tbuckley/cabot-search huggingface dataset:
Simply Adjusting for Schedulers’ Bias in Estimated Case Durations Can Accomplish the Same Objectives of Improving Predictions as Use of Machine Learning—Reply
Authors: Christopher T. Strömblad, Roger S. Wilson
Journal: JAMA Surgery (2021)

In Reply We appreciate Dexter and Epstein for their interest in our article. Prior to developing the randomized clinical trial,1 we explored different modeling approaches and data inputs. We selected the random forest model because it provided the best results on a testing set.
光干渉断層計(OCT)を用いた薬物溶出ステント埋込後の新生内膜の特性の解析
Authors: Ikuta Shinichiro, Tsujimoto Toshikazu, Nakauchi Yoshihumi, Ohe Kentaro, Yamaji Kenji, Miyazaki Shunichi
Journal: Circulation (2009)
Abstract 664: Development and validation of a glycolysis-related gene signature to predict overall survival in lung adenocarcinoma patients
Authors: Shengguang Wang, Zhang Bei
Journal: Cancer Research (2021)

Abstract Background: Genomic expression profiles have enabled the classification of lung adenocarcinoma (LUAD) into molecular sub-types and provide prognostic information, which have implications for the personalized treatment of LUAD beyond clinical and pathological features. Methods: Gene-expression profiling was performed on 459 patients in TCGA-LUAD(I-IIIa) for which RNA sequencing data and clinical covariates were available. A single-sample gene set enrichment analysis (ssGSEA) algorithm were used to quantified the levels of various hallmarks of cancer. And LASSO Cox regression model was used to screen robust prognostic biomarkers to identify the best set of survival-associated gene signatures in LUAD. Statistical analyses were performed using R version 3.4.4. Results: We identified glycolysis as the primary risk factor for survival(HR=0.55 [0.38-0.8], P&amp;lt;0.001)among various hallmarks of cancer in TCGA-LUAD. And glycolysis ssGESA scores were significantly elevated in patients who died during follow up (P&amp;lt;0.001). Kaplan-Meier analysis showed that patients with high ssGSEA scores of glycolysis exhibited worse OS ( HR=1.9,P= 0.001).Adjusted for stage,age,gender, our signature was an independent risk factor for overall survival in TCGA cohorts (HR=1.67[1.19-2.30],P= 0.003). We then apply the glycolysis -related gene signature to classify patients into the high risk group and the low risk group with the cutoff of median. In external independent cohorts, similar results were observed. In the validation cohort GEO31210, the multivariate Cox regression analysis showed that glycolysis -related gene signature exhibited an independent risk prediction for overall survival in 226 patients with stage I-II LUAD (HR=2.5 [1.11-5.5], P =0.025). Conclusions: By analyzing the gene-expression data with bioinformation approach, we developed and validated a risk prediction model with glycolysis -related expression scores in early stage LUAD, which have the potential to identify patients who could have better overall survival. Furthmore, our study confirmed that tumor glycolysis has wide-ranging effects, would become an attractive therapeutic target. Citation Format: Shengguang Wang, Zhang Bei. Development and validation of a glycolysis-related gene signature to predict overall survival in lung adenocarcinoma patients [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 664.
Abstract 714: From cancer to COVID-19- development of a dendritic cell-targeted nano-vaccine for prevention and therapy of COVID-19
Authors: Daniella Vaskovich-Koubi, Ron Kleiner, Yulia Liubomirski, Eilam Yeini, Galia Tiram, Sabina Pozzi, Anat Eldar-Boock, Helena F. Florindo, Ronit Satchi-Fainaro
Journal: Cancer Research (2021)

