Hematology
COHORT
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Imatinib treatment reduces inflammatory marker in CML patients in small study
Frontiers in Medicine
Published April 1, 2026
Researchers at a hospital in New Delhi studied 40 patients with chronic myeloid leukemia (CML) who were starting standard treatment with the drug imatinib. They wanted to see if levels of a protein in the blood called TNF-α, which is linked to inflammation, changed during treatment and if those changes were connected to how well patients responded.
They found that after 5 to 7 months of treatment, TNF-α levels dropped significantly in the patients. More importantly, they saw a pattern: patients whose TNF-α levels did not fall much were very likely to have a poor response to imatinib. This suggests that measuring TNF-α might one day give doctors an extra clue about how treatment is working.
It is crucial to understand this is a very early finding. The study was small, only looked at patients at one hospital, and simply observed what happened without testing an intervention. The authors themselves say this idea needs proper, larger studies to confirm it. For now, TNF-α is not a replacement for the standard tests doctors use to monitor CML. This research is a first step in exploring a possible new tool, especially in places where advanced testing is harder to get.
View Original Abstract ↓
PurposeChronic Myeloid Leukemia (CML) is characterized by the BCR-ABL1 fusion gene and is effectively managed with tyrosine kinase inhibitors (TKIs). However, therapeutic resistance and the persistence of leukemic stem cells pose challenges to achieving long-term remission. Tumor Necrosis Factor-alpha (TNF-α), a pro-inflammatory cytokine, is implicated in leukemogenesis and resistance, yet its clinical relevance in Indian CML cohorts remains underexplored.ObjectiveThis study investigates the pharmacodynamic and prognostic role of serum TNF-α levels in chronic-phase CML patients receiving first-line imatinib, aiming to evaluate its utility as a biomarker for treatment response.MethodsWe conducted a prospective observational study on 40 CML patients treated at Safdarjung Hospital, New Delhi. Blood samples were taken before treatment and 5–7 months after starting imatinib. ELISA was used to quantify TNF-α levels, and qRT-PCR was used to monitor BCR-ABL1 transcripts. We analyzed clinical and hematologic parameters using appropriate statistical methods.ResultsImatinib treatment significantly reduced serum TNF-α (259.5 to 129.8 pg/mL; p < 0.0001), mirroring the observed decrease in BCR-ABL1 transcripts. Basically, if TNF-α stuck around (r = 0.87), patients responded poorly, whereas good outcomes correlated with its quicker clearance (r = 0.45).ConclusionOur data suggest that TNF-α represents a clinically relevant pharmacodynamic and prognostic biomarker for patients with chronic-phase CML receiving imatinib therapy. A decline in TNF-α levels was associated with a favorable therapeutic outcome, whereas failure of TNF-α to decline was indicative of an inferior outcome. TNF-α does not replace qRT-PCR–based monitoring of BCR-ABL1; however, it may be useful as an adjunctive prognostic marker, especially in resource-poor environments, pending appropriate prospective confirmation.
