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Showing 1–19 of 19 results
Advanced filters: Author: Siddhartha Jaiswal Clear advanced filters

  • Siddhartha Jaiswal is an assistant professor at Stanford University School of Medicine, where he is also a member of the Immunology Program and the Institute for Stem Cell Biology and Regenerative Medicine.

    • Siddhartha Jaiswal
    Comments & Opinion
    Nature Medicine
    Volume: 25, P: 1184

  • Analysis of 97,691 high-coverage human blood DNA-derived whole-genome sequences enabled simultaneous identification of germline and somatic mutations that predispose individuals to clonal expansion of haematopoietic stem cells, indicating that both inherited and acquired mutations are linked to age-related cancers and coronary heart disease.

    • Alexander G. Bick
    • Joshua S. Weinstock
    • Pradeep Natarajan
    Research
    Nature
    Volume: 586, P: 763-768

  • Using data from a single time point, passenger-approximated clonal expansion rate (PACER) estimates the fitness of common driver mutations that lead to clonal haematopoiesis and identifies TCL1A activation as a mediator of clonal expansion.

    • Joshua S. Weinstock
    • Jayakrishnan Gopakumar
    • Siddhartha Jaiswal
    Research
    Nature
    Volume: 616, P: 755-763

  • Rauch et al. show that loss-of-function mutations in the epigenetic regulator Dnmt3a lead to accelerated atherosclerosis, as previously shown for Tet2, and that loss of either gene leads to similar changes in atheroma composition, with the emergence of a distinct population of chemokine-enriched, resident-like macrophages infiltrating the adventitia, as revealed by single-cell transcriptomics and spatial proteomic analyses.

    • Philipp J. Rauch
    • Jayakrishnan Gopakumar
    • Siddhartha Jaiswal
    Research
    Nature Cardiovascular Research
    Volume: 2, P: 805-818

  • Here, the authors use passenger mutations to quantify expansion rate in ~6,000 people with mosaic chromosomal alterations in the NHLBI TOPMed cohort, finding associations between growth rate and blood counts along with germline genetic modulators of growth rate.

    • Yash Pershad
    • Taralynn Mack
    • Alexander G. Bick
    ResearchOpen Access
    Nature Communications
    Volume: 15, P: 1-10

  • A study shows that clonal haematopoiesis of indeterminate potential is associated with an increased risk of chronic liver disease specifically through the promotion of liver inflammation and injury.

    • Waihay J. Wong
    • Connor Emdin
    • Pradeep Natarajan
    Research
    Nature
    Volume: 616, P: 747-754

  • Exploring the clonal expansion of somatically mutated hematopoietic stem cells with aging, Mack, Raddatz et al. quantify rates of clonal expansion in 4,370 individuals in the Trans-Omics for Precision Medicine cohort, observing epigenetic and proteomic patterns associated with clonal hematopoiesis of indeterminate potential.

    • Taralynn M. Mack
    • Michael A. Raddatz
    • Alexander G. Bick
    Research
    Nature Aging
    Volume: 4, P: 1043-1052

  • Clonal hematopoiesis, often caused by mutations in DNMT3A and TET2, is associated with blood cancer and coronary artery disease. Here, the authors conduct an epigenome-wide association study, finding that clonal hematopoiesis caused by DNMT3A vs. TET2 mutations has directionally opposing changes in DNA methylation profiles, with both promoting stem cell self-renewal.

    • M d Mesbah Uddin
    • Ngoc Quynh H. Nguyen
    • Karen N. Conneely
    ResearchOpen Access
    Nature Communications
    Volume: 13, P: 1-16

  • Clonal hematopoiesis is a risk factor for hematological cancers, cardiovascular diseases and death. Two papers now use new experimental and mathematical tools to quantify changes in the clonal composition of human blood over time, and the results have implications for the risk of cardiovascular diseases.

    • Siddhartha Jaiswal
    • Alexander G. Bick
    News & Views
    Nature Cardiovascular Research
    Volume: 1, P: 537-538

  • Clonal haematopoiesis of indeterminate potential (CHIP) commonly occurs as a result of mutations in transcriptional regulators and is associated with a doubling of the risk of atherosclerotic cardiovascular disease. Jaiswal and Libby propose that CHIP contributes to the increased inflammation seen in ageing and thereby explains some of the age-related risk of cardiovascular disease.

    • Siddhartha Jaiswal
    • Peter Libby
    Reviews
    Nature Reviews Cardiology
    Volume: 17, P: 137-144

  • Clonal haematopoiesis of indeterminate potential (CHIP) is defined as an expansion of mutant blood stem cells in individuals without haematological malignancies. CHIP is linked to an increased risk of non-cancerous disorders such as atherosclerotic cardiovascular disease, possibly because mutant innate immune cells have pro-inflammatory phenotypes. Prospective studies are needed to determine whether individuals with CHIP might benefit from anti-inflammatory therapies.

    • Herra Ahmad
    • Siddhartha Jaiswal
    Comments & Opinion
    Nature Reviews Cardiology
    Volume: 20, P: 437-438

  • The number, identity, and burden of mutations in clonal hematopoiesis are associated with the risk and timing of progression to acute myeloid leukemia.

    • Rob S. Sellar
    • Siddhartha Jaiswal
    • Benjamin L. Ebert
    News & Views
    Nature Medicine
    Volume: 24, P: 904-906