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Molecular differences between RER+ and RER sporadic endometrial carcinomas in a large population-based series
  1. N. D. Macdonald*,
  2. H. B. Salvesen,,
  3. A. Ryan*,
  4. S. Malatos*,
  5. I. Stefansson,
  6. O. E. Iversen,
  7. L. A. Akslen,
  8. S. Das§ and
  9. I. J. Jacobs*
  1. * The Gynaecological Oncology Unit, St Bartholomew's and The London Hospitals, Queen Mary School of Medicine and Dentistry, Charterhouse Square, London, UK
  2. Department of Gynaecology and Obstetrics, Haukeland University Hospital, Bergen, Norway
  3. Department of Pathology, The Gade Institute, Haukeland University Hospital, Bergen, Norway
  4. § Department of Human Genetics, The University of Chicago, Chicago, IL, USA
  1. Address correspondence and reprint requests to: Dr Nicola MacDonald, Subspecialty Trainee in Gynecological Oncology, Elizabeth Garrett Anderson & Obstetric Hospital, Huntley Street, London, WC1E 6AU, UK. Email: ndmacdonald{at}


Studies, to date, have suggested that there are distinct molecular differences between microsatellite stable (RER) and unstable (RER+) solid tumors, such as colorectal carcinoma. We investigated a range of molecular events including mutation frequency of K-ras, microsatellite instability within the coding region of TGF-βRII, BAX, and IGF-IIR, loss of expression of p53, hMLH1, hMSH2, hMSH6, and PTEN, and methylation of hMLH1, hMSH2, and PTEN within a large population-based series of sporadic endometrial carcinomas to establish whether there are distinct differences between replication error repair (RER+) and RER cases. RER+ endometrial carcinomas tended to be diploid with normal p53 expression, compared with RER cases. Mutations in TGF-βRII, IGF-IIR, and BAX were rare, but there was a strong association between mutation and RER+ status. Methylation and loss of hMLH1 expression were significantly more common in RER+ cases, as was methylation of PTEN. K-ras mutations were equally frequent in RER+ and RER cases. Despite the absence of distinct clinicopathological differences between RER+ and RER cases in this series of sporadic endometrial carcinomas, our results confirm that there are molecular differences between RER+ and RER cases, but the molecular events occurring in RER+ endometrial carcinomas differ from those seen in RER+ colorectal carcinomas.

  • endometrial carcinoma
  • K-ras
  • microsatellite instability
  • mismatch repair
  • target genes

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