TY - JOUR
T1 - Modulating the heat stress response to improve hyperthermia-based anticancer treatments
AU - Scutigliani, Enzo M.
AU - Liang, Yongxin
AU - Crezee, Hans
AU - Kanaar, Roland
AU - Krawczyk, Przemek M.
N1 - Funding Information:
This research was funded by the Dutch Cancer Society (grant number 11143). PMK and HC are members of the H2020 European Training Network ?HYPERBOOST: Hyperthermia boosting the effect of Radiotherapy? (grant number 955625). This work was also supported by the Gravitation program CancerGenomiCs.nl from the Netherlands Organisation for Scientific Research (NWO), which is part of the Oncode Institute. The Oncode Institute is partly financed by the Dutch Cancer Society.
Publisher Copyright:
© 2021 by the authors. Licensee MDPI, Basel, Switzerland.
PY - 2021/3/2
Y1 - 2021/3/2
N2 - Cancer treatments based on mild hyperthermia (39–43◦C, HT) are applied to a widening range of cancer types, but several factors limit their efficacy and slow down more widespread adoption. These factors include difficulties in adequate heat delivery, a short therapeutic window and the acquisition of thermotolerance by cancer cells. Here, we explore the biological effects of HT, the cellular responses to these effects and their clinically-relevant consequences. We then identify the heat stress response—the cellular defense mechanism that detects and counteracts the effects of heat—as one of the major forces limiting the efficacy of HT-based therapies and propose targeting this mechanism as a potentially universal strategy for improving their efficacy.
AB - Cancer treatments based on mild hyperthermia (39–43◦C, HT) are applied to a widening range of cancer types, but several factors limit their efficacy and slow down more widespread adoption. These factors include difficulties in adequate heat delivery, a short therapeutic window and the acquisition of thermotolerance by cancer cells. Here, we explore the biological effects of HT, the cellular responses to these effects and their clinically-relevant consequences. We then identify the heat stress response—the cellular defense mechanism that detects and counteracts the effects of heat—as one of the major forces limiting the efficacy of HT-based therapies and propose targeting this mechanism as a potentially universal strategy for improving their efficacy.
UR - http://www.scopus.com/inward/record.url?scp=85102376653&partnerID=8YFLogxK
U2 - 10.3390/cancers13061243
DO - 10.3390/cancers13061243
M3 - Review article
AN - SCOPUS:85102376653
VL - 13
SP - 1
EP - 20
JO - Cancers
JF - Cancers
SN - 2072-6694
IS - 6
M1 - 1243
ER -
