tbuckley/cabot-search huggingface dataset:
Influence of inflammation-based prognostic score on mortality of patients undergoing chemotherapy for far advanced or recurrent unresectable colorectal cancer
Authors: M. Ishizuka, H. Nagata, K. Takagi, K. Kubota
Journal: Journal of Clinical Oncology (2009)

11084 Background: Recent studies have revealed that the Glasgow prognostic score (GPS), an inflammation-based prognostic score that includes only C-reactive protein (CRP) and albumin, is a useful tool for predicting postoperative outcome in cancer patients. However, few studies have investigated the GPS in patients undergoing chemotherapy for far advanced or recurrent unresectable colorectal cancer (AR-UCRC). Objective: To demonstrate the influence of the GPS for prognostication of patients undergoing chemotherapy for AR-UCRC. Methods: The GPS was calculated as follows: patients with both an elevated level of CRP (&gt;1.0 mg/dl) and hypoalbuminemia (&lt;3.5 g/dl) were allocated a score of 2, and patients showing one or none of these blood chemistry abnormalities were allocated a score of 1 or 0, respectively. Results: One hundred twelve patients who had undergone chemotherapy for AR-UCRC with regimens such as such as FOLFIRI (5-fluorouracil [5-FU]/l-leucovorin [LV]/irinotecan hydrochloride [CPT-11]) or FOLFOX (5-FU/LV/oxialiplatin [L-OHP]) were evaluated retrospectively. Kaplan-Meier analysis and log rank test revealed that GPS2 predicted a higher risk of mortality than GPS0 or 1 (P &lt;0.0001). Univariate analyses revealed that the neutrophil ratio (P = 0.0411), CA19–9 (P = 0.0473), CRP (P = 0.0477), albumin (P = 0.0043) and GPS (0,1/2) (P &lt; 0.0001) were associated with mortality. Multivariate analyses using these five factors revealed that only GPS (0,1/2) (odds ratio, 6.071; 95% C.I., 1.625–22.68; P = 0.0073) was an independent risk factor of mortality. Conclusions: GPS is considered the most important and independent predictor of mortality in patients undergoing chemotherapy for AR-UCRC. No significant financial relationships to disclose.
Factors Influencing Long-Term Hematopoietic Function Following Autologous Stem Cell Transplantation
Authors: Alissa Visram, Natasha Kekre, Christopher N. Bredeson, Jason Tay, Lothar B. Huebsch, Sheryl McDiarmid, Ranjeeta Mallick, Mitchell Sabloff, Harold Atkins, David S. Allan, Alan Tinmouth, Linda Hamelin, Lisa Martin, Dawn Maze
Journal: Blood (2016)
How to run survival-endpoint phase II trials with 25% to 40% fewer patients.
Authors: Michael J. Schell, Eric B. Haura, Jongphil Kim, Gang Han, George R. Simon
Journal: Journal of Clinical Oncology (2012)

2544 Background: New molecular information, whether arising from expression profiling, identification of key mutations, or proteomic analyses is making the personalization of therapy increasingly feasible. This leads to the fragmentation of common disease entities into multiple molecular subtypes. Having sufficient numbers of patients to demonstrate the effectiveness of novel targeted therapies for each subtype has therefore become challenging, essentially impeding progress. Methods: Use of sample size determination software allows for comparison of phase II trials with a target survival proportion at a given time T based upon Kaplan-Meier versus exponential survival methods. Results: The use of exponential survival fitting methods, in lieu of the currently implemented trial designs, to single arm phase II studies can routinely reduce patient numbers by 25-40% (Table) without compromising the statistical power. The biggest advantage is that survival information both before and after time T reduces the variability for the exponential fit estimate. This approach will lead to the saving of financial and patient resources for researchers. Moreover, the time saved will accelerate the approval of agents making the proposed trial designs ethically attractive. However, this approach is only applicable if the exponential distribution assumption behind the approach is valid. Conclusions: The exponential survival fitting method should replace the current standard approach in all instances unless the exponential distribution assumption is known to be false. Detailed examples and analysis will be presented. [Table: see text]
A phase I study of everolimus in combination with cetuximab and cisplatin as first-line therapy inrecurrent and metastatic (R/M) head and neck squamous cell carcinoma (HNSCC).
