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Research groups

Khan Lab: Engineering Human Pre-Clinical Models

Abdullah Khan

BSc (Hons) MRes PhD

Wellcome Trust Career Development Fellow, RDM Principal Investigator, MRC WIMM Group Leader

I'm a bioengineer interested in the basic processes that drive blood and immune cell production, and how these processes change in ageing and disease.

Biography and Background

I am a Group Leader in the MRC Molecular Haematology Unit at the MRC Weatherall Institute of Molecular Medicine, and a Wellcome Career Development Fellow. I’m interested in how blood and immune cells are produced, and particularly in how the systems that drive that production change with ageing and disease. To explore these questions, I engineer human model systems—mini organs or organoids.

I completed my PhD at the Institute of Cardiovascular Sciences, University of Birmingham, where I established a method for generating CRISPR-edited megakaryocytes (platelet-producing cells) from human induced pluripotent stem cells (iPSCs). I also developed a CRISPR-based approach to express photo-switchable tags in iPSCs and their progeny, enabling single-molecule imaging.

After completing my PhD in 2019, I was awarded a Sir Henry Wellcome Fellowship to develop a bone marrow organoid model for studying myeloid cancers. That award began at the University of Birmingham in 2020. In 2022, I undertook a six-month secondment at Boston Children’s Hospital (Harvard Medical School) in the Machlus/Italiano lab. I then joined Beth Psaila’s group at the MRC WIMM in 2023 and have since established my own research group, supported by a Wellcome Trust Career Development Award.

My recent research has focused on developing and applying vascularised human organoid models, with a particular emphasis on the bone marrow—the system responsible for blood and immune cell generation throughout adult life. I developed the first human bone marrow organoid model that captured the myeloid niche and, together with the Oxford team, have since advanced this system to better reflect the complexity of the native environment. We use these models to dissect healthy, aged, and diseased biology, and to develop human pre-clinical platforms that we believe will accelerate both basic and translational research.

More recently, we’ve begun coupling different organoid systems to model, for the first time, how injury to other tissues (e.g. cardiac tissue) drives immune cell recruitment, and how that immune response influences tissue injury and repair.

Outside of research, I’m overly fond of reading, music, eating, and dangling from precarious rock faces by my fingertips—questioning all my life choices.

Key publications

Human Multi-Organoid Platform to Model Immune Dynamics in Cardiac Injury and Disease.

Reyat JS. et al, (2025), Circ Res, 137, 1133 - 1136

proinflammatory stem cell niche drives myelofibrosis through a targetable galectin-1 axis.

Li R. et al, (2024), Sci Transl Med, 16

Human Bone Marrow Organoids for Disease Modeling, Discovery, and Validation of Therapeutic Targets in Hematologic Malignancies.

Khan AO. et al, (2023), Cancer Discov, 13, 364 - 385

Modelling the pathology and treatment of cardiac fibrosis in vascularised atrial and ventricular cardiac microtissues.

Reyat JS. et al, (2023), Front Cardiovasc Med, 10

Recent publications

Supp Table 3 from Human Bone Marrow Organoids for Disease Modeling, Discovery, and Validation of Therapeutic Targets in Hematologic Malignancies

Khan AO. et al, (2025)

Supp Table 7 from Human Bone Marrow Organoids for Disease Modeling, Discovery, and Validation of Therapeutic Targets in Hematologic Malignancies

Khan AO. et al, (2025)

Figure 6 from Human Bone Marrow Organoids for Disease Modeling, Discovery, and Validation of Therapeutic Targets in Hematologic Malignancies

Khan AO. et al, (2025)

Figure 4 from Human Bone Marrow Organoids for Disease Modeling, Discovery, and Validation of Therapeutic Targets in Hematologic Malignancies

Khan AO. et al, (2025)

Figure 7 from Human Bone Marrow Organoids for Disease Modeling, Discovery, and Validation of Therapeutic Targets in Hematologic Malignancies

Khan AO. et al, (2025)

Figure 3 from Human Bone Marrow Organoids for Disease Modeling, Discovery, and Validation of Therapeutic Targets in Hematologic Malignancies

Khan AO. et al, (2025)

Figure 1 from Human Bone Marrow Organoids for Disease Modeling, Discovery, and Validation of Therapeutic Targets in Hematologic Malignancies

Khan AO. et al, (2025)

Supp Table 4 from Human Bone Marrow Organoids for Disease Modeling, Discovery, and Validation of Therapeutic Targets in Hematologic Malignancies

Khan AO. et al, (2025)

Supplementary Information from Human Bone Marrow Organoids for Disease Modeling, Discovery, and Validation of Therapeutic Targets in Hematologic Malignancies

Khan AO. et al, (2025)

