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Peer-reviewedCC BYEJHaem

Nodal T Follicular Helper Cell Lymphoma With Epstein–Barr Virus‐Positive Neoplastic T Cells Derived From Clonal Hematopoiesis

  • Daichi Kishi1
  • Nobuhiro Hiramoto1
  • Daisuke Yamashita2
  • Hayato Maruoka3
  • Yumi Shiroishi3
  • Masashi Nishikubo1
  • Yoshimitsu Shimomura1
  • Ryusuke Yamamoto1
  • Yuya Nagai1
  • Yuka Torii4
  • Hiroshi Kimura5
  • Yasuhito Nannya6,7
2 more authors
  • Seishi Ogawa6,8
  • Tadakazu Kondo1
8 affiliations
  1. 1Department of Hematology Kobe City Medical Center General Hospital Kobe Japan.
  2. 2Department of Pathology Kobe City Medical Center General Hospital Kobe Japan.
  3. 3Department of Clinical Laboratory Kobe City Medical Center General Hospital Kobe Japan.
  4. 4Department of Pediatrics Nagoya University Graduate School of Medicine Nagoya Japan.
  5. 5Department of Virology Nagoya University Graduate School of Medicine Nagoya Japan.
  6. 6Department of Pathology and Tumor Biology Kyoto University Kyoto Japan.
  7. 7Division of Hematopoietic Disease Control Institute of Medical Science The University of Tokyo Tokyo Japan.
  8. 8Institute For the Advanced Study of Human Biology (WPI-ASHBi) Kyoto University Kyoto Japan.
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Abstract

Introduction

Nodal T follicular helper cell lymphoma (nTFHL) with Epstein-Barr virus (EBV)-positive neoplastic T cells is rare.Methods

We report a woman with nTFHL and analyzed EBV-infected cells using an immunobead-based method and assessed somatic mutations in lymphoma and lymphoma-uninvolved bone marrow by targeted sequencing.Results

EBV DNA was enriched in the CD4-positive fraction containing neoplastic T cells. Shared TET2 mutation was identified in both lymphoma and bone marrow, whereas additional TET2 and RHOA G17V mutations were restricted to the lymphoma.Conclusion

These findings support a stepwise model of EBV-positive nTFHL arising from TET2-mutated clonal hematopoiesis with subsequent acquisition of a RHOA mutation.Trial registration

The authors have confirmed clinical trial registration is not needed for this submission.

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Cite

BibTeXRIS
BibTeX
@article{kishi2026nodal,
  title = {{Nodal T Follicular Helper Cell Lymphoma With Epstein–Barr Virus‐Positive Neoplastic T Cells Derived From Clonal Hematopoiesis}},
  author = {Daichi Kishi and Nobuhiro Hiramoto and Daisuke Yamashita and Hayato Maruoka and Yumi Shiroishi and Masashi Nishikubo and Yoshimitsu Shimomura and Ryusuke Yamamoto and Yuya Nagai and Yuka Torii and Hiroshi Kimura and Yasuhito Nannya and Seishi Ogawa and Tadakazu Kondo},
  journal = {EJHaem},
  year = {2026},
  month = oct,
  doi = {10.1002/jha2.70449},
  url = {https://europepmc.org/article/PMC/PMC13717066},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Nodal T Follicular Helper Cell Lymphoma With Epstein–Barr Virus‐Positive Neoplastic T Cells Derived From Clonal Hematopoiesis
AU  - Daichi Kishi
AU  - Nobuhiro Hiramoto
AU  - Daisuke Yamashita
AU  - Hayato Maruoka
AU  - Yumi Shiroishi
AU  - Masashi Nishikubo
AU  - Yoshimitsu Shimomura
AU  - Ryusuke Yamamoto
AU  - Yuya Nagai
AU  - Yuka Torii
AU  - Hiroshi Kimura
AU  - Yasuhito Nannya
AU  - Seishi Ogawa
AU  - Tadakazu Kondo
PY  - 2026
DA  - 2026/10/28
JO  - EJHaem
DO  - 10.1002/jha2.70449
UR  - https://europepmc.org/article/PMC/PMC13717066
AB  - Introduction  Nodal T follicular helper cell lymphoma (nTFHL) with Epstein-Barr virus (EBV)-positive neoplastic T cells is rare.Methods  We report a woman with nTFHL and analyzed EBV-infected cells using an immunobead-based method and assessed somatic mutations in lymphoma and lymphoma-uninvolved bone marrow by targeted sequencing.Results  EBV DNA was enriched in the CD4-positive fraction containing neoplastic T cells. Shared TET2 mutation was identified in both lymphoma and bone marrow, whereas additional TET2 and RHOA G17V mutations were restricted to the lymphoma.Conclusion  These findings support a stepwise model of EBV-positive nTFHL arising from TET2-mutated clonal hematopoiesis with subsequent acquisition of a RHOA mutation.Trial registration  The authors have confirmed clinical trial registration is not needed for this submission.
SN  - 2688-6146
ER  -