tbuckley/cabot-search huggingface dataset:
Retracted: A novel fully automated MRI-based deep-learning method for classification of IDH mutation status in brain gliomas
Authors: Chandan Ganesh Bangalore Yogananda, Bhavya R Shah, Maryam Vejdani-Jahromi, Sahil S Nalawade, Gowtham K Murugesan, Frank F Yu, Marco C Pinho, Benjamin C Wagner, Bruce Mickey, Toral R Patel, Baowei Fei, Ananth J Madhuranthakam, Joseph A Maldjian
Journal: Neuro-Oncology (2019)

Isocitrate dehydrogenase (IDH) mutation status has emerged as an important prognostic marker in gliomas. Currently, reliable IDH mutation determination requires invasive surgical procedures. The purpose of this study was to develop a highly accurate, MRI-based, voxelwise deep-learning IDH classification network using T2-weighted (T2w) MR images and compare its performance to a multicontrast network.Multiparametric brain MRI data and corresponding genomic information were obtained for 214 subjects (94 IDH-mutated, 120 IDH wild-type) from The Cancer Imaging Archive and The Cancer Genome Atlas. Two separate networks were developed, including a T2w image-only network (T2-net) and a multicontrast (T2w, fluid attenuated inversion recovery, and T1 postcontrast) network (TS-net) to perform IDH classification and simultaneous single label tumor segmentation. The networks were trained using 3D Dense-UNets. Three-fold cross-validation was performed to generalize the networks' performance. Receiver operating characteristic analysis was also performed. Dice scores were computed to determine tumor segmentation accuracy.T2-net demonstrated a mean cross-validation accuracy of 97.14% ± 0.04 in predicting IDH mutation status, with a sensitivity of 0.97 ± 0.03, specificity of 0.98 ± 0.01, and an area under the curve (AUC) of 0.98 ± 0.01. TS-net achieved a mean cross-validation accuracy of 97.12% ± 0.09, with a sensitivity of 0.98 ± 0.02, specificity of 0.97 ± 0.001, and an AUC of 0.99 ± 0.01. The mean whole tumor segmentation Dice scores were 0.85 ± 0.009 for T2-net and 0.89 ± 0.006 for TS-net.We demonstrate high IDH classification accuracy using only T2-weighted MR images. This represents an important milestone toward clinical translation.
P2.17-24 Minimally Invasive Surgery for Lung Cancer Improves Short Term Outcomes in Patients with History of Head and Neck Carcinoma
Authors: D. Boulate, T. Kassegne, J. Chenesseau, M. Ammi, S. Mussot, D. Fabre, D. Mitilian, A. Crutu, S. Temam, O. Mercier, E. Fadel
Journal: Journal of Thoracic Oncology (2019)
How Certain Foods Affect Cognition, Seizures, and Cardiometabolic Disease
Authors: Rebecca Voelker
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 Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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) 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
P2.04-52 Impact of Corticosteroids and Antibiotics on Efficacy of Immune-Checkpoint Inhibitors in Patients with Advanced Non-Small Cell Lung Cancer
Authors: M. Riudavets, J. Mosquera, R. Garcia Campelo, J. Serra, G. Anguera, P. Gallardo, I.G. Sullivan, A. Barba, M. Majem
Journal: Journal of Thoracic Oncology (2019)
MA05.10 Pembrolizumab in the Treatment of Patients with Malignant Pleural Mesothelioma Following Progression After Initial Chemotherapy
Authors: K. Cengel, S. Katz, L. Roshkovan, S. Mcnulty, J. Lian, D. Aleynick, M. Culligan, J. Friedberg, S. Singhal, C. Simone Li, C. Ciunci, M. Marmarelis, E. Alley, C. Langer
Journal: Journal of Thoracic Oncology (2019)
P2.14-60 Afatinib in EGFR Mutation-Positive NSCLC: Activity in Patients with Brain Metastases, and Impact on CNS Progression/Spread
Authors: K. O'Byrne, J.C. Yang, Y. Wu, V. Hirsh, N. Yamamoto, S. Popat, A. Tamiya, A. Märten, M. Schuler
