Tumor Evolution in a Patient with Recurrent Endometrial Cancer and Synchronous Neuroendocrine Cancer and Response to Checkpoint Inhibitor Treatment

Nikolaos A. Trikalinos, Deyali Chatterjee, Kyle Winter, Matthew Powell, Motoyo Yano

Research output: Contribution to journalArticlepeer-review

2 Scopus citations

Abstract

Both metachronous and synchronous tumors pose a diagnostic and clinical challenge, more so when one of the specimens demonstrates the rare neuroendocrine histology. We describe a patient with sarcoidosis who was treated for endometrial and ovarian neoplasm, recurred with two separate histologies (adenocarcinoma and high grade neuroendocrine), both associated with microsatellite instability (MSI)-high status. Targeted next-generation sequencing of tumor with synonymous somatic alterations pointed to a common ancestry of all three tumors and patient was successfully treated with a tailored immunotherapy regimen. Her sarcoidosis worsened only slightly, and immunotherapy did not need to be discontinued. This case highlights the importance of molecular testing for the optimal therapy of complex synchronous tumors and the need for communication between surgical and medical oncologists in patients with MSI-high cancer. Key Points: The case of a patient with a recurrent gynecological cancer presenting as microsatellite instability (MSI)-high endometrial adenocarcinoma and MSI-high neuroendocrine tumor is reported. This case demonstrated a common genetic lineage with good response to checkpoint inhibition without clinical worsening of autoimmune disease. This article adds to the literature, suggesting tumor evolution with neuroendocrine differentiation in some cancers, and argues that a molecular-based approach to treatment might achieve better understanding and possibly superior treatment outcomes.

Original languageEnglish
Pages (from-to)90-96
Number of pages7
JournalOncologist
Volume26
Issue number2
DOIs
StatePublished - Feb 2021

Fingerprint

Dive into the research topics of 'Tumor Evolution in a Patient with Recurrent Endometrial Cancer and Synchronous Neuroendocrine Cancer and Response to Checkpoint Inhibitor Treatment'. Together they form a unique fingerprint.

Cite this