Authors: Christine H. Chung, Hao Wang, Nancy Tsottles, Christine Gail Gourin, Nishant Agrawal, Alfredo Molinolo, Silvio Gutkind, Arlene A. Forastiere, Shanthi Marur
Journal: Journal of Clinical Oncology (2012)

e16061 Background: The AKT/mTOR pathway emerged as a promising therapeutic target and as a potential mechanism of EGFR inhibitors in HNSCC. To assess the prevalence of AKT/mTOR pathway activation, HNSCC tumors were stained with phospho-specific AKT (pAKT) antibody. To test a hypothesis that resistance to an EGFR inhibitor, cetuximab, can be overcome by mTOR inhibition, we conducted a phase I clinical trial combining everolimus, cetuximab and cisplatin in R/M HNSCC. Methods: A TMA of 153 cores from 51 HNSCC was stained with a pAKT antibody (Ser473), and digitally quantified with TMAJ software. For the trial, patients with ECOG PS 0-2 with no prior systemic therapy for R/M HNSCC were enrolled and escalating doses of everolimus (2.5, 5, or 10mg) were administered daily, cetuximab 250mg/m 2 weekly, and cisplatin 40mg/m 2 days 1 and 8. Each cycle was 28 days. Response was evaluated with CT/MRI and PET scans after every 2 cycles. Biospecimens to analyze the EGFR and AKT/mTOR pathways were collected. Results: pAKT staining data were evaluable in 123 cores from 45 tumors. Nine patients were accrued before the study was terminated. Five evaluable patients progressed rapidly within 12 weeks after enrolling in the study (median PFS=2.8 months, 95% CI [1.6, 13.9]). Two patients received everolimus at 5mg, and both patients were dose reduced to 2.5mg for grade 3 hypophosphatemia, infection and mucositis. Among the 7 patients enrolled to receive 2.5mg, 3 patients received the treatment until progression of disease, 2 patients were taken off the study due to grade 4 infusion reaction to the first dose of cetuximab and non-adherence to everolimus, and 2 patients withdrew consent. The 5 evaluable patients had a PET response after 2 cycles. The proposed biomarker results will be available at the time of presentation. Conclusions: While AKT/mTOR is a promising therapeutic target, a combination of everolimus, cetuximab and cisplatin was poorly tolerated even at the lowest dose level of 2.5mg daily with unexpected toxicities suggesting that this combination should be studied with a caution in patients with R/M HNSCC.
Blinatumomab for Relapsed/Refractory Acute Lymphocytic Leukemia: A Single Center Experience
Authors: Tara L. Lin, Zahra Mahmoudjafari, Omar S. Aljitawi, Anurag K. Singh, Leyla Shune, Siddhartha Ganguly, Sunil Abhyankar, Joseph McGuirk
Journal: Blood (2015)
SWOG S0307 phase III trial of bisphosphonates as adjuvant therapy in primary breast cancer: Comparison of toxicities and patient-stated preference for oral versus intravenous delivery.
Authors: Julie Gralow, William E. Barlow, Alexander H. G. Paterson, Danika Lew, Alison Stopeck, Daniel F. Hayes, Dawn L. Hershman, Mark Schubert, Mark Clemons, Catherine H. Van Poznak, Elizabeth Claire Dees, James N. Ingle, Carla Isadora Falkson, Anthony D. Elias, Michael J. Messino, Jeffrey H. Margolis, Shaker R. Dakhil, Helen K. Chew, Robert B. Livingston, Gabriel N. Hortobagyi
Journal: Journal of Clinical Oncology (2014)

