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Ascl2 and 11p15.5 amplification in colorectal cancer
  1. Adrian M Jubb1,
  2. Klaus P Hoeflich2,
  3. Peter M Haverty3,
  4. Jennifer Wang4,
  5. Hartmut Koeppen4
  1. 1Nuffield Department of Clinical Laboratory Sciences, Oxford University, Oxford, UK
  2. 2Department of Cancer Signaling and Translational Oncology, Genentech Inc, South San Francisco, California, USA
  3. 3Department of Bioinformatics, Genentech Inc, South San Francisco, California, USA
  4. 4Department of Pathology, Genentech Inc, South San Francisco, California, USA
  1. Correspondence to Dr Adrian Jubb, Nuffield Department of Clinical Laboratory Sciences, University of Oxford, Level 4 – Academic Block, John Radcliffe Hospital, Headley Way, Headington, Oxford OX3 9DU, UK; adrian.jubb{at}ndcls.ox.ac.uk

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We read with interest the recent article by Stange et al1 describing gain of 11p or 11p15.5 in approximately one-quarter of colorectal cancer liver metastases compared with matched primary adenocarcinomas. Stange et al speculated that this event may be targeting several putative oncogenes and focused on achaete scute-like (Ascl)2 in particular.1 However, on examining our own published2 3 and unpublished data, we reached different conclusions regarding the role of Ascl2 in colorectal cancer.

We queried two series of primary colorectal cancers with both expression microarray and array comparative genomic hybridisation data. The first dataset relates to 37 cases (experiments conducted at Genentech; 100 k single nucleotide polymorphism array and HG-U133B GeneChip expression microarray (Affymetrix, Santa Clara, California, USA)). The second dataset relates to 30 cases from the commercial GeneLogic (Gaithersburg, Maryland, USA) database available at …

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    Daniel E Stange Bernhard Radlwimmer