Abstract Dendritic cells (DC) are antigen-presenting cells with an important role in the initiation and regulation of the innate and adaptive arms of the immune system. By efficient presentation of antigens, DC elicit an antigen-specific immune response. Therefore, we previously established in our laboratory a melanoma-DC-targeted NP that was evaluated and validated against aggressive melanoma. Although DC-therapy is mainly exploited in the treatment of cancer, DC are becoming a key therapeutic target in other pathologies such as infectious diseases. Viral pathogens, similarly, to cancer, modulate the host defense mechanisms to their benefit. COVID-19, an ongoing pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has spread globally and is already infecting tens of millions of people worldwide. Historically, vaccines are among therapies with the greatest impact in health and constitute an unmet medical need against coronavirus disease-19 (COVID-19) pandemic. To that end, we repurposed our recently published melanoma-targeted NP to co-deliver modulators of host immune response and SARS-CoV-2 specific antigen epitopes discovered by a computational approach integrating 3D information with large-scale statistical analysis. The immune response kinetics in patients infected with SARS-CoV-2 is poorly understood, but recent reports show that germinal B cells and active follicular T-helper cells, IgM/IgG SARS-CoV-2 antibodies, in addition to an enhanced cellular immunity, are found in patients with mild-to-moderate SARS-CoV-2 infection. Our preliminary data demonstrated that our nano-vaccine was able to activate specific immune cell response of effector T cells and B cells and decrease the regulatory activity of T cells, compared to controls. Moreover, we found that our DC-targeted SARS-CoV-2 NP successfully induced antigen-specific secretion of IgM and IgG antibodies with high binding affinity to the antigens. Importantly, our nano-vaccine elicited specific neutralization of Spike virus like particles (VLPs) by sera of immunized mice. We hypothesize that implementing our novel nano-vaccine platform for COVID-19 will lead to a safe and efficacious COVID-19 vaccine ready for first-in-human clinical trials. Citation Format: Daniella Vaskovich-Koubi, Ron Kleiner, Yulia Liubomirski, Eilam Yeini, Galia Tiram, Sabina Pozzi, Anat Eldar-Boock, Helena F. Florindo, Ronit Satchi-Fainaro. From cancer to COVID-19- development of a dendritic cell-targeted nano-vaccine for prevention and therapy of COVID-19 [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 714.
Abstract 2273: MAPK signaling pathway disruption explains the anticancer mechanism for polyisoprenylated cysteinyl amide inhibitors (PCAIs)
Authors: Nada Tawfeeq, Yonghao Jin, Nazarius Lamango
Journal: Cancer Research (2021)

Abstract The Mitogen-activated protein kinase (MAPK) pathway is one of the key signaling pathways that regulates normal cell proliferation, differentiation, and survival. Abnormalities of the pathway play vital roles in cancer initiation and progression. Ras small GTPases that are key upstream mediators of the MAPK pathway are mutated in 20%-30% of human tumors. KRAS is the most frequently mutated isoform of the RAS proteins, accounting for up to 86% of RAS mutant cancer cases. Mutant KRAS is prevalent in lung, colon, and pancreatic cancers, which considered to be the most aggressive and account for the most cancer deaths in the US. To help mitigate this problem and fill the therapeutic need that has lingered for decades, polyisoprenylated cysteinyl amide inhibitors (PCAIs) were designed and synthesized to target the hyperactivity of aberrant monomeric G-Proteins. Recently, the PCAIs underwent a synthetic optimization to mitigate the excessive hydrophobicity of the earlier analogs. While the newer agents are more polar and have maintained the effectiveness of the earlier PCAIs against cancer cell lines driven by mutant KRAS proteins, the specific anticancer mechanisms are still unclear. Thus, we explored the effects of the newer PCAIs on the MAPK pathway using lung cancer A549 cells which harbor the KRAS mutation. When the cells were treated with NSL-YHJ-2-27 for 48 h, the KRAS protein levels dropped by 40% at 5μM compared to the controls. However, no significant difference was observed in the levels of total or phosphorylated B- and C-Raf proteins. Moreover, it was observed that the PCAIs immensely stimulated the MAPK pathway in a concentration-dependent manner following treatment with 1, 2, and 5μM of NSL-YHJ-2-27. The phosphorylation of MEK1/2, ERK1/2, and p90RSK significantly increased by 84%, 59%, and 160%, respectively, relative to controls following treatment for 48h at 5 µM of NSL-YHJ-2-27. Interestingly, a non-farnesylated analog, NSL-YHJ-2-62, did not elicit similar effects on the MAPK pathway. Although ERK stimulation has mostly been associated with cell survival and proliferation, various studies show that ERK activation can also mediate apoptosis depending on the intensity and duration of the stimulation. These data reveal that the Ras-MAPK signaling axis is involved in the anticancer effects of the PCAIs. The PCAIs may thus be considered as possible agents for the unmet therapeutic needs of patients with aberrantly hyperactive G-proteins. Citation Format: Nada Tawfeeq, Yonghao Jin, Nazarius Lamango. MAPK signaling pathway disruption explains the anticancer mechanism for polyisoprenylated cysteinyl amide inhibitors (PCAIs) [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 2273.
Abstract 1918: Coxsackievirus A11 elicits a potent oncolytic activity in human malignant pleural mesothelioma via ICAM-1 receptor
Authors: Koji Okamura, Hiroyuki Inoue, Yuki Ikematsu, Rie Furukawa, Keiichi Ota, Yasuto Yoneshima, Eiji Iwama, Kentaro Tanaka, Isamu Okamoto
Journal: Cancer Research (2021)

