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Downregulation of CDX2 in gastrointestinal neoplasia
  1. S J Hayes1,2,
  2. P K Wright3,
  3. Y Ang2,
  4. G L Carlson4
  1. 1 Department of Histopathology, Salford Royal NHS Foundation Trust, Salford, UK
  2. 2 Faculty of Medical and Human Sciences, University of Manchester, Manchester, UK
  3. 3 Department of Histopathology, Manchester Royal Infirmary, Manchester, UK
  4. 4 Department of Surgery, Salford Royal NHS Foundation Trust, Salford, UK
  1. Correspondence to Dr Stephen Hayes, Department of Histopathology, Salford Royal NHS Foundation Trust, Stott Lane, Salford M6 8HD, UK; stephen.hayes{at}

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Research in the field of cancer immunity, which is of increasing credence, suggests that cancer is a disorder that manifests with characteristics also present in reproductive physiology—effectively a somatic cell pregnancy.1 This paradigm complements the conventional somatic mutation theory, proposing tumorigenesis to be initiated by mutations in a growth control gene, followed by alteration of further genes with resultant malignant clonal development.2

The former paradigm is supported by the expression of oncofetal, cancer-embryonic and cancer testis antigens in cancer, such as α-fetoprotein, carcinoembryonic antigen and NY-ESO-1. Moreover, characteristics of cancer are shared by gametogenesis and placentation; namely, invasion, angiogenesis, immune evasion and resistance to apoptosis.

With regard to gastrointestinal neoplasia and the former paradigm, it is of interest to assess expression for CDX2; this is a transcription factor belonging to the caudal-related homeobox gene family. It …

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  • Competing interests None.

  • Patient consent Obtained.

  • Provenance and peer review Not commissioned; internally peer reviewed.

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