A new mild hyperthermia device to treat vascular involvement in cancer surgery

Matthew J. Ware, Lam P. Nguyen, Justin J. Law, Martyna Krzykawska-Serda, Kimberly M. Taylor, Hop S.Tran Cao, Andrew O. Anderson, Merlyn Pulikkathara, Jared M. Newton, Jason C. Ho, Rosa Hwang, Kimal Rajapakshe, Cristian Coarfa, Shixia Huang, Dean Edwards, Steven A. Curley, Stuart J. Corr

Research output: Contribution to journalArticlepeer-review

15 Scopus citations


Surgical margin status in cancer surgery represents an important oncologic parameter affecting overall prognosis. The risk of disease recurrence is minimized and survival often prolonged if margin-negative resection can be accomplished during cancer surgery. Unfortunately, negative margins are not always surgically achievable due to tumor invasion into adjacent tissues or involvement of critical vasculature. Herein, we present a novel intra-operative device created to facilitate a uniform and mild heating profile to cause hyperthermic destruction of vessel-encasing tumors while safeguarding the encased vessel. We use pancreatic ductal adenocarcinoma as an in vitro and an in vivo cancer model for these studies as it is a representative model of a tumor that commonly involves major mesenteric vessels. In vitro data suggests that mild hyperthermia (41-46 °C for ten minutes) is an optimal thermal dose to induce high levels of cancer cell death, alter cancer cell's proteomic profiles and eliminate cancer stem cells while preserving non-malignant cells. In vivo and in silico data supports the well-known phenomena of a vascular heat sink effect that causes high temperature differentials through tissues undergoing hyperthermia, however temperatures can be predicted and used as a tool for the surgeon to adjust thermal doses delivered for various tumor margins.

Original languageEnglish (US)
Article number11299
JournalScientific reports
Issue number1
StatePublished - Dec 1 2017
Externally publishedYes

Bibliographical note

Funding Information:
MJW, SC and SJC acknowledge the financial support from Kanzius Cancer Research Foundation. SH, CC and KR acknowledges the financial support from Cancer Prevention & Research Institute of Texas Proteomics & Metabolomics Core Facility Support Award (RP120092) (DPE and SH) and NCI Cancer Center Support Grant to Antibody-based Proteomics Core/Shared Resource (P30CA125123) (DPE and SH). JMN acknowledges financial support from award number 2T32GM088129 from the National Institute of General Medical Sciences. JCH acknowledges support from Baylor College of Medicine Oncology Scholars (T32CA174647). We thank Dr Qianxing Mo for data normalization on RPPA data. We would also like to thanks Dr Paul Johnson and Dr Dalis Collins from the Center for Comparative Medicine at Baylor College of Medicine and Deborah Taylor and Ebony Lewis from the Experimental Surgery Program at Baylor College of Medicine for their support during large animal experiments. We thank Fuli Jia, Kimberley Holloway, and Davis So from the Antibody-based Proteomics Core/Shared Resource for their excellent technical assistance in performing RPPA experiments. We Thank students Kateřina Klimánková, Poornima Ramesh, Rukshikah Loganathan, Chloe Marie Johnson, Chimdi Tiffany Ndukwe, Alexander Fish and George Adam Wygant from the Department of Surgery Incubator Summer Intern Research Program at Baylor College of Medicine in Collaboration with Swansea University, United Kingdom and University of Houston, Texas who assisted in acquiring data. Finally, thanks are extended to Dr. R. Hwang of the Department of Surgical Oncology, University of Texas MD Anderson Cancer who kindly provided the Pancreatic stellate cells.

Publisher Copyright:
© 2017 The Author(s).


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