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Radiother Oncol ; 128(2): 283-300, 2018 08.
Article in English | MEDLINE | ID: mdl-29929859

ABSTRACT

Radiation therapy is used to treat cancer by radiation-induced DNA damage. Despite the best efforts to eliminate cancer, some cancer cells survive irradiation, resulting in cancer progression or recurrence. Alteration in DNA damage repair pathways is common in cancers, resulting in modulation of their response to radiation. This article focuses on the recent findings about molecules and pathways that potentially can be targeted to sensitize prostate cancer cells to ionizing radiation, thereby achieving an improved therapeutic outcome.


Subject(s)
DNA Damage/radiation effects , DNA Repair/radiation effects , Prostatic Neoplasms/radiotherapy , Ataxia Telangiectasia Mutated Proteins/genetics , Ataxia Telangiectasia Mutated Proteins/radiation effects , Aurora Kinases/radiation effects , Cell Cycle/radiation effects , Checkpoint Kinase 1/radiation effects , Cyclin-Dependent Kinases/radiation effects , Cyclins/radiation effects , HSP90 Heat-Shock Proteins/radiation effects , Histone Deacetylases/radiation effects , Humans , Hyaluronan Receptors/radiation effects , Hypoxia-Inducible Factor 1, alpha Subunit/radiation effects , Male , Mutation/radiation effects , NEDD8 Protein/radiation effects , Neoplasm Recurrence, Local/etiology , Neoplasm Recurrence, Local/radiotherapy , Neoplasm, Residual , Neoplastic Stem Cells/radiation effects , Phosphatidylinositol 3-Kinases/radiation effects , Poly(ADP-ribose) Polymerases/radiation effects , Proto-Oncogene Proteins c-met/radiation effects , Radiation Tolerance , Radiation, Ionizing , Receptors, Androgen/radiation effects , TOR Serine-Threonine Kinases/radiation effects , Zinc Finger Protein GLI1/radiation effects
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