tbuckley/cabot-search huggingface dataset:
SARS-CoV-2 vaccination and ITP in patients with de novo or preexisting ITP
Authors: Eun-Ju Lee, Marina Beltrami-Moreira, Hanny Al-Samkari, Adam Cuker, Jennifer DiRaimo, Terry Gernsheimer, Alexandra Kruse, Craig Kessler, Caroline Kruse, Andrew D. Leavitt, Alfred I. Lee, Howard A. Liebman, Adrian C. Newland, Ashley E. Ray, Michael D. Tarantino, Jecko Thachil, David J. Kuter, Douglas B. Cines, James B. Bussel
Journal: Blood (2021)

Cases of de novo immune thrombocytopenia (ITP), including a fatality, following SARS-CoV-2 vaccination in previously healthy recipients led to studying its impact in preexisting ITP. In this study, 4 data sources were analyzed: the Vaccine Adverse Events Reporting System (VAERS) for cases of de novo ITP; a 10-center retrospective study of adults with preexisting ITP receiving SARS-CoV-2 vaccination; and surveys distributed by the Platelet Disorder Support Association (PDSA) and the United Kingdom (UK) ITP Support Association. Seventy-seven de novo ITP cases were identified in VAERS, presenting with median platelet count of 3 [1-9] ×109/L approximately 1 week postvaccination. Of 28 patients with available data, 26 responded to treatment with corticosteroids and/or intravenous immunoglobulin (IVIG), and/or platelet transfusions. Among 117 patients with preexisting ITP who received a SARS-CoV-2 vaccine, 19 experienced an ITP exacerbation (any of: ≥50% decline in platelet count, nadir platelet count <30 × 109/L with >20% decrease from baseline, and/or use of rescue therapy) following the first dose and 14 of 70 after a second dose. Splenectomized persons and those who received 5 or more prior lines of therapy were at highest risk of ITP exacerbation. Fifteen patients received and responded to rescue treatment. In surveys of both 57 PDSA and 43 UK patients with ITP, prior splenectomy was associated with worsened thrombocytopenia. ITP may worsen in preexisting ITP or be identified de novo post-SARS-CoV2 vaccination; both situations responded well to treatment. Proactive monitoring of patients with known ITP, especially those postsplenectomy and with more refractory disease, is indicated.
Antimicrobial peptides – Unleashing their therapeutic potential using nanotechnology
Authors: Sonia Gera, Esko Kankuri, Karin Kogermann
Journal: Pharmacology & Therapeutics (2021)

Antimicrobial peptides (AMPs) are potent, mostly cationic, and amphiphilic broad-spectrum host defense antimicrobials that are produced by all organisms ranging from prokaryotes to humans. In addition to their antimicrobial actions, they modulate inflammatory and immune responses and promote wound healing. Although they have clear benefits over traditional antibiotic drugs, their wide therapeutic utilization is compromised by concerns of toxicity, stability, and production costs. Recent advances in nanotechnology have attracted increasing interest to unleash the AMPs' immense potential as broad-spectrum antibiotics and anti-biofilm agents, against which the bacteria have less chances to develop resistance. Topical application of AMPs promotes migration of keratinocytes and fibroblasts, and contributes significantly to an accelerated wound healing process. Delivery of AMPs by employing nanotechnological approaches avoids the major disadvantages of AMPs, such as instability and toxicity, and provides a controlled delivery profile together with prolonged activity. In this review, we provide an overview of the key properties of AMPs and discuss the latest developments in topical AMP therapy using nanocarriers. We use chronic hard-to-heal wounds-complicated by infections, inflammation, and stagnated healing-as an example of an unmet medical need for which the AMPs' wide range of therapeutic actions could provide the most potential benefit. The use of innovative materials and sophisticated nanotechnological approaches offering various possibilities are discussed in more depth.
870P Comparison of PD-L1 and VISTA expression levels in head and neck cancers in primary and recurrent tumor tissue after radiotherapy/chemoradiotherapy
Authors: G. Yazıcı Şener, O. Sutcuoglu, B. Öğüt, D.C. Guven, A. Kavuncuoğlu, A. Özet, N. Özdemir, Y.G. Güler Tezel, N. Akyurek, O. Yazıcı
Journal: Annals of Oncology (2021)
In ASCVD, 81 mg and 325 mg of aspirin did not differ for CV or bleeding events
Authors: Lucas McCarthy
Journal: Annals of Internal Medicine (2021)

