کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
6182784 1254032 2014 6 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
The role of FOXL2 in the pathogenesis of adult ovarian granulosa cell tumours
کلمات کلیدی
موضوعات مرتبط
علوم پزشکی و سلامت پزشکی و دندانپزشکی زنان، زایمان و بهداشت زنان
پیش نمایش صفحه اول مقاله
The role of FOXL2 in the pathogenesis of adult ovarian granulosa cell tumours
چکیده انگلیسی


- The 402C>G mutation in FOXL2 is critical for the development of adult granulosa cell tumours.
- We suggest that FOXL2 may behave as an oncogene or tumour suppressor gene depending on genetic context.

ObjectiveIt has been four years since the discovery of the FOXL2 402C>G mutation in adult ovarian granulosa cell tumours. Yet to date, there have been few studies which have investigated the precise role of the mutation in tumour pathogenesis. This review aims to summarise the research in this area, proposes a mechanism of action for the mutation, and explores the implications for clinical practice and future therapeutics.MethodsA literature search was performed with the keywords 'granulosa cell tumour' and 'FOXL2' on PubMed.ResultsAlthough the search returned 52 articles, of these only nine publications investigate the pathogenic effect of the mutant FOXL2 allele. Mutant FOXL2 maintains some of the transcriptional activity of the wildtype allele, but there is a subtle alteration of the expression in a unique suite of cancer-related genes. The mutation appears to deregulate the anti-proliferative transforming growth factor beta (TGF-β) pathway and this may contribute to the pathogenesis of adult GCTs. The inability of mutant FOXL2 to elicit an effective apoptotic signalling cascade may also be important in GCT pathogenesis.ConclusionThe 402C>G mutation in FOXL2 is central to the development of adult granulosa cell tumours. Based on the evidence, we suggest that FOXL2 is an oncogene or tumour suppressor depending on the genetic context that is the GCT subtype.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Gynecologic Oncology - Volume 133, Issue 2, May 2014, Pages 382-387
نویسندگان
, , ,