Journal: Journal of Thoracic Oncology (2019)
Apolipoprotein B Particles and Cardiovascular Disease
Authors: Allan D. Sniderman, George Thanassoulis, Tamara Glavinovic, Ann Marie Navar, Michael Pencina, Alberico Catapano, Brian A. Ference
Journal: JAMA Cardiology (2019)

<h3>Importance</h3> The conventional model of atherosclerosis presumes that the mass of cholesterol within very low-density lipoprotein particles, low-density lipoprotein particles, chylomicron, and lipoprotein (a) particles in plasma is the principal determinant of the mass of cholesterol that will be deposited within the arterial wall and will drive atherogenesis. However, each of these particles contains one molecule of apolipoprotein B (apoB) and there is now substantial evidence that apoB more accurately measures the atherogenic risk owing to the apoB lipoproteins than does low-density lipoprotein cholesterol or non–high-density lipoprotein cholesterol. <h3>Observations</h3> Cholesterol can only enter the arterial wall within apoB particles. However, the mass of cholesterol per apoB particle is variable. Therefore, the mass of cholesterol that will be deposited within the arterial wall is determined by the number of apoB particles that are trapped within the arterial wall. The number of apoB particles that enter the arterial wall is determined primarily by the number of apoB particles within the arterial lumen. However, once within the arterial wall, smaller cholesterol-depleted apoB particles have a greater tendency to be trapped than larger cholesterol-enriched apoB particles because they bind more avidly to the glycosaminoglycans within the subintimal space of the arterial wall. Thus, a cholesterol-enriched particle would deposit more cholesterol than a cholesterol-depleted apoB particle whereas more, smaller apoB particles that enter the arterial wall will be trapped than larger apoB particles. The net result is, with the exceptions of the abnormal chylomicron remnants in type III hyperlipoproteinemia and lipoprotein (a), all apoB particles are equally atherogenic. <h3>Conclusions and Relevance</h3> Apolipoprotein B unifies, amplifies, and simplifies the information from the conventional lipid markers as to the atherogenic risk attributable to the apoB lipoproteins.
The role of exosomal PD-L1 in tumor progression and immunotherapy
Authors: Feiting Xie, Mengxue Xu, Jian Lu, Lingxiang Mao, Shengjun Wang
Journal: Molecular Cancer (2019)

Abstract Programmed death ligand 1 (PD-L1), a type I transmembrane protein, binds to its receptor PD-1 to suppress the activation of T cells, thereby maintaining immunological homeostasis. In contrast, tumor cells highly express PD-L1, which binds to receptor PD-1 expressed on activated T cells, leading to immune escape. Anti-PD-1/PD-L1 immune checkpoint therapy blocks the binding of PD-1/PD-L1 to reinvigorate the exhausted T cells, thereby inhibiting tumor growth. Exosomes are biologically active lipid-bilayer nanovesicles secreted by various cell types that mediate intercellular signal communication. Numerous studies have shown that tumor cells are able to promote tumor epithelial-mesenchymal transition, angiogenesis, and immune escape by releasing exosomes. Recent studies imply that tumor-derived exosomes could carry PD-L1 in the same membrane topology as the cell surface, thereby resisting immune checkpoint therapy. In this review, we mainly discuss the role of exosomes in the regulation of tumor progression and the potential resistance mechanism to immunotherapy via exosomal PD-L1. In addition, we propose that exosomal PD-L1 may have the potential to be a target to overcome resistance to anti-PD-1/PD-L1 antibody therapy.