558 Background: Bone metastases are a common site of distant recurrence in breast cancer. Evidence from randomized trials, including a recent meta-analysis, suggests that adjuvant bisphosphonates can decrease recurrence and death. SWOG S0307 compares efficacy of 3 bisphosphonates in early stage breast cancer. Methods: Patients with stage I-III breast cancer receiving adjuvant systemic therapy were randomized to receive 3 years of clodronate (CLOD) (1600 mg po qd), ibandronate (IBAN) (50 mg po qd) or zoledronic acid (ZA) (4 mg IV q month x 6, then q3 months x 2.5 years). The primary endpoint is disease-free survival. Overall survival, sites of first recurrence, and adverse events are secondary endpoints. Results: Between Nov 2005 and Feb 2010 6,097 patients were enrolled. Survival data are maturing with 50% of the expected events occurring to date. Annual interim analyses are being conducted. 5,752 patients are assessable for toxicity. Median age was 53. 78% of tumors were ER positive, 16% HER2 positive, 16% triple negative. 34% were stage I, 45% stage II, and 21% stage III. Planned adjuvant treatment included chemotherapy in 80%, endocrine therapy in 76%, and both in 56%. 25 (0.4%) and 494 (8.6%) patients experienced grade 4 or 3 toxicities, respectively. The most common adverse events were musculoskeletal, pain, gastrointestinal, metabolic/laboratory (creatinine, calcium), and constitutional symptoms (acute phase reactions). There have been 40 reported cases of osteonecrosis of the jaw (ONJ): ZA 24/2094 (1.15%), CLOD 6/2151 (0.28%), and IBAN 10/1507 (0.66%) (p=0.003). Fractures have been reported in 4.5% of patients in ZA arm, 4.8% in CLOD arm, and 4.1% in IBAN arm (p= ns). Prior to randomization, 76% preferred oral medication versus 24% for intravenous if drugs proved equal in efficacy. Preferences changed little at completion of therapy, although some switched preference. Conclusions: Grade 3 and 4 toxicities were low in S0307. ONJ, a rare but serious complication, was statistically highest for ZA and lowest for CLOD. Fractures were equal across arms. The majority of patients indicated a preference for oral formulation. Clinical trial information: NCT00127205.
Survivorship in WM: Identification of Factors Associated with Survival of More Than a Decade and with Early WM-Related Death
Authors: Efstathios Kastritis, Marie-Christine Kyrtsonis, Maria Gavriatopoulou, Evdoxia Hatjiharissi, Eirini Katodritou, Panagiotis Repousis, Argiris Symeonidis, Michalis Michael, Anastasia Pouli, Nikolaos Giannakoulas, Dimitrios Christoulas, Aikaterini Megalakaki, Panagiotis Tsirigotis, Stavroula Giannouli, Panayiotis Panayiotidis, Amalia Vassou, Elina Vervessou, Sossana Delimpasi, Georgia D Kaiafa, Konstantinos Tsatalas, Evangelos Terpos, Meletios A Dimopoulos
Journal: Blood (2016)
PD-L1 on tumor cells is sufficient for immune evasion in immunogenic tumors and inhibits CD8 T cell cytotoxicity
Authors: Vikram R. Juneja, Kathleen A. McGuire, Robert T. Manguso, Martin W. LaFleur, Natalie Collins, W. Nicholas Haining, Gordon J. Freeman, Arlene H. Sharpe
Journal: The Journal of Experimental Medicine (2017)

It is unclear whether PD-L1 on tumor cells is sufficient for tumor immune evasion or simply correlates with an inflamed tumor microenvironment. We used three mouse tumor models sensitive to PD-1 blockade to evaluate the significance of PD-L1 on tumor versus nontumor cells. PD-L1 on nontumor cells is critical for inhibiting antitumor immunity in B16 melanoma and a genetically engineered melanoma. In contrast, PD-L1 on MC38 colorectal adenocarcinoma cells is sufficient to suppress antitumor immunity, as deletion of PD-L1 on highly immunogenic MC38 tumor cells allows effective antitumor immunity. MC38-derived PD-L1 potently inhibited CD8+ T cell cytotoxicity. Wild-type MC38 cells outcompeted PD-L1–deleted MC38 cells in vivo, demonstrating tumor PD-L1 confers a selective advantage. Thus, both tumor- and host-derived PD-L1 can play critical roles in immunosuppression. Differences in tumor immunogenicity appear to underlie their relative importance. Our findings establish reduced cytotoxicity as a key mechanism by which tumor PD-L1 suppresses antitumor immunity and demonstrate that tumor PD-L1 is not just a marker of suppressed antitumor immunity.
