tbuckley/cabot-search huggingface dataset:
Abstract 1969: PTEN plays a role in histone modifications during mitosis
Authors: Byeong Hyeok Choi, Tania Marlyn Colon, Eunji Lee, Ziyue Kou, Wei Dai
Journal: Cancer Research (2021)

Abstract The tumor suppressor PTEN plays an important role in the regulation of cell survival, proliferation, and angiogenesis. Deregulated expression and/or activities of PTEN frequently result in tumor development. PTEN is a plasma-membrane lipid-phosphatase, functioning to antagonize the PI3K/AKT signaling pathway. It also has a role in the nucleus regulating mitotic progression and suppressing chromosomal instability during cell division. To date, the exact function of nuclear PTEN remains not entirely clear. Several recent studies have revealed that PTEN physically interacts with histones and regulates their post-translational modifications. We previously found that PTEN is heavily phosphorylated by Plk1, which regulates mototic progression and chromosomal instability through its physical interaction with mitotic checkpoint complex (MCC). Therefore, we asked whether PTEN directly interacted with epigenetic regulators and mediated histone modifications and whether PTEN-mediated histone modifications functioned as an important regulatory mechanism during the cell cycle. Here we demonstrated that PTEN was associated with Chromobox Homolog proteins (CBXs) which are part of PRC1 complex that mediates histone modifications. Among CBXs, CBX8 levels were high in mitosis, which were correlated with an increase in PTEN mono-ubiquitination, suggesting its potential involvement in mitotic progression. Supporting this notion, we showed that CBX8 was required for cell proliferation and mitotic progression. Moreover, CBX8 was associated with PTEN/MCC during mitosis and mediated histone H2AK119 mono-ubiquitination. Combined, these results strongly suggest that CBX8/PTEN/MCC plays a significant role in modifying histones and suppressing chromosomal instability during mitotic progression. Citation Format: Byeong Hyeok Choi, Tania Marlyn Colon, Eunji Lee, Ziyue Kou, Wei Dai. PTEN plays a role in histone modifications during mitosis [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2021; 2021 Apr 10-15 and May 17-21. Philadelphia (PA): AACR; Cancer Res 2021;81(13_Suppl):Abstract nr 1969.
The Effects of Renin-Angiotensin System Blockers on Atrial Fibrillation Recurrence Following Pulmonary Vein Isolation
Authors: Hirayama H, Nanasato M, Tatematsu Y, Inoue N, Takigawa M, Aoyama Y, Hashimoto T, Yamamoto T, Yoshida L, Kanemura N, Yoshida Y, Ishikawa K
Journal: Journal of the American College of Cardiology (2009)
Abstract 3107: HSB-1216, A Novel Agent for the Treatment of Chemotherapy-Resistant ES-SCLC
Authors: Anees Mohammad, Sachchidanand Tiwari, Neha Mehrotra, Bozena Korczak, Steve Laumas, Sireesh Appajosyula, Harpal Singh, Surender M. Kharbanda
Journal: Cancer Research (2021)

Abstract Small cell lung cancer (SCLC) is a highly malignant form of lung cancer that accounts for 15% of lung cancer cases. The tumor has a tendency to disseminate early resulting in ~ 85% patients being diagnosed with extensive stage disease (ES-SCLC). Chemotherapy has been the mainstay of treatment for many decades, until recently when immunotherapeutic agents have been approved as first-line agents. However, resistance to anti-cancer drugs represents the main cause of cancer-related deaths. Thus, new therapeutic approach to suppress chemotherapy-resistant ES-SCLC constitutes a significant unmet medical need. We have generated novel biodegradable QUATRAMERTM polymeric nanoparticles comprised of a polyethylene glycol (PEG)-polypropylene glycol (PPG)-PEG- polylactic acid (PLA)-tetra-block copolymer for the intracellular delivery of salinomycin (HSB-1216). Here we studied the HSB-1216 activity in a resistant SCLC cell line (NCI-H69AR). Compared to cisplatin and irinotecan, a second-line agent often used in ES-SCLC, HSB-1216 exhibited a ~7-fold and ~2-fold decrease in IC50in the aggressive and resistant variant of NCI-H69AR cell line and ~30-fold and ~18-fold decrease in a non-resistant NCI-H69 SCLC line. The tumorsphere formation assay has become an essential tool for quantifying cancer stem cells (CSC) and testing of anti-cancer agents. We used this assay to estimate an effect of HSB-1216 on NCI-H69AR tumorspheres .Our results demonstrated significant dose-dependent inhibition of tumorosphere formation in response to HSB-1216. In addition, exposure to HSB-1216 resulted in substantial decrease in number of CD44+/CD24- cells in comparison to untreated control. Furthermore, significant reduction in the expression of CSC markers such as ALDH1 and Oct3/Oct4 was seen when chemotherapy-resistant NCI-H69AR cells were treated with HSB-1216.Taken together, based on these findings, HSB-1216 is being developed as a novel agent in the treatment of second-line ES-SCLC in chemo-resistant tumors, where a gap exists in current standards of care. Further work of this novel agent is planned to outline its effect when combined with targeted and non-targeted therapies in both first- and third-line SCLC. Citation Format: Anees Mohammad, Sachchidanand Tiwari, Neha Mehrotra, Bozena Korczak, Steve Laumas, Sireesh Appajosyula, Harpal Singh, Surender M. Kharbanda. HSB-1216, A Novel Agent for the Treatment of Chemotherapy-Resistant ES-SCLC [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2021; 2021 Apr 10-15 and May 17-21. Philadelphia (PA): AACR; Cancer Res 2021;81(13_Suppl):Abstract nr 3107.
Prevention of Morbidity in Sickle Cell Disease Phase II (Improvement of Pain and Quality of Life in Children with Sickle Cell Disease with Auto-adjusting Continuous Positive Airways Pressure: Phase II) (POMS 2b pediatric cohort)
Authors: April E Slee, Jamie M Kawadler, Melanie Koelbel, Hanne Stotesbury, David C Rees, Maria Pelidis, Jo Howard, Swee Lay Thein, Simon Skene, Sahota Sati, Carol Nwosu, Maureen Gwam, Dawn Saunders, Johanna C Gavlak, Gupta Atul, Simrat Sarkaria, Christina Liossi, Fenella J Kirkham, Baba Inusa
Journal: Blood (2017)
An international cohort study spanning five decades assessed outcomes of nephropathic cystinosis
Authors: Francesco Emma, William van’t Hoff, Katharina Hohenfellner, Rezan Topaloglu, Marcella Greco, Gema Ariceta, Chiara Bettini, Detlef Bockenhauer, Koenraad Veys, Lars Pape, Sally Hulton, Suzanne Collin, Fatih Ozaltin, Aude Servais, Georges Deschênes, Robert Novo, Aurélia Bertholet-Thomas, Jun Oh, Elisabeth Cornelissen, Mirian Janssen, Dieter Haffner, Lucilla Ravà, Corinne Antignac, Olivier Devuyst, Patrick Niaudet, Elena Levtchenko
Journal: Kidney International (2021)
Abstract 1275: Potent ENPP1 inhibitors activating STING pathway in tumor microenvironment
Authors: Zhiyuan Peng, Kun Guo, Ying-Ying Li, Deming Kong, Jinfu Yang, Xiaoli (Shelley) Qin, Xiaolin Hao
Journal: Cancer Research (2021)

Abstract Cyclic GMP-AMP synthase (cGAS) recognizes and binds double-stranded DNA (dsDNA) in the cytosol to generate 2′3′-cGAMP, a cyclic dinucleotide and an activator of STING-dependent innate immunity. Emerging studies revealed that tumor derived 2′3′-cGAMP could act as an immune transmitter and directly trigger anti-tumor immunity. Up to date, Ecto-nucleotide pyrophosphatase/phosphodiesterase-1 (ENPP1/NPP1), a membrane-bound nucleotide hydrolase, was discovered as the predominant enzyme hydrolyzing 2'3'cGAMP. The breakdown of 2'3' cGAMP by ENPP1 may dampen STING-dependent anti-tumor innate immune response. Employing genomic approach, we found that ENPP1 expression varies dramatically among different tumor tissues. Interestingly, ENPP1 expression in breast cancer tissues is overall double the level in normal breast tissues. These results made ENPP1 an attractive cancer immunotherapy target, to enhance STING-dependent innate immunity in tumor microenvironment.We have discovered a novel class of potent ENPP1 inhibitors with pico-molar IC50 in rhENPP1 enzymatic assay. In a cell-based enzymatic assay, compound ZXP-8202 showed an EC50 of 20 nM. To further assess its efficacy on STING-dependent interferon production, 2'3'-cGAMP was added to the culture medium of a high ENPP1-expressing cell line MDA-MB-231 in the absence and presence of ZXP-8202. IFNB1 production in THP1 monocyte was induced when THP-1 cells were incubated with the conditioned medium from MDA-MB-231 cells. In this IFNB1 assay, ZXP-8202 had an EC50 of 10nM. To confirm the ZXP-8202 