Abstract Malignant pleural mesothelioma (MPM) is an aggressive solid cancer with dismal prognosis. Oncolytic virotherapy is a promising anticancer treatment that directly lyses tumor cells. Coxsackievirus A11 (CVA11) is an emerging oncolytic virus against solid cancers. Herein we tested whether CVA11 infection has an oncolytic activity in human MPM cell lines and identified its cognate receptor. We found that CVA11 infection shows a remarkable oncolytic activity in six of six human MPM cell lines. MPM cells having higher intercellular adhesion molecule-1 (ICAM-1) expression showed higher CVA11-induced cytotoxicity, and that identified ICAM-1 as its surface receptor because coinfection with neutralizing ICAM-1 antibody substantially abrogated CVA11-triggered cytotoxicity in MPM cells. In addition, we unraveled that the activations of both phosphoinositide 3-kinase/Akt and mitogen-activated protein (MAP)/extracellular signal-regulated (ERK) kinase (MEK) signaling pathways partially but significantly contributed to the CVA11-triggered cytotoxicity of CVA11 as evidenced by treating with respective inhibitors. Taken together, our findings show a novel oncolytic virotherapy using CVA11 could be an alternative therapeutic modality for human MPM. Citation Format: Koji Okamura, Hiroyuki Inoue, Yuki Ikematsu, Rie Furukawa, Keiichi Ota, Yasuto Yoneshima, Eiji Iwama, Kentaro Tanaka, Isamu Okamoto. Coxsackievirus A11 elicits a potent oncolytic activity in human malignant pleural mesothelioma via ICAM-1 receptor [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 1918.
Abstract 2064: Homologous recombination repair somatic/germline mutation detection in plasma by next-generation sequencing in Chinese solid tumor patients
Authors: Wei Zhu, Hui Chen, Bei Zhang, Xiaochen Zhao, Yuezong Bai
Journal: Cancer Research (2021)

Abstract Purpose: PARP inhibitors (PARPis) have been approved for germline and/or somatic BRCA-mutated ovarian cancer, breast cancer, pancreatic cancer and homologous recombination repair gene (HRR)-mutated prostate cancer. Emerging evidence has shown that antitumor activity of PARPis could expand to other HRR-mutated solid tumors. Therefore, efficient and timely methods to detect both somatic and germline HRR mutations using tissue or blood are urgently needed. Here, we first specially reported the prevalence of HRR mutation in plasma samples using Next-generation sequencing (NGS). Methods: A total of 1601 paired plasma-white blood cell samples and 3404 paired tumor-white blood from Chinese solid tumor patients were collected between October 2019 and October 2020. The samples were assessed with targeted NGS of circulating tumor DNA (ctDNA) or tumor tissue DNA (ttDNA) to detect deleterious somatic and germline mutations in 16 core HR genes in a CLIA-certified laboratory. Results: Overall, 165/1601 (10.3%) patients had at least one somatic or germline HRR gene mutations by ctDNA-based NGS analysis. The most commonly mutated tumor types were endometrium (42.9%, n=7), ovary (38.5%, n=13), prostate (27.8%, n=108), neuroendocrine (20%, n=5), breast (19%, n=42), melanoma (16.7%, n=6), stomach (15.8%, n=101), biliary tract (15.6%, n=64), cervix (12.5%, n=8), pancreas (11.4%, n=70), colorectum (9.8%, n=174) and bladder urinary tract (9.5%, n=21). Except for the four tumor types (endometrium, neuroendocrine, melanoma and cervix) with less than ten samples, the prevalence of HRR mutation was comparable with the ttDNA-based NGS data. Among HRR mutations, BRCA2 was the most commonly mutated gene (3.2%), followed by ATM (2.4%), BRCA1 (1.4%), CHEK2 (1.2%), BARD1 (0.7%), PALB2 (0.7%), CDK12 (0.7%) and FANCA (0.5%). Most of these data was similar to the results of ttDNA-based NGS. Moreover, slightly higher prevalence was found in BRCA2 (3.2% vs 2.5%) and CHEK2 (1.2% vs 0.7%), and slightly lower prevalence was found in ATM (2.4% vs 3.2%) and CDK12 (0.7% vs 1.4%). Conclusion: We first described the prevalence of somatic and/or germline HRR mutations detected by ctDNA-based NGS in a Chinese solid tumor cohort. Further prospective study is needed to compare the impact of the HRR status identified by ctDNA and ttDNA NGS on PARPis efficacy. Citation Format: Wei Zhu, Hui Chen, Bei Zhang, Xiaochen Zhao, Yuezong Bai. Homologous recombination repair somatic/germline mutation detection in plasma by next-generation sequencing in Chinese solid tumor patients [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 2064.
Heat wave causes hundreds of deaths and hospitalisations in Pacific north west
Authors: Joanne Silberner
Journal: BMJ (2021)

Governments in south western Canada and the north west corner of the US are now counting the dead and considering the region’s ability to respond to extreme temperatures after an unprecedented heat wave in late June. The weather in this part of the world is usually temperate.

Warnings of a massive “heat dome”1 started a few days before the thermometers began to rise on 27 June. Meteorologists predicted temperatures near 38°C in Seattle, Washington, and 43°C in Portland, Oregon. Many areas began setting up wading pools, spray parks, and cooling centres. The heat dome, which lasted five days, turned out to be worse than expected. Seattle hit a record high of 42°C and Portland reported temperatures of 47°C. In British Columbia, temperatures …
Abstract 1681: Correlation of <i>BRCA1/2</i> mutations with response to immune checkpoint inhibitors in colorectal cancer
Authors: Dong-Dong Jia, Yanling Niu, Tonghui Ma, Min Shi
Journal: Cancer Research (2021)

