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Life sciences · Journal article
Frontiers in Cell and Developmental Biology · November 6, 2026
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Clonal hematopoiesis (CH) introduces a hematopoietic component into the molecular and immune landscape of solid tumors. Its interpretation depends on whether a variant is measured in blood, plasma or tumor tissue, which cells carry it, and when sampling occurs relative to treatment. Existing reviews have examined cancer-associated inflammation, therapy-related clonal selection and clinical outcomes; a less developed question is how these observations can be compared when they measure different aspects of the same clone. This focused narrative review connects source attribution with immune-cell state, tissue localization and longitudinal change, separating human associations from cellular localization and experimental perturbation. Paired leukocyte analysis can identify hematopoietic variants that would otherwise be assigned to cancer cells. Mutation-resolved tissue measurements add information about local immune interactions, whereas serial blood measurements help distinguish clonal selection from the relative prominence of CH when tumor-derived plasma DNA declines. Genotype-specific findings, particularly involving TET2 and myeloid function, provide mechanistic explanations for some treatment associations, but aggregate CH has shown inconsistent relationships with immune-checkpoint efficacy and toxicity. The resulting framework links each measurement to its appropriate biological or clinical use: source correction is already actionable, while treatment prediction and organ-specific risk assessment require evidence that CH adds information beyond established tumor and patient characteristics.