potency in this culture system reflecting cellular ENPP1 activity, MDA-MB-231 was also treated with 2'3'-cGAMP(PS)2(Rp/Sp), a potent activator of STING but resistant to ENPP1 hydrolysis. The presence of ZXP-8202 showed no effect on 2'3'-cGAMP(PS)2(Rp/Sp) stimulated IFNB1 production in THP-1 cells when cultured in conditioned medium. These results demonstrated ZXP-8202 as a potent ENPP1 inhibitor, blocking 2'3-cGAMP hydrolysis by ENPP1, subsequently activating STING pathway. ZXP-8202 was dosed in CT26 syngeneic mouse model for 14 days and achieved about 70% tumor growth inhibition. No body weight loss was observed at this efficacious dose during treatment. The studies on further characterization of ENPP1 inhibitors and their mechanism of actions are ongoing and the results will be reported in due course. Citation Format: Zhiyuan Peng, Kun Guo, Ying-Ying Li, Deming Kong, Jinfu Yang, Xiaoli (Shelley) Qin, Xiaolin Hao. Potent ENPP1 inhibitors activating STING pathway in tumor microenvironment [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2021; 2021 Apr 10-15 and May 17-21. Philadelphia (PA): AACR; Cancer Res 2021;81(13_Suppl):Abstract nr 1275.
Abstract 495: TNFR2 and PD-1/PD-L1/TNFR2 humanized mice aiding exploration of combination strategies to overcome tumor immune escape mechanisms
Authors: Huilin Li, Xiaofei Zhou, Jing Zhang, Veronika Chromikova, Qingcong Lin
Journal: Cancer Research (2021)

Abstract Tumor necrosis factor receptor 2 (TNFR2), also known as tumor necrosis factor receptor superfamily member 1B (TNFRSF1B), is a transmembrane protein, which can mediate both pro- and anti-inflammatory activities of T cells. TNFR2 is mainly expressed on the surface of activated effector T cells and regulatory T cells (Tregs) and promotes proliferation and survival of Tregs through nuclear factor kappa B (NF-κB). Blockade of TNF-TNFR2 interaction with monoclonal antibodies can inhibit the activation of Tregs, possibly resulting in inhibition of their function and/or reduction of their numbers. Yet, until recently the potential of TNFR2 as a therapeutic target for cancer therapy has been underappreciated. Discovery of anti-TNFR2 antibodies, developed to inhibit NF-κB driven growth, has revived excitement for the use of TNFR2as a cancer therapy target and stressed the demand for suitable pre-clinical models to evaluate the safety and efficacy of TNFR2-targeted therapeutics. Biocytogen has generated a humanized TNFR2 mouse model for both in vitro function validation of signaling pathways and in vivo efficacy evaluation of TNFR2 antibodies. In this model, the exons 2~6 of mouse Tnfrsf1b gene which encode the extracellular domain were replaced by human TNFRSF1B counterparts. In the humanized mouse, human TNFR2 was detectable on Tregs in the spleen and the anti-human TNFR2 antibodies associated well with the splenocytes. In addition, anti-human TNFR2 antibodies bound well to CD3+ T cells and inhibited tumor growth. Furthermore, Biocytogen has also generated PD-1/PD-L1/TNFR2 multi-gene humanized mice, in which blood cell composition, morphology and the levels of ALT, AST and other indicators were similar to the wild-type counterpart. Basal leukocyte subpopulations including T/B/NK cells, DC, granulocytes, and monocytes/macrophages, were similar between humanized and wild-type mice. Moreover, using the MC38 tumor model, the combination of anti-TNFR2 antibody and anti-PD-1 (or anti-PD-L1) shows enhanced effect compared to the individual groups, demonstrating that the PD-1/PD-L1/TNFR2 humanized mice have a potential to provide a powerful preclinical model for in vivo evaluation of combination therapies. In conclusion, TNFR2 and PD-1/PD-L1/TNFR2 humanized mice are a useful tool to explore anti-PD-1, anti-PD-L1 and anti-TNFR2 combination therapy strategies with promising activity and low cytotoxicity. Citation Format: Huilin Li, Xiaofei Zhou, Jing Zhang, Veronika Chromikova, Qingcong Lin. TNFR2 and PD-1/PD-L1/TNFR2 humanized mice aiding exploration of combination strategies to overcome tumor immune escape mechanisms [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2021; 2021 Apr 10-15 and May 17-21. Philadelphia (PA): AACR; Cancer Res 2021;81(13_Suppl):Abstract nr 495.
