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Xanthohumol kills B‐chronic lymphocytic leukemia cells by an apoptotic mechanism
Author(s) -
Lust Sofie,
Vanhoecke Barbara,
Janssens Ann,
Philippe Jan,
Bracke Marc,
Offner Fritz
Publication year - 2005
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.200500045
Subject(s) - chronic lymphocytic leukemia , cancer research , apoptosis , annexin , biology , leukemia , in vitro , cd20 , immunology , microbiology and biotechnology , antibody , genetics
B‐chronic lymphocytic leukemia (B‐CLL) is an indolent lymphoid malignancy with variable prognosis. Adverse prognostic factors comprise treatment resistance, cytogenetics (11q‐ and 17p‐), the presence of unmutated Ig genes, and the more comprehensive activation marker Zap70. In contrast to diminished sensitivity to chemotherapy, Zap70+ B‐CLL cells retain their responsiveness to manipulation of signal transduction and monoclonals. Xanthohumol (XA) has recently been documented to have an impact on breast cancer cell growth and invasiveness in vitro . Based on these observations, lymphocytes from patients with B‐CLL were cultured in the presence of XA in vitro . XA induced a dose‐dependent killing of B‐CLL cells at an LD 50 (24 h) of 24.4 ± 6.6 μM, independent of known adverse prognostic factors including functional loss of p53. Cell death was associated with poly (ADP)‐ribose polymerase cleavage and annexin V positivity, suggestive of an apoptotic mechanism. Surprisingly, p70 S6K phosphorylation was stimulated upon XA treatment. In conclusion, XA has an antitumor activity on B‐CLL cells in vitro . The molecular mechanisms behind this pro‐apoptotic effect deserve further investigation.