Radiation-induced Adaptive Response: New Potential for Cancer Treatment.
Journal
Clinical cancer research : an official journal of the American Association for Cancer Research
ISSN: 1557-3265
Titre abrégé: Clin Cancer Res
Pays: United States
ID NLM: 9502500
Informations de publication
Date de publication:
15 11 2020
15 11 2020
Historique:
received:
17
02
2020
revised:
24
04
2020
accepted:
11
06
2020
pubmed:
20
6
2020
medline:
23
11
2021
entrez:
20
6
2020
Statut:
ppublish
Résumé
Radiotherapy is highly effective due to its ability to physically focus the treatment to target the tumor while sparing normal tissue and its ability to be combined with systemic therapy. This systemic therapy can be utilized before radiotherapy as an adjuvant or induction treatment, during radiotherapy as a radiation "sensitizer," or following radiotherapy as a part of combined modality therapy. As part of a unique concept of using radiation as "focused biology," we investigated how tumors and normal tissues adapt to clinically relevant multifraction (MF) and single-dose (SD) radiation to observe whether the adaptations can induce susceptibility to cell killing by available drugs or by immune enhancement. We identified an adaptation occurring after MF (3 × 2 Gy) that induced cell killing when AKT-mTOR inhibitors were delivered following cessation of radiotherapy. In addition, we identified inducible changes in integrin expression 2 months following cessation of radiotherapy that differ between MF (1 Gy × 10) and SD (10 Gy) that remain targetable compared with preradiotherapy. Adaptation is reflected across different "omics" studies, and thus the range of possible molecular targets is not only broad but also time, dose, and schedule dependent. While much remains to be studied about the radiation adaptive response, radiation should be characterized by its molecular perturbations in addition to physical dose. Consideration of the adaptive effects should result in the design of a tailored radiotherapy treatment plan that accounts for specific molecular changes to be targeted as part of precision multimodality cancer treatment.
Identifiants
pubmed: 32554542
pii: 1078-0432.CCR-20-0572
doi: 10.1158/1078-0432.CCR-20-0572
pmc: PMC7669567
mid: NIHMS1603488
doi:
Substances chimiques
MTOR protein, human
EC 2.7.1.1
Oncogene Protein v-akt
EC 2.7.11.1
TOR Serine-Threonine Kinases
EC 2.7.11.1
Types de publication
Journal Article
Research Support, N.I.H., Intramural
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
5781-5790Subventions
Organisme : Intramural NIH HHS
ID : Z99 CA999999
Pays : United States
Organisme : Intramural NIH HHS
ID : ZIA BC010670
Pays : United States
Informations de copyright
©2020 American Association for Cancer Research.
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