Impact of Ruxolitinib-Response Feature on Outcome in Myelofibrosis: A Multicentre Study on 356 Patients
Authors: Giulia Benevolo, Giuseppe A Palumbo, Massimiliano Bonifacio, Mario Tiribelli, Maura Nicolosi, Andrea Evangelista, Bruno Martino, Elisabetta Abruzzese, Mariella D'adda, Nicola Polverelli, Micaela Bergamaschi, Alessandra Tieghi, Francesco Cavazzini, Adalberto Ibatici, Monica Crugnola, Costanza Bosi, Roberto Latagliata, Lucia Catani, Franco Aversa, Francesco Di Raimondo, Umberto Vitolo, Roberto Massimo Lemoli, Renato Fanin, Francesco Merli, Antonio Cuneo, Michele Cavo, Massimo Breccia, Nicola Vianelli, Florian Heidel, Francesca Palandri
Journal: Blood (2017)
Abstract 2046: Binding of FANCD2 to SRSF1 splicing factor prevents genomic instability through R-loop regulation
Authors: Anne Olazabal-Herrero, Allison M. Green, Xiaoyong Chen, Patrick Sung, Pillai M. Manoj, Gary M. Kupfer
Journal: Cancer Research (2021)

Abstract BACKGROUND. Fanconi Anemia (FA) is a rare disease characterized by congenital abnormalities, bone marrow failure and cancer susceptibility. The pivotal role of the FA pathway is DNA interstrand crosslink (ICL) repair, where FANCD2-FANCI complex monoubiquitination is the key regulatory step. Recent studies have linked defects in the FA pathway to R-loop metabolism and implicated R-loops as an endogenous source of genomic instability that contributes to the FA phenotype, although the mechanism remains elusive. Splicing factors, such as SRSF1 (ASF/SF2), have also been linked to R-loops, cancer, and myelodysplastic syndrome (MDS), so we hypothesized a link between SRSF1 and FA. METHODS. Cells: FA-D2 mutant (PD20) and corrected (D2), HeLa. siRNA transfections were used to reduce SRSF1 and FANCD2 protein levels. Survival assays were performed to determine cell sensitivity to DNA damaging agents. In vitro immunoprecipitation was performed using SRSF1 purified from bacteria and FANCD2-FANCI purified from insect cells. R-loops were studied using the Damage At RNA Transcription (DART) assay and S9.6 immunofluorescence. RNA FISH was used to measure mRNA export. RESULTS. In order to study the involvement of splicing factors in the FA pathway, we knocked down SRSF1 by using siRNA. SRSF1 knockdown leads to impaired FANCD2 monoubiquitination after DNA damage as well as diminished cell survival, thus creating a FA-like phenotype. In addition, immunoprecipitation in cells and in vitro showed direct interaction between FANCD2 and SRSF1. We found that FANCD2 and SRSF1 knockdown leads to increased R-loops visualized by S9.6 immunofluorescence. Besides, DART assay revealed colocalization of SRSF1 and FANCD2 with R-loops in highly transcribed genomic sites, known to be R-loop hotspots. Additionally, we found that SRSF1 interacts with the mRNA export factor NXF1 in a FANCD2-dependent fashion and through RNA. Interestingly, SRSF1-NXF1 interaction is enhanced upon DNA damage. Finally, we found that FANCD2-deficient cells present defects in mRNA export, suggesting that SRSF1 and FANCD2 could cooperate in the prevention of R-loop formation by exporting accumulated RNA in the nucleus. CONCLUSION. Our findings suggest a novel non-canonical mechanism of FANCD2 via regulation of SRSF1 in R-loop prevention via facilitation of mRNA export, thus preventing genomic instability. Citation Format: Anne Olazabal-Herrero, Allison M. Green, Xiaoyong Chen, Patrick Sung, Pillai M. Manoj, Gary M. Kupfer. Binding of FANCD2 to SRSF1 splicing factor prevents genomic instability through R-loop regulation [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2021; 2021 Apr 10-15 and May 17-21. Philadelphia (PA): AACR; Cancer Res 2021;81(13_Suppl):Abstract nr 2046.