Supp Table 1 from Human Bone Marrow Organoids for Disease Modeling, Discovery, and Validation of Therapeutic Targets in Hematologic Malignancies

Khan AO. et al, (2025)

Figure 2 from Human Bone Marrow Organoids for Disease Modeling, Discovery, and Validation of Therapeutic Targets in Hematologic Malignancies

Khan AO. et al, (2025)

Figure 5 from Human Bone Marrow Organoids for Disease Modeling, Discovery, and Validation of Therapeutic Targets in Hematologic Malignancies

Khan AO. et al, (2025)

Supp Table 6 from Human Bone Marrow Organoids for Disease Modeling, Discovery, and Validation of Therapeutic Targets in Hematologic Malignancies

Khan AO. et al, (2025)

Data from Human Bone Marrow Organoids for Disease Modeling, Discovery, and Validation of Therapeutic Targets in Hematologic Malignancies

Khan AO. et al, (2025)

Supp Table 5 from Human Bone Marrow Organoids for Disease Modeling, Discovery, and Validation of Therapeutic Targets in Hematologic Malignancies

Khan AO. et al, (2025)

Supp Table 2 from Human Bone Marrow Organoids for Disease Modeling, Discovery, and Validation of Therapeutic Targets in Hematologic Malignancies

Khan AO. et al, (2025)

comBO: A combined human bone and lympho-myeloid bone marrow organoid for pre-clinical modelling of haematopoietic disorders

Shen Y. et al, (2025)

Development of a First-in-Class CAR-T Therapy Against Calreticulin-Mutant Neoplasms and Evaluation in the Relevant Human Tissue Environment

Rampotas A. et al, (2024), BLOOD, 144, 871 - 872

Implementing human bone marrow organoids to interrogate microenvironmental influences on the efficacy of blood cancer immunotherapies

Wong ZC. et al, (2024), CANCER RESEARCH, 84

Blood Coagulation and Beyond: Position Paper from the Fourth Maastricht Consensus Conference on Thrombosis.

Akbulut AC. et al, (2023), Thromb Haemost, 123, 808 - 839

Efficient megakaryopoiesis and platelet production require phospholipid remodeling and PUFA uptake through CD36.

Barrachina MN. et al, (2023), Nat Cardiovasc Res, 2, 746 - 763

Supp Table 5 from Human Bone Marrow Organoids for Disease Modeling, Discovery, and Validation of Therapeutic Targets in Hematologic Malignancies

Khan AO. et al, (2023)

Supp Table 2 from Human Bone Marrow Organoids for Disease Modeling, Discovery, and Validation of Therapeutic Targets in Hematologic Malignancies

Khan AO. et al, (2023)

Supp Table 7 from Human Bone Marrow Organoids for Disease Modeling, Discovery, and Validation of Therapeutic Targets in Hematologic Malignancies

Khan AO. et al, (2023)

Data from Human Bone Marrow Organoids for Disease Modeling, Discovery, and Validation of Therapeutic Targets in Hematologic Malignancies

Khan AO. et al, (2023)

Supplementary Information from Human Bone Marrow Organoids for Disease Modeling, Discovery, and Validation of Therapeutic Targets in Hematologic Malignancies

Khan AO. et al, (2023)

Supp Table 3 from Human Bone Marrow Organoids for Disease Modeling, Discovery, and Validation of Therapeutic Targets in Hematologic Malignancies

Khan AO. et al, (2023)

Supplementary Information from Human Bone Marrow Organoids for Disease Modeling, Discovery, and Validation of Therapeutic Targets in Hematologic Malignancies

Khan AO. et al, (2023)

Supp Table 4 from Human Bone Marrow Organoids for Disease Modeling, Discovery, and Validation of Therapeutic Targets in Hematologic Malignancies

Khan AO. et al, (2023)

Supp Table 3 from Human Bone Marrow Organoids for Disease Modeling, Discovery, and Validation of Therapeutic Targets in Hematologic Malignancies

Khan AO. et al, (2023)

Supp Table 1 from Human Bone Marrow Organoids for Disease Modeling, Discovery, and Validation of Therapeutic Targets in Hematologic Malignancies

Khan AO. et al, (2023)

Supp Table 7 from Human Bone Marrow Organoids for Disease Modeling, Discovery, and Validation of Therapeutic Targets in Hematologic Malignancies

Khan AO. et al, (2023)

Supp Table 5 from Human Bone Marrow Organoids for Disease Modeling, Discovery, and Validation of Therapeutic Targets in Hematologic Malignancies

Khan AO. et al, (2023)

Supp Table 3 from Human Bone Marrow Organoids for Disease Modeling, Discovery, and Validation of Therapeutic Targets in Hematologic Malignancies

Khan AO. et al, (2023)