COMPARISON OF PROCEDURAL EFFICACY OF CORONARY ANGIOGRAPHY IN OCTOGENARIAN, NONAGENARIAN AND GENERAL POPULATION
Authors: Amornpol Anuwatworn, Alexander Pham, Udit Bhatnagar, Shenjing Li, Vishesh Kumar, Jimmy Yee, James Higgins, Terezia Petraskova, Julia Stys, Paul Thompson, Adam Stys, Tomasz Stys
Journal: Journal of the American College of Cardiology (2017)
Clinical Manifestations and Treatment Results in Accordance with Frontline Treatment Modalities for Ocular Adnexal Mucosa-Associated Lymphoid Tissue Lymphoma (OAML)
Authors: Young-Woo Jeon, Jae-Ho Yoon, Sung-Eun Lee, Ki-Seong Eom, Yoo-Jin Kim, Hee-Je Kim, Seok Lee, Chang-Ki Min, Jong Wook Lee, Woo-Sung Min, Seok-Goo Cho
Journal: Blood (2015)
PLATELET REACTIVITY AND OUTCOMES AFTER PCI OF LESIONS WITH AND WITHOUT IN-STENT RESTENOSIS: THE ADAPT-DES STUDY
Authors: Bjorn Redfors, Philippe Genereux, Ajay Kirtane, Bernhard Witzenbichler, Akiko Maehara, Giora Weisz, Thomas McAndrew, Roxana Mehran, Gregg Stone
Journal: Journal of the American College of Cardiology (2017)
Exosomal protein FAM3C as a potential novel biomarker for non-small cell lung cancer.
Authors: Ling-Zhi Wang, Ross A. Soo, Win Lwin Thuya, Ting Ting Wang, Tiannan Guo, Jieying Amelia Lau, Fang Cheng Wong, Andrea Li Ann Wong, Soo Chin Lee, Siu Kwan Sze, Boon C. Goh
Journal: Journal of Clinical Oncology (2014)

e22162 Background: Low-dose computed tomography screening has been shown to reduce lung cancer-specific mortality, but has a high false-positive detection rate. The discovery of biomarkers for lung cancer is therefore urgently needed. Exosomes are small membrane bound vesicles extruded from cells that mediate local and systemic cell communications via the transfer of proteins, miRNAs and RNAs. Circulating exosomal proteins may thus have diagnostic and prognostic potential. We conducted a study to determine the utility of exosomes as non-invasive diagnostic and prognostic markers in non-small cell lung cancer (NSCLC). Methods: Quantitative proteomic profiling of exosomes using LTQ-FT mass spectrometer was performed in NSCLC cell lines and normal lung fibroblast as study models. Potential biomarkers were verified in lung cancer patients by western blot (WB), ELISA and immunohistochemistry (IHC). Results: More than 1,000 exosomal proteins were identified for each cell line. 158 proteins were detectable only in the exosomes of NSCLC cell lines but not in those of normal lung fibroblast. Five were selected for further investigation and WB showed that FAM3C, a secreted exosomal protein, was the most promising protein. There was FAM3C over-expression in the exosomes of 2 other lung cancer cell lines, demonstrating its widespread existence in lung cancer cells-derived exosomes. The mean plasma concentration of FAM3C in 20 patients with NSCLC was two-fold higher than that of 10 healthy subjects; FAM3C was also detectable in pleural fluid exosomes in a subset of NSCLC patients (n=7). Furthermore, in NSCLC tissue arrays, IHC revealed granular FAM3C staining was significantly associated with improved lung cancer specific survival in squamous cell carcinoma patients (median: not reached vs 19.1 months, p= 0.021). Functional studies showed that silencing of FAM3C gene reduced cell migration in a K-ras mutant cell line but not in wild-type cells, suggesting that it may have an oncogenic ras addictive role in NSCLC. Conclusions: FAM3C in exosomes may be a potential non-invasive prognostic biomarker for lung cancer and further studies are warranted to investigate it as a diagnostic biomarker for NSCLC.
Triple-negative breast cancer subtypes and pathologic complete-response rate to neoadjuvant chemotherapy: Results from the GEICAM/2006-2003 study.
