Oncotarget

Case Reports:

Genomic analysis of exceptional responder to regorafenib in treatment-refractory metastatic rectal cancer: a case report and review of the literature

Krittiya Korphaisarn _, Jonathan M. Loree, Van Nguyen, Ryanne Coulson, Vijaykumar Holla, Beate C. Litzenburger, Ken Chen, Gordon B. Mills, Dipen M. Maru, Funda Meric-Bernstan, Kenna R. Mills Shaw and Scott Kopetz

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Oncotarget. 2017; 8:57882-57888. https://doi.org/10.18632/oncotarget.18357

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Abstract

Krittiya Korphaisarn1,2, Jonathan M. Loree1, Van Nguyen3, Ryanne Coulson1, Vijaykumar Holla4, Beate C. Litzenburger4 , Ken Chen4, Gordon B. Mills4, Dipen M. Maru5, Funda Meric-Bernstan4, Kenna R. Mills Shaw4 and Scott Kopetz1

1 Department of Gastrointestinal Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA

2 Department of Medicine, Division of Medical Oncology, Faculty of Medicine Siriraj Hospital, Bangkok, Thailand

3 Department of Pharmacy, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA

4 Sheikh Khalifa Bin Zayed Al Nahyan Institute for Personalized Cancer Therapy (IPCT), The University of Texas MD Anderson Cancer Center, Houston, Texas, USA

5 Department of Pathology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA

Correspondence to:

Scott Kopetz, email:

Keywords: metastatic colorectal cancer, regorafenib, survival, biomarker, response

Received: March 29, 2017 Accepted: May 20, 2017 Published: June 03, 2017

Abstract

We present the case of a 53-year-old male with metastatic rectal cancer who was treatment resistant to FOLFOX and FOLFOXIRI. Due to a Kirsten rat sarcoma viral oncogene homolog (KRAS) mutation, regorafenib was given in the third line setting. Surprisingly, the patient had a prolonged partial response that lasted 27 months. Mutational status was extensively evaluated to identify potential alterations that might play a role as predictive markers for this unusual event. A poorly characterized but nontransforming mutation in Fms-like tyrosine kinase 4 (FLT4) was present in the tumor. Prior to and at the time of clinical progression, we found amplification of fibroblast growth factor receptor 1 (FGFR1) and epidermal growth factor receptor (EGFR), loss of the FLT4 mutation, and gain of KIT proto-oncogene receptor tyrosine kinase (KIT) G961S suggesting potential roles in acquired resistance.


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