Ovarian development and disease: The known and the unexpected.
Fribourg, Switzerland. In Semin Cell Dev Biol, Sep 2015
The role and interactions of WNT4, RSPO1 and other factors, such as FOXL2 as well as the possible role of chromatin modifiers such as the polycomb protein CBX2 in ovarian development and function will be discussed.
Sexual Fate Reprogramming in the Steroid-Induced Bi-Directional Sex Change in the Protogynous Orange-Spotted Grouper, Epinephelus coioides.
Chi-lung, Taiwan. In Plos One, 2014
These male characteristics included increased plasma 11-ketotestosterone (11-KT), decreased estradiol (E2) levels, increased male-related gene (dmrt1, sox9, and cyp11b2) expression, and decreased female-related gene (figla, foxl2, and cyp19a1a) expression.
Adult granulosa cell tumours of the ovary.
Roma, Italy. In Curr Opin Oncol, 2014
RECENT FINDINGS: Novel biomarkers, including FOXL2, SMAD3 and GATA4, have been identified as potential diagnostic and therapeutic targets for this type of tumour.
Characterising novel pathways in testis determination using mouse genetics.
United Kingdom. In Sex Dev, 2013
Studies in 2 broad areas have been especially revealing: (i) identification of pathways required for the appropriate expression of Sry, and (ii) characterisation of the antagonistic interactions between the core testis- (SRY-SOX9-FGF9) and ovary- (RSPO1-WNT4-CTNNB1-FOXL2) determining gene regulatory networks.
FOXL2 mutations in granulosa cell tumors occurring in males.
Rochester, United States. In Arch Pathol Lab Med, 2012
The FOXL2 402C-->G (C134W) mutation is also present in adult-type granulosa cell tumors occurring in men, although in a smaller proportion when compared with women. FOXL2 can be a helpful in the diagnosis of granulosa cell tumors of the testis.
Mutation of FOXL2 in granulosa-cell tumors of the ovary.
Vancouver, Canada. In N Engl J Med, 2009
identified a single, recurrent somatic mutation (402C-->G) in FOXL2 that was present in almost all morphologically identified adult-type GCTs. Mutant FOXL2 is a potential driver in the pathogenesis of adult-type GCTs