Abstract Background: BRCA1 and BRCA2 are involved in homologous recombination (HR) DNA repair. They have been found to promote both tumor initiation and progression. BRCA1/2 mutations lead to genomic instability and higher tumor mutation burden (TMB). Therefore, we hypothesized that BRCA1/2 mutations may be a predictor of immune checkpoint inhibitors (ICIs) efficacy. In the present work, we explored the correlation of BRCA1/2 mutations with TMB, high microsatellite instability (MSI-H), PD-L1 expression, tumor-infiltrating lymphocytes (TILs), and ICIs efficacy in colorectal cancer. Methods: A total of 509 Chinese colorectal cancer patients were enrolled from January 2017 to January 2020 in our center. Targeted next-generation sequencing and PD-L1 immunohistochemistry (22C3 antibody) were performed in the tissues from patients. TCGA colorectal cancer cohort was used for characterizing TILs with CIBERSORT. The ICIs treatment cohort from the Memorial Sloan Kettering Cancer Center (MSKCC) was selected to analyze the association of BRCA1/2 mutations with ICIs efficacy. Results: In our cohort, the mutational frequency of BRCA1/2 genes was 9.04%. The median TMB was significantly higher in the BRCA1/2 mutations (Mut) group compared to the wild type (WT) group (52.4 vs 5.7 muts/Mb, P &amp;lt; 0.0001). About 41.30% of patients have MSI-H in the Mut group, while 3.67% of patients display MSI-H in the WT group (P &amp;lt; 0.0001). There was no association of BRCA1/2 mutations with PD-L1 expression (P = 0.172). In TCGA cohort, BRCA1/2 mutations can down-regulate regulatory T (T reg) cells (P = 0.0176) and up-regulate T follicular helper cells (P = 0.0042) and macrophages M1 (P &amp;lt;0.0001). In MSKCC cohort, patients in the Mut group had significantly longer median overall survival after ICIs therapy (34 vs 13 months, HR: 0.37 [95%CI: 0.19-0.72], P = 0.0234). Conclusions: Our data indicated that BRCA1/2 mutations are associated with increased TMB and MSI-H, but not with PD-L1 expression. And BRCA1/2 mutations can regulate TILs. Furthermore, BRCA1/2 mutations are associated with better response to ICIs, suggesting that they may be a useful predictor for ICIs efficacy in colorectal cancer. Citation Format: Dong-Dong Jia, Yanling Niu, Tonghui Ma, Min Shi. Correlation of BRCA1/2 mutations with response to immune checkpoint inhibitors in colorectal cancer [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 1681.
Transcription-coupled structural dynamics of topologically associating domains regulate replication origin efficiency
Authors: Yongzheng Li, Boxin Xue, Mengling Zhang, Liwei Zhang, Yingping Hou, Yizhi Qin, Haizhen Long, Qian Peter Su, Yao Wang, Xiaodong Guan, Yanyan Jin, Yuan Cao, Guohong Li, Yujie Sun
Journal: Genome biology (2021)

Metazoan cells only utilize a small subset of the potential DNA replication origins to duplicate the whole genome in each cell cycle. Origin choice is linked to cell growth, differentiation, and replication stress. Although various genetic and epigenetic signatures have been linked to the replication efficiency of origins, there is no consensus on how the selection of origins is determined.
Real-world data shows increased reactogenicity in adults after heterologous compared to homologous prime-boost COVID-19 vaccination, March−June 2021, England
Authors: Annabel A Powell, Linda Power, Samantha Westrop, Kelsey McOwat, Helen Campbell, Ruth Simmons, Mary E Ramsay, Kevin Brown, Shamez N Ladhani, Gayatri Amirthalingam
Journal: Eurosurveillance (2021)

Adults receiving heterologous COVID-19 immunisation with mRNA (Comirnaty) or adenoviral-vector (Vaxzevria) vaccines had higher reactogenicity rates and sought medical attention more often after two doses than homologous schedules. Reactogenicity was higher among ≤ 50 than &gt; 50 year-olds, women and those with prior symptomatic/confirmed COVID-19. Adults receiving heterologous schedules on clinical advice after severe first-dose reactions had lower reactogenicity after dose 2 following Vaxzevria/Comirnaty (93.4%; 95% confidence interval: 90.5–98.1 vs 48% (41.0–57.7) but not Comirnaty/Vaxzevria (91.7%; (77.5–98.2 vs 75.0% (57.8–87.9).
Diagnosis and treatment of COVID-19 associated pulmonary apergillosis in critically ill patients: results from a European confederation of medical mycology registry
Authors: Juergen Prattes, Joost Wauters, Daniele Roberto Giacobbe, Katrien Lagrou, Martin Hoenigl, Philipp Koehler, Jon Salmanton-García, Riina Rautemaa-Richardson, Stefan Hatzl, Johan Maertens, Yves Debaveye, Marc Bourgeois, Marijke Reynders, Lynn Rutsaert, Niels Van Regenmortel, Piet Lormans, Simon Feys, Alexander Christian Reisinger, Oliver A Cornely, Tobias Lahmer, Maricela Valerio, Laurence Delhaes, Kauser Jabeen, Joerg Steinmann, Mathilde Chamula, Matteo Bassetti
Journal: Intensive Care Medicine (2021)
Abstract LB211: Epstein-Barr virus BART lncRNAs induce <i>IKZF3</i>/Aiolos to maintain EBV latency and promote tumorigenicity in nasopharyngeal carcinoma
Authors: Songtao HE, Jiayan Liu, Honglin Chen
Journal: Cancer Research (2021)

