Alone against the crowd: Individual differences in referees' ability to cope under pressure

This paper contributes to the recent debate about the role of referees in the home advantage phenomenon. Specifically, it aims to provide a convincing answer to the newly posed question of the existence of individual differences among referees in terms of the home advantage (Boyko, Boyko, & Boyko, 2007; Johnston, 2008). Using multilevel modelling on a large and representative dataset we find that (1) the home advantage effect differs significantly among referees, and (2) this relationship is moderated by the size of the crowd. These new results suggest that a part of the home advantage is due to the effect of the crowd on the referees, and that some referees are more prone to be influenced by the crowd than others. This provides strong evidence to indicate that referees are a significant contributing factor to the home advantage. The implications of these findings are discussed both in terms of the relevant social psychological research, and with respect to the selection, assessment, and training of referees.

FGFR2 mutations are rare across histologic subtypes of ovarian cancer

OBJECTIVE: Ovarian cancer is the leading cause of death from gynecologic malignancies in the Western world. Fibroblast growth factor receptor (FGFR) signaling has been implicated to play a role in ovarian tumorigenesis. Mutational activation of one member of this receptor family, FGFR2, is a frequent event in endometrioid endometrial cancer. Given the similarities in the histologic and molecular genetics of ovarian and endometrial cancers, we hypothesized that activating FGFR2 mutations may occur in a subset of endometrioid ovarian tumors, and possibly other histotypes. METHODS: Six FGFR2 exons were sequenced in 120 primary ovarian tumors representing the major histologic subtypes. RESULTS: FGFR2 mutation was detected at low frequency in endometrioid (1/46, 2.2%) and serous (1/41, 2.4%) ovarian cancer. No mutations were detected in clear cell, mucinous, or mixed histology tumors or in the ovarian cancer cell lines tested. Functional characterization of the FGFR2 mutations confirmed that the mutations detected in ovarian cancer result in receptor activation. CONCLUSIONS: Despite the low incidence of FGFR2 mutations in ovarian cancer, the two FGFR2 mutations identified in ovarian tumors (S252W, Y376C) overlap with the oncogenic mutations previously identified in endometrial tumors, suggesting activated FGFR2 may contribute to ovarian cancer pathogenesis in a small subset of ovarian tumors.