In:
Cancer Research, American Association for Cancer Research (AACR), Vol. 71, No. 8_Supplement ( 2011-04-15), p. 331-331
Abstract:
Endometrial cancer is among the most common gynaecological malignancies in industrialized countries. Although 75% of cancers are treated at an early stage, 15% to 20% recur. Due to these recurrences the demand for systemic therapies and better prognostic markers are vital. Our recent study of global genetic characterisation has identified that C-MYC amplifications associate with aggressive phenotype in uterine cancers (Salvesen et al., PNAS 2009). The present study was conducted to validate the phenotype associated with C-MYC amplification in a large population based prospectively collected sample series from primary tumours and corresponding metastatic lesions from patients with endometrial cancer. Primary tumours from 399 patients and 80 corresponding metastatic lesions were analysed for amplification of the C-MYC gene using fluorescence in situ hybridization (FISH). We found that 5% of primary endometrial cancer tumors have C-MYC amplifications or gains. C-MYC amplification is correlated with high FIGO stage (P = 0.003), non-endometroid subtype (P = 0.002), and high grade (P & lt;0.001). Patients with C-MYC amplifications had a significantly poorer recurrence free- (P = 0.002) and disease specific survival (P = & lt;0.001). These data suggest that C-MYC amplification might be one important mechanism involved in endometrial cancer tumourigenesis. Further characterization of C-MYC amplifications in corresponding metastatic lesions are in progress. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 331. doi:10.1158/1538-7445.AM2011-331
Type of Medium:
Online Resource
ISSN:
0008-5472
,
1538-7445
DOI:
10.1158/1538-7445.AM2011-331
Language:
English
Publisher:
American Association for Cancer Research (AACR)
Publication Date:
2011
detail.hit.zdb_id:
2036785-5
detail.hit.zdb_id:
1432-1
detail.hit.zdb_id:
410466-3
