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Jabbour, E.

Publications and source records attributed to Jabbour, E..

6 recordsLinked to original sources

H3K27me3 spreading organizes canonical PRC1 chromatin architecture to regulate developmental programs

Polycomb Repressive Complex 2 (PRC2)-mediated histone H3K27 tri-methylation (H3K27me3) recruits canonical PRC1 (cPRC1) to maintain heterochromatin. In early development, polycomb-regulated genes are connected through long-range 3D interactions which resolve upon differentiation. Here, we report that polycomb looping is controlled by H3K27me3 spreading and regulates target gene silencing and cell fate specification. Using glioma-derived H3 Lys-27-Met (H3K27M) mutations as tools to restrict H3K27me3 deposition, we show that H3K27me3 confinement concentrates the chromatin pool of cPRC1, resulting in heightened 3D interactions mirroring chromatin architecture of pluripotency, and stringent gene repression that maintains cells in progenitor states to facilitate tumor development. Conversely, H3K27me3 spread in pluripotent stem cells, following neural differentiation or loss of the H3K36 methyltransferase NSD1, dilutes cPRC1 concentration and dissolves polycomb loops. These results identify the regulatory principles and disease implications of polycomb looping and nominate histone modification-guided distribution of reader complexes as an important mechanism for nuclear compartment organization. Highlights{square} The confinement of H3K27me3 at PRC2 nucleation sites without its spreading correlates with increased 3D chromatin interactions. {square}The H3K27M oncohistone concentrates canonical PRC1 that anchors chromatin loop interactions in gliomas, silencing developmental programs. {square}Stem and progenitor cells require factors promoting H3K27me3 confinement, including H3K36me2, to maintain cPRC1 loop architecture. {square}The cPRC1-H3K27me3 interaction is a targetable driver of aberrant self-renewal in tumor cells.

molecular biology↗

Epigenomic mapping in B-cell acute lymphoblastic leukemia identifies transcriptional regulators and noncoding variants promoting distinct chromatin architectures

B-cell lineage acute lymphoblastic leukemia (B-ALL) is comprised of diverse molecular subtypes and while transcriptional and DNA methylation profiling of B-ALL subtypes has been extensively examined, the accompanying chromatin landscape is not well characterized for many subtypes. We therefore mapped chromatin accessibility using ATAC-seq for 10 B-ALL molecular subtypes in primary ALL cells from 154 patients. Comparisons with B-cell progenitors identified candidate B-ALL cell-of-origin and AP-1-associated cis-regulatory rewiring in B-ALL. Cis-regulatory rewiring promoted B-ALL-specific gene regulatory networks impacting oncogenic signaling pathways that perturb normal B-cell development. We also identified that over 20% of B-ALL accessible chromatin sites exhibit strong subtype enrichment, with transcription factor (TF) footprint profiling identifying candidate TFs that maintain subtype-specific chromatin architectures. Over 9000 inherited genetic variants were further uncovered that contribute to variability in chromatin accessibility among individual patient samples. Overall, our data suggest that distinct chromatin architectures are driven by diverse TFs and inherited genetic variants which promote unique gene regulatory networks that contribute to transcriptional differences among B-ALL subtypes. HIGHLIGHTSO_LIPro-B progenitor cells as the most common cell-of-origin for B-ALL C_LIO_LIAP-1 TF-associated cis-regulatory rewiring in B-ALL C_LIO_LISubtype-specific accessible chromatin signatures representing 20% of all B-ALL sites C_LIO_LIRole for distinct TFs in promoting subtype-specific chromatin architectures C_LIO_LIThousands of inherited genetic variants identified impacting chromatin state C_LI

cancer biology↗

Leukemia stemness and co-occurring mutations drive resistance to IDH inhibitors in acute myeloid leukemia

Allosteric inhibitors of mutant IDH1 or IDH2 induce terminal differentiation of the mutant leukemic blasts and provide durable clinical responses in approximately 40% of acute myeloid leukemia (AML) patients with the mutations. However, primary resistance and acquired resistance to the drugs are major clinical issues. To understand the molecular underpinnings of clinical resistance to IDH inhibitors (IDHi), we performed multipronged genomic analyses (DNA sequencing, RNA sequencing and cytosine methylation profiling) in longitudinally collected specimens from 68 IDH1- or IDH2-mutant AML patients treated with the inhibitors. The analysis revealed that leukemia stemness is a major driver of primary resistance to IDHi, whereas selection of mutations in RUNX1/CEBPA or RAS-RTK pathway genes was the main driver of acquired resistance to IDHi, along with BCOR, homologous IDH gene, and TET2. These data suggest that targeting stemness and certain high-risk co-occurring mutations may overcome resistance to IDHi in AML.

