PIK3CA and PTEN gene and exon mutation-specific clinicopathologic and molecular associations in Colorectal cancer

FL Day; RN Jorissen; L Lipton; D Mouradov; A Sakthianandeswaren; M Christie; S Li; C Tsui; J Tie; J Desai; ZZ Xu; P Molloy; V Whitehall; BA Leggett; IT Jones; S McLaughlin; RL Ward; NJ Hawkins; AR Ruszkiewicz; J Moore; D Busam; Q Zhao; RL Strausberg; P Gibbs; OM Sieber

Journal article

PIK3CA and PTEN gene and exon mutation-specific clinicopathologic and molecular associations in Colorectal cancer

FL Day, RN Jorissen, L Lipton, D Mouradov, A Sakthianandeswaren, M Christie, S Li, C Tsui, J Tie, J Desai, ZZ Xu, P Molloy, V Whitehall, BA Leggett, IT Jones, S McLaughlin, RL Ward, NJ Hawkins, AR Ruszkiewicz, J Moore Show all

Clinical Cancer Research | Published : 2013

DOI: 10.1158/1078-0432.CCR-12-3614

Abstract

Purpose: PIK3CA and PTEN mutations are prevalent in colorectal cancer and potential markers of response to mitogen-activated protein/extracellular signal-regulated kinase inhibitors and anti-EGF receptor antibody therapy. Relationships between phosphoinositide 3-kinase (PI3K) pathway mutation, clinicopathologic characteristics, molecular features, and prognosis remain controversial. Experimental Design: A total of 1,093 stage I-IV colorectal cancers were screened for PIK3CA (exons 9 and 20), KRAS (codons 12-13), BRAF (codon 600) mutations, and microsatellite instability (MSI). PTEN (exons 3-8) and CpG island methylator phenotype (CIMP) status were determined in 744 and 489 cases. PIK3CA data..

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University of Melbourne Researchers

Michael Christie Author

Jeanne Tie Author

Jayesh Desai Author

Peter Gibbs Author

Grants

Funding Acknowledgements

This study was supported by the CSIRO Preventative Health Flagship through an Australian Cancer Grid Project Grant (to L. Lipton, P. Gibbs, and O.M. Sieber), the National Health and Medical Research Council through a Project Grant (Application ID 489418; to L. Lipton, O.M. Sieber, P. Gibbs, and R. L. Ward), the Hilton Ludwig Cancer Metastasis Initiative (to L. Lipton, P. Gibbs, and O.M. Sieber), and the Victorian Government through a Victorian Cancer Agency Translation Cancer Research Grant (to L. Lipton, P. Gibbs, and O.M. Sieber). F. L. Day and M. Christie are supported by the Cancer Council Victoria through a Postgraduate Cancer Research Scholarship and L. Lipton by the CSIRO Preventative Health Flagship through a Clinical Researcher Fellowship. J. Tie is supported by the Victorian Government through a Victorian Cancer Agency Researcher Fellowship and an ASCO Cancer Foundation Young Investigator Award.