Radiation can induce DNA double-stranded breaks, which are typically detected by the fluorescence of phosphorylated histone H2AX. In this study, we examined the usefulness of the dynamics of radiation-induced gamma-H2AX foci of peripheral blood lymphocytes (PBLs), as a marker of DNA repair ability, in predicting late adverse events from radiotherapy. A total of 46 patients with cervical, vaginal and anal canal cancers treated with radical radiotherapy between 2014 and 2019 were included in this analysis. Concurrent chemotherapy was administered in 36 cases (78.3%). Peripheral blood was obtained before treatment, and then irradiated ex vivo with 1 Gy X-ray. The ratio of radiation-induced gamma-H2AX foci in PBLs measured at 30 min and at 4 h was defined as the foci decay ratio (FDR). With a median follow-up of 54 months, 9 patients (19.6%) were observed to have late genitourinary or gastrointestinal (GU/GI) toxicity. The FDR ranged from 0.51 to 0.74 (median 0.59), with a significantly higher incidence of Grade 1 or higher late adverse events in the FDR ≥ 0.59 group. In multivariate analysis, FDR ≥ 0.59 and hypertension also emerged as significant factors associated with the development of late toxicities. Overall, our results suggest that measurement of radiation-induced gamma-H2AX foci in PBLs may predict the risk of late GU/GI toxicities from chemoradiotherapy, which can enable tailoring the radiation dose to minimize adverse effects.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10665300PMC
http://dx.doi.org/10.1093/jrr/rrad079DOI Listing

Publication Analysis

Top Keywords

radiation-induced gamma-h2ax
16
gamma-h2ax foci
16
late adverse
12
adverse events
12
peripheral blood
8
foci pbls
8
foci
5
late
5
prediction late
4
adverse
4

Similar Publications

Radiation therapy is crucial for cancer treatment, but it often causes tissue damage. The kidney, which is sensitive to radiation, is under-researched in this context. This study aimed to develop a mouse model for radiation-induced acute kidney injury (AKI) using a small animal radiation research platform (SARRP) to mimic clinical radiation conditions.

View Article and Find Full Text PDF

We previously reported endogenous activation of the DNA damage response (DDR) in the epidermis surrounding basal cell carcinoma resected from Nagasaki atomic bomb survivors, suggesting the presence of genomic instability (GIN) in the survivors as a late effect of radiation. Dual-color immunofluorescence (IF) analysis of TP53-binding protein-1 (53BP1) and a proliferative indicator, Ki-67, to elucidate GIN in tumor tissues revealed that abnormal 53BP1 expression is closely associated with carcinogenesis in several organs. The present study aimed to confirm the presence of radiation-induced GIN in the non-neoplastic epidermis of patients with radiation-induced skin cancer.

View Article and Find Full Text PDF

Trichostatin A mitigates acute and late effects of radiation in intestine by regulation of DNA damage repair and Wnt/TGFβ/Smad signaling.

Int J Radiat Biol

January 2025

Radiomitigation Research Department, Institute of Nuclear Medicine and Allied Sciences (INMAS), Defence Research and Development Organization (DRDO), Brig. S.K Mazumdar Marg, Delhi, India.

Purpose: Radiation accidents and misuse of nuclear weapons elevate the risk of development of acute life-threatening injuries as well as their late effects are noted in survivors. Currently, no countermeasure agents are available for the management of radiation-induced GI injury (RIGI) in humans. In the present study, the radiomitigative potential of Trichostatin A (TSA) was evaluated against acute and late RIGI.

View Article and Find Full Text PDF

Objectives: Single-strand DNA-binding protein 1 (SSB1) plays a crucial role in the cellular response to DNA damage. This study aimed to explore the expression and regulation of SSB1 in normal rat salivary gland tissues and tissues following radiation, with a specific emphasis on its involvement in the repair of salivary gland injury.

Methods: A total of 45 adult SD rats were randomly assigned to one control group or eight experimental groups.

View Article and Find Full Text PDF

S6K1 Controls DNA Damage Signaling Modulated by the MRN Complex to Induce Radioresistance in Lung Cancer.

Int J Mol Sci

September 2024

Department of Radiation Oncology, Sidney Kimmel Comprehensive Cancer Center, Thomas Jefferson University, Philadelphia, PA 19107, USA.

Radiation is a mainstay of lung cancer treatment; however, resistance frequently develops. Identifying novel therapeutic targets to increase radiation sensitivity is crucial. S6K1 is a serine/threonine kinase known to regulate protein translation which is associated with radioresistance, but the mechanisms involved are unknown.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!