G Transversions and Acute Lymphoid Leukemia Development
Supp_Tables_S1-S13 from The DNA Methyltransferase Inhibitor 5-Aza-4′-thio-2′-Deoxycytidine Induces C>G Transversions and Acute Lymphoid Leukemia Development Open
Supp_Tables_S1-S13
View article: Supplementary Table S7 from Plasma Proteomic Signature Predicts Myeloid Neoplasm Risk
Supplementary Table S7 from Plasma Proteomic Signature Predicts Myeloid Neoplasm Risk Open
Association between plasma protein levels and individual clonal hematopoiesis (CH) genes with frequency greater than 20 (N=13 genes).
View article: Supplementary Table S9 from Plasma Proteomic Signature Predicts Myeloid Neoplasm Risk
Supplementary Table S9 from Plasma Proteomic Signature Predicts Myeloid Neoplasm Risk Open
Association between plasma protein levels and blood count measurements.
View article: Supplementary Table S2 from Plasma Proteomic Signature Predicts Myeloid Neoplasm Risk
Supplementary Table S2 from Plasma Proteomic Signature Predicts Myeloid Neoplasm Risk Open
Association between protein levels (N=1,463), myeloid neoplasm (MN) risk and clonal hematopoesisis (CH).
View article: Supp_Tables_S1-S13 from The DNA Methyltransferase Inhibitor 5-Aza-4′-thio-2′-Deoxycytidine Induces C>G Transversions and Acute Lymphoid Leukemia Development
Supp_Tables_S1-S13 from The DNA Methyltransferase Inhibitor 5-Aza-4′-thio-2′-Deoxycytidine Induces C>G Transversions and Acute Lymphoid Leukemia Development Open
Supp_Tables_S1-S13
View article: Supplementary Figure S2 from Plasma Proteomic Signature Predicts Myeloid Neoplasm Risk
Supplementary Figure S2 from Plasma Proteomic Signature Predicts Myeloid Neoplasm Risk Open
Association between MN and plasma protein levels stratified by MN subtype (MPN vs. MDS/AML).
View article: Supplementary Table S10 from Plasma Proteomic Signature Predicts Myeloid Neoplasm Risk
Supplementary Table S10 from Plasma Proteomic Signature Predicts Myeloid Neoplasm Risk Open
Asociation between polygenic risk score and risk of myeloid neoplasm (MN) with and without adjusting for CH.
View article: Supplementary Table S6 from Plasma Proteomic Signature Predicts Myeloid Neoplasm Risk
Supplementary Table S6 from Plasma Proteomic Signature Predicts Myeloid Neoplasm Risk Open
Association between plasma protein levels and clonal hematopoiesis (CH) stratified by VAF.
View article: Data from The DNA Methyltransferase Inhibitor 5-Aza-4′-thio-2′-Deoxycytidine Induces C>G Transversions and Acute Lymphoid Leukemia Development
Data from The DNA Methyltransferase Inhibitor 5-Aza-4′-thio-2′-Deoxycytidine Induces C>G Transversions and Acute Lymphoid Leukemia Development Open
DNA methyltransferase inhibitors (DNMTi), most commonly cytidine analogs, are compounds that decrease 5′-cytosine methylation. DNMTi are used clinically based on the hypothesis that cytosine demethylation will lead to re-expression of tumo…
View article: Supp_Fig_S1-S19 from The DNA Methyltransferase Inhibitor 5-Aza-4′-thio-2′-Deoxycytidine Induces C>G Transversions and Acute Lymphoid Leukemia Development
Supp_Fig_S1-S19 from The DNA Methyltransferase Inhibitor 5-Aza-4′-thio-2′-Deoxycytidine Induces C>G Transversions and Acute Lymphoid Leukemia Development Open
Supp_Fig_S1-S19
View article: Supplementary Figure S4 from Plasma Proteomic Signature Predicts Myeloid Neoplasm Risk
Supplementary Figure S4 from Plasma Proteomic Signature Predicts Myeloid Neoplasm Risk Open
Association between plasma proteins and common CH genes.
View article: Supplementary Figure S7 from Plasma Proteomic Signature Predicts Myeloid Neoplasm Risk
Supplementary Figure S7 from Plasma Proteomic Signature Predicts Myeloid Neoplasm Risk Open
Prediction of MN risk using clinical, CH, and proteomics data.
View article: Supplementary Figure S1 from Plasma Proteomic Signature Predicts Myeloid Neoplasm Risk
Supplementary Figure S1 from Plasma Proteomic Signature Predicts Myeloid Neoplasm Risk Open
Association between myeloid neoplasm and plasma protein levels stratified by disease subtype.
View article: Supplementary Table S9 from Plasma Proteomic Signature Predicts Myeloid Neoplasm Risk
Supplementary Table S9 from Plasma Proteomic Signature Predicts Myeloid Neoplasm Risk Open
Association between plasma protein levels and blood count measurements.
View article: Supplementary Table S3 from Plasma Proteomic Signature Predicts Myeloid Neoplasm Risk
Supplementary Table S3 from Plasma Proteomic Signature Predicts Myeloid Neoplasm Risk Open
Significantly enriched Reactome gene sets after multiple hypothesis testing correction (pFDR <= 0.05).
View article: Supplementary Figure S4 from Plasma Proteomic Signature Predicts Myeloid Neoplasm Risk
Supplementary Figure S4 from Plasma Proteomic Signature Predicts Myeloid Neoplasm Risk Open
Association between plasma proteins and common CH genes.
View article: Supplementary Table S1 from Plasma Proteomic Signature Predicts Myeloid Neoplasm Risk
Supplementary Table S1 from Plasma Proteomic Signature Predicts Myeloid Neoplasm Risk Open
List of genes with known relevance to hematologic cancer.
View article: Supplementary Figure S7 from Plasma Proteomic Signature Predicts Myeloid Neoplasm Risk
Supplementary Figure S7 from Plasma Proteomic Signature Predicts Myeloid Neoplasm Risk Open
Prediction of MN risk using clinical, CH, and proteomics data.
View article: Supplementary Figure S10 from Plasma Proteomic Signature Predicts Myeloid Neoplasm Risk
Supplementary Figure S10 from Plasma Proteomic Signature Predicts Myeloid Neoplasm Risk Open
Two-sample Mendelian randomization (MR) analyses of the causal effect of plasma protein levels on myeloid neoplasm (MN) risk in the UKBB (N=381,485).
View article: Supplementary Methods S1 from Plasma Proteomic Signature Predicts Myeloid Neoplasm Risk
Supplementary Methods S1 from Plasma Proteomic Signature Predicts Myeloid Neoplasm Risk Open
Supplementary Methods
View article: Supplementary Table S2 from Plasma Proteomic Signature Predicts Myeloid Neoplasm Risk
Supplementary Table S2 from Plasma Proteomic Signature Predicts Myeloid Neoplasm Risk Open
Association between protein levels (N=1,463), myeloid neoplasm (MN) risk and clonal hematopoesisis (CH).
View article: Supplementary Table S11 from Plasma Proteomic Signature Predicts Myeloid Neoplasm Risk
Supplementary Table S11 from Plasma Proteomic Signature Predicts Myeloid Neoplasm Risk Open
Two-sample Mendelian randomization analyses of the causal effect of plasma protein levels on myeloid neoplasm (MN) risk in the UKBB.
View article: Supplementary Figure S9 from Plasma Proteomic Signature Predicts Myeloid Neoplasm Risk
Supplementary Figure S9 from Plasma Proteomic Signature Predicts Myeloid Neoplasm Risk Open
Discrimination of MN risk integrating Clonal Hematopoiesis Risk Score (CHRS) and proteomics.
View article: Supplementary Table S5 from Plasma Proteomic Signature Predicts Myeloid Neoplasm Risk
Supplementary Table S5 from Plasma Proteomic Signature Predicts Myeloid Neoplasm Risk Open
Association between plasma protein levels and risk of myeloid neoplasm (MN) with and without adjustment for clonal hematopoiesis (CH).