ACP Journal ClubOctober 2021In ASCVD, 81 mg and 325 mg of aspirin did not differ for CV or bleeding eventsLucas McCarthy, MD, MScLucas McCarthy, MD, MScVirginia Mason Medical Center, Seattle, Washington, USA (L.M.)Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/ACPJ202110190-118 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail Source CitationJones WS, Mulder H, Wruck LM, et al. Comparative effectiveness of aspirin dosing in cardiovascular disease. N Engl J Med. 2021;384:1981-90. https://pubmed.ncbi.nlm.nih.gov/33999548Clinical Impact RatingsGIM/FP/GP: Cardiology: Neurology: Reference1. Serebruany VL, Steinhubl SR, Berger PB, et al. Analysis of risk of bleeding complications after different doses of aspirin in 192,036 patients enrolled in 31 randomized controlled trials. Am J Cardiol. 2005;95:1218-22. [PMID: 15877994] Google Scholar Author, Article, and Disclosure InformationAffiliations: Virginia Mason Medical Center, Seattle, Washington, USA (L.M.)Disclosures: The commentator has reported no disclosures of interest. The form can be viewed at www.acponline.org/authors/icmje/ConflictOfInterestForms.do?msNum=M20-7321.This article was published at Annals.org on 5 October 2021. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics October 2021Volume 174, Issue 10Page: JC118 ePublished: 5 October 2021 Issue Published: October 2021 Copyright & PermissionsCopyright © 2021 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Nonnutritive Sweeteners and Neural Reward Response in Women and Individuals With Obesity
Authors: Stephanie Kullmann
Journal: JAMA Network Open (2021)

Alexandra G. Yunker, BA; Jasmin M. Alves, PhD; Shan Luo, PhD; Brendan Angelo, MS; Alexis DeFendis, BA; Trevor A. Pickering, PhD; John R. Monterosso, PhD; Kathleen A. Page, MD
714P Prognostic factors in stage I seminoma: Data from the phase III, randomised TRial of Imaging and Surveillance in Seminoma Testis (TRISST)
Authors: E.C. James, J.K. Joffe, R.A. Huddart, G.J. Rustin, S.A. Sohaib, L. Murphy, D.A. Noor, S.D. Wade, F. Schiavone, R.S. Kaplan, F.H. Cafferty
Journal: Annals of Oncology (2021)
Obesity-Associated <i>GNAS</i> Mutations and the Melanocortin Pathway
Authors: Edson Mendes de Oliveira, Julia M. Keogh, Fleur Talbot, Elana Henning, Rachel Ahmed, Aliki Perdikari, Rebecca Bounds, Natalia Wasiluk, Vikram Ayinampudi, Inês Barroso, Jacek Mokrosiński, Deepthi Jyothish, Sharon Lim, Sanjay Gupta, Melanie Kershaw, Cristina Matei, Praveen Partha, Tabitha Randell, Antoinette McAulay, Louise C. Wilson, Tim Cheetham, Elizabeth C. Crowne, Peter Clayton, I. Sadaf Farooqi
Journal: New England Journal of Medicine (2021)

