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A pathological study of tumour regression in oesophageal adenocarcinoma treated with preoperative chemoradiotherapy
  1. S K Suvarna,
  2. T J Stephenson
  1. Department of Histopathology, Northern General Hospital, Sheffield S5 7AU, UK; s.k.suvarna{at}sheffield.ac.uk

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    We read with interest the study of adenocarcinomas treated by preoperative chemoradiotherapy by Dunne et al.1 This broadly parallelled our study into the subject of adjuvant treatment before surgery for oesophageal carcinoma. These results have been published in abstract form previously,2 and may be summarised as follows.

    We studied a series of 29 patients (23 men, six women; average age, 59 years for men, 62 years for women) over a period of three years (1998 to 2000), who had confirmed oesophageal carcinoma (adenocarcinoma, squamous carcinoma) and were treated with radiotherapy (30 in 10 fractions or 45 Gy in 25 fractions) and chemotherapy of cisplatin (80 mg/m2) and 5 fluorouracil (1 gm/m2) in weekly cycles for four weeks. Four patients did not undergo resection; three showing disseminated disease and one dying of gastrointestinal haemorrhage before surgery. The remaining nine patients with squamous carcinoma and 16 patients with adenocarcinoma underwent resection of the tumours with local node sampling.

    Five of the patients with squamous carcinoma and five with adenocarcinoma showed no viable tumour after preoperative adjuvant treatment. In a manner similar to the above study, we found standard features of radiotherapy in the form of fibrosis, vascular changes, radiation fibroblasts, and occasional zones of necrosis containing amorphous matter. We determined the pretreatment level of tumour spread by means of identifying either degenerate keratin (derived from the squamous carcinomas) or mucin pools (in cases of adenocarcinoma). Residual viable tumour could be staged in the normal fashion, depending on whether one used TRG or TNM methods. We would emphasise the usefulness of a mucin stain to determine pools of mucin within lymphatic channels and or lymph nodes as a method of highlighting the extent of adenocarcinoma spread, but would also advocate the need for a cytokeratin or equivalent stain to identify single residual tumour cells. This parallels the concept of “skip metastases” described by Hosch et al.3

    All of the tumours studied were completely excised at the peripheral plane of resection, but seven cases revealed metastatic nodal disease (one squamous, six adenocarcinoma). In several of these cases the metastatic tumour was determined as being outside the field of radiotherapy. At the time of the last analysis, 18 of these 25 patients were alive with follow up periods ranging between four and 30 months. Overall, we concur that these studies, and others,4 appear to indicate a survival advantage in the arena of oesophageal carcinoma treatment.

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