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We present the case of a 91 years old patient diagnosed through biopsy with temporal arteritis who, in addition, had scalp necrosis. We briefly review the literature for published cases. [ABSTRACT FROM AUTHOR]

Abstract: Nucleoside transporters (NTs) are essential for the uptake of therapeutic nucleoside analogs, broadly used in cancer treatment. The mechanisms responsible for NT regulation are largely unknown. IL-4 is a pro-survival signal for chronic lymphocytic leukemia (CLL) cells and has been shown to confer resistance to nucleoside analogs. The aim of this study was to investigate whether IL-4 is able to modulate the expression and function of the human equilibrative NT1 (hENT1) in primary cultures of CLL cells and, consequently, to affect cytotoxicity induced by therapeutic nucleosides analogs. We found that treatment with IL-4 (20ng/ml for 24h) increased mRNA hENT1 expression in CLL cells without affecting that of normal B cells. Given that the enhanced mRNA levels of hENT1 in CLL cells did not result in increased transport activity, we examined the possibility that hENT1 induced by IL-4 may require post-translational modifications to become active. We found that the acute stimulation of PKC in IL-4-treated CLL cells by short-term incubation with PMA significantly increased hENT1 transport activity and favoured fludarabine-induced apoptosis. By contrast, and in line with previous reports, IL-4 plus PMA protected CLL cells from a variety of cytotoxic agents. Our findings indicate that the combined treatment with IL-4 and PMA enhances hENT1 activity and specifically sensitizes CLL cells to undergo apoptosis induced by fludarabine. [Copyright &y& Elsevier]

Abstract: Two main isoforms of Fcγ receptor II (CD32) have been described in humans: activatory FcγRIIA and inhibitory FcγRIIB. We have previously reported that B cells from a subset of chronic lymphocytic leukemia (B-CLL) patients express not only FcγRIIB, as normal B lymphocytes, but also the myeloid FcγRIIA. The aim of this study was to evaluate the signaling capacity of both FcγRII isoforms in B-CLL cells. We found that FcγRIIA expressed by leukemic cells failed to induce Ca2+ mobilization or protein tyrosine phosphorylation, suggesting that the receptor is not functional. By contrast, FcγRIIB effectively diminished BCR-triggered ERK1 phosphorylation, which indicates that it is able to transduce inhibitory signals in B-CLL cells. Moreover, we found that FcγRIIB homoaggregation in either B-CLL or non-malignant tonsillar B cells did not result in apoptosis as was reported for murine B splenocytes. Together, these results show that FcγRIIB, but not FcγRIIA is biologically active in B-CLL cells and might influence leukemic cell physiology in vivo. [Copyright &y& Elsevier]