tbuckley/cabot-search huggingface dataset:
Targeting MDM2 for novel molecular therapy: Beyond oncology
Authors: Wei Wang, Jiang‐Jiang Qin, Mehrdad Rajaei, Xin Li, Xiaoyi Yu, Courtney Hunt, Ruiwen Zhang
Journal: Medicinal Research Reviews (2019)

The murine double minute 2 (MDM2) oncogene exerts major oncogenic activities in human cancers; it is not only the best-documented negative regulator of the p53 tumor suppressor, but also exerts p53-independent activities. There is an increasing interest in developing MDM2-based targeted therapies. Several classes of MDM2 inhibitors have been evaluated in preclinical models, with a few entering clinical trials, mainly for cancer therapy. However, noncarcinogenic roles for MDM2 have also been identified, demonstrating that MDM2 is involved in many chronic diseases and conditions such as inflammation and autoimmune diseases, dementia and neurodegenerative diseases, heart failure and cardiovascular diseases, nephropathy, diabetes, obesity, and sterility. MDM2 inhibitors have been shown to have promising therapeutic efficacy for treating inflammation and other nonmalignant diseases in preclinical evaluations. Therefore, targeting MDM2 may represent a promising approach for treating and preventing these nonmalignant diseases. In addition, a better understanding of how MDM2 works in nonmalignant diseases may provide new biomarkers for their diagnosis, prognostic prediction, and monitoring of therapeutic outcome. In this review article, we pay special attention to the recent findings related to the roles of MDM2 in the pathogenesis of several nonmalignant diseases, the therapeutic potential of its downregulation or inhibition, and its use as a biomarker.
Abstract 1602: Strain-derived and Tissue velocity-derived Dyssynchrony Indexes for Prediction of Reverse Remodeling with Cardiac Resynchronization Therapy
Authors: Chinami Miyazaki, Margaret M Redfield, Raul E Espinosa, Charles J Bruce, David L Hayes, Fletcher A Miller, Jae K Oh
Journal: Circulation (2007)

Background : Dyssynchrony indexes derived from time to peak systolic velocity and time to peak strain have been reported to predict left ventricular reverse remodeling (RR) after cardiac resynchronization therapy (CRT). The predictive characteristics of these indices have not been validated in a variety of clinical settings. Our objective was to determine the predictive value of strain and tissue velocity derived dyssynchrony indices for RR or clinical response to CRT in a prospective single-center CRT registry. Methods : Prospective registry of all heart failure patients (pts) undergoing CRT with echo before and 3 and 6 months after CRT. Color -coded tissue Doppler imaging in 12 segments was used to calculate the standard deviation of time to peak strain (Tϵ-SD) and time to peak systolic velocity (Tv-SD). RR was defined as a decrease in end systolic volume (ESV; biplane Simpson’s method) ≥15%. Indices were assessed with receiver-operating characteristics (ROC) analysis and the area under the curve (AUC) calculated in all pts and excluding those with atrial fibrillation at implant. Results : To date, of the first 87 patients, 4 died (classified as non-responder); 83 pts had 3 and 59 pts had 6 month echocardiography follow-up. Tϵ-SD (93%) and Tv-SD (98%) were feasible in most pts. RR occurred in 42 pts (51%) at 3 month and 32 patients (54%) at 6 month follow-up. See table . Tϵ-SD was superior to Tv-SD for prediction of RR in all pts and in those without atrial fibrillation. Findings were similar regardless of ischemic (68% of patients) or non-ischemic etiology. Neither baseline Tϵ-SD nor Tv-SD correlated with the improvement in clinical response measured by the change in six minute walk distance or peak VO 2 at 3 or 6 month after CRT (data not shown). Conclusions : In this single center experience, mechanical dyssynchrony measured by strain imaging but not tissue velocity imaging was predictive of RR. Neither index predicted clinical response.
Metformin for Type 2 Diabetes
Authors: Alfredo Caturano, Raffaele Galiero, Pia Clara Pafundi
Journal: JAMA (2019)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
A Comparative Modeling Analysis of Risk-Based Lung Cancer Screening Strategies
Authors: Kevin ten Haaf, Mehrad Bastani, Pianpian Cao, Jihyoun Jeon, Iakovos Toumazis, Summer S Han, Sylvia K Plevritis, Erik F Blom, Chung Yin Kong, Martin C Tammemägi, Eric J Feuer, Rafael Meza, Harry J de Koning
Journal: JNCI Journal of the National Cancer Institute (2019)