GNAS encodes the Gαs (stimulatory G-protein alpha subunit) protein, which mediates G protein-coupled receptor (GPCR) signaling. GNAS mutations cause developmental delay, short stature, and skeletal abnormalities in a syndrome called Albright's hereditary osteodystrophy. Because of imprinting, mutations on the maternal allele also cause obesity and hormone resistance (pseudohypoparathyroidism).We performed exome sequencing and targeted resequencing in 2548 children who presented with severe obesity, and we unexpectedly identified 22 GNAS mutation carriers. We investigated whether the effect of GNAS mutations on melanocortin 4 receptor (MC4R) signaling explains the obesity and whether the variable clinical spectrum in patients might be explained by the results of molecular assays.Almost all GNAS mutations impaired MC4R signaling. A total of 6 of 11 patients who were 12 to 18 years of age had reduced growth. In these patients, mutations disrupted growth hormone-releasing hormone receptor signaling, but growth was unaffected in carriers of mutations that did not affect this signaling pathway (mean standard-deviation score for height, -0.90 vs. 0.75, respectively; P = 0.02). Only 1 of 10 patients who reached final height before or during the study had short stature. GNAS mutations that impaired thyrotropin receptor signaling were associated with developmental delay and with higher thyrotropin levels (mean [±SD], 8.4±4.7 mIU per liter) than those in 340 severely obese children who did not have GNAS mutations (3.9±2.6 mIU per liter; P = 0.004).Because pathogenic mutations may manifest with obesity alone, screening of children with severe obesity for GNAS deficiency may allow early diagnosis, improving clinical outcomes, and melanocortin agonists may aid in weight loss. GNAS mutations that are identified by means of unbiased genetic testing differentially affect GPCR signaling pathways that contribute to clinical heterogeneity. Monogenic diseases are clinically more variable than their classic descriptions suggest. (Funded by Wellcome and others.).
541P Ezabenlimab (BI 754091), an anti-PD-1 antibody, in combination with BI 836880, a VEGF/Ang2-blocking nanobody, in patients (pts) with previously treated advanced solid tumours
Authors: M. Hussein, I. Percent, E. Arrowsmith, H-T. Arkenau, Q. Chu, A.R. Hansen, D. Erzen, S. Qiu, A. Lucarelli, S. Ulahannan
Journal: Annals of Oncology (2021)
421P FOLFIRINOX with or without targeted therapy as first line for metastatic colorectal cancer: An AGEO multicenter real-world study
Authors: R. Varnier, C. Toullec, M. Fonnesu, S. Philonenko, P. Artru, E. Hafliger, A. Drouillard, C. Torregrosa, S. Pernot, P. McLellan, T. Lecomte, V. Moulin, C. Lecaille, Y. Touchefeu, C. Locher, A. Turpin, J. Taieb, C. Coutzac
Journal: Annals of Oncology (2021)
Deep learning in cancer diagnosis, prognosis and treatment selection
Authors: Khoa A. Tran, Olga Kondrashova, Andrew Bradley, Elizabeth D. Williams, John V. Pearson, Nicola Waddell
Journal: Genome Medicine (2021)

Abstract Deep learning is a subdiscipline of artificial intelligence that uses a machine learning technique called artificial neural networks to extract patterns and make predictions from large data sets. The increasing adoption of deep learning across healthcare domains together with the availability of highly characterised cancer datasets has accelerated research into the utility of deep learning in the analysis of the complex biology of cancer. While early results are promising, this is a rapidly evolving field with new knowledge emerging in both cancer biology and deep learning. In this review, we provide an overview of emerging deep learning techniques and how they are being applied to oncology. We focus on the deep learning applications for omics data types, including genomic, methylation and transcriptomic data, as well as histopathology-based genomic inference, and provide perspectives on how the different data types can be integrated to develop decision support tools. We provide specific examples of how deep learning may be applied in cancer diagnosis, prognosis and treatment management. We also assess the current limitations and challenges for the application of deep learning in precision oncology, including the lack of phenotypically rich data and the need for more explainable deep learning models. Finally, we conclude with a discussion of how current obstacles can be overcome to enable future clinical utilisation of deep learning.
1015P A phase I dose-escalation study of HBM4003: An anti-CTLA-4 heavy-chain-only mAb
Authors: P. de Souza, J. Park, D. Day, S. Frentzas, A.M. Haydon, J. Ji, M.M. de Assis, X. Chen, X. Gan, X. Tao, R. Zuo, G. Ross, L. Lu
Journal: Annals of Oncology (2021)
1658P Clinical characteristics of long-term survivors (LTS) in small cell lung cancer (SCLC) patients (p) with extended disease (ED)
Authors: A. Plaja, T. Moran, E. Carcereny, A. Bernat, A. Martinez Cardus, A. Hernández, M. Saigi, A. Estival Gonzalez, M. Cucurull, M. Domenech Vinolas
Journal: Annals of Oncology (2021)
Adult sucrase-isomaltase deficiency masquerading as IBS
Authors: Anna Foley, Emma Phoebe Halmos, Diab M Husein, Sasha Rachel Fehily, Britt-Sabina Löscher, Andre Franke, Hassan Y Naim, Peter R Gibson, Mauro D'Amato
Journal: Gut (2021)

Recently in Gut, several publications reported an increased prevalence of hypomorphic (defective) sucrase-isomaltase ( SI ) gene variants in patients with irritable bowel syndrome (IBS),1 2 and the association with impaired cell-surface expression and reduced digestive function of the corresponding enzyme.3 In addition, hypomorphic SI carriers have shown reduced response compared with non-carriers in a low-FODMAP (fermentable oligo- di- mono-saccharides and polyols) trial of IBS patients with diarrhoea.4 These and other studies,5 6 including recent large population-based surveys,7 raise the question whether genetic defects in the SI gene may be sought to explain abdominal symptoms in some patients with IBS.

A 23-year-old patient was referred with a diagnosis of IBS due to his long-standing postprandial diarrhoea associated with bloating, abdominal pain and nausea. He also had marked fatigue, headaches and mouth ulcers. He had symptoms since infancy without signs of malnutrition or failure-to-thrive. Extensive investigations excluded alternate causes of diarrhoea, including coeliac and inflammatory bowel disease, pancreatic exocrine insufficiency and bile acid diarrhoea. A low FODMAP diet worsened symptoms and psychological interventions were not helpful.

We hypothesised the involvement of SI defects. Resequencing of the gene identified three coding variants of interest (H1684Q, G1760V and V15F), which were assigned to …
1040O Phase II trial of ipilimumab, nivolumab and tocilizumab for unresectable metastatic melanoma
Authors: J.S. Weber, T. Muramatsu, O. Hamid, J. Mehnert, F.S. Hodi, S. Krishnarajapet, S. Malatyali, E. Buchbinder, J. Goldberg, R. Sullivan, M. Faries, I. Mehmi
Journal: Annals of Oncology (2021)
1349P Application of a classifier combining bronchial transcriptomics and chest CT features facilitates the diagnostic evaluation of lung cancer in smokers and non-smokers
Authors: W. Li, Y. Xia, S. Ying, R. Jin, H. Wu, Y. Shen, T. Yin, F. Yan, W. Zhang, F. Lan, B. Zhang, C. Zhu, C. Li, H. Shen
Journal: Annals of Oncology (2021)
Abstract 10872: Soluble Programed Cell Death Ligand-1 is Associated With Acute Coronary Syndrome
Authors: Koichiro Fujisue, Eiichiro Yamamoto, Daisuke Sueta, Masafumi Takae, Taiki Nishihara, Fumi Oike, Takashi Komorita, Hiroki Usuku, Seiji Takashio, Kenji Sakamoto, Koichi Kaikita, Kenichi Tsujita
Journal: Circulation (2019)

Backgrounds: Immune checkpoint by programmed cell death (PD)-1 plays crucial role in T cell tolerance toward vascular wall. Its ligand (PD-L1) is widely expressed on immune cells and vascular endot...
111In-Pentetreotide Uptake Due to COVID-19 Vaccination
Authors: Sho Koyasu, Yuji Nakamoto
Journal: Clinical Nuclear Medicine (2021)

Abstract A 72-year-old woman was referred for whole-body 111 In-pentetreotide scintigraphy with SPECT/CT. There was increased uptake of lymphadenopathy in the left axilla and left deltoid muscle. The patient's history revealed that the patient received the first dose of the COVID-19 vaccine 3 days before the 111 In-pentetreotide scintigraphy with SPECT/CT. This case demonstrates that the COVID-19 vaccine can cause 111 In-pentetreotide uptake in the lymph nodes and the deltoid muscle.
141P Gene-expression pathways and dynamics during neoadjuvant chemo-free therapy predict pathologic complete response in ER+/HER2+ breast cancer (BC)
Authors: M. Dugo, B. Gyorffy, G. Bisagni, M.A. Colleoni, M. Mansutti, C. Zamagni, L. Del Mastro, S. Zambelli, A. Frassoldati, L. Licata, B. Galbardi, O.M. Biasi, L. Viganò, A. Locatelli, G. Viale, P. Valagussa, G. Viale, M. Callari, L. Gianni, G. Bianchini
Journal: Annals of Oncology (2021)
1286P Senescent immune phenotype (SIP) status predicts resistance to immune checkpoint blockers (ICB) among CMV+ advanced non-small cell lung cancer (aNSCLC) patients
Authors: M. Naigeon, C. de Oliveira, F-X. Danlos, B. Duchemann, L. Boselli, S. Farhane, S. Messayke, L. Bedouda, C. Mohamed-Djalim, F. Griscelli, A. Marabelle, L. Cassard, B. Besse, N. Chaput
Journal: Annals of Oncology (2021)
Abstract 458: Critical Role of Bone Marrow Nox2-based NADPH Oxidase in Neovascularization in Response to Hindlimb Ischemia: Impact on Endothelial Progenitor Cells Function
Authors: Norifumi Urao, Hyoe Inomata, Ha Won Kim, Ronald Mckinney, Mazooma Razvi, Tohru Fukai, Masuko Ushio-Fukai
Journal: Circulation (2007)

Bone marrow (BM) is the major reservoir for endothelial progenitor cells (EPCs). Postnatal neovascularization involves not only angiogenesis but also mobilization of EPCs from BM and their recruitment to the ischemic sites. We demonstrated that reactive oxygen species (ROS) derived from Nox2-based NADPH oxidase play an important role in reparative angiogenesis induced by hindlimb ischemia. However, role of Nox2-derived ROS in BM and EPC function in postnatal neovascularization is unknown. Here we show that Nox2 is the most highly expressed Nox enzymes in mouse BM cells (BMCs) and EPCs. Hindlimb ischemia of mice significantly increases Nox2 mRNA expression (2.3-fold) and ROS production (7.2-fold) in BMCs at 3 days after surgery, which is associated with an increase in number of EPC-like c-kit+Flk-1+ cells in peripheral blood (3.9-fold). Nox2-deficient mice show impairment of ischemia-induced flow recovery (68% inhibition) and significant reduction of ROS levels in BM (98% decrease) and EPC mobilization, as assessed by EPC culture assay (76% decrease) and FACS analysis of c-kit+Flk-1+ cells (33% decrease). Transplantation of wild-type (WT)-BM into Nox2-deficient mice rescues the defective neovascularization. Conversely, WT mice transplanted with Nox2-deficient BM show significant decrease of flow recovery (41% decrease) and capillary density (24% decrease) compared to WT-BM transplanted control. Intravenous infusion of WT-BM-mononuclear cells (MNCs), but not Nox2-deficient MNCs, into WT mice at 1 day after hindlimb ischemia significantly promotes neovascularization (37% increase). Infusion of fluorescent dye-labeled WT- and Nox2-deficient BMCs reveals that homing capacity of Nox2-deficient BMCs in ischemic border zone is significantly reduced (52% decrease). In vitro, VEGF-induced EPC migration (48% decrease) and BMCs invasion (68% decrease) are significantly inhibited in Nox2-deficient cells. In conclusion, Nox2-derived ROS in BM play a critical role in mobilization, homing and angiogenic capacity of EPCs, thereby promoting revascularization of ischemic tissue. Thus, NADPH oxidase in BM and EPCs is potential therapeutic targets for ischemic cardiovascular diseases.
1562MO Effectiveness of COVID-19 vaccination in cancer patients: A nationwide Veterans Affairs study
Authors: J.T-Y. Wu, J. La, W. Branch-Elliman, L.B. Huhmann, S. Han, G. Parmigiani, D. Tuck, M. Brophy, N. Do, A. Lin, N. Munshi, N. Fillmore
Journal: Annals of Oncology (2021)
Metabolic dysregulation and emerging therapeutical targets for hepatocellular carcinoma
Authors: Danyu Du, Chan Liu, Mengyao Qin, Xiao Zhang, Tao Xi, Shengtao Yuan, Haiping Hao, Jing Xiong
Journal: Acta Pharmaceutica Sinica B (2021)

Hepatocellular carcinoma (HCC) is an aggressive human cancer with increasing incidence worldwide. Multiple efforts have been made to explore pharmaceutical therapies to treat HCC, such as targeted tyrosine kinase inhibitors, immune based therapies and combination of chemotherapy. However, limitations exist in current strategies including chemoresistance for instance. Tumor initiation and progression is driven by reprogramming of metabolism, in particular during HCC development. Recently, metabolic associated fatty liver disease (MAFLD), a reappraisal of new nomenclature for non-alcoholic fatty liver disease (NAFLD), indicates growing appreciation of metabolism in the pathogenesis of liver disease, including HCC, thereby suggesting new strategies by targeting abnormal metabolism for HCC treatment. In this review, we introduce directions by highlighting the metabolic targets in glucose, fatty acid, amino acid and glutamine metabolism, which are suitable for HCC pharmaceutical intervention. We also summarize and discuss current pharmaceutical agents and studies targeting deregulated metabolism during HCC treatment. Furthermore, opportunities and challenges in the discovery and development of HCC therapy targeting metabolism are discussed.
599P A phase I dose-escalation study of LAE001/prednisone plus afuresertib in patients with metastatic castration-resistant prostate cancer (mCRPC) following standard of care (SOC) treatment
Authors: A. Bessudo, X. Wang, J.F. Strauss, D.E. Slater, C. Pieczonka, P. Guo, J. Liu, Y. Yue, C. Lu
Journal: Annals of Oncology (2021)
920P The sarcopenia skeletal muscle mass index (SMI) has a three-tier survival effect in HNSCC, which can be predicted by hemoglobin (Hb), lymphocytes (Ly) and creatinine (Cre)
Authors: S. Guerriero, C. Morelli, M. Rofei, S. Riondino, R. Argirò, D. Morosetti, F. Gasparrini, D. Nitti, M. Benassi, S. Di Girolamo, R.M. D'Angelillo, V. Formica, M. Roselli
Journal: Annals of Oncology (2021)
Critical care management of chimeric antigen receptor T‐cell therapy recipients
Authors: Alexander Shimabukuro‐Vornhagen, Boris Böll, Peter Schellongowski, Sandrine Valade, Victoria Metaxa, Elie Azoulay, Michael von Bergwelt‐Baildon
Journal: CA A Cancer Journal for Clinicians (2021)

Abstract Chimeric antigen receptor (CAR) T‐cell therapy is a promising immunotherapeutic treatment concept that is changing the treatment approach to hematologic malignancies. The development of CAR T‐cell therapy represents a prime example for the successful bench‐to‐bedside translation of advances in immunology and cellular therapy into clinical practice. The currently available CAR T‐cell products have shown high response rates and long‐term remissions in patients with relapsed/refractory acute lymphoblastic leukemia and relapsed/refractory lymphoma. However, CAR T‐cell therapy can induce severe life‐threatening toxicities such as cytokine release syndrome, neurotoxicity, or infection, which require rapid and aggressive medical treatment in the intensive care unit setting. In this review, the authors provide an overview of the state‐of‐the‐art in the clinical management of severe life‐threatening events in CAR T‐cell recipients. Furthermore, key challenges that have to be overcome to maximize the safety of CAR T cells are discussed.
966P Diabetes therapy burden as proxy of impairment of immune checkpoint inhibitors efficacy
Authors: A. Cortellini, D. Mallardo, S. Cleary, M. Bersanelli, D. Santini, M.G. Tucci, A. Russo, F. Rastelli, M. Filetti, A.J. Gelibter, R. Marconcini, R. Chiari, F. Grossi, M. De Tursi, P. Queirolo, F. Zoratto, E.T. Tanda, G. Porzio, P.A. Ascierto, D.J. Pinato
Journal: Annals of Oncology (2021)
Introducing a Special Series: Addressing Racial and Ethnic Disparities in Kidney Disease
Authors: Josephine P. Briggs, Donald Wesson
Journal: Journal of the American Society of Nephrology (2021)

It has been more than a year and a half since the murder of George Floyd precipitated our ongoing national discussion on racial and ethnic inequity. This has been a difficult and at times polarizing conversation, but there is widespread recognition that addressing racial and ethnic inequity is as
1405P Efficacy and safety of perioperative FLOT (5-FU, LV, oxaliplatin, docetaxel) chemotherapy in gastric and gastroesophageal junction adenocarcinoma: Real-life data from Turkish oncology group
Authors: C. Erol, T. Basoglu, A. Sakin, E. Ozden, D. Cubuk, P.F. Yumuk, M. Dogan, B. Oksuzoglu, H.C. Yildirim, I. Oner, M. Karakurt Eryilmaz, O. Dulgar, E. Turkmen Bekmez, N. Dogan, M. Ozen, F. Gurler, N. Paksoy, A. Aksoy, M. Hizal, M.A.N. Sendur
Journal: Annals of Oncology (2021)