Clinico-pathological features and p53 expression in left-sided sporadic colorectal cancers with and without microsatellite instability

M Ilyas, I P Tomlinson, M R Novelli, A Hanby, W F Bodmer, I C Talbot

Research output: Contribution to journalArticlepeer-review


Defects in mismatch repair (MMR) can result in the development of a 'mutator phenotype', manifest as an increase in DNA replication errors (RERs). Patients with hereditary non-polyposis colorectal cancer (HNPCC) have germline mutations in MMR genes. These patients develop carcinomas of the colon and other specific sites at a significantly earlier age than patients with sporadic carcinomas. RERs are found in the cancers from patients with HNPCC and have been demonstrated in 10-20 per cent of sporadic colorectal cancers (CRCs). Loss of MMR may simply accelerate tumour development, but it is also possible that these tumours follow a different carcinogenetic pathway from tumours with intact MMR. In particular, it has been suggested that p53 mutations occur less often in RER-positive (RER+) sporadic colorectal cancers. In this study, the clinico-pathological features and frequency of p53 overexpression in 17 left-sided RER+ CRCs were compared with 35 left-sided RER- CRCs. No differences were found in the age and tumour stage at presentation, mucinous differentiation, or Jass prognostic grouping between these two types of CRC. Thirteen out of 17 (76 per cent) RER+ and 19/35 (54 per cent) RER- tumours showed overexpression of p53, a non-significant difference (chi 2 test). Although some previous studies have suggested differences in the clinico-pathological features and p53 expression of RER+ and RER- right-sided CRCs, our results show that these differences do not exist in left-sided cancers.

Original languageEnglish
Pages (from-to)370-5
Number of pages6
JournalThe Journal of Pathology
Issue number4
Publication statusPublished - Aug 1996


  • Aged
  • Colorectal Neoplasms/genetics
  • DNA Replication
  • DNA, Neoplasm/genetics
  • Humans
  • Immunoenzyme Techniques
  • Microsatellite Repeats/genetics
  • Neoplasm Proteins/metabolism
  • Polymerase Chain Reaction
  • Prognosis
  • Tumor Suppressor Protein p53/metabolism


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