tbuckley/cabot-search huggingface dataset:
Relation of the BIM deletion polymorphism to intrinsic EGFR-TKI resistance of Chinese patients with EGFR mutant advanced non-small cell lung cancer.
Authors: Shuang Xin, YuanYuan Zhao, Yuxiang Ma, Xueding Wang, Yan Huang, Hongyun Zhao, Chen Zhu, Yunpeng Yang, Li Zhang, Min Huang
Journal: Journal of Clinical Oncology (2016)

e14095 Background: In order to identify the influence of BCL2-like 11 (BIM) gene deletion polymorphism, which results in expression of BIM isoforms lacking the proapoptotic BCL2-homology domain 3 (BH3), on EGFR-TKI responses, we detected Bim deletion polymorphism in Chinese patients with EGFR mutant NSCLC. Methods: The blood sample and clinical data of a group of 295 EGFR mutant NSCLC patients who were administrated with gefitinib or erlotinib were collected retrospectively. BIM polymorphism was identified by Sanger sequencing. Results: BIM deletion polymorphism was detected in blood of 8.1% (24 of 295) patients,2 patients were found to be mutation homozygous, 22 patients were mutation heterozygous. The PFS were not significantly different between BIM deletion carriers and those without BIM deletion (median, 14.17 months versus 19.37 months; p = 0.394). Multivariate Cox regression analysis showed that BIM deletion was not an independent indicator of shorter PFS (hazard ratio, 1.326; 95% confidence interval, 0.691-2.543). Conclusions: We conclude that the BIM deletion polymorphism cannot account for intrinsic EGFR-TKI resistance of Chinese patients with EGFR mutant NSCLC. Our result suggests that the mechanism of primary resistance might be heterogeneous.
Institutional treatment volume and outcomes in salivary gland cancer.
Authors: Conor Ernst Steuer, Jeffrey M. Switchenko, Christopher C Griffith, Mihir Patel, Richard John Cassidy, Theresa Wicklin Gillespie, Mark William McDonald, Kristin Ann Higgins, Jonathan Jay Beitler, Taofeek Kunle Owonikoko, Zhuo Georgia Chen, Dong Moon Shin, Nabil F. Saba
Journal: Journal of Clinical Oncology (2017)

6082 Background: Salivary gland cancer (SGC) is a rare malignancy and has been understudied in the literature. Given the rarity of SGC, we sought to compare outcomes of SGC within high volume (HV) and low volume (LV) centers, utilizing the National Cancer Database (NCDB). Methods: The NCDB was queried from 2004 to 2014 for SGC using ICD-O-3 codes for the 4 most common histologies: (mucoepidermoid carcinoma (ME), adenoid cystic carcinoma (AdCC), acinic cell carcinoma(ACC), and adenocarcinoma NOS(A)) for consistency. The number of cases treated at each facility was calculated, and the threshold for distinguishing high volume vs. low volume was determined using the 80 th percentile of the number of cases treated per facility. Patient characteristics were compared using chi-squared tests and ANOVA. Overall survival was estimated using the Kaplan-Meier method, and was compared using log-rank tests. Statistical analyses were performed using SAS 9.4. Results: There were 31,189 SG patients overall; 16,373 were either ME, AdCC, ACC, or A and were included in the analysis. There were 6534 patients treated in LV (41%) and 9839 in HV (59%). HV centers were more likely to be academic and integrated network cancer programs (p &lt; .001). The median age for LV vs. HV was 61y vs. 58y (p &lt; .001), 49% vs. 47% male (p = .007), and 84% vs. 80% White (p &lt; .001), respectively. Patients presented with slightly more advanced disease at HV, with 24.4% having stage 3-4 disease, vs 23% in LV (p = .004). The majority of patients underwent surgical resection (57% LV vs. 64% HV). HV had more negative margins (59% vs 55%, p &lt; .001), more neck dissections (72% vs. 64%, p &lt; .001), and longer hospital stays (mean 2.21d vs 1.55d, p &lt; .001). More patients in LV received radiation than HV (55% vs. 52%, p &lt; .001), but there was no difference in chemotherapy use (p = 0.650). Patients had better survival (m1 disease excluded) in HV as compared to LV (5-year OS HV 77.4% vs LV 75.5%, HR 0.89, p = 0.002). Conclusions: Our results indicate that survival of SGC is affected by institutional treatment volume and the significant differences in treatment at LV vs. HV institutions urges for the need of better standardization of care.
Effect of adequate hypomethylating agent (HMA) therapy on adverse prognostic factors in very elderly patients (>75 yrs) with myelodysplastic syndrome (MDS).
Authors: Vipin Lohiya, Garrett Sherwood, Bradford E. Jackson, Uma Borate
Journal: Journal of Clinical Oncology (2016)