Authors: Angela Santonja, Joan Albanell, Jose Ignacio Chacon, Ana Lluch, Alfonso Sanchez-Muñoz, Federico Rojo, Antonio Anton, Laura G. Estevez, Beatriz Cirauqui, V. de Luque, Lourdes Calvo, Miguel Angel Seguí-Palmer, Arrate Plazaola, Sonia Gonzalez, Ana Santaballa, Juan de la Haba-Rodriguez, Cesar Rodriguez, Rosalia Caballero, Eva Maria Carrasco, Emilio Alba
Journal: Journal of Clinical Oncology (2014)

1024 Background: Triple negative breast cancer (TNBC) is a heterogeneous disease with distinct molecular subtypes that differentially respond to chemotherapy (CHT) and targeted agents. In a recent study, Lehmann et al. (JCI 2011) identified six molecular subtypes of TNBC, characterized on the basis of gene ontologies and differential gene expression. However, their clinical utility remains unclear. We aimed to explore the clinical relevance of these molecular subtypes in TNBC determining differences in response to neoadjuvant chemotherapy in a randomized phase II trial, the GEICAM/ 2006-03. Methods: The GEICAM/ 2006-03 study evaluated a regimen of anthracyclines and taxanes +/- carboplatin in the neoadjuvant treatment of patients (pts) with TNBC (Alba, BCRT 2012). We determined TNBC molecular subtypes in FFPE pre-treatment tumor biopsies from pts recruited in this study. Gene expression profile was determined using HTA 2.0 arrays (Illumina). Subtypes were identified with the online tool TNBC type (http://cbc.mc.vanderbilt.edu/tnbc). Finally, we explored the association of the Lehmann subtypes with the pathological complete response (pCR) in breast and axilla (Miller and Payne criteria) using Fisher's exact test. Results: From the 94 enrolled pts, we processed 46 pre-treatment tumor samples in a central lab and isolated high-quality RNA for microarray analysis in 39 (42%); 7 samples are still pending to be analyzed. Tumors were classified as follows: 4 BL1, 2 BL2, 8 IM, 5 LAR, 3 M, 3 ML with 7 pts that couldn't be assigned to any subtype and were not included in this analysis. Three (75%) of the BL1 subtype pts achieved a pCR (p-value=0.075). In contrast, IM and LAR achieved the lowest pCR rates (12% and 20%, respectively). In the carboplatin-treated patients, 100% of BL1 patients showed pCR (p-value=0.033) in contrast with none of the IM and LAR pts. Conclusions: Our preliminary findings suggest that TNBC subtypes can predict tumor response to neoadjuvant CHT, supporting their potential clinical utility in diagnosis, treatment selection and drug development, bringing TNBC pts a step closer to personalized medicine.
PREDICTORS OF TRUE ST-SEGMENT ELEVATION MYOCARDIAL INFARCTION IN COCAINE POSITIVE PATIENTS
Authors: Ikechukwu Ifedili, Siri Kadire, Tamunoinemi Bob-Manuel, Britney Heard, Leah John, Benjamin Zambetti, Mark Heckle, Fridjof Thomas, Showkat Haji, Rami Khouzam, Guy Reed, Uzoma Ibebuogu
Journal: Journal of the American College of Cardiology (2017)
Establishment of a baseline to measure academic clinical trial activity in Canada.
Authors: Karen E. Arts, Diana Kato, Janet Dancey
Journal: Journal of Clinical Oncology (2015)

e17547 Background: The Canadian Cancer Clinical Trials Network (3CTN) was created in 2013 in response to the State of Cancer Clinical Trials in Canada Report recommendation for pan-Canadian program to facilitate initiation and conduct of academic cancer clinical trials. Goals are 1) strengthen capability and capacity for multi-centre trials developed by the academic sector; 2) improve patient outcomes. Methods: To establish 3CTN: 1) Sites were surveyed about current trial activities, personnel and resources; 2) the 2011-2013 academic trials portfolio was created from cancer registries; 3) recruitment data was collected . Results: 47 Canadian sites responded to the survey. Atlantic Canada had the fewest numbers of trials, phase 1 trials, biospecimens and novel imaging capacity. Ontario conducted the most academic trials. Most sites did not have clinical trial management systems. Average time from protocol receipt ranged from 85 - 198 days. All sites had SOPs and training programs. The most commonly cited requirement to increase trial activity was funding. 67 sites in 9 provinces reported recruitment (Table). From 2011-2014, 172 new trials opened and 211 trials were closed; a loss of 39 trials to the portfolio. Conclusions: Canadian academic clinical trials activity is declining. Trial capabilities are diverse. 3CTN will direct activity and resources to increase capacity and efficiency to improve patient outcomes. Recruitment to 3CTN portfolio trials. Recruitment by Region Centres 2011 2012 2013 Mean Alberta 2 187 171 175 178 Atlantic Canada 8 145 116 79 113 British Columbia 6 177 183 127 162 Manitoba 1 111 90 95 99 Ontario 21 1548 1263 1232 1348 Quebec 12 618 654 823 704 Pediatrics 17 361 374 394 376 Total 67 3147 2851 2925 2974 Trials All Open Academic 616 620 624 559 single-center 366 352 373 336 multi-center 250 268 251 223 New trials 40 55 29 47 Closed trials 37 46 62 66 * Canadian Cancer Research Alliance (2011). Report on the State of Cancer Clinical Trials in Canada. Toronto: CCRA.
Sporadic Notch1 Mutations Found in Human T-ALL Drive T Cell Development but Not Leukemogenesis in Murine Models: Implications for Pathogenesis and gamma-Secretase Inhibitor (GSI) Therapy.
Authors: Mark Y. Chiang, Olga Shestova, Gavin Histin, Mina Xu, Warren S. Pear, Jon C. Aster
Journal: Blood (2006)
OUTCOME OF ELDERLY PATIENTS UNDERGOING EXTRACORPOREAL LIFE SUPPORT IN REFRACTORY CARDIOGENIC SHOCK
Authors: Suzanne de Waha, Steffen Desch, Tobias Graf, Georg Fuernau, Ingo Eitel, Janine Poess, Thomas Stiermaier, Alexander Jobs, Jakob Ledwoch, Philipp Lurz, Gerhard Schuler, Holger Thiele
Journal: Journal of the American College of Cardiology (2017)
Abstract A23: AMPK's role in glioblastoma survival: An insight into its regulation on transcription factors and mTOR
Authors: Rishi Raj Chhipa, Biplab Dasgupta
Journal: Cancer Research (2017)

Abstract AMP kinase (AMPK) is an evolutionarily conserved enzyme required for adaptive responses to various physiological and pathological conditions. The multisubunit structure and sensitivity to various stresses confer complexity to AMPK function which scores beyond energy sensing. Here we show that inhibition of AMPK reduces viability of patient-derived primary Glioblastoma Multiforme (GBM) lines and tumors. We demonstrate that primary GBM cells coopt the AMPK-CREB1 pathway to coordinate global bioenergetics program through control of the transcription factors HIF1alpha and GABPA. But a growing number of AMPK activators are being developed to treat human diseases such as cancer and diabetes. This may be because AMPK activity can inhibit biosynthetic kinases like mammalian target of rapamycin (mTOR) and acetyl Co-A carboxylase (ACC). We found that AMPK silencing in glioma cells did not affect mTOR or downstream targets. AMPK is not absolutely necessary for mTOR inhibition, suggesting that in certain contexts, activated AMPK and mTOR may coexist. Indeed, this is what we observed in glioblastoma suggesting that basally active AMPK may not be sufficient to put a brake on mTOR. Further analysis of our preliminary data from primary tumor cells on Cap-dependent and well reported procancer IRES dependent translation under tumor microenvironment context will demonstrate significance of AMPK in translational machinery in GBM and will benefit in finding new therapeutic targets. Citation Format: Rishi Raj Chhipa, Biplab Dasgupta. AMPK's role in glioblastoma survival: An insight into its regulation on transcription factors and mTOR. [abstract]. In: Proceedings of the AACR Special Conference on Translational Control of Cancer: A New Frontier in Cancer Biology and Therapy; 2016 Oct 27-30; San Francisco, CA. Philadelphia (PA): AACR; Cancer Res 2017;77(6 Suppl):Abstract nr A23.
TREATMENT OF LEFT MAIN CORONARY ARTERY DISEASE IN PATIENTS WITH DIABETES: 3-YEAR OUTCOMES COMPARING CABG AND PCI WITH EVEROLIMUS-ELUTING STENTS FROM THE EXCEL STUDY
Authors: A. Pieter Kappetein, Milan Milojevic, Patrick Serruys, Joseph Sabik, Stuart Head, David Kandzari, Eric Schampaert, David Taggart, Ferenc Horkay, Kovacs Imre Laszlo, Samer Mansour, Adrian Banning, Manel Sabate, Andrezj Bochenek, Jose Pomar, Nicholas Lembo, Nicolas Noiseux, John Puskas, Ioanna Kosmidou, Roxana Mehran, Ori Ben-Yehuda, Philippe Genereux, Charles Simonton, Stuart Pocock, Gregg Stone, Erasmus MC
Journal: Journal of the American College of Cardiology (2017)