scholarly journals Particle therapy in prostate cancer: a review

2007 ◽  
Vol 10 (4) ◽  
pp. 323-330 ◽  
Author(s):  
C Greco
2020 ◽  
Vol 117 (26) ◽  
pp. 15172-15181 ◽  
Author(s):  
Mesude Bicak ◽  
Katharina Lückerath ◽  
Teja Kalidindi ◽  
Michael E. Phelps ◽  
Sven-Erik Strand ◽  
...  

Hu11B6 is a monoclonal antibody that internalizes in cells expressing androgen receptor (AR)-regulated prostate-specific enzyme human kallikrein-related peptidase 2 (hK2;KLK2). In multiple rodent models, Actinium-225–labeled hu11B6-IgG1([225Ac]hu11B6-IgG1) has shown promising treatment efficacy. In the present study, we investigated options to enhance and optimize [225Ac]hu11B6 treatment. First, we evaluated the possibility of exploiting IgG3, the IgG subclass with superior activation of complement and ability to mediate FC-γ-receptor binding, for immunotherapeutically enhanced hK2 targeted α-radioimmunotherapy. Second, we compared the therapeutic efficacy of a single high activity vs. fractionated activity. Finally, we used RNA sequencing to analyze the genomic signatures of prostate cancer that progressed after targeted α-therapy. [225Ac]hu11B6-IgG3was a functionally enhanced alternative to [225Ac]hu11B6-IgG1but offered no improvement of therapeutic efficacy. Progression-free survival was slightly increased with a single high activity compared to fractionated activity. Tumor-free animals succumbing after treatment revealed no evidence of treatment-associated toxicity. In addition to up-regulation of canonical aggressive prostate cancer genes, such asMMP7,ETV1,NTS, andSCHLAP1, we also noted a significant decrease in bothKLK3(prostate-specific antigen ) andFOLH1(prostate-specific membrane antigen) but not inARandKLK2, demonstrating efficacy of sequential [225Ac]hu11B6 in a mouse model.


2019 ◽  
Vol 26 (10) ◽  
pp. 971-979 ◽  
Author(s):  
Hitoshi Ishikawa ◽  
Hiroshi Tsuji ◽  
Shigeyuki Murayama ◽  
Mikio Sugimoto ◽  
Nobuo Shinohara ◽  
...  

2021 ◽  
Vol 11 ◽  
Author(s):  
Stine Elleberg Petersen ◽  
Morten Høyer

PurposeThere is high-level evidence for addition of androgen deprivation therapy to photon-based radiotherapy of the prostate in intermediate- and high-risk prostate cancer. Little is known about the value of ADT in particle therapy of prostate cancer. We are conducting a systematic review on biochemical disease-free survival, overall survival, and morbidity after combined particle therapy and ADT for prostate cancer.MethodsA thorough search in PubMed, Embase, Scopus, and Web of Science databases were conducted, searching for relevant studies. Clinical studies on prostate cancer and the treatment combination of particle therapy and androgen deprivation therapy were included. The review was conducted according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines and registered on PROSPERO (CRD42021230801).ResultsA total of 298 papers were identified. Fifteen papers reporting on 7,202 patients after proton or carbon-ion therapy for localized prostate cancer where a fraction or all patients received ADT were selected for analysis. Three thousand five hundred and nineteen (49%) of the patients had received combined ADT and particle therapy. Primarily high-risk (87%), to a lesser extent intermediate-risk (34%) and low-risk patients (12%) received ADT. There were no comparative studies on the effect of ADT in patients treated with particles and no studies identified ADT as an independent prognostic factor related to survival outcomes.ConclusionsThe review found no evidence to support that the effects on biochemical disease-free survival and morbidity of combining ADT to particle therapy differs from the ADT effects in conventional photon based radiotherapy. The available data on the topic is limited.


2013 ◽  
Vol 8 (1) ◽  
Author(s):  
Antoni Ruciński ◽  
Julia Bauer ◽  
Patrick Campbell ◽  
Stephan Brons ◽  
Daniel Unholtz ◽  
...  

Author(s):  
Curtis M. Bryant ◽  
Randal H. Henderson ◽  
R. Charles Nichols ◽  
William M. Mendenhall ◽  
Bradford S. Hoppe ◽  
...  

Abstract Proton therapy is a promising but controversial treatment in the management of prostate cancer. Despite its dosimetric advantages when compared with photon radiation therapy, its increased cost to patients and insurers has raised questions regarding its value. Multiple prospective and retrospective studies have been published documenting the efficacy and safety of proton therapy for patients with localized prostate cancer and for patients requiring adjuvant or salvage pelvic radiation after surgery. The Particle Therapy Co-Operative Group (PTCOG) Genitourinary Subcommittee intends to address current proton therapy indications, advantages, disadvantages, and cost effectiveness. We will also discuss the current landscape of clinical trials. This consensus report can be used to guide clinical practice and research directions.


2016 ◽  
Vol 119 ◽  
pp. S265-S266
Author(s):  
C. Stokkevåg ◽  
M. Fukahori ◽  
T. Nomiya ◽  
N. Matsufuji ◽  
G. Engeseth ◽  
...  

2019 ◽  
Author(s):  
Mesude Bicak ◽  
Katharina Lückerath ◽  
Teja Kalidindi ◽  
Sven-Erik Strand ◽  
Michael Morris ◽  
...  

AbstractHu11B6 is a monoclonal antibody that internalizes in cells expressing androgen receptor (AR)-regulated prostate specific enzyme human kallikrein 2 (hK2; KLK2). In multiple rodent models, Actinium-225 labeled hu11B6-IgG1 ([225Ac]hu11B6-IgG1) has shown promising treatment efficacy. In the current study we investigated options to enhance and optimize [225Ac]hu11B6 treatment. Firstly, we evaluated the possibility of exploiting IgG3, the immunoglobulin G (IgG) subclass with superior activation of complement and ability to mediate FC-gamma-receptor binding, for immunotherapeutically enhanced hK2 targeted alpha-radioimmunotherapy. Secondly, we compared the therapeutic efficacy of a single high activity vs. fractionated activity. Finally, we used RNA sequencing to analyze the genomic signatures of prostate cancer that progressed after targeted alpha therapy. [225Ac]hu11B6-IgG3 was a functionally enhanced alternative to [225Ac]hu11B6-IgG1 but offered no improvement of therapeutic efficacy. Progression free survival was slightly increased with a single high activity compared to fractionated activity. Tumor free animals succumbing after treatment revealed no evidence of treatment associated toxicity. In addition to upregulation of canonical aggressive prostate cancer genes, such as MMP7, ETV1, NTS and SCHLAP1, we also noted a significant decrease in both KLK3 (PSA) and FOLH1 (PSMA) but not in AR and KLK2, demonstrating efficacy of sequential [225Ac]hu11B6 in a mouse model.


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