e18553Background: Very elderly MDS patients ( ≥ 75 years) have limited therapeutic options. We studied the impact of available MDS therapies in very elderly MDS patients and their correlation with ...
Effect of knockdown of eukaryotic initiation factor 4A2 (eIF4A2) on growth, metastasis, and oxaliplatin sensitivity in colorectal cancer.
Authors: Zhan-Hong Chen, Qinian Wu, Jiahuan Lu, Jingjing QI, Zexian Liu, Yun Wang, Xiangyuan Wu, Ya Chen, Zhao-Lei Zeng, Huaiqiang Ju, Rui-hua Xu
Journal: Journal of Clinical Oncology (2018)

e15658 Background: Our previous study found that eIF4A2 was highly expressed in colorectal cancer and high eIF4A2 expression predicted poor prognosis, which was reported in ASCO GI 2018. However, the regulating mechanism of eIF4A2 in colorectal cancer remains unknown. Methods: We knockdowned eIF4A2 in HCT116 and DLD1 cell lines. We used sphere formation test. We used quantitative real-time polymerase chain reaction(RT-PCR) to compare expression of stemness-associated genes (Nanog, Oct-4, Bmi-1, Notch-1 and Smo), multiple drug-resistant transporter genes (ABCC2, ABCG2) and surface antigens associated with cancer stem cells (CD24, CD44, CD105 and CD133). We used western-blot(WB) to identify change of CD133 and OCT4. We identified the downstream target genes by using a human tumor metastasis profiler PCR array and the top three downstream genes with the most significant decrease were further verified by WB. We carried out MTT test to calculate IC50 changes when HCT116 and DLD1 cells with eIF4A2 knockdown were treated with oxaliplatin. The impact of eIF4A2 knockdown on tumor growth, metastasis and sensitivity to oxaliplatin was also determined in nude mouse model. Results: Knockdown of eIF4A2 significantly reduced the sphere formation in HCT116 and DLD1 cells (P < 0.05). Real-time PCR analysis showed knockdown of eIF4A2 markedly decreased the mRNA level of Nanog, Oct-4, Bmi-1, Notch-1, Smo, ABCC2, ABCG2, CD24, CD44, CD105 and CD133(P < 0.05). RT-PCR array showed that C-MYC, MTA1 and KRAS mRNA level significantly decreased after knockdown of eIF4A2 (P < 0.05). WB showed OCT4 and C-MYC significantly decreased butCD133, MTA1 and KRAS remained unchanged. When HCT116 and DLD1 cells with eIF4A2 knockdown were treated with oxaliplatin, IC50 significantly decreased and inhibition rate significantly increased(P < 0.05). Knockdown of eIF4A2 significantly inhibits tumor growth, lung metastasis and improves oxaliplatin sensitivity in vivo(P < 0.05). Conclusions: Knockdown of eIF4A2 inhibits growth, metastasis and improves oxaliplatin sensitivity in colorectal cancer.
Searching for predictive biomarkers on the efficacy of cetuximab plus chemotherapy for patients with unresectable colorectal liver-limited metastases: An expended biomarker analysis based on BELIEF study.
Authors: Jianmin Xu, Ye Wei, Li Ren, Peng Zheng, Le-chi Ye, Qingyang Feng, Dexiang Zhu, Wenju Chang, Meiling Ji
Journal: Journal of Clinical Oncology (2016)