Magnesium implantation or supplementation ameliorates bone disorder in CFTR-mutant mice through an ATF4-dependent Wnt/β-catenin signaling
Authors: Jiankun Xu, Peijie Hu, Xiaotian Zhang, Junjiang Chen, Jiali Wang, Jieting Zhang, Ziyi Chen, Mei Kuen Yu, Yiu Wa Chung, Yan Wang, Xiaohu Zhang, Yifeng Zhang, Nianye Zheng, Hao Yao, Jiang Yue, Hsiao Chang Chan, Ling Qin, Ye Chun Ruan
Journal: Bioactive Materials (2021)

Magnesium metal and its alloys are being developed as effective orthopedic implants; however, the mechanisms underlying the actions of magnesium on bones remain unclear. Cystic fibrosis, the most common genetic disease in Caucasians caused by the mutation of CFTR, has shown bone disorder as a key clinical manifestation, which currently lacks effective therapeutic options. Here we report that implantation of magnesium-containing implant stimulates bone formation and improves bone fracture healing in CFTR-mutant mice. Wnt/β-catenin signaling in the bone is enhanced by the magnesium implant, and inhibition of Wnt/β-catenin by iCRT14 blocks the magnesium implant to improve fracture healing in CFTR-mutant mice. We further demonstrate that magnesium ion enters osteocytes, increases intracellular cAMP level and activates ATF4, a key transcription factor known to regulate Wnt/β-catenin signaling. In vivo knockdown of ATF4 abolishes the magnesium implant-activated β-catenin in bones and reverses the improved-fracture healing in CFTR-mutant mice. In addition, oral supplementation of magnesium activates ATF4 and β-catenin as well as enhances bone volume and density in CFTR-mutant mice. Together, these results show that magnesium implantation or supplementation may serve as a potential anabolic therapy for cystic fibrosis-related bone disease. Activation of ATF4-dependent Wnt/β-catenin signaling in osteocytes is identified as a previously undefined mechanism underlying the beneficial effect of magnesium on bone formation.
Severe consequences of a high-lipid diet include hydrogen sulfide dysfunction and enhanced aggression in glioblastoma
Authors: Daniel J. Silver, Gustavo A. Roversi, Nazmin Bithi, Sabrina Z. Wang, Katie M. Troike, Chase K.A. Neumann, Grace K. Ahuja, Ofer Reizes, J. Mark Brown, Christopher Hine, Justin D. Lathia
Journal: Journal of Clinical Investigation (2021)

Glioblastoma (GBM) remains among the deadliest of human malignancies, and the emergence of the cancer stem cell (CSC) phenotype represents a major challenge to durable treatment response. Because the environmental and lifestyle factors that impact CSC populations are not clear, we sought to understand the consequences of diet on CSC enrichment. We evaluated disease progression in mice fed an obesity-inducing high-fat diet (HFD) versus a low-fat, control diet. HFD resulted in hyperaggressive disease accompanied by CSC enrichment and shortened survival. HFD drove intracerebral accumulation of saturated fats, which inhibited the production of the cysteine metabolite and gasotransmitter, hydrogen sulfide (H2S). H2S functions principally through protein S-sulfhydration and regulates multiple programs, including bioenergetics and metabolism. Inhibition of H2S increased proliferation and chemotherapy resistance, whereas treatment with H2S donors led to death of cultured GBM cells and stasis of GBM tumors in vivo. Syngeneic GBM models and GBM patient specimens present an overall reduction in protein S-sulfhydration, primarily associated with proteins regulating cellular metabolism. These findings provide clear evidence that diet-modifiable H2S signaling serves to suppress GBM by restricting metabolic fitness, while its loss triggers CSC enrichment and disease acceleration. Interventions augmenting H2S bioavailability concurrent with GBM standard of care may improve outcomes for patients with GBM.