cancer biology↗

Clinicopathologic Correlates and Natural History of Atypical Chronic Myeloid Leukemia

There is limited data on the clonal mechanisms underlying leukemogenesis, prognostic factors, and optimal therapy for atypical chronic myeloid leukemia (aCML). We evaluated the clinicopathological features, outcomes, and responses to therapy of 65 patients with aCML. Median age was 67 years (range 46-89). The most frequently mutated genes included ASXL1 (83%), SRSF2 (68%), and SETBP1 (58%). Mutations in SETBP1, SRSF2, TET2, and GATA2 tended to appear within dominant clones, with frequent SRSF2 and SETBP1 codominance, while other RAS pathway mutations were more likely to appear as minor clones. Acquisition of new, previously undetectable mutations at transformation was observed in 63% of evaluable patients, the most common involving signaling pathway mutations. Hypomethylating agents were associated with the highest response rates and duration. With a median overall survival of 25 months (95% CI 20-30), intensive chemotherapy was associated with worse OS than other treatment modalities, and allogeneic stem cell transplantation was the only therapy associated with improved outcomes (HR 0.044, 95% CI 0.035-0.593, p=0.007). Age, platelet count, BM blast percentage, and serum LDH levels were independent predictors of survival and were integrated in a multivariable model which allowed to predict 1-year and 3-year survival.

cancer biology↗

Only SF3B1 Mutation involving K700E (And Not Other Codons), Independently Predicts Overall Survival in Myelodysplastic Syndromes