e15079 Background: To identify predictive biomarkers for the efficacy of cetuximab. Materials and Methods: The DNA samples from 106 patients were sequenced for single nucleotide polymorphisms (SNPs) of biomarkers including the well-known
A new clinical variant of acquired reactive perforating dermatosis‐like bullous pemphigoid
Authors: F. Schauer, J.S. Kern, O. Virtic, K. Technau‐Hafsi, F. Meiss, K. Thoma, I. Athanasiou, C. Sitaru, G. Di Zenzo, K. Izumi, W. Nishie, H. Shimizu, L. Bruckner‐Tuderman, D. Kiritsi
Journal: British Journal of Dermatology (2018)
How sensitive are epidermal growth factor receptor-tyrosine kinase inhibitor for lung adenosquamous cell carcinoma harboring EGFR mutation? A bicenter research and pooled analysis of published reports.
Authors: Yong-Mei Liu, Xueming Xia, Wei Du, Yan Zhang, Jianlin Xu, You-Ling Gong, Yong Xu, Jiang Zhu, Zhen-Yu Ding, Feng Peng, Meijuan Huang, Jin Wang, Li Ren, You Lu, Baohui Han, Yongsheng Wang
Journal: Journal of Clinical Oncology (2017)

e20571 Background: Lung adenosquamous cell carcinoma (ASC) is a rare subtype of lung cancer. Little is known about the efficacy of epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) for lung ASC with EGFR mutation. Methods: We retrospectively analyzed 44 patients with advanced or recurrent lung ASC harboring EGFR mutation who were treated with EGFR-TKI from two cancer centers to investigate the efficacy. Then a pooled analysis on the efficacy of EGFR-TKI was performed in 74 patients including 30 patients selected from 11 published reports. Results: In our bicenter research, for the ASC patients treated with EGFR-TKI, the objective response rate (ORR), the disease control rate (DCR), the median progression free survival (mPFS) and the median overall survival (mOS) were 54.5%, 79.5%, 8.8 months and 19.43 months, respectively. In pooled analysis, the ORR, DCR, mPFS and mOS of ASC patients were 63.4%, 85.9%, 10.00 months and 21.37 months, respectively. Similar PFS (11.0 vs. 10.0 months; P= 0.771) and OS (23.67 vs. 20.33 months; P= 0.973) were found in patients with deletion in exon 19 and exon 21 L858R mutation. The patients treated with erlotinib or gefitinib had a trend of better OS than those treated with icotinib. Conclusions: EGFR-TKI is an effective treatment for ASC harboring EGFR mutation, comparing with historical data, similar to EGFR-mutated adenocarcinoma (ADC). Further study is needed to identify the different role of the two components of ASC in EGFR treatment.
Combined encapsulation of a tumor antigen and immune cells using a self-assembling immunostimulatory DNA hydrogel to enhance antigen-specific tumor immunity
Authors: Yuka Umeki, Masaaki Saito, Kosuke Kusamori, Mari Tsujimura, Moeka Nishimura, Yuki Takahashi, Yoshinobu Takakura, Makiya Nishikawa
Journal: Journal of Controlled Release (2018)
Abstract B09: Evaluating transcription factor networks as targets for the treatment of small cell lung cancer
Authors: Karine Pozo, Rahul K. Kollipara, John D. Minna, Adi F. Gazdar, Jane E. Johnson
Journal: Clinical Cancer Research (2018)