Abstract Background Risk-prediction models have been proposed to select individuals for lung cancer screening. However, their long-term effects are uncertain. This study evaluates long-term benefits and harms of risk-based screening compared with current United States Preventive Services Task Force (USPSTF) recommendations. Methods Four independent natural history models were used to perform a comparative modeling study evaluating long-term benefits and harms of selecting individuals for lung cancer screening through risk-prediction models. In total, 363 risk-based screening strategies varying by screening starting and stopping age, risk-prediction model used for eligibility (Bach, PLCOm2012, or Lung Cancer Death Risk Assessment Tool [LCDRAT]), and risk threshold were evaluated for a 1950 US birth cohort. Among the evaluated outcomes were percentage of individuals ever screened, screens required, lung cancer deaths averted, life-years gained, and overdiagnosis. Results Risk-based screening strategies requiring similar screens among individuals ages 55–80 years as the USPSTF criteria (corresponding risk thresholds: Bach = 2.8%; PLCOm2012 = 1.7%; LCDRAT = 1.7%) averted considerably more lung cancer deaths (Bach = 693; PLCOm2012 = 698; LCDRAT = 696; USPSTF = 613). However, life-years gained were only modestly higher (Bach = 8660; PLCOm2012 = 8862; LCDRAT = 8631; USPSTF = 8590), and risk-based strategies had more overdiagnosed cases (Bach = 149; PLCOm2012 = 147; LCDRAT = 150; USPSTF = 115). Sensitivity analyses suggest excluding individuals with limited life expectancies (&amp;lt;5 years) from screening retains the life-years gained by risk-based screening, while reducing overdiagnosis by more than 65.3%. Conclusions Risk-based lung cancer screening strategies prevent considerably more lung cancer deaths than current recommendations do. However, they yield modest additional life-years and increased overdiagnosis because of predominantly selecting older individuals. Efficient implementation of risk-based lung cancer screening requires careful consideration of life expectancy for determining optimal individual stopping ages.
Potential role of a clinical, taxonomical classification and RNA expression integrated signature to predict response to neoadjuvant platinum-based chemotherapy in muscle-invasive bladder cancer (MIBC) patients
Authors: A. Font, M. Domenech, J.L. Ramirez, J. Gago, C. Carrato, B. Cadenas, R. Benítez, T. Lobato, S. Pineda, V. Ruiz de Porras, M.L. Calle, N. Malats, F.X. Real
Journal: Annals of Oncology (2019)
Switch maintenance gemcitabine after first-line chemotherapy in patients with malignant mesothelioma: A multicenter open label phase II trial (NVALT19)
Authors: S.A. Burgers, C. de Gooijer, R. Cornelissen, J.G. Aerts, B. Biesma, R.V. Heemst, M. Youssef-El Soud, H.J.M. Groen, A.J. Staal-van den Brekel, G. Bootsma, J H E M Schijen, P. Baas, E. Giovannetti, J.F. de Vries, F.A. Hogenboom, D.C.M. de Wit, M.C.W. Mahn- Schaefers, F. Lalezari, V. van de Noort, J. Stigt
Journal: Annals of Oncology (2019)
ADAPTeR: A phase II study of anti-PD1 (nivolumab) therapy as pre- and post-operative therapy in metastatic renal cell carcinoma
Authors: L. Au, K. Litchfield, A. Rowan, S. Horswell, F. Byrne, D. Nicol, N. Fotiadis, R.F. Salgado, S. Hazell, J.I. Lopez, E. Hatipoglu, L. Del Rosario, L. Pickering, M. Gore, B. Chain, S. Quezada, J.M.G. Larkin, C. Swanton, S. Turajlic
Journal: Annals of Oncology (2019)
Synthesis and characterization of the biological activity of the cisplatin analogs cis-PtCl2(dexrazoxane) and cis-PtCl2(levrazoxane) of the topoisomerase II inhibitors dexrazoxane (ICRF-187) and levrazoxane (ICRF-186).
Authors: Brian B. Hasinoff, Xing Wu
Journal: Cancer Research (2004)

3077  The bisdioxopiperazines dexrazoxane and levrazoxane are strong catalytic inhibitors of mammalian DNA topoisomerase II. The individual stereoisomers of their platinum(II) complexes, cis-PtCl2(dexrazoxane) and cis-PtCl2(levrazoxane), were synthesized and their structures were determined by x-ray crystallography. Dexrazoxane and levrazoxane inhibit cell growth because they inhibit topoisomerase II, whereas cisplatin acts through the formation of DNA cross-links. It was hypothesized that platinum(II) complexes of dexrazoxane and levrazoxane would retain both activities and yield drugs with a dual mode of action. Both cis-PtCl2(dexrazoxane) and cis-PtCl2(levrazoxane) inhibited Chinese hamster ovary cell growth, but more weakly than dexrazoxane and levrazoxane did. Based on the inability of these platinum complexes to inhibit the catalytic activity of topoisomerase II it was concluded that these compounds did not inhibit cell growth by. targeting topoisomerase II. The recent x-ray structure of dexrazoxane bound to the ATPase region of a yeast topoisomerase II has been used to model the platinum complexes into the bisdioxopiperazine binding site. A comparison of the conformation of cis-PtCl2(dexrazoxane) to that of dexrazoxane bound to the dimer interface of topoisomerase II showed that the highly constrained cis-PtCl2(dexrazoxane) was in a highly unfavorable conformation for binding. Also neither of the platinum complexes were able to cross-link DNA. Thus the cell growth inhibitory activity of these complexes were also not likely due to any cisplatin-type cross-linking activity. Support: CIHR and a Canada Research Chair in Drug Development.
Preventive Cardiology as a Subspecialty of Cardiovascular Medicine
Authors: Michael D. Shapiro, David J. Maron, Pamela B. Morris, Mikhail Kosiborod, Pratik B. Sandesara, Salim S. Virani, Amit Khera, Christie M. Ballantyne, Seth J. Baum, Laurence S. Sperling, Deepak L. Bhatt, Sergio Fazio
Journal: Journal of the American College of Cardiology (2019)
A pan-ErbB family inhibitor, AF8c, promotes apoptosis by DR5/Nrf2 activation via ROS in colorectal cancer cells
Authors: S. Jeong, H.K. Yun, Y.A. Jeong, D.Y. Kim, M.J. Jo, S.H. Park, B.R. Kim, J.L. Kim, Y.J. Na, D.-H. Lee, S.C. Oh
Journal: Annals of Oncology (2019)
Feasibility study of a ctEGFR prototype assay on the fully automated Idylla™ platform
Authors: M. Reijans, S.V. Gestel, E.D. Haes, C. Vandesteene, J.M. Castro Gomez, C. Gouedard, S. Patera, S. Murray, G.G. Maertens
Journal: Annals of Oncology (2019)
Does the Hematopoietic Cell Transplantation Specific Comorbidity Index (HCT-CI) Predict Transplant Outcomes?: A Prospective Multicenter Validation Study of the Kanto Study Group for Cell Therapy (KSGCT)
Authors: Aya Nakaya, Takehiko Mori, Masatsugu Tanaka, Naoto Tomita, Chiaki Nakaseko, Shingo Yano, Shin Fujisawa, Hisashi Sakamaki, Nobuyuki Aotsuka, Akira Yokota, Yoshinobu Kanda, Toru Sakura, Yasuhito Nannya, Takayuki Saitoh, Heiwa Kanamori, Satoshi Takahashi, Shinichiro Okamoto
Journal: Blood (2012)
Evaluating polygenic risk score prediction model for melanoma prognosis
Authors: M. Potrony, N. Calbet-llopart, M. Combalia, G. Tell-Martí, J.A. Puig-Butille, A. Barreiro, S. Podlipnik, C. Carrera, J. Malvehy, S. Puig
Journal: Annals of Oncology (2019)
Antitumor activity, immunogenicity and safety of a novel PD-1 vaccine in combination with two chimeric HER-2 peptide vaccine in syngeneic Balb/c, C57Bl/6 models and in beagle dogs
Authors: P.T.P. Kaumaya, J. Overholser, L. Guo, Y. Yang, M. Penichet, B. Sayanjali, N. Ede, L. Chong, T. Bekaii-Saab
Journal: Annals of Oncology (2019)
HORMONET: Study of tamoxifen in well differentiated neuroendocrine tumours and hormone receptor positive expression
Authors: M. Barros, T.C. Felismino, V.H.F. de Jesus, C.A. Mello, V.S. Silva, M. Camandaroba, N. Rodrigues, M.D. Donadio, E. Nobrega, L. Chinen, L. De Brot, R.F. Weschenfelder, J.F. Rego, J.B. Carvalheira, R.P. Riechelmann
Journal: Annals of Oncology (2019)
Preliminary results from the TRITON2 study of rucaparib in patients (pts) with DNA damage repair (DDR)-deficient metastatic castration-resistant prostate cancer (mCRPC): Updated analyses
Authors: W. Abida, D. Campbell, A. Patnaik, B. Sautois, J. Shapiro, N.J. Vogelzang, A.H. Bryce, R. McDermott, F. Ricci, J. Rowe, J. Zhang, A.D. Simmons, D. Despain, M. Dowson, T. Golsorkhi, S. Chowdhury
Journal: Annals of Oncology (2019)
Zebrafish MITF-Low Melanoma Subtype Models Reveal Transcriptional Subclusters and MITF-Independent Residual Disease
Authors: Jana Travnickova, Sonia Wojciechowska, Ava Khamseh, Philippe Gautier, Daniel V. Brown, Thomas Lefevre, Alessandro Brombin, Ailith Ewing, Amy Capper, Michaela Spitzer, Ramile Dilshat, Colin A. Semple, Marie E. Mathers, James A. Lister, Eiríkur Steingrimsson, Thierry Voet, Chris P. Ponting, E. Elizabeth Patton
Journal: Cancer Research (2019)

Abstract The melanocyte-inducing transcription factor (MITF)–low melanoma transcriptional signature is predictive of poor outcomes for patients, but little is known about its biological significance, and animal models are lacking. Here, we used zebrafish genetic models with low activity of Mitfa (MITF-low) and established that the MITF-low state is causal of melanoma progression and a predictor of melanoma biological subtype. MITF-low zebrafish melanomas resembled human MITF-low melanomas and were enriched for stem and invasive (mesenchymal) gene signatures. MITF-low activity coupled with a p53 mutation was sufficient to promote superficial growth melanomas, whereas BRAFV600E accelerated MITF-low melanoma onset and further promoted the development of MITF-high nodular growth melanomas. Genetic inhibition of MITF activity led to rapid regression; recurrence occurred following reactivation of MITF. At the regression site, there was minimal residual disease that was resistant to loss of MITF activity (termed MITF-independent cells) with very low-to-no MITF activity or protein. Transcriptomic analysis of MITF-independent residual disease showed enrichment of mesenchymal and neural crest stem cell signatures similar to human therapy-resistant melanomas. Single-cell RNA sequencing revealed MITF-independent residual disease was heterogeneous depending on melanoma subtype. Further, there was a shared subpopulation of residual disease cells that was enriched for a neural crest G0-like state that preexisted in the primary tumor and remained present in recurring melanomas. These findings suggest that invasive and stem-like programs coupled with cellular heterogeneity contribute to poor outcomes for MITF-low melanoma patients and that MITF-independent subpopulations are an important therapeutic target to achieve long-term survival outcomes. Significance: This study provides a useful model for MITF-low melanomas and MITF-independent cell populations that can be used to study the mechanisms that drive these tumors as well as identify potential therapeutic options.
Dissociated responses in patients with metastatic solid tumours treated with immunotherapy
Authors: P. Vaflard, X. Paoletti, V. Servois, E. Pons-Tostivint, M.P. Sablin, F. Ricci, D. Loirat, S. Hescot, N. Torossian, E. Borcoman, C. Le Tourneau
Journal: Annals of Oncology (2019)
Abstract 10504: Patient, Medical and Laboratory Characteristics Associated With a Decline in Physical Functioning in Children and Adolescents After the Fontan Procedure
Authors: Brian W McCrindle, Victor Zak, Roger E Breitbart, Lynn Mahony, Peter Shrader, Wyman W Lai, Kristin M Burns, Steven D Colan, Richard V Williams, David J Goldberg, Kevin D Hill, Svetlana Khaikin, Andrew M Atz
Journal: Circulation (2013)