BackgroundSF3B1 mutations (SF3B1mut) in myelodysplastic syndromes (MDS) frequently involve codon K700E and have a favorable prognosis. The prognostic effect of non-K700E SF3B1mut is uncertain. MethodsWe analyzed the clinical-pathologic features and outcomes of a single-institutional series of 94 SF3B1mut and 415 SF3B1wt newly diagnosed untreated MDS patients and explored the differences between K700E and non-K700E subgroups. FindingsNinety-four (19%) patients had SF3B1mut: median age, 74 years. Fifty-five (60%) patients carried K700E. Recurrent non-K700E mutations (39, 40%) included R625, H662 and K666. Compared to SF3B1mut K700E, non-K700E patients had a lower median ANC (1{middle dot}8 vs. 2{middle dot}4, p=0{middle dot}005) and were frequently "high" R-IPSS (revised International Prognostic Scoring System) [7(19%) vs. 2(4%), p=0{middle dot}031]. Non-K700E MDS frequently associated with RUNX1 (26% vs. 7%, p=0{middle dot}012) and exclusively with BCOR, IDH2, and SRSF2 mutations. There was no significant difference in karyotype or SF3B1 variant allele frequency. Most ([~]80%) were treated with hypomethylating agents. SF3B1mut had superior overall survival (OS) than SF3B1wt in all MDS categories [not-reached vs. 25{middle dot}2 months, p=0{middle dot}0003], low-grade MDS, and MDS with ring sideroblasts (MDS-RS). Compared to SF3B1wt, SF3B1mut K700E had superior outcomes in all MDS categories (25 months vs. not-reached, p=0{middle dot}0001), low-grade MDS, and MDS-RS, but no significant difference was seen with non-K700E. By multivariate analysis, absence of SF3B1mut K700E (not non-K700E) independently associated with prognosis. InterpretationSF3B1mut MDS show distinct clinical and mutational profiles, with K700E showing a significantly better OS compared to non-K700E mutations and SF3B1wt. Our study highlights the importance of SF3B1 mutation type in MDS risk assessment. Data Sharing StatementThe datasets generated during and/or analyzed during the current study are not publicly available due to patient privacy concerns but are available from the corresponding author on reasonable request. Research in ContextO_ST_ABSEvidence before this studyC_ST_ABSWe designed this study based on the collective evidence from a systematic search of the literature for outcomes of patients MDS with SF3B1 mutations (SF3B1mut) from January 2013 to June 2020. Both the International Working Group for the Prognosis of MDS (IWG-PM) proposal and 2016 revisions to the World Health Organization (WHO) Classification of Myelodysplastic Syndromes recognize SF3B1mut MDS with <5% blasts (or ring sideroblasts >5% for WHO) as a distinct sub-category, in the absence of other unfavorable features. This was largely based on favorable prognostic outcomes, a distinct gene expression profile, and association with ring sideroblasts. However, the natural history of SF3B1mut MDS is heterogeneous. A high proportion of SF3B1 mutations occur within codon K700, leading to large-scale mRNA downregulation due to branch point recognition error, while the rest occur outside of this codon. The downstream functional effects of SF3B1 mutations outside of the K700 codon are unclear. The clinical course of SF3B1mut MDS patients likely depends on the type of SF3B1 mutation and other features such as variant allele frequency, concomitant gene mutations, and karyotype. Until now, the effects of the different types of SF3B1 mutations were largely unknown. Added value of this studyIn this study, we report distinctive clinicopathologic characteristics and outcomes of MDS patients with SF3B1 mutations segregated based on mutation type: K700E vs. non-K700E. We show that [~]40% of SF3B1 mutated MDS patients have non-K700E mutations. Non-K700E SF3B1mut MDS have distinct clinico-pathologic features, such as lower ANC and frequent association with mutations in RUNX1, BCOR, IDH2, and SRSF2. There was no significant difference in karyotype or SF3B1 variant allele frequency. Importantly, K700E SF3B1mut MDS had superior overall survival compared to SF3B1wt, in all MDS, low-grade MDS, and MDS with ring sideroblasts, but no significant difference was seen with non-K700E. By multivariate analysis, absence of SF3B1mut K700E, but not non-K700E, independently associated with prognosis. Implications of all the available evidenceTo the best of our knowledge, this is the first study to report these findings from a single-institutional series of MDS primarily treated with hypomethylating agents. Our study highlights the importance of determining the SF3B1 mutation type in MDS risk assessment. These findings are important in light of the recent FDA approval of luspatercept based on the results of the MEDALIST trial that suggested sustained hematological responses in SF3B1mut MDS patients.

cancer biology↗

Clonal Evolution of Acute Myeloid Leukemia Revealed by High-Throughput Single-Cell Genomics

One of the pervasive features of cancer is the diversity of mutations found in malignant cells within the same tumor; a phenomenon called clonal diversity or intratumor heterogeneity. Clonal diversity allows tumors to adapt to the selective pressure of treatment and likely contributes to the development of treatment resistance and cancer recurrence. Thus, the ability to precisely delineate the clonal substructure of a tumor, including the evolutionary history of its development and the co-occurrence of its mutations, is necessary to understand and overcome treatment resistance. However, DNA sequencing of bulk tumor samples cannot accurately resolve complex clonal architectures. Here, we performed high-throughput single-cell DNA sequencing to quantitatively assess the clonal architecture of acute myeloid leukemia (AML). We sequenced a total of 556,951 cells from 77 patients with AML for 19 genes known to be recurrently mutated in AML. The data revealed clonal relationship among AML driver mutations and identified mutations that often co-occurred (e.g., NPM1/FLT3-ITD, DNMT3A/NPM1, SRSF2/IDH2, and WT1/FLT3-ITD) and those that were mutually exclusive (e.g., NRAS/KRAS, FLT3-D835/ITD, and IDH1/IDH2) at single-cell resolution. Reconstruction of the tumor phylogeny uncovered history of tumor development that is characterized by linear and branching clonal evolution patterns with latter involving functional convergence of separately evolved clones. Analysis of longitudinal samples revealed remodeling of clonal architecture in response to therapeutic pressure that is driven by clonal selection. Furthermore, in this AML cohort, higher clonal diversity ([&ge;]4 subclones) was associated with significantly worse overall survival. These data portray clonal relationship, architecture, and evolution of AML driver genes with unprecedented resolution, and illuminate the role of clonal diversity in therapeutic resistance, relapse and clinical outcome in AML.

cancer biology↗