Abstract
BackgroundDespite the introduction of novel effective treatment regimens like gemcitabine plus nab-paclitaxel and FOLFIRINOX, pancreatic ductal adenocarcinoma (PDAC) remains one of the most aggressive epithelial tumors. Among the genetic alterations frequently found in PDAC, mutations in the KRAS gene might play a prognostic role regarding overall survival and may also have the potential to predict the efficacy of anti-EGFR treatment.Case presentationWe report the clinical case of a 69 year old Caucasian female that was diagnosed with histologically confirmed locally advanced PDAC with lymph node involvement in August 2010. At the time of first diagnosis, tumor tissue obtained from an open regional lymph node biopsy showed a poorly differentiated adenocarcinoma with a wild type sequence within exon 2 (codon 12/13) of the KRAS gene. The patient initially received single-agent gemcitabine and a subsequent 5-FU-based chemoradiotherapy with a sequential maintenance chemotherapy with oral capecitabine resulting in a long term disease control. Local disease progression occurred in May 2014 and the patient underwent pancreaticoduodenectomy in September 2014. A novel KRAS gene mutation (c.35G > T, p.G12 V) in exon 2 (codon 12) was detected within the surgical specimen. As of January 2016 the patient is still alive and without evidence of the underlying disease.ConclusionsSpecifically in the context of clinical trials and translational research in PDAC a re-assessment of molecular biomarkers, i. e. KRAS, at defined time points (e. g. relapse, disease progression, unusual clinical course) may be indicated in order to detect a potential switch in biomarker status during the course of disease.
Highlights
Despite the introduction of novel effective treatment regimens like gemcitabine plus nab-paclitaxel and FOLFIRINOX, pancreatic ductal adenocarcinoma (PDAC) remains one of the most aggressive epithelial tumors
Kirsten rat sarcoma viral oncogene homologue (KRAS), at defined time points (e. g. relapse, disease progression, unusual clinical course) may be indicated in order to detect a potential switch in biomarker status during the course of disease
Several studies showed that constitutively activating KRAS mutations are associated with worse overall survival (OS), whereas KRAS wildtype status is associated with improved OS in Pancreatic ductal adenocarcinoma (PDAC) [7, 10, 11]
Summary
KRAS mutational status may change during the course of disease in PDAC. in well-defined clinical scenarios (e. g. relapse after surgery in curative intent, disease progression during/after chemotherapy, unusual clinical course) a re-assessment of the KRAS status should be discussed, within the setting of controlled clinical and translational trials. As KRAS is not yet established as a clinically relevant biomarker in Consent for publication The patient reported here was included in a single-center translational study protocol of the Ludwig-Maximilians-University of Munich, named “The Informative Patient” (Patient number 1303). By signing the official consent form provided by BMC Cancer (http://resourcecms.springer.com/springer-cms/rest/v1/content/6621850/data/v1/ConsentForm-PDF), the patient gave written informed consent for publication of her data in form of this case report. Both a copy of the original informed consent for study participation, data analysis and publication (in German language only) as well as a copy of the original BMC Cancer consent to publish form are available for review through the editors of this journal.
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