Background: Despite hypothesized concerns about deterioration beginning in adolescence, longitudinal data and associated factors regarding standardized assessment of physical functioning are not av...
Nurse Practitioners
Authors: LEWIS J. RUBIN
Journal: Annals of Internal Medicine (1975)

Comments and Correction1 August 1975Nurse PractitionersLEWIS J. RUBIN, M.D., ROBERT S. KATZ, M.D.LEWIS J. RUBIN, M.D.Search for more papers by this author, ROBERT S. KATZ, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-83-2-278_2 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: As recent graduates of a medical school whose affiliated hospitals are involved in the training and employment of nurse practitioners in the clinics and emergency rooms, we have had the opportunity to observe and work along with many nurse practitioners. Thus, we read with great interest the article by Dr. Bates (Ann Intern Med 82:702-706, 1975).She accurately describes the problems of transition from performing routine nursing duties to participating in the diagnostic and therapeutic process. We take issue, however, with several points.We do not believe that the nurse practitioner has an edge over the house... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited ByInternational Collaboration: Initial Steps and Strategies 1 August 1975Volume 83, Issue 2Page: 278-279KeywordsEmergency departmentGraduate medical educationHospitalsNurses Issue Published: 1 August 1975 PDF DownloadLoading ...
Medical school places must double by 2029, says Royal College of Psychiatrists
Authors: Anna Harvey
Journal: BMJ (2019)

The number of medical school places in England should double from 7500 to 15 000 by 2029, the Royal College of Psychiatrists has said. This echoes a 2018 statement from the Royal College of Physicians calling for the same increase.1

The Royal College of Psychiatrists warned that, without an increase in medical school places, mental health services would implode. It said that the extra medical students could lead to around 4497 additional consultant psychiatrists, helping the government to meet its aim to expand mental health services as set out in the NHS long term plan.

Wendy Burn, president …
Evaluation of different diagnostic methods for identification of FGFR alteration in advanced urothelial carcinomas: Proficiency results based on multiple RNA extraction kits and mutation detection methods
Authors: V.E.J. Weyerer, R. Stoehr, H. Juette, R. Wirtz, M. Eckstein, F. Roghmann, J. Breyer, S. Porubsky, D. Sikic, C. Bolenz, M.C. Kriegmair, A. Hartmann, P. Erben
Journal: Annals of Oncology (2019)
Holding replication studies to mainstream standards of evidence
Authors: Duane T. Wegener, Leandre R. Fabrigar
Journal: Behavioral and Brain Sciences (2018)

Abstract Replications can make theoretical contributions, but are unlikely to do so if their findings are open to multiple interpretations (especially violations of psychometric invariance). Thus, just as studies demonstrating novel effects are often expected to empirically evaluate competing explanations, replications should be held to similar standards. Unfortunately, this is rarely done, thereby undermining the value of replication research.
Abstract 20266: Riata Lead Failure in Pediatric and Congenital Heart Disease Patients
Authors: Carolina A Escudero, Sunjidatul Islam, Douglas Mah, Christina Y Miyake, Elizabeth A Stephenson, Martin J LaPage, Joseph Atallah
Journal: Circulation (2016)

