Self reported skin morbidity and ethnicity: a population-based study in a Western community

<p>Abstract</p> <p>Background</p> <p>Recent studies have shown ethnic differences concerning cardio-vascular disease, diabetes and mental health. Little is known about ethnic differences in skin morbidity. The purpose of this study was to describe possible ethnic differences in self-reported skin morbidity in a Western urban community.</p> <p>Methods</p> <p>The design was cross sectional. 40 888 adults in Oslo, Norway, received a postal questionnaire providing information on socio-demographic factors and self-reported health, including items on skin complaints.</p> <p>Results</p> <p>18770 individuals answered the questionnaire. In the sample 84% were from Norway. The largest immigrant group was from Western countries (5%) and the Indian Subcontinent (3%). Itch was the most prevalent reported skin symptom (7%), and was significantly more reported by men from East Asia (18%) and Middle East/North Africa (13%). The same observations were seen for reported dry and sore skin. Hair loss was a dominating complaint for men from the Indian Subcontinent and the Middle East/North Africa (23% and 25%) and for women from the same ethnic groups. Women from Sub-Saharan Africa reported significantly more pimples than in the other groups (17%).</p> <p>Conclusion</p> <p>The study showed that there were significant differences in self-reported skin complaints among ethnic groups. Issues concerning the cultural value of some skin symptoms should be examined further.</p

Overexpression of CD44 accompanies acquired tamoxifen resistance in MCF7 cells and augments their sensitivity to the stromal factors, heregulin and hyaluronan

Background: Acquired resistance to endocrine therapy in breast cancer is a significant problem with relapse being associated with local and/or regional recurrence and frequent distant metastases. Breast cancer cell models reveal that endocrine resistance is accompanied by a gain in aggressive behaviour driven in part through altered growth factor receptor signalling, particularly involving erbB family receptors. Recently we identified that CD44, a transmembrane cell adhesion receptor known to interact with growth factor receptors, is upregulated in tamoxifen-resistant (TamR) MCF7 breast cancer cells. The purpose of this study was to explore the consequences of CD44 upregulation in an MCF7 cell model of acquired tamoxifen resistance, specifically with respect to the hypothesis that CD44 may influence erbB activity to promote an adverse phenotype. Methods: CD44 expression in MCF7 and TamR cells was assessed by RT-PCR, Western blotting and immunocytochemistry. Immunofluorescence and immunoprecipitation studies revealed CD44-erbB associations. TamR cells (± siRNA-mediated CD44 suppression) or MCF7 cells (± transfection with the CD44 gene) were treated with the CD44 ligand, hyaluronon (HA), or heregulin and their in vitro growth (MTT), migration (Boyden chamber and wound healing) and invasion (Matrigel transwell migration) determined. erbB signalling was assessed using Western blotting. The effect of HA on erbB family dimerisation in TamR cells was determined by immunoprecipitation in the presence or absence of CD44 siRNA. Results: TamR cells overexpressed CD44 where it was seen to associate with erbB2 at the cell surface. siRNA-mediated suppression of CD44 in TamR cells significantly attenuated their response to heregulin, inhibiting heregulin-induced cell migration and invasion. Furthermore, TamR cells exhibited enhanced sensitivity to HA, with HA treatment resulting in modulation of erbB dimerisation, ligand-independent activation of erbB2 and EGFR and induction of cell migration. Overexpression of CD44 in MCF7 cells, which lack endogenous CD44, generated an HA-sensitive phenotype, with HA-stimulation promoting erbB/EGFR activation and migration. Conclusions: These data suggest an important role for CD44 in the context of tamoxifen-resistance where it may augment cellular response to erbB ligands and HA, factors that are reported to be present within the tumour microenvironment in vivo. Thus CD44 may present an important determinant of breast cancer progression in the setting of endocrine resistance

CD44: a multitude of isoforms with diverse functions.

The CD44 transmembrane glycoprotein of 90 kD has been known for more than ten years under such diverse designations as lymphocyte homing receptor gp90Hermes, phagocytic glycoprotein Pgp-1, extracellular matrix receptor III (ECMRIII) and hyaluronate receptor H-CAM (see reviews by Haynes et al., 1989 and 1991). Studies with monoclonal antibodies revealed similarity, and most likely identity among these molecules (Omary et al., 1988; Gallatin et al., 1989; Picker et al., 1989; Aruffo et al., 1990; Miyake et al., 1990; Culty et al., 1990). When the human, baboon and murine cDNA sequences were established identity was confirmed. However, the cDNA sequence codes only for about 360 amino acids, revealing a just 37 kD encompassing protein core (Stamenkovic et al., 1989; Goldstein et al., 1989; Idzerda et al., 1989; Nottenburg et al., 1989; Zhou et al., 1989; Wolffe et al., 1990). This protein core is highly glycosylated by N- and O-linked sugars to yield a 85 to 90 kD form and is sometimes additionally linked to chondroitin sulfate side chains to produce a 180 - 200 kD form (Jalkanen et al., 1988; Stamenkovic et al., 1989). Concomitant with the diverse names for CD44, the description of functions was as diverse: CD44 molecules were described to participate in cell-cell and cell-matrix interactions such as lymphocyte recirculation and prothymocyte homing, hematopoiesis, lymphocyte and monocyte activation, cell migration and metastasis (reviewed in Haynes et al., 1989 and 1991). It seemed rather unlikely that all these functions were associated with one and the same molecule, though differences in the posttranslational modification may as well modulate the adhesive properties (Brown et al., 1991). Thus, the description of new extracellular regions led to the assumption that the multitude of functions may be attributed to the various isoforms (Günthert et al., 1991; Brown et al., 1991; Hofmann et al., 1991; He et al., 1992; Matsumura and Tarin, 1992). The aim of this review article is to describe the ever growing family of isoforms and their organization and to discuss possible functional implications