Hijacking the helpers: platelet and neutrophil trafficking in AML and therapeutic exploitation

Acute myeloid leukemia (AML) remains one of the most aggressive and treatment-resistant hematologic malignancies, driven by clonal expansion of immature myeloid blasts in the bone marrow and peripheral blood. Current therapies-chemotherapy and targeted agents-are limited by poor marrow penetration, systemic toxicity, and rapid development of resistant clones, leaving long-term survival rates low. Clinicians face the persistent challenge of delivering effective therapy while minimizing harm. Platelets and neutrophils-beyond their classical roles in hemostasis and innate immunity-actively support leukemic niches, suppress anti-tumor immunity, and protect malignant cells from cytotoxic attack. These interactions highlight an untapped opportunity: harnessing endogenous cellular networks to deliver therapeutics with precision and potency. Conventional carriers, including liposomes and nanoparticles, fail to exploit these natural trafficking and immune-modulatory mechanisms, limiting marrow-specific targeting and therapeutic durability. We propose cellular hitchhiking using patient-derived platelets and neutrophils as a transformative, patient-tailored strategy. These carriers leverage intrinsic homing mechanisms, immune interface modulation, and prolonged circulation to deliver cytotoxic, immunomodulatory, or gene-based therapeutics directly to marrow and sanctuary sites. Ex vivo priming, biomaterial functionalization, and patient-specific engineering can enhance marrow-targeted drug concentration by several-fold, reduce systemic exposure, and minimize thrombo-inflammatory complications. By converting circulating blood cells into programmable delivery vectors, this approach offers a biologically rational platform with translational potential; however, immediate clinical relevance requires validation in controlled early-phase human studies. Preclinical evidence indicates that cellular hitchhiking can substantially increase bone-marrow drug delivery and reduce systemic exposure; whether these improvements will translate into higher remission rates or lower relapse in patients remains to be established in prospective clinical studies. Integrated into AML management, this strategy provides a biologically rational platform with translational potential; careful preclinical de-risking and early-phase clinical trials are required to determine clinical relevance.

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Publication Details

Journal
Experimental Hematology and Oncology
Published
2026-01-27
DOI
https://doi.org/10.1186/s40164-026-00744-w
Primary Topic
Immune cells in cancer
Type
article
Field-Weighted Citation Impact
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article

Hijacking the helpers: platelet and neutrophil trafficking in AML and therapeutic exploitation

Jalal Naghinezhad, Michael R. Hamblin, Farshad Heydari
Experimental Hematology and Oncology
Immune cells in cancer
article

Hijacking the helpers: platelet and neutrophil trafficking in AML and therapeutic exploitation

Jalal Naghinezhad, Michael R. Hamblin, Farshad Heydari
article en

Abstract

Acute myeloid leukemia (AML) remains one of the most aggressive and treatment-resistant hematologic malignancies, driven by clonal expansion of immature myeloid blasts in the bone marrow and peripheral blood. Current therapies-chemotherapy and targeted agents-are limited by poor marrow penetration, systemic toxicity, and rapid development of resistant clones, leaving long-term survival rates low. Clinicians face the persistent challenge of delivering effective therapy while minimizing harm. Platelets and neutrophils-beyond their classical roles in hemostasis and innate immunity-actively support leukemic niches, suppress anti-tumor immunity, and protect malignant cells from cytotoxic attack. These interactions highlight an untapped opportunity: harnessing endogenous cellular networks to deliver therapeutics with precision and potency. Conventional carriers, including liposomes and nanoparticles, fail to exploit these natural trafficking and immune-modulatory mechanisms, limiting marrow-specific targeting and therapeutic durability. We propose cellular hitchhiking using patient-derived platelets and neutrophils as a transformative, patient-tailored strategy. These carriers leverage intrinsic homing mechanisms, immune interface modulation, and prolonged circulation to deliver cytotoxic, immunomodulatory, or gene-based therapeutics directly to marrow and sanctuary sites. Ex vivo priming, biomaterial functionalization, and patient-specific engineering can enhance marrow-targeted drug concentration by several-fold, reduce systemic exposure, and minimize thrombo-inflammatory complications. By converting circulating blood cells into programmable delivery vectors, this approach offers a biologically rational platform with translational potential; however, immediate clinical relevance requires validation in controlled early-phase human studies. Preclinical evidence indicates that cellular hitchhiking can substantially increase bone-marrow drug delivery and reduce systemic exposure; whether these improvements will translate into higher remission rates or lower relapse in patients remains to be established in prospective clinical studies. Integrated into AML management, this strategy provides a biologically rational platform with translational potential; careful preclinical de-risking and early-phase clinical trials are required to determine clinical relevance.

Experimental Hematology and OncologyVol. 15(1)
University of Johannesburg (ZA), High Institute for Education and Research in Transfusion Medicine (IR)
Openalex Percentile: Top 77%
Immune cells in cancer
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