Abstract Achaete-scute homolog 1 (ASCL1) is a transcription factor that is highly expressed in most small cell lung cancer (SCLC) tumors and cell lines and is critical for their proliferation. Inhibiting ASCL1 transcriptional activity may thus be a valid therapeutic strategy for SCLC. However, transcription factors (TFs) have been historically difficult to target. Given that TFs belong to complex regulatory networks, we propose to identify and target multiple components within an ASCL1-transcriptional network rather than ASCL1 alone. We have previously detected ASCL1-bound genomic regions associated with the active chromatin epigenetic mark, H3K27Ac in SCLC cells. Here we report the identification of an ASCL1-containing transcriptional network in SCLC cells and evaluate its targeting by the transcriptional inhibitor, mithramycin. We conducted chromatin immunoprecipitation (ChIP) by immunoprecipitating the H3K27Ac chromatin mark from NCI-H2107 and NCI-H69 SCLCs (5X107 cells) nuclear lysates with10 μg H3K27Ac antibodies (Abcam-Ab4729), and sequenced ChIP libraries on an Illumina High-Seq2000. Further characterization using siRNA transfections, immunoblotting and MTS-cell proliferation assays were conducted following standard procedures. We found 82 overlapping TF genes, including lineage-specific TF genes for ASCL1, Forkhead box protein A2 (FOXA2), and nuclear factor 1 B-type (NFIB), associated with the active chromatin epigenetic marks H3K27Ac in SCLC cell lines. This suggests that ASCL1, FOXA2, and NFIB may belong to the same transcriptional network. siRNA-mediated knockdown of ASCL1 leads to decreased FOXA2 levels, but it has no effect on NFIB levels, implicating ASCL1 as a transcriptional regulator of FOXA2 but not NFIB. Mithramycin stops cell proliferation and reduces ASCL1, FOXA2 but not NFIB protein levels. In conclusion, our studies identify the beginning of a transcriptional network necessary for SCLC proliferation in which ASCL1 regulates FOXA2. Targeting multiple TFs within a network with mithramycin can stop cell proliferation and as such suggests a therapeutic strategy for SCLC. Because of the importance of NFIB in mediating metastatic behavior of SCLC, these data indicate that approaches other than targeting ASCL1 and use of mithramycin will be needed to target NFIB. Citation Format: Karine Pozo, Rahul K. Kollipara, John D. Minna, Adi F. Gazdar, Jane E. Johnson. Evaluating transcription factor networks as targets for the treatment of small cell lung cancer [abstract]. In: Proceedings of the Fifth AACR-IASLC International Joint Conference: Lung Cancer Translational Science from the Bench to the Clinic; Jan 8-11, 2018; San Diego, CA. Philadelphia (PA): AACR; Clin Cancer Res 2018;24(17_Suppl):Abstract nr B09.
Preliminary single-dose clinical pharmacokinetics of an anti–PD-L1 Probody therapeutic (Pb-Tx) in cancer patients.
Authors: Mark Stroh, Laura Serwer, Hong Lu, Vanessa Huels, Chihunt Wong, Beiyao Zheng, Bjorn L. Millard, Joshua F. Apgar, Nancy Zheng, Jennifer Hope Richardson, Matthias Will, Rachel W. Humphrey
Journal: Journal of Clinical Oncology (2018)

e14558 Background: CX-072 is a protease-activatable antibody prodrug directed against programmed cell death ligand 1 (PD-L1). Probody therapeutics (Pb-Txs) are designed to be preferentially activated by tumor-associated proteases but not in healthy tissue. Once activated, the Pb-Tx can bind with high affinity to target antigen on tumor cells. Pb-Txs are thus designed to widen the therapeutic index by minimizing target interaction in healthy tissue while retaining antitumor activity. Methods: The phase 1-2 PROCLAIM-CX-072 (Probody Clinical Assessment In Man; NCT03013491) trial is a first-in-human study of CX-072 to characterize the safety, tolerability, pharmacokinetics (PK), and antitumor activity of CX-072 administered intravenously as a single agent or in combination with ipilimumab or vemurafenib in adult patients (pts) with cancer. Here the PK results of the dose-escalation segment of the trial in pts receiving a single dose of CX-072 monotherapy are reported. PK samples were collected intensively following the first dose of CX-072, with sparse collection thereafter. Analytes quantified in plasma samples are Intact Pb-Tx, representing the prodrug form of CX-072, and Total Pb-Tx, representing the sum of intact and activated species. Results: Preliminary single-dose PK data are available for pts enrolled in the dose-escalation segment of PROCLAIM-CX-072 receiving one dose of 0.03-30 mg/kg CX-072 as a single agent. Single-dose PK data suggest CX-072 circulates predominantly as the intact, prodrug species; there does not appear to be monotonic trending of the estimates of clearance and the volume of distribution across the 0.1-30 mg/kg dose levels. A mechanistic PK model suggests target-mediated drug disposition (TMDD) may not be an important contributor to the clearance of intact, protected CX-072 across the dose range evaluated. Single-agent CX-072 plasma PK and tumor biopsy data continue to be collected, and updated data will be presented. Conclusions: Preliminary single-agent, single-dose CX-072 PK data suggest that CX-072 behaves as designed: it circulates predominantly as the intact prodrug species, and TMDD does not strongly influence its PK. Clinical trial information: NCT03013491.
The characteristics of c-MET and HER2 expression in gastric carcinoma and its correlation with clinical-pathological parameters.
Authors: Patrick Stuebs, Florian Dittmar, Kathrin Zierau, Joerg Fahlke, Karsten Ridwelski, Ann Kristin Geers, Jana Lessel, Doerthe Jechorek
Journal: Journal of Clinical Oncology (2017)

