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Biology subjects

Slager, S. L.

Publications and source records attributed to Slager, S. L..

2 recordsLinked to original sources

Unified somatic calling and machine learning-based classification enhance the discovery of clonal hematopoiesis of indeterminate potential

Clonal hematopoiesis (CH) of indeterminate potential (CHIP), driven by somatic mutations in leukemia-associated genes, confers increased risk of hematologic malignancies, cardiovascular disease and all-cause mortality. In blood of healthy individuals, small CH clones can expand over time to reach 2% variant allele frequency (VAF), the current threshold for CHIP. Nevertheless, reliable detection of low-VAF CHIP mutations is challenging, often relying on deep targeted sequencing. Here, we present UNISOM, a streamlined workflow for CHIP detection from whole-genome and whole-exome sequencing data that are underpowered, especially for low VAFs. UNISOM utilizes a meta-caller for variant detection, in couple with machine learning models which classify variants into CHIP, germline and artifact. In whole-exome data, UNISOM recovered nearly 80% of the CHIP mutations identified via deep targeted sequencing in the same cohort. Applied to whole-genome data from Mayo Clinic Biobank, it recapitulated the patterns previously established in much larger cohorts, including the most frequently mutated CHIP genes, predominant mutation types and signatures, as well as strong associations of CHIP with age and smoking status. Notably, 30% of the identified CHIP mutations had <5% VAFs, demonstrating its high sensitivity toward small mutant clones. This workflow is applicable to CHIP screening in population genomic studies.

bioinformatics↗

B Cell Receptor Signaling Drives APOBEC3 Expression Via Direct Enhancer Regulation in Chronic Lymphocytic Leukemia B Cells

Constitutively activated B cell receptor (BCR) signaling is a primary biological feature of chronic lymphocytic leukemia (CLL). The biological events controlled by BCR signaling in CLL are not fully understood and need investigation. To make inroads we obtained blood samples from CLL patients before and after Brutons tyrosine kinase inhibitors (BTKi) treatment and used them to study BCR signaling regulated genes. Here, by analysis of the chromatin states and gene expression profiles of CLL B cells from patients before and after BTKi ibrutinib treatment, we show that BTKi treatment leads to a decreased expression of APOBEC3 family genes in an enhancer regulation dependent manner. BTKi treatment reduces enrichment of enhancer markers (H3K4me1, H3K27ac) and chromatin accessibility at putative APOBEC3 enhancers. CRISPR-Cas9 directed deletion or inhibition of the putative APOBEC3 enhancers leads to reduced APOBEC3 expression. We further find that transcription factor NFATc1 couples BCR signaling with the APOBEC3 enhancer activity to control APOBEC3 expression. Importantly, enhancer regulated APOBEC3 expression contributes to replication stress in malignant B cells. We also demonstrate a novel mechanism for BTKi suppression of APOBEC3 expression via direct enhancer regulation in a NFATc1 dependent manner, implicating BCR signaling as a potential regulator of leukemic genomic instability. Key pointsO_LIBCR signaling pathway regulates APOBEC3 expression via direct enhancer regulation. C_LIO_LIAOPEBC3 enhancers are involved in the process of DNA replication stress, implicating a potential role in B cell genomic instability and CLL evolution C_LI

cancer biology↗