2021
DOI: 10.1038/s41375-021-01337-8
|View full text |Cite
|
Sign up to set email alerts
|

Clonal hematopoiesis and its emerging effects on cellular therapies

Abstract: The accumulation of somatic mutations in hematopoietic stem cells during aging, leading to clonal expansion, is linked to a higher risk of cardiovascular mortality and hematologic malignancies. Clinically, clonal hematopoiesis is associated with a pro-inflammatory phenotype of hematopoietic cells and their progeny, inflammatory conditions and a poor outcome for patients with hematologic neoplasms and solid tumors. Here, we review the relevance and complications of clonal hematopoiesis for the treatment of hema… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
1
1
1

Citation Types

1
19
0

Year Published

2022
2022
2024
2024

Publication Types

Select...
7
1
1

Relationship

2
7

Authors

Journals

citations
Cited by 31 publications
(20 citation statements)
references
References 101 publications
1
19
0
Order By: Relevance
“…For instance, the functional decline of the lymphoid compartment, responsible for a defective adaptive immunity in old age, has been observed also in human-aged HSPC leading to the common interpretation that, likewise in mice, human HSPC aging is associated with a prominent myeloid skewing 1921 . Additionally, the increased incidence of myeloproliferative disorders and hematopoietic myeloid malignancies in aged individuals 2226 further supports the above-mentioned shift in myeloid output during aging. Moreover, there is evidence in humans that aging is associated with anemia 27 and clonal hematopoiesis 23 which may act as additional cofactors in the development of myelodysplasia and hematopoietic malignancies 28,29 .…”
Section: Introductionsupporting
confidence: 56%
“…For instance, the functional decline of the lymphoid compartment, responsible for a defective adaptive immunity in old age, has been observed also in human-aged HSPC leading to the common interpretation that, likewise in mice, human HSPC aging is associated with a prominent myeloid skewing 1921 . Additionally, the increased incidence of myeloproliferative disorders and hematopoietic myeloid malignancies in aged individuals 2226 further supports the above-mentioned shift in myeloid output during aging. Moreover, there is evidence in humans that aging is associated with anemia 27 and clonal hematopoiesis 23 which may act as additional cofactors in the development of myelodysplasia and hematopoietic malignancies 28,29 .…”
Section: Introductionsupporting
confidence: 56%
“…Nevertheless, other cellular therapies in patients with lymphoma were reported to be influenced negatively by CHIP, which we did not observe. 11 In the future, larger studies with longitudinal single-cell analysis of various immune cells, including the CAR T cells themselves, are necessary to perform reliable multivariate analyses and to elucidate the influence of CHIP-associated somatic mutations on the outcome of CAR T-cell treatment.…”
Section: Resultsmentioning
confidence: 99%
“…The relevance of CHIP in the context of CAR T-cell treatment is widely unknown. 11,12 Therefore, we longitudinally evaluated the prevalence of CHIP in patients with r/r B-cell non-Hodgkin lymphoma undergoing CAR T-cell treatment and assessed the influence on clinical inflammation syndromes (CRS/ICANS), cytopenia after CAR T-cell therapy, and outcome.…”
Section: Introductionmentioning
confidence: 99%
“…However, most scholars only focus on heart damage caused by anti-tumor therapy ( 25 , 26 ). Cardiotoxicity during the treatment of AL patients has been extensively reported ( 27 ), including radiotherapy ( 28 , 29 ), conventional chemotherapies (e.g., anthracyclines, antimetabolites, and cyclophosphamide) ( 30 32 ), immune checkpoint inhibitors (programmed cell death 1, programmed death ligand 1, or CTL-associated protein 4) ( 33 , 34 ), and many targeted therapies, particularly monoclonal antibodies and tyrosine kinase inhibitors ( 35 , 36 ), CART therapy ( 37 39 ), natural killer cell immunotherapy ( 40 ), and hematopoietic stem cell transplantation ( 41 43 ). Possible mechanisms are mediated by reactive oxygen species generated in iron-dependent chemical reactions ( 44 ), mitochondrial dysfunction ( 45 ), increased calcium flux in cardiomyocytes ( 46 ), and disorders of DNA topoisomerase 2-beta metabolism ( 47 ).…”
Section: Discussionmentioning
confidence: 99%