e15566 Background: The aim of this study was to determine whether overexpression of c-MET or HER2 had an effect on the clinical-pathological parameters and / or the prognosis of gastric carcinoma, as well as a direct correlation among those parameters. Methods: 134 gastric resectates were archived between 2007-2012 and retrospectively examined for c-MET and HER2 expression via immunohistochemistry (IHC). The HER2 status IHC2 + was additionally verified by means of Chromogenic in situ hybridization (CISH). Statistical data analysis was performed on the basis of the parameters acquired in the prospective multicentre observation study QCGC'07 / 09. Results: A total of 71 patients (53%) were found to express c-MET low and 63 patients (47%) expressed c-MET high, 122 patients (91%) were found to be HER2 negative and 12 persons (9%) were HER2 positive. C-MET high was significantly more pronounced in the Lauren intestinal type (63.8%, p = 0.001) and moderately to poorly differentiated tumour tissue (G2 50.9%, G3 43.9%, p = 0.038) as well es tissue with lymph vessel infiltration (L1 59.1%, p = 0.039). HER2 showed no significant effect on the clinical-pathological parameters. The median overall survival was shown to be shortened for the c-MET high-expressing (c-MET low 56 months, SD: ± 24.67; 95% CI: 7.65-104.36 vs. c-MET high 32 months, SD: ± (median-OS HER2 negative 38 months, SD: ± 14.11, 95% CI: 10.35-65, p = 0.839), and HER2 negative, 65, median-OS HER2 positive not reached, p = 0.305) patients. 8/134 resectates (5.97%, p = 0.135) were high and positive in both expression patterns, showing no significant difference to the OS (p = 0.393). Conclusions: In our studies, c-MET high or HER2 negative expression was associated with a poorer OS. However, no direct correlation between HER2 and c-MET could be demonstrated
TCT-158 Post-implantation Strut Protrusion and Neointimal Thickness at follow-up in Absorn Bioresorbable Scaffold: A serial Shear Stress Analysis Up to Five Years
Authors: Erhan Tenekecioglu, Ryo Torii, Vikas Thondapu, Yuki Katagiri, Ply Chichareon, Yosuke Miyazaki, Taku Asano, Rodrigo Modolo, Eric Poon, Frank Gijsen, David Klaveren, Andrew Ooi, Peter Barlis, Yoshinobu Onuma, Christos Bourantas, Patrick Serruys
Journal: Journal of the American College of Cardiology (2018)
Phase 2 trial of SL-701 in relapsed/refractory (r/r) glioblastoma (GBM): Correlation of immune response with longer-term survival.
Authors: David M. Peereboom, Louis B. Nabors, Priya Kumthekar, Michael A. Badruddoja, Karen L. Fink, Frank S. Lieberman, Surasak Phuphanich, Erin M. Dunbar, Tobias Walbert, David Schiff, David Dinh Tran, Lynn Stuart Ashby, Nicholas A. Butowski, Fabio Massaiti Iwamoto, Ross Lindsay, John Bullington, Michael Schulder, Jonathan Sherman, Trishna Goswami, David A. Reardon
Journal: Journal of Clinical Oncology (2018)

