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Cancer is a major public health problem worldwide. Over two-thirds of cancer-related deaths could most probably be prevented through lifestyle modification, particularly through dietary means. Proanthocyanidins (PAs), the most abundant polyphenolic substances after lignin in the plant kingdom, have been widely investigated for their chemopreventive potential. The PAs literature has, however, been mostly concerned with positive cardiovascular activities, and recent reviews about cancer chemoprevention are scarce. The present review highlights a series of in vitro and in vivo studies indicating ( 1 ) that PAs can act as anticarcinogenic agents through their antioxidant, apoptosis-inducing, immuno-modulating, and/or enzyme modulating properties, effects on epigenetics; and ( 2 ) that PAs could be particularly safe dietary compounds. These convergent data encourage further research to better understand the many aspects of cancer chemoprevention by PAs.

The role of the CD44 cytoplasmic domain in cells displaying constitutive or inducible hyalu ronan (HA) binding mediated by wild-type CD44 was investigated using mutant CD44 constructs with the cytoplasmic domain truncated or replaced by foreign sequences. In cell lines in which wild-type CD44 bound HA constitutively, chimeric constructs consisting of the CD44 external domain and the transmembrane plus cytoplasmic domains of beta5 integrin bound as well as wild-type CD44, arguing that the specific sequence of the cytoplasmic and transmembrane domains was not critical for HA binding by the external domain. The cytoplasmic domain sequence did not contribute to the 'inducible' phenotype in cell lines which did not bind HA constitutively, but which could be induced to bind by CD44-specific mAb. Tailless CD44 was inducible in these cells, as was chimeric CD44 with the integrin beta5 cytoplasmic domain. Dimer- or oligomerization of CD44 by addition of AP1510 to cells containing CD44 / FKBP chimeric constructs caused a modest enhancement of HA binding in cells that bound constitutively, but did not alter the inducible phenotype. This result suggests that clustering of CD44 from inside the cell is not a sufficient 'inside-out' signal to activate HA binding in inducible cells.

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