Journal article

Transducin-Like Enhancer of Split 3 (TLE3) Expression Is Associated with Taxane Sensitivity in Nonserous Ovarian Carcinoma in a Three-Cohort Study

Brian Z Ring, Rajmohan Murali, Robert A Soslow, David DL Bowtell, Sian Fereday, Anna Defazio, Nadia Traficante, Catherine J Kennedy, Alison Brand, Raghwa Sharma, Paul Harnett, Goli Samimi

CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION | AMER ASSOC CANCER RESEARCH | Published : 2018

Abstract

Background: Chemoresistance is a major challenge in ovarian cancer treatment, resulting in poor survival rates. Identifying markers of treatment response is imperative for improving outcome while minimizing unnecessary side effects. We have previously demonstrated that expression of transducin-like enhancer of split 3 (TLE3) is associated with favorable progression-free survival in taxane-treated ovarian cancer patients with nonserous histology. The purpose of this study was to perform an independent evaluation of the association of TLE3 expression with response to taxane-based chemotherapy in nonserous ovarian cancer, to validate its role as a potential therapeutic response marker for taxan..

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Grants

Awarded by U.S. Army Medical Research and Materiel Command


Awarded by National Health and Medical Research Council of Australia (NHMRC)


Awarded by NIH/NCI Cancer Center Support Grant


Awarded by National Health and Medical Research Council Enabling


Awarded by Cancer Institute NSW


Awarded by NATIONAL CANCER INSTITUTE


Funding Acknowledgements

AOCS: The AOCS gratefully acknowledges the cooperation of the participating institutions in Australia, and also acknowledges the contribution of the study nurses, research assistants, and all clinical and scientific collaborators. A complete list of the AOCS Study Group can be found at www.aocstudy.org. AOCS was supported by the U.S. Army Medical Research and Materiel Command under DAMD17-01-1-0729, The Cancer Council Victoria, Queensland Cancer Fund, The Cancer Council New South Wales, The Cancer Council South Australia, The Cancer Foundation of Western Australia, The Cancer Council Tasmania and the National Health and Medical Research Council of Australia (NHMRC; ID400413, ID400281). The AOCS gratefully acknowledges additional support from Ovarian Cancer Australia and the Peter MacCallum Foundation. MSKCC: This research was funded in part through the NIH/NCI Cancer Center Support Grant P30 CA008748. Westmead: We acknowledge the Gynaecological Oncology Biobank at Westmead (GynBiobank), a member of the Australasian Biospecimen Network-Oncology group, which was funded by the National Health and Medical Research Council Enabling Grants ID 310670 & ID 628903 and the Cancer Institute NSW Grant ID 12/RIG/117 & 15/RIG/1-16.