P2.09-18 Lymphocyte Infiltration Pattern and STING Expression Identify Different Prognostic Groups in Early Stage NSCLC
Authors: F. Tabbò, F. Guerrera, P. Bironzo, M. Gagliasso, C. Cartia, A. Rigutto, S. Izzo, F. Veneziano, F. Arizio, F. Ardissone, M. Papotti, M. Volante, S. Novello, L. Righi
Journal: Journal of Thoracic Oncology (2019)
EP1.04-31 Immunotherapy in Advanced Non-Small Cell Lung Cancer Previously Treated: Real World Data
Authors: F. Ferreira Pereira, A.R. Lopes, A. Cruz, M. Cassiano, A. Rosinha, C. Oliveira, A. Rodrigues, J. Oliveira, I. Pousa, I. Azevedo, M. Soares
Journal: Journal of Thoracic Oncology (2019)
Energy Metabolism of Leukemia Cells: Glycolysis Vs Oxidative Phosphorylation
Authors: Hiroshi Miwa, Kazuto Suganuma, Masato Shikami, Norikazu Imai, Mayuko Sakai, Akihito Hiramatsu, Hidesuke Yamamoto, Motohiro Wakabayashi, Masaya Watarai, Ichiro Hanamura, Akira Imamura, Hidetsugu Mihara, Masakazu Nitta
Journal: Blood (2008)
OA14.04 Five-Year Outcomes From the Randomized, Phase 3 Trials CheckMate 017/057: Nivolumab vs Docetaxel in Previously Treated NSCLC
Authors: S. Gettinger, H. Borghaei, J. Brahmer, L. Chow, M. Burgio, J. De Castro Carpeno, A. Pluzanski, O. Arrieta, O. Aren Frontera, R. Chiari, C. Butts, J. Wojcik-Tomaszewska, B. Coudert, M. Garassino, N. Ready, E. Felip, M. Alonso Garcia, D. Waterhouse, M. Domine, F. Barlesi, S. Antonia, M. Wohlleber, D. Gerber, G. Czyzewicz, D. Spigel, L. Crino, W. Eberhardt, A. Li, S. Marimuthu, E. Vokes
Journal: Journal of Thoracic Oncology (2019)
P2.01-99 A Phase IIIb Open-Label Study of Afatinib in EGFR TKI-Naïve Patients with EGFR Mutation-Positive NSCLC: Final Analysis
Authors: Y. Wu, H. Tu, J. Feng, M. Shi, J. Zhao, Y. Wang, J. Chang, J. Wang, Y. Cheng, J. Zhu, E. Tan, Y. Zhang, V. Lee, C. Yang, W. Su, D.C. Lam, B. Srinivasa, S. Rajappa, C. Ho, K.C. Lam, Y. Hu, S.A. Bondarde, X. Liu, K. Pang, Y. Tian, A. Cseh, D.C. Huang, C. Zhou
Journal: Journal of Thoracic Oncology (2019)
P1.01-73 An Explorative Analysis of Pemetrexed +/- Pembrolizumab Maintenance from KEYNOTE-189 Versus PARAMOUNT, PRONOUNCE, and JVBL
Authors: E. Garon, R. Govindan, V. Papadimitrakopoulou, C. Wang, R. Varea, J.S. Kim, J. Aerts
Journal: Journal of Thoracic Oncology (2019)
Convergent Evolution of Hydrogenosomes from Mitochondria by Gene Transfer and Loss
Authors: William H Lewis, Anders E Lind, Kacper M Sendra, Henning Onsbring, Tom A Williams, Genoveva F Esteban, Robert P Hirt, Thijs J G Ettema, T Martin Embley
Journal: Molecular Biology and Evolution (2019)

Abstract Hydrogenosomes are H2-producing mitochondrial homologs found in some anaerobic microbial eukaryotes that provide a rare intracellular niche for H2-utilizing endosymbiotic archaea. Among ciliates, anaerobic and aerobic lineages are interspersed, demonstrating that the switch to an anaerobic lifestyle with hydrogenosomes has occurred repeatedly and independently. To investigate the molecular details of this transition, we generated genomic and transcriptomic data sets from anaerobic ciliates representing three distinct lineages. Our data demonstrate that hydrogenosomes have evolved from ancestral mitochondria in each case and reveal different degrees of independent mitochondrial genome and proteome reductive evolution, including the first example of complete mitochondrial genome loss in ciliates. