一组荷兰科研人员已经证明了一点热量可以在很大程度上让某些类型的癌症疗法增效。一些临床医生使用局部体温过高（让肿瘤升温到41-43摄氏度，即大约106-109华氏度）的方法增加某些癌症疗法的疗效，诸如放射性疗法和化学疗法。然而，迄今为止科研人员不清楚体温过高如何起到了帮助作用。Przemek M. Krawczyk及其同事证明了体温过高阻断了一种关键的DNA修复路径，如果没有体温过高，这种修复路径就会妨碍放射性疗法和化学疗法，温度增加导致了在DNA修复中起到关键作用的BRCA2蛋白降解，并且让放射性疗法和化学疗法更有效地阻止肿瘤生长。目前，能够抑制PARP-1酶（这是另一种参与DNA修复的蛋白）的药物正在被用于治疗BRCA基因没有激活的罕见癌症。这组作者说，体温过高是一种非侵入性、非毒性的工具，可能有助于改善PARP-1抑制剂的效果，而且还可能改善与正常的BRCA基因有关的其他癌症的当前疗法的效果。（生物谷Bioon.com）
生物谷推荐原文出处：
PNAS doi: 10.1073/pnas.1101053108
Mild hyperthermia inhibits homologous recombination, induces BRCA2 degradation, and sensitizes cancer cells to poly (ADP-ribose) polymerase-1 inhibition
Przemek M. Krawczyka,1, Berina Eppinkb,1, Jeroen Essersb,c,d,1, Jan Stapa,1, Hans Rodermonde, Hanny Odijkb, Alex Zelenskyb, Chris van Breee, Lukas J. Stalpersf, Marrije R. Buistg, Thomas Soulliéh, Joost Rensh, Hence J. M. Verhagend, Mark J. O'Connori, Nicolaas A. P. Frankene,f, Timo L. M. ten Hagenh, Roland Kanaarb,c,2, and Jacob A. Atena
Abstract
Defective homologous recombination (HR) DNA repair imposed by BRCA1 or BRCA2 deficiency sensitizes cells to poly (ADP-ribose) polymerase (PARP)-1 inhibition and is currently exploited in clinical treatment of HR-deficient tumors. Here we show that mild hyperthermia (41–42.5 °C) induces degradation of BRCA2 and inhibits HR. We demonstrate that hyperthermia can be used to sensitize innately HR-proficient tumor cells to PARP-1 inhibitors and that this effect can be enhanced by heat shock protein inhibition. Our results, obtained from cell lines and in vivo tumor models, enable the design of unique therapeutic strategies involving localized on-demand induction of HR deficiency, an approach that we term induced synthetic lethality.
