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Bone Marrow Transplantation Procedures in Mice to Study Clonal Hematopoiesis

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Aging in the bone marrow: when hematopoiesis gets clonal.

Dawn M E Bowdish^1,2, Candice Quin³

¹Firestone Institute for Respiratory Health, St. Joseph's Healthcare Hamilton.

Current Opinion in Hematology

|May 6, 2026

Summary

Elevated tumor necrosis factor alpha (TNF) drives myeloid expansion and clonal hematopoiesis of indeterminate potential (CHIP) in aging. Anti-TNF drugs may reduce CHIP clones but are not a direct treatment, necessitating further research into other anti-inflammatory strategies.

Keywords:

aging clonal hematopoiesis of indeterminate potential hematopoiesis inflammation tumor necrosis factor alpha

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Characterizing Mutational Load and Clonal Composition of Human Blood

Characterizing Mutational Load and Clonal Composition of Human Blood

Published on: July 11, 2019

Area of Science:

Hematology
Immunology
Aging Research

Background:

Cytokine tumor necrosis factor alpha (TNF) has a long-established role in influencing hematopoiesis.
Increased TNF in the aging microenvironment promotes myeloid progenitor expansion, particularly those with mutations linked to clonal hematopoiesis of indeterminate potential (CHIP).

Purpose of the Study:

To review seminal and recent studies on how TNF affects hematopoietic development during aging.
To examine TNF's influence on clonal dynamics in CHIP.

Main Methods:

Literature review of studies investigating TNF, aging, hematopoiesis, and CHIP.
Analysis of findings related to TNF levels, myeloid progenitor behavior, and CHIP mutations.

Main Results:

Elevated TNF promotes the engraftment and expansion of CHIP-mutant clones, with variations based on specific mutations.
Sex differences in TNF levels may correlate with variations in CHIP mutation frequency and type between males and females.
Anti-TNF inhibitors have demonstrated a reduction in CHIP mutation-containing clones across various inflammatory conditions.

Conclusions:

Elevated TNF, associated with aging and chronic inflammation, contributes to myeloid skewing and CHIP.
Anti-TNF therapies can mitigate detrimental changes in myeloid hematopoiesis.
Current anti-TNF drugs are not a direct treatment for CHIP; further investigation into other anti-inflammatory approaches like diet and exercise is warranted.