Research Papers:
Somatic mutations in salivary duct carcinoma and potential therapeutic targets
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Abstract
Timothy K. Khoo1,*, Bing Yu1,2,*, Joel A. Smith3, Angus J. Clarke1, Peter P. Luk4, Christina I. Selinger4, Kate L. Mahon1,5, Spiridoula Kraitsek2, Carsten Palme1,3, Michael J. Boyer1,5, Marcel E. Dinger6, Mark J. Cowley6, Sandra A. O’Toole1,4, Jonathan R. Clark1,3,7,* and Ruta Gupta1,3,4,*
1Central Clinical School, The University of Sydney, Australia
2Department of Medical Genomics, Royal Prince Alfred Hospital, Sydney, Australia
3The Sydney Head and Neck Cancer Institute, Chris O’Brien Lifehouse, Sydney, Australia
4Department of Tissue Pathology and Diagnostic Oncology, Royal Prince Alfred Hospital, Sydney, Australia
5The Department of Medical Oncology, Chris O’Brien Lifehouse, Sydney, Australia
6Kinghorn Cancer Centre and Garvan Institute of Medical Research, Darlinghurst, Sydney, Australia
7South West Clinical School, University of New South Wales, Sydney, Australia
*These authors contributed equally to this work
Correspondence to:
Ruta Gupta, email: [email protected]
Keywords: salivary duct carcinoma, somatic mutation analysis, targeted therapies, androgen receptor, HER2
Received: January 10, 2017 Accepted: March 20, 2017 Published: May 25, 2017
ABSTRACT
Background: Salivary duct carcinomas (SDCa) are rare highly aggressive malignancies. Most patients die from distant metastatic disease within three years of diagnosis. There are limited therapeutic options for disseminated disease.
Results: 11 cases showed androgen receptor expression and 6 cases showed HER2 amplification. 6 Somatic mutations with additional available targeted therapies were identified: EGFR (p.G721A: Gefitinib), PDGFRA (p.H845Y: Imatinib and Crenolanib), PIK3CA (p.H1047R: Everolimus), ERBB2 (p.V842I: Lapatinib), HRAS (p.Q61R: Selumetinib) and KIT (p.T670I: Sorafenib). Furthermore, alterations in PTEN, PIK3CA and HRAS that alter response to androgen deprivation therapy and HER2 inhibition were also seen.
Materials and Methods: Somatic mutation analysis was performed on DNA extracted from 15 archival cases of SDCa using the targeted Illumina TruSeq Amplicon Cancer Panel. Potential targetable genetic alterations were identified using extensive literature and international somatic mutation database (COSMIC, KEGG) search. Immunohistochemistry for androgen receptor and immunohistochemistry and fluorescent in situ hybridization for HER2 were also performed.
Conclusions: SDCa show multiple somatic mutations, some that are amenable to pharmacologic manipulation and others that confer resistance to treatments currently under investigation. These findings emphasize the need to develop testing and treatment strategies for SDCa.
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