Abstract PO-213: Financial implication of prostate cancer hypofractionated radiotherapy

Author(s):  
Suryakanta Acharya
BMC Cancer ◽  
2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Wei Guo ◽  
Yun-Chuan Sun ◽  
Jian-Qiang Bi ◽  
Xin-Ying He ◽  
Li Xiao

Abstract Background Prostate cancer is one of the most common cancers in the world. The results of treatment after hypofractionated radiotherapy only have been reported from several small randomized clinical trials. Therefore, we conducted a meta-analysis to compare clinical outcomes of hypofractionated radiotherapy versus conventional radiotherapy in the treatment of intermediate- to high-risk localized prostate cancer. Methods Relevant studies were identified through searching related databases till August 2018. Hazard ratio (HR) or risk ratio (RR) with its corresponding 95% confidence interval (CI) was used as pooled statistics for all analyses. Results The meta-analysis results showed that overall survival (HR = 1.12, 95% CI: 0.93–1.35, p = 0.219) and prostate cancer-specific survival (HR = 1.29, 95% CI: 0.42–3.95, p = 0.661) were similar in two groups. The pooled data showed that biochemical failure was RR = 0.90, 95% CI: 0.76–1.07, p = 0.248. The incidence of acute adverse gastrointestinal events (grade ≥ 2) was higher in the hypofractionated radiotherapy (RR = 1.70, 95% CI: 1.12–2.56, p = 0.012); conversely, for late grade ≥ 2 gastrointestinal adverse events, a significant increase in the conventional radiotherapy was found (RR = 0.75, 95% CI: 0.61–0.91, p = 0.003). Acute (RR = 1.01, 95% CI: 0.89–1.15, p = 0.894) and late (RR = 0.98, 95% CI: 0.86–1.10, p = 0.692) genitourinary adverse events (grade ≥ 2) were similar for both treatment groups. Conclusion Results suggest that the efficacy and risk for adverse events are comparable for hypofractionated radiotherapy and conventional radiotherapy in the treatment of intermediate- to high-risk localized prostate cancer.


2010 ◽  
Vol 106 (10) ◽  
pp. 1458-1462 ◽  
Author(s):  
Mario Di Staso ◽  
Pierluigi Bonfili ◽  
Giovanni L. Gravina ◽  
Milena Di Genesio Pagliuca ◽  
Pietro Franzese ◽  
...  

2021 ◽  
Vol 161 ◽  
pp. S1117-S1118
Author(s):  
M. Miszczyk ◽  
Ł. Magrowski ◽  
J. Rembak-Szynkiewicz ◽  
P. Rajwa ◽  
A. Namysł-Kaletka ◽  
...  

2018 ◽  
Vol 127 ◽  
pp. S1250-S1251
Author(s):  
L. Larrea ◽  
E. López-Muñoz ◽  
P. Antonini ◽  
V. González-Vidal ◽  
M.C. Baños ◽  
...  

2020 ◽  
Vol 123 (7) ◽  
pp. 1089-1100 ◽  
Author(s):  
Yiannis Philippou ◽  
Hanna T. Sjoberg ◽  
Emma Murphy ◽  
Said Alyacoubi ◽  
Keaton I. Jones ◽  
...  

Abstract Background Radiotherapy enhances innate and adaptive anti-tumour immunity. It is unclear whether this effect may be harnessed by combining immunotherapy with radiotherapy fractions used to treat prostate cancer. We investigated tumour immune microenvironment responses of pre-clinical prostate cancer models to radiotherapy. Having defined this landscape, we tested whether radiotherapy-induced tumour growth delay could be enhanced with anti-PD-L1. Methods Hypofractionated radiotherapy was delivered to TRAMP-C1 and MyC-CaP flank allografts. Tumour growth delay, tumour immune microenvironment flow-cytometry, and immune gene expression were analysed. TRAMP-C1 allografts were then treated with 3 × 5 Gy ± anti-PD-L1. Results 3 × 5 Gy caused tumour growth delay in TRAMP-C1 and MyC-CaP. Tumour immune microenvironment changes in TRAMP-C1 at 7 days post-radiotherapy included increased tumour-associated macrophages and dendritic cells and upregulation of PD-1/PD-L1, CD8+ T-cell, dendritic cell, and regulatory T-cell genes. At tumour regrowth post-3 × 5 Gy the tumour immune microenvironment flow-cytometry was similar to control tumours, however CD8+, natural killer and dendritic cell gene transcripts were reduced. PD-L1 inhibition plus 3 × 5 Gy in TRAMP-C1 did not enhance tumour growth delay versus monotherapy. Conclusion 3 × 5 Gy hypofractionated radiotherapy can result in tumour growth delay and immune cell changes in allograft prostate cancer models. Adjuncts beyond immunomodulation may be necessary to improve the radiotherapy-induced anti-tumour response.


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