HiJAKing the hematopoietic system: a low-frequency JAK2V617F clone drives myeloproliferative neoplasm pathology

D Dennis M. Bonal (1Brown University Pathobiology Graduate Program, Brown University, Providence, RI) A Alissa Oakes (2Department of Medicine, Division of Hematology-Oncology, Warren Alpert Medical School of Brown University and Rhode Island Hospital, Providence, RI) A Anna Chorzalska (2Department of Medicine, Division of Hematology-Oncology, Warren Alpert Medical School of Brown University and Rhode Island Hospital, Providence, RI) M Makayla Pardo (1Brown University Pathobiology Graduate Program, Brown University, Providence, RI) M Max Petersen (2Department of Medicine, Division of Hematology-Oncology, Warren Alpert Medical School of Brown University and Rhode Island Hospital, Providence, RI) M Michael Y. Clarke (2Department of Medicine, Division of Hematology-Oncology, Warren Alpert Medical School of Brown University and Rhode Island Hospital, Providence, RI) S Seo-Ho Lee (2Department of Medicine, Division of Hematology-Oncology, Warren Alpert Medical School of Brown University and Rhode Island Hospital, Providence, RI) A Adam J. Olszewski (10Department of Medicine, Brown University, Providence, RI) D Diana O. Treaba (1Brown University Pathobiology Graduate Program, Brown University, Providence, RI) J John L. Reagan (2Department of Medicine, Division of Hematology-Oncology, Warren Alpert Medical School of Brown University and Rhode Island Hospital, Providence, RI) M Mark Dooner (2Department of Medicine, Division of Hematology-Oncology, Warren Alpert Medical School of Brown University and Rhode Island Hospital, Providence, RI) J John Morgan (2Department of Medicine, Division of Hematology-Oncology, Warren Alpert Medical School of Brown University and Rhode Island Hospital, Providence, RI) P Paul Bertone (2Department of Medicine, Division of Hematology-Oncology, Warren Alpert Medical School of Brown University and Rhode Island Hospital, Providence, RI) T Ting C. Zhao (7Department of Surgery, Warren Alpert Medical School of Brown University, Providence, RI) W Wentian Yang (5Legorreta Cancer Center, Brown University, Providence, RI) C Corey E. Ventetuolo (9Department of Medicine, Division of Pulmonary, Critical Care, and Sleep Medicine, Warren Alpert Medical School of Brown University, Providence, RI) G Gabriela S. Hobbs (10Department of Hematology-Oncology, Massachusetts General Hospital Cancer Center and Harvard Medical School, Boston, MA) J Joslyn Mills (11Department of Biological Sciences, Bartlett College of Science and Mathematics, Bridgewater State University, Bridgewater, MA) P Patrycja M. Dubielecka (1Brown University Pathobiology Graduate Program, Brown University, Providence, RI)

Abstract

Abstract JAK2V617F is one of the most common mutations in clonal hematopoiesis of indeterminate potential (CHIP) and a major driver of myeloproliferative neoplasms (MPNs). To determine the impact of a low-frequency JAK2V617F clone on both the hematopoietic system and the bone marrow (BM) stroma, we developed a traceable murine MPN model, in which whole BM transplantation (BMT) was performed using CD45.2 5.0 × 106 JAK2V617F donor cells transplanted into unconditioned CD45.1 recipient mice. BMT recipients developed a polycythemia vera–like phenotype (elevated hematocrit and leukocytosis) with a 2.7% average donor cell chimerism in peripheral blood. Eight months after BMT, RNA sequencing (RNA-seq) analysis of BM cells sorted according to CD45.1/CD45.2 expression showed significant upregulation of early erythroblast- and myeloid cell–specific transcripts, and downregulation of lymphoid transcripts in donor-derived cells compared to controls. Surprisingly, recipient-derived cells also showed upregulation of myeloid- and erythroblast-related transcripts, indicating a skewing of the non–JAK2V617F-carrying recipient hematopoietic system toward an MPN-like phenotype. In addition, RNA-seq analysis of the BM stroma from JAK2V617F BMT recipients indicated significant loss of osteomesenchymal transcripts. Consistently, micro–computed tomography imaging indicated loss of trabecular bone. In sum, our results indicate that low-frequency MPN-driving cells in unconditioned recipients not only impact hematopoiesis-supporting stroma but also profoundly influence unmutated cells, uniquely altering their transcriptomic and phenotypic profiles. These observations are challenging our current understanding of the etiology and therapeutic approaches to MPNs and other CHIP-associated diseases.

Article Details

Journal Blood
Volume / Issue Vol. 146, Issue 20
Published November 13, 2025
Pages 2428-2442
ISSN 0006-4971
Publisher Elsevier BV

Journal Info

Blood

Elsevier BV

ISSN: 0006-4971 Health Sciences

Authors (19)

D

Dennis M. Bonal

1Brown University Pathobiology Graduate Program, Brown University, Providence, RI

A

Alissa Oakes

2Department of Medicine, Division of Hematology-Oncology, Warren Alpert Medical School of Brown University and Rhode Island Hospital, Providence, RI

A

Anna Chorzalska

2Department of Medicine, Division of Hematology-Oncology, Warren Alpert Medical School of Brown University and Rhode Island Hospital, Providence, RI

M

Makayla Pardo

1Brown University Pathobiology Graduate Program, Brown University, Providence, RI

M

Max Petersen

2Department of Medicine, Division of Hematology-Oncology, Warren Alpert Medical School of Brown University and Rhode Island Hospital, Providence, RI

M

Michael Y. Clarke

2Department of Medicine, Division of Hematology-Oncology, Warren Alpert Medical School of Brown University and Rhode Island Hospital, Providence, RI

S

Seo-Ho Lee

2Department of Medicine, Division of Hematology-Oncology, Warren Alpert Medical School of Brown University and Rhode Island Hospital, Providence, RI

A

Adam J. Olszewski

10Department of Medicine, Brown University, Providence, RI

D

Diana O. Treaba

1Brown University Pathobiology Graduate Program, Brown University, Providence, RI

J

John L. Reagan

2Department of Medicine, Division of Hematology-Oncology, Warren Alpert Medical School of Brown University and Rhode Island Hospital, Providence, RI

M

Mark Dooner

2Department of Medicine, Division of Hematology-Oncology, Warren Alpert Medical School of Brown University and Rhode Island Hospital, Providence, RI

J

John Morgan

2Department of Medicine, Division of Hematology-Oncology, Warren Alpert Medical School of Brown University and Rhode Island Hospital, Providence, RI

P

Paul Bertone

2Department of Medicine, Division of Hematology-Oncology, Warren Alpert Medical School of Brown University and Rhode Island Hospital, Providence, RI

T

Ting C. Zhao

7Department of Surgery, Warren Alpert Medical School of Brown University, Providence, RI

W

Wentian Yang

5Legorreta Cancer Center, Brown University, Providence, RI

C

Corey E. Ventetuolo

9Department of Medicine, Division of Pulmonary, Critical Care, and Sleep Medicine, Warren Alpert Medical School of Brown University, Providence, RI

G

Gabriela S. Hobbs

10Department of Hematology-Oncology, Massachusetts General Hospital Cancer Center and Harvard Medical School, Boston, MA

J

Joslyn Mills

11Department of Biological Sciences, Bartlett College of Science and Mathematics, Bridgewater State University, Bridgewater, MA

P

Patrycja M. Dubielecka

1Brown University Pathobiology Graduate Program, Brown University, Providence, RI