Hyperthermia, Radiation and Chemotherapy: The Role of Heat in Multidisciplinary Cancer Care

Hurwitz, Mark; Stauffer, Paul R.

doi:10.1053/j.seminoncol.2014.09.014

Cited by 123 publications

(107 citation statements)

References 93 publications

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“…After rewarming, the recovery is far from complete (44) and therefore may affect CIN. Also it has been demonstrated that hyperthermia may lead to damage and death of cancer cells, enhancing the effectiveness of cancer treatments (45,46). Therefore in separate experiments we checked if such treatment might increase CIN induced by anticancer drugs.…”

Section: Resultsmentioning

confidence: 99%

Effects of Anticancer Drugs on Chromosome Instability and New Clinical Implications for Tumor-Suppressing Therapies

Lee

Kouprina

et al. 2016

Cancer Research

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Whole-chromosomal instability (CIN), manifested as unequal chromosome distribution during cell division, is a distinguishing feature of most cancer types. CIN is generally considered to drive tumorigenesis, but a threshold level exists whereby further increases in CIN frequency in fact hinder tumor growth. While this attribute is appealing for therapeutic exploitation, drugs that increase CIN beyond this therapeutic threshold are currently limited. In our previous work, we developed a quantitative assay for measuring CIN based on the use of a non-essential human artificial chromosome (HAC) carrying a constitutively expressed EGFP transgene. Here, we used this assay to rank 62 different anticancer drugs with respect to their effects on chromosome transmission fidelity. Drugs with various mechanisms of action such as antimicrotubule activity, histone deacetylase (HDAC) inhibition, mitotic checkpoint inhibition, and targeting of DNA replication and damage responses were included in the analysis. Ranking of the drugs based on their ability to induce HAC loss revealed that paclitaxel, gemcitabine, dactylolide, LMP400, talazoparib, olaparib, peloruside A, GW843682, VX-680, and cisplatin were the top ten drugs demonstrating HAC loss at a high frequency. Therefore, identification of currently used compounds that greatly increase chromosome mis-segregation rates should expedite the development of new therapeutic strategies to target and leverage the CIN phenotype in cancer cells.

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Section: Resultsmentioning

confidence: 99%

Effects of Anticancer Drugs on Chromosome Instability and New Clinical Implications for Tumor-Suppressing Therapies

Lee

Kouprina

et al. 2016

Cancer Research

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“…These have been very well summarized in various reviews [7][8][9]. Primarily, the thermal sensitizing effects with radiotherapy are due to (a) increased sensitivity of hypoxic, nutritionally deficient cells in low pH (b) inhibition of radiation induced DNA damage repair (c) sensitization of the ''S'' phase cells and (d) an enhanced intrinsic sensitivity of some tumor cells to hyperthermia (e.g.…”

Section: Mode Of Action Of Hyperthermiamentioning

confidence: 99%

“…Temperatures beyond this are considered as thermal ablation. The resurgence of hyperthermia for cancer therapy came subsequent to the several in vitro and in vivo studies carried out during the latter half of the last century following systematic evidence of a thermal dependence of cell kill and its potentiation by radiotherapy [7][8][9]. This prompted clinicians to use http://dx.doi.org/10.1016/j.ctrv.2015.05.009 0305-7372/Ó 2015 Elsevier Ltd. All rights reserved.…”

Section: Introductionmentioning

confidence: 97%

Local hyperthermia combined with radiotherapy and-/or chemotherapy: Recent advances and promises for the future

Datta

Ordóñez

Gaipl

et al. 2015

Cancer Treatment Reviews

464

393

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“…used for the treatment of various cancers. The capacity of hyperthermia to potentiate the action of chemotherapeutic drugs contributes to improved and more effective therapeutic strategies in terms of using lower but equally effective drug doses, a fact which is essential in druginduced cytotoxic side effects and the overall benefit to patients' health outcome [82].…”

Section: Mismatch Repair (Mmr)mentioning

confidence: 99%

Effects of hyperthermia as a mitigation strategy in DNA damage-based cancer therapies

Mantso

Goussetis

Franco

et al. 2016

Seminars in Cancer Biology

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Utilization of thermal therapy (hyperthermia) is defined as the application of exogenous heat induction and represents a concept that is far from new as it goes back to ancient times when heat was used for treating various diseases, including malignancies. Such therapeutic strategy has gained even more popularity (over the last few decades) since various studies have shed light into understanding hyperthermia's underlying molecular mechanism(s) of action. In general, hyperthermia is applied as complementary (adjuvant) means in therapeutic protocols combining chemotherapy and/or irradiation both of which can induce irreversible cellular DNA damage. Furthermore, according to a number of in vitro, in vivo and clinical studies, hyperthermia has been shown to enhance the beneficial effects of DNA targeting therapeutic strategies by interfering with DNA repair response cascades. Therefore, the continuously growing evidence supporting hyperthermia's beneficial role in cancer treatment can also encourage its application as a DNA repair mitigation strategy. In this review article, we aim to provide detailed information on how hyperthermia acts on DNA damage and repair pathways and thus potentially contributing to various adjuvant therapeutic protocols relevant to more efficient cancer treatment strategies.

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Hyperthermia, Radiation and Chemotherapy: The Role of Heat in Multidisciplinary Cancer Care

Cited by 123 publications

References 93 publications

Effects of Anticancer Drugs on Chromosome Instability and New Clinical Implications for Tumor-Suppressing Therapies

Effects of Anticancer Drugs on Chromosome Instability and New Clinical Implications for Tumor-Suppressing Therapies

Local hyperthermia combined with radiotherapy and-/or chemotherapy: Recent advances and promises for the future

Effects of hyperthermia as a mitigation strategy in DNA damage-based cancer therapies

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