2058 Background: SL-701 is a novel immunotherapy comprised of synthetic peptides designed to elicit an anti-tumor immune response against GBM targets: interleukin-13 receptor alpha-2, EphrinA2 and Survivin. Updated Phase 2 data are reported. Methods: Patients with r/r GBM HLA-A2+, bevacizumab (bev)-naive and KPS > 60, enrolled. Stage 1: SL-701 with adjuvants GM-CSF and imiquimod dosed biweekly for 6 months, then q28 days. Stage 2: SL-701 with adjuvant poly-ICLC dosed biweekly with bev (10 mg/kg) for 6 months, then q28 days. Primary objectives: safety, tolerability, investigator assessed objective response rate (ORR, RANO criteria) and 12-month OS rate (OS-12). SL-701-specific CD8+ T-cell frequency was assessed by flow cytometry. PBMCs were isolated by density gradient and stimulated for 4h with SL-701 peptides (1mg/ml/peptide) before intracellular staining with live/dead, CD3, CD4, CD8, IFNγ, TNFα, IL-2, and PD-1. Results: As of 2/7/18, 74 bev-naive patients received median of 8.5 SL-701 doses. Most frequent treatment-related adverse events (TRAEs) were fatigue (22%) and injection site reaction (18%). Grade 3 TRAE was fatigue (3%); no other grade 3 TRAEs. In Stage 1, 1 partial response (PR) (duration: 78 wks) and 15 stable disease (SD) (median 16 wks; range: 1.3–99) seen in 46 patients. In Stage 2, 2 complete responses (CR) (duration: 30, 46 wks), 4 PRs (median 31 wks; range 12–47) and 19 SDs (median 14 wks; range 0.1-41) seen in 28 patients. OS-12: 43% (median 11.7 mos) in Stage 2 and 37% (median 11 mos) in Stage 1. 5 patients receive SL-701 on compassionate use basis. Preliminary flow cytometry analysis of subset of Stage 2 patients: 5/6 responders (CR, PR or SD of ≥6 mos) had SL-701-specific T cell responses, with 1 CR patient at wk 16 generating > 6% SL-701-specific CD8+ T cells by wk 58. Conclusions: SL-701 with immunostimulants, alone and in combination with bev, was well-tolerated and demonstrated anti-tumor activity including multiple major responses. There is also a preliminarily promising survival tail in r/r GBM patients who received SL-701 with bev Further analyses ongoing; updated data to be presented. Clinical trial information: NCT02078648.
Phase II study of the effect of the topical corticosteroid fluocinonide in patients on endocrine therapy for breast cancer or breast cancer prevention with symptoms of vaginal dryness and dyspareunia.
Authors: Evthokia A. Hobbs, Kristine Lethert, Deirdre J. Nauman, Jenna Bucher, Emile Latour, Motomi Mori, Stephen Y. Chui, Kathleen A. Kemmer
Journal: Journal of Clinical Oncology (2017)

10105 Background: Gynecologic symptoms and sexual dysfunction from endocrine therapy are troublesome side effects for a significant number of patients. This study explored amelioration of vaginal dryness and dyspareunia with fluocinonide cream, a strong topical corticosteroid. Methods: A single-arm, open-label phase II trial of topical fluocinonide 0.05% cream to improve vaginal symptoms in women on endocrine therapy in the adjuvant setting for early stage breast cancer was performed. Patients with vaginal symptoms applied topical vaginal fluocinonide 0.05% cream twice a day for two weeks then once daily for two weeks. Patients were assessed for symptoms by weekly completion of the Mayo/North Central Cancer Treatment Group Patient Pretreatment Questionnaire. The primary outcome was a change from baseline in patient-reported effects of vaginal dryness and dyspareunia on a scale from 0 (no symptoms) to 4 (very severe symptoms) from time of enrollment and at 4 weeks. Secondary outcomes were decrease in vaginal itching and total vaginal index score. Comparisons were made with Wilcoxon sign rank test with 2.5% significance level. Results: Thirty-four women were accrued. At 4 weeks compared with baseline, vaginal dryness improved from a median score of 2 (moderate symptoms) to 0 (no symptoms) ( P &lt; .001) and dyspareunia from 3 (severe symptoms) compared with 1 (mild symptoms) ( P = .002). Percentage of patients who had &gt; 2 point improvement in vaginal dryness and dyspareunia was 69.0% and 75% respectively. Secondary analysis showed decrease in vaginal itching score from 1 to 0 ( P = .001) and vaginal index score of 6 to 1 ( P = .002). Twenty-one patients experienced low-grade toxicities which were mostly limited to skin irritation. Conclusions: Fluocinonide 0.05% cream improves vaginal dryness and dyspareunia experienced by women receiving endocrine therapy and has the potential to improve quality of life of cancer survivors and compliance of endocrine therapy. Clinical trial information: NCT00297011.
CD8+ T cells modulate autosomal dominant polycystic kidney disease progression
Authors: Emily K. Kleczko, Kenneth H. Marsh, Logan C. Tyler, Seth B. Furgeson, Bonnie L. Bullock, Christopher J. Altmann, Makoto Miyazaki, Berenice Y. Gitomer, Peter C. Harris, Mary C.M. Weiser-Evans, Michel B. Chonchol, Eric T. Clambey, Raphael A. Nemenoff, Katharina Hopp
Journal: Kidney International (2018)