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Loss of CD7, independent of galectin‐3 expression, implies a worse prognosis in adult T‐cell leukaemia/lymphoma
Author(s) -
Liu TingYun,
Chen ChienYuan,
Tien HweiFang,
Lin ChungWu
Publication year - 2009
Publication title -
histopathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.626
H-Index - 124
eISSN - 1365-2559
pISSN - 0309-0167
DOI - 10.1111/j.1365-2559.2008.03199.x
Subject(s) - lymphoma , expression (computer science) , medicine , oncology , cancer research , immunohistochemistry , pathology , computer science , programming language
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.