Navigating the Changing Multiple Myeloma (MM) Treatment Landscape: Real-World Data on Clinical Practice Patterns in 287 MM Patients Treated in and Outside German DSMM (Deutsche Studiengruppe Multiples Myelom) Study Group Trials
Authors: Laura Gengenbach, Heike Reinhardt, Stefanie Ajayi, Magdalena Szymaniak-Vits, Martin Köhler, Stefan J. Müller, Sandra M. Dold, Martin J. Hug, Markus Ruch, Martin Boeker, Hermann Einsele, Justus Duyster, Ralph Wäsch, Monika Engelhardt
Journal: Blood (2017)
En bloc laser enucleation technique using holmium pulse modulation (virtual basket and bubble blast effects), for the treatment of Benign Prostatic Enlargement (BPE)
Authors: M.E. Rodríguez Socarrás, J. Fernandez Del Alamo, L. Llanes Gonzalez, J. Gomez Rivas, D. Carrion, J. Reinoso Elbers, V. Cuadros Rivera, P. Juarez Del Dago, F. Gomez Sancha
Journal: European Urology (2021)
Abstract 1652: Co-targeting distinct hallmark capabilities for therapeutic benefit in pre-clinical GBM models
Authors: Agnieszka Chryplewicz, Douglas Hanahan
Journal: Cancer Research (2021)

Abstract Glioblastoma (GBM) is the most common primary tumor arising in the central nervous system (CNS). The currently approved standard of care has transient clinical benefit as GBM tends to be exceedingly aggressive. Despite pronounced efforts to identify novel therapies, curative options for GBM do not exist and the survival rate of diagnosed patients is very low. Therefore, there is an urgent need for new treatment strategies, and one approach would be to co-target and thereby disrupt distinct hallmarks of cancer, aiming to elicit sustained therapeutic responses. We have assessed this concept by combining a tricyclic antidepressant -imipramine - with drugs targeting VEGF-A ligand or VEGF-Receptor in mice bearing de novo GBM. All monotherapies were ineffective. In notable contradistinction, we found that combinatorial regimens significantly increased survival benefit and regressed established tumors. Investigation of the basis for the therapeutic efficacy revealed that combining the VEGF pathway inhibitor with imipramine hyperactivated autophagy to the level of eliciting cancer cell-intrinsic autophagy-associated cell death, whilst modifying the tumor vasculature to be more normal-like. In addition, imipramine downregulated an M2-like phenotype of tumor-associated macrophages and reprogramed them to express chemokines attracting otherwise rare CD8 T cells, which were demonstrably contributing to the observed efficacy. As such, these hallmark co-targeting combinations served to reprogram the GBM microenvironment from immunosuppressive to pro-inflammatory, thereby sensitizing the tumors to immune checkpoint blockade, as evidenced by enhanced responses when an anti-PD-L1 therapy was included in the mix. The results to be presented will elaborate a provocative new therapeutic approach for glioblastoma that has prospect to motivate clinical evaluation in this daunting form of human cancer. Citation Format: Agnieszka Chryplewicz, Douglas Hanahan. Co-targeting distinct hallmark capabilities for therapeutic benefit in pre-clinical GBM models [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2021; 2021 Apr 10-15 and May 17-21. Philadelphia (PA): AACR; Cancer Res 2021;81(13_Suppl):Abstract nr 1652.
The real impact of the delay in presenting to the emergency department with acute renal colic: which patients are at risk?
Authors: S. Tappero, S. Parodi, G. Mantica, D.M. Carrion, M. Antón-Juanilla, K.H. Pang, A. Rodriguez-Serrano, V. Crespo-Atìn, R. Cansino, R.M. Scarpa, S. Nikles, J.G. Rivas, N. Suardi, F. Esperto, C. Terrone
Journal: European Urology (2021)