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Early relapse on adjuvant gemcitabine associated with an exceptional response to 2nd line capecitabine chemotherapy in a patient with pancreatic adenosquamous carcinoma with strong intra-tumoural expression of cytidine deaminase: a case report

Authors
  • Connell, Claire M.1, 2
  • Brais, Rebecca1
  • Whitaker, Hayley3
  • Upponi, Sara1
  • Beh, Ian1
  • Risdall, Jane1
  • Corrie, Pippa1
  • Janowitz, Tobias1, 2
  • Jodrell, Duncan I.1, 2
  • 1 Addenbrooke’s Hospital, Cambridge University Hospitals NHS Foundation Trust, Cambridge, CB2 0QQ, UK , Cambridge (United Kingdom)
  • 2 CRUK Cambridge Institute, Li Ka Shing Centre, University of Cambridge, Cambridge, CB2 0RE, UK , Cambridge (United Kingdom)
  • 3 University College London, Charles Bell House, 43-45 Foley Street, London, W1W 7TS, UK , London (United Kingdom)
Type
Published Article
Journal
BMC Cancer
Publisher
Springer (Biomed Central Ltd.)
Publication Date
Jan 15, 2020
Volume
20
Issue
1
Identifiers
DOI: 10.1186/s12885-020-6516-1
Source
Springer Nature
Keywords
License
Green

Abstract

BackgroundPancreatic adenosquamous carcinoma has a poor prognosis, with limited prospective trial data to guide optimal treatment. The potential impact of drug metabolism on the treatment response of patients with pancreatic adenosquamous carcinoma is largely unknown.Case presentationWe describe the case of a 51 year old woman with pancreatic adenosquamous carcinoma who, following surgical resection, experienced early disease relapse during adjuvant gemcitabine therapy. Paradoxically, this was followed by an exceptional response to capecitabine therapy lasting 34.6 months. Strong expression of cytidine deaminase was detected within the tumour.ConclusionsThis case study demonstrates that early relapse during adjuvant chemotherapy for pancreatic adenosquamous carcinoma may be compatible with a subsequent exceptional response to second line chemotherapy, an important observation given the poor overall prognosis of patients with adenosquamous carcinoma. Cytidine deaminase is predicted to inactivate gemcitabine and, conversely, catalyze capecitabine activation. We discuss strong intra-tumoural expression of cytidine deaminase as a potential mechanism to explain this patient’s disparate responses to gemcitabine and capecitabine therapy, and highlight the benefit that may be gained from considering similar determinants of response to chemotherapy in clinical practice.

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