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    Clinical and molecular characterization of HER2 amplified-pancreatic cancer

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    Author
    Chou, A; Waddell, N; Cowley, MJ; Gill, AJ; Chang, DK; Patch, A-M; Nones, K; Wu, J; Pinese, M; Johns, AL; ...
    Date
    2013-08-31
    Source Title
    Genome Medicine: medicine in the post-genomic era
    Publisher
    BMC
    University of Melbourne Author/s
    Grimmond, Sean
    Affiliation
    Centre for Cancer Research
    Metadata
    Show full item record
    Document Type
    Journal Article
    Citations
    Chou, A., Waddell, N., Cowley, M. J., Gill, A. J., Chang, D. K., Patch, A. -M., Nones, K., Wu, J., Pinese, M., Johns, A. L., Miller, D. K., Kassahn, K. S., Nagrial, A. M., Wasan, H., Goldstein, D., Toon, C. W., Chin, V., Chantrill, L., Humphris, J. ,... Biankin, A. V. (2013). Clinical and molecular characterization of HER2 amplified-pancreatic cancer. GENOME MEDICINE, 5 (8), https://doi.org/10.1186/gm482.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/258240
    DOI
    10.1186/gm482
    Abstract
    BACKGROUND: Pancreatic cancer is one of the most lethal and molecularly diverse malignancies. Repurposing of therapeutics that target specific molecular mechanisms in different disease types offers potential for rapid improvements in outcome. Although HER2 amplification occurs in pancreatic cancer, it is inadequately characterized to exploit the potential of anti-HER2 therapies. METHODS: HER2 amplification was detected and further analyzed using multiple genomic sequencing approaches. Standardized reference laboratory assays defined HER2 amplification in a large cohort of patients (n = 469) with pancreatic ductal adenocarcinoma (PDAC). RESULTS: An amplified inversion event (1 MB) was identified at the HER2 locus in a patient with PDAC. Using standardized laboratory assays, we established diagnostic criteria for HER2 amplification in PDAC, and observed a prevalence of 2%. Clinically, HER2- amplified PDAC was characterized by a lack of liver metastases, and a preponderance of lung and brain metastases. Excluding breast and gastric cancer, the incidence of HER2-amplified cancers in the USA is >22,000 per annum. CONCLUSIONS: HER2 amplification occurs in 2% of PDAC, and has distinct features with implications for clinical practice. The molecular heterogeneity of PDAC implies that even an incidence of 2% represents an attractive target for anti-HER2 therapies, as options for PDAC are limited. Recruiting patients based on HER2 amplification, rather than organ of origin, could make trials of anti-HER2 therapies feasible in less common cancer types.

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