Abstract Epstein-Barr virus (EBV) infection is one of the main causative factors of nasopharyngeal carcinoma (NPC), which is prevalent in southern China and some Southeast Asian countries. EBV infection in NPC cells is characteristically type II latency, where very few viral proteins (EBNA1, LMP1 and LMP2A) but high levels of noncoding RNAs (especially BARTs: BamHI-A rightward transcripts) are expressed. Our previous study found that BART lncRNAs modulate transcription of IKZF3, which encodes Aiolos, through epigenetic pathways in NPC cells. However, the biological significance functional mechanism of IKZF3/Aiolos are not yet clearly defined. We now further show that IKZF3/Aiolos expression levels are associated with copy numbers of EBV episomes in the EBV-harboring NPC cell line, NPC43, and specifically correlate to the level of lnc-BARTs, as demonstrated using CRISPR systems. Transcriptomic analysis of IKZF3-knockout C666-1 NPC cells revealed that 17 EBV-encoded microRNAs and 53 lytic genes were significantly downregulated or upregulated (FDR p value &amp;lt;0.05 and posterior fold changes &amp;gt;1.5). Immunoblot testing showed that the EBV lytic reactivator Zta and antigen BMRF1 are upregulated following knockout of IKZF3 in C666-1 cells, suggesting involvement of IKZF3/Aiolos in maintaining EBV latency in NPC. Gene ontology and KEGG (Kyoto Encyclopaedia of Genes and Genomes) analysis of IKZF3-knockout C666-1 cells found that most of the host genes with differential expression that are enriched in Epstein-Barr virus infection are associated with apoptosis, focal adhesion, cancer cell growth and mammary neoplasm (p value &amp;lt;0.01). In addition, a soft agar assay demonstrated that oncogenic transformation of C666-1 cells was attenuated after knocking down expression of lnc-BARTs, knocking out IKZF3, or treatment with the IKZF3 inhibitor lenalidomide. Immunoprecipitation (IP) testing showed that Aiolos interacted with core elements (HDAC1 and MTA2) of the Mi-2/NuRD (nucleosome remodelling deacetylase) complex in NPC cells. Our findings suggest that Aiolos may recruit Mi-2/NuRD complexes for deacetylation of histone lysine residues bordering promoter regions of EBV lytic genes and host tumour suppressor genes, leading to inhibition of reactivation of EBV lytic infection, thereby preventing apoptosis of NPC cells. Citation Format: Songtao HE, Jiayan Liu, Honglin Chen. Epstein-Barr virus BART lncRNAs induce IKZF3/Aiolos to maintain EBV latency and promote tumorigenicity in nasopharyngeal carcinoma [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 LB211.
ステント内再狭窄(ISR)病変に対して再PCI後の血流障害の決定因子
Authors: Koiwaya Hiroshi, Shibata Yoshisato, Nishino Shun, Ogata Kenji, Kimura Toshiyuki, Inoue Yohei, Fukushima Yusuke, Nakama Tatsuya, Furugen Makoto, Sagara Shuichiro, Ashikaga Keiichi, Kuriyama Nehiro, Matsuyama Akihiko, Ueno Takafumi, Fukumoto Yoshihiro
Journal: Circulation (2014)
Very low risk of severe complications after a single, post-operative instillation of intravesical chemotherapy in patients with low- or intermediate risk urothelial carcinoma of the bladder
Authors: L.M.C. van Hoogstraten, J.A. Witjes, T.M. Ripping, R.I. Nooter, L.A. Kiemeney, K.K.H. Aben
Journal: European Urology (2021)