Loss of CD7, independent of galectin-3 expression, implies a worse prognosis in adult T-cell leukaemia/lymphoma

Authors

  • Ting-Yun Liu,

    1. Departments of Pathology & Internal Medicine, National Taiwan University Hospital, National Taiwan University College of Medicine, Taipei, Taiwan
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  • Chien-Yuan Chen,

    1. Departments of Pathology & Internal Medicine, National Taiwan University Hospital, National Taiwan University College of Medicine, Taipei, Taiwan
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  • Hwei-Fang Tien,

    1. Departments of Pathology & Internal Medicine, National Taiwan University Hospital, National Taiwan University College of Medicine, Taipei, Taiwan
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  • Chung-Wu Lin

    1. Departments of Pathology & Internal Medicine, National Taiwan University Hospital, National Taiwan University College of Medicine, Taipei, Taiwan
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Chung-Wu Lin, Department of Pathology, National Taiwan University College of Medicine, 1-1 Jen-Ai Road, Taipei, Taiwan 10016. e-mail: chungwulin@yahoo.com

Abstract

Aims:  Loss of CD7 is characteristic of adult T-cell lymphoma/leukaemia (ATLL). Galectin-3 (Gal-3) is strongly induced in cultured human T lymphotropic virus-1-infected T lymphocytes, and may cause apoptosis through interaction with CD7. The aim was to investigate the clinical relevance of the Gal-3–CD7 pathway in ATLL.

Methods and results:  Immunohistochemistry for Gal-3 and CD7 was performed on 22 cases of ATLL in the leukaemic phase. We found that the lymphoma cells were not necessarily Gal-3+, but Gal-3+ stromal cells could always be found. Independent of the status of Gal-3, there was an association of loss of CD7 with a worse prognosis.

Conclusions:  These data suggest that, by down-regulating CD7, ATLL cells could have escaped Gal-3-induced apoptosis to run a more aggressive clinical course.

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