Supp Table 4 from Human Bone Marrow Organoids for Disease Modeling, Discovery, and Validation of Therapeutic Targets in Hematologic Malignancies

Khan AO. et al, (2023)

Supp Table 3 from Human Bone Marrow Organoids for Disease Modeling, Discovery, and Validation of Therapeutic Targets in Hematologic Malignancies

Khan AO. et al, (2023)

Supplementary Information from Human Bone Marrow Organoids for Disease Modeling, Discovery, and Validation of Therapeutic Targets in Hematologic Malignancies

Khan AO. et al, (2023)

Supp Table 7 from Human Bone Marrow Organoids for Disease Modeling, Discovery, and Validation of Therapeutic Targets in Hematologic Malignancies

Khan AO. et al, (2023)

Efficient megakaryopoiesis and platelet production require phospholipid remodeling and PUFA uptake through CD36.

Barrachina MN. et al, (2023), bioRxiv

Human Bone Marrow Organoids for Disease Modeling, Discovery, and Validation of Therapeutic Targets in Hematologic Malignancies.

Khan AO. et al, (2023), Cancer Discov, 13, 364 - 385

Preferential uptake of SARS-CoV-2 by pericytes potentiates vascular damage and permeability in an organoid model of the microvasculature.

Khan AO. et al, (2022), Cardiovasc Res, 118, 3085 - 3096

Rare missense variants in Tropomyosin-4 (TPM4) are associated with platelet dysfunction, cytoskeletal defects, and excessive bleeding.

Stapley RJ. et al, (2022), J Thromb Haemost, 20, 478 - 485

Post-translational polymodification of β1-tubulin regulates motor protein localisation in platelet production and function.

Khan AO. et al, (2022), Haematologica, 107, 243 - 259

Case of ST-Elevation Myocardial Infarction With Right Bundle Branch Block, an Ominous Sign of Critical Coronary Occlusion.

Basit H. et al, (2022), Cureus, 14

Human bone marrow organoids for disease modelling, discovery and validation of therapeutic targets in hematological malignancies

Khan A. et al, (2022)

Cross-Talk between Hematopoietic Cells and Fibroblast Subsets Drives Inflammation and Remodelling of the Bone Marrow Microenvironment in Myeloproliferative Neoplasms

Li R. et al, (2022), BLOOD, 140, 1091 - 1092

Human Bone Marrow Organoids Enable the Study of Hematopoietic Cell-Stromal Interactions and Support the Survival of Malignant Cells from Patients

Khan A. et al, (2022), BLOOD, 140, 1679 - 1681

Neutrophil extracellular traps and inflammasomes cooperatively promote venous thrombosis in mice.

Campos J. et al, (2021), Blood Adv, 5, 2319 - 2324

Heterozygous mutation SLFN14 K208N in mice mediates species-specific differences in platelet and erythroid lineage commitment.

Stapley RJ. et al, (2021), Blood Adv, 5, 377 - 390

n adaptable analysis workflow for characterization of platelet spreading and morphology.

Pike JA. et al, (2021), Platelets, 32, 54 - 58

Novel gene variants in patients with platelet-based bleeding using combined exome sequencing and RNAseq murine expression data.

Khan AO. et al, (2021), J Thromb Haemost, 19, 262 - 268

Surface Chemistry-Dependent Evolution of the Nanomaterial Corona on TiO2 Nanomaterials Following Uptake and Sub-Cellular Localization.

Khan AO. et al, (2020), Nanomaterials (Basel), 10

n adaptable analysis workflow for characterization of platelet spreading and morphology

Pike J. et al, (2020)

Optimised insert design for improved single-molecule imaging and quantification through CRISPR-Cas9 mediated knock-in.

Khan AO. et al, (2019), Sci Rep, 9

Post-translational polymodification of β1 tubulin regulates motor protein localisation in platelet production and function

Khan A. et al, (2019)

TREM-like transcript 1: a more sensitive marker of platelet activation than P-selectin in humans and mice.

Smith CW. et al, (2018), Blood Adv, 2, 2072 - 2078

Role of the novel endoribonuclease SLFN14 and its disease-causing mutations in ribosomal degradation.

Fletcher SJ. et al, (2018), RNA, 24, 939 - 949

Microscopy-based high-throughput assays enable multi-parametric analysis to assess adverse effects of nanomaterials in various cell lines.

Hansjosten I. et al, (2018), Arch Toxicol, 92, 633 - 649

Multimerin-2 is a ligand for group 14 family C-type lectins CLEC14A, CD93 and CD248 spanning the endothelial pericyte interface.

Khan KA. et al, (2017), Oncogene, 36, 6097 - 6108

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Contact information

Research groups

Abdullah Khan

Biography and Background

Key publications

Recent publications