Introduction: ICD lead failures are relatively common with higher failure rates identified in pediatric and congenital heart disease (CHD) patients. Our study aim was to determine the rate and timi...
Molecular subtypes of metastatic (met) gastric cancer (GC) (MoTriGastric): New biomarkers closer to the clinics
Authors: M. Alsina Maqueda, F. Ruiz, S. Landolfi, C. Viaplana, J.M. Miquel, J. Jimenez, M. Diez, I. Gullo, O. Mirallas, J. Tabernero, F. Carneiro, P.G. Nuciforo, A. Vivancos, R. Dienstmann
Journal: Annals of Oncology (2019)
Insights from pharmacokinetic models of host-microbiome drug metabolism
Authors: Maria Zimmermann-Kogadeeva, Michael Zimmermann, Andrew L. Goodman
Journal: Gut Microbes (2019)

Increasing evidence suggests a role of the gut microbiota in patients' response to medicinal drugs. In our recent study, we combined genomics of human gut commensals and gnotobiotic animal experiments to quantify microbiota and host contributions to drug metabolism. Informed by experimental data, we built a physiology-based pharmacokinetic model of drug metabolism that includes intestinal compartments with microbiome drug-metabolizing activity. This model successfully predicted serum levels of metabolites of three different drugs, quantified microbial contribution to systemic drug metabolite exposure, and simulated the effect of different parameters on host and microbiota drug metabolism. In this addendum, we expand these simulations to assess the effect of microbiota on the systemic drug and metabolite levels under conditions of altered host physiology, microbiota drug-metabolizing activity or physico-chemical properties of drugs. This work illustrates how and under which circumstances the gut microbiome may influence drug pharmacokinetics, and discusses broader implications of expanded pharmacokinetic models.
Bone Marrow Stromal Cells Induce ALDH+ Stem Cell Phenotype and Chemotherapy Resistance in AML Cells through TGF-β1 Mediated Signaling: Reversal By TGFβ Inhibitor Galunisertib
Authors: Ximin Zhou, Bin Yuan, Yuanqing Yan, Khoa Nguyen, Vivian Ruvolo, Hong Mu, Teresa McQueen, Elizabeth J Shpall, Kim-Ann Do, Marina Konopleva, Michael Andreeff, Venkata Lokesh Battula
Journal: Blood (2017)
Mechanisms Underlying Superior Efficacy of Co-Targeting BET Proteins and Anti-Apoptotic BCL2 or MCL1 Protein Against AML Blast Progenitor Cells
Authors: Christopher Peter Mill, Tianyu Cai, Warren Fiskus, Gautam Borthakur, Steven M. Kornblau, Tapan M. Kadia, Courtney D. DiNardo, Agnieszka J Nowak, Dyana T. Saenz, David N Saenz, Baohua Sun, Thurika Ganesh, Wendy Jin, Vaishnavi Rao, Joseph David Khoury, Yu Shen, Marina Y. Konopleva, Kapil N. Bhalla
Journal: Blood (2018)
Presence of a T383G Mutation in the Vitamin K Epoxide Reductase Gene (VKORC1) in a Patient Resistant to Four Different Vitamin K Antagonists.
Authors: Michel-Meyer M.M. Samama, Laurent L. Bodin, Marie Helene M.H. Horellou, Florence F. Parent, Anne A. Kereveur, Philippe P. Beaune, Marie Anne M.A. Loriot, Jacqueline J. Conard
Journal: Blood (2004)
Prognostic significance of tumour tissue NeuGcGM3 ganglioside expression and predictive value of circulating tumour cell count monitoring in patients receiving racotumomab immunotherapy
Authors: N. Üskent, S. Ayla, N Molinas Mandel, M. Ozkan, M. Teomete, H. Baloglu, C. Aydıncer, H. Yergok, E. Dogan, B. Berk, A. Yazar
Journal: Annals of Oncology (2019)