Age-related clonal hematopoiesis associated with adverse outcomes.
By Siddhartha Jaiswal, P. Fontanillas, Jason Flannick, A. Manning, Peter V. Grauman, B. Mar, R. C. Lindsley, Craig H. Mermel, N. Burtt, A. Chavez and 24 more. New England Journal of Medicine, 2014
4,169 citations recorded by the source corpus.
Subfields: Cancer Research, Hematology, Public Health, Environmental and Occupational Health
View Paper: https://www.semanticscholar.org/paper/1d07f0078aab6cc51ef5c807c3457341ca7a5f43
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Cancer Research
- K. Walsh
- Trey Ideker
- Lawrence Loeb
- Benjamin L. Ebert
- Siddhartha Jaiswal
- J. Salk
- Michael W. Schmitt
- Wolf Reik
In Hematology
- J. Apperley
- Trey Ideker
- J. Baselga
- Benjamin L. Ebert
- Andreas Hochhaus
- Siddhartha Jaiswal
- H. Kantarjian
- Brian J. Druker
In Public Health, Environmental and Occupational Health
Citations in the corpus
- Standards and Guidelines for the Interpretation and Reporting of Sequence Variants in Cancer: A Joint Consensus Recommendation of the Association for Molecular Pathology, American Society of Clinical Oncology, and College of American Pathologists. (2017, background): “Special care should be taken when evaluating possible hematological malignancies because many commonly mutated genes in leukemia and myelodysplastic syndromes may also be somatically mutated in the blood of otherwise healthy individuals and, therefore, may be incorrectly annotated as polymorphisms.(”
- The 2016 revision to the World Health Organization classification of myeloid neoplasms and acute leukemia. (2016, neutral): “Importantly, acquired clonal mutations identical to those seen inMDS can occur in the hematopoietic cells of apparently healthy older individuals without MDS, so-called “clonal hematopoiesis of indeterminate potential” (CHIP).(30,31,61) Although some patients with CHIP subsequently developMDS, the n”
- Monocyte-Macrophages and T Cells in Atherosclerosis (2017, neutral): “One of the consequences of aging is an accumulation of somatic mutations in hematopoietic stem cells (HSCs) which has been linked to increased clonal hematopoiesis and cardiovascular disease (Jaiswal et al., 2014; Jaiswal et al., 2017) (Figure 2).”
- Circulating Tumor DNA Analysis in Patients With Cancer: American Society of Clinical Oncology and College of American Pathologists Joint Review. (2018, background): “These variants are observed with increasing frequency from approximately the fifth decade of life, detected in approximately 5% of persons 60 to 69 years of age and 10% of persons $ 70 years of age.(33) The substantial majority of individuals with clonal hematopoiesis do not have hematologic cancer,”
- Tet2-mediated Clonal Hematopoiesis Accelerates Heart Failure through a Mechanism Involving the IL-1β/NLRP3 Inflammasome (2018, background): “Recent longitudinal studies have reported that detectable clonal hematopoiesis in non-symptomatic individuals is associated with all-cause mortality (6,7,9).”
- The 5th edition of the World Health Organization Classification of Haematolymphoid Tumours: Myeloid and Histiocytic/Dendritic Neoplasms (2022, background): “The incidence of CH increases with age [6].”
- DNA methylation aging clocks: challenges and recommendations (2019, background): “These clones are pathogenically associated with not only hematological cancers [179, 180] but also non-cancer disease risks such as atherosclerosis [181].”
- Clonal hematopoiesis in human aging and disease (2019, background): “Indeed, some individuals with clonal hematopoiesis have nearly all of their blood cells arising from a single mutated HSC (29).”
- Role of TET enzymes in DNA methylation, development, and cancer (2016, background): “Second, TET2 mutations are frequently observed in aged healthy individuals with clonal hematopoiesis and increase the propensity to develop hematopoieticmalignancies (Busque et al. 2012; Genovese et al. 2014; Jaiswal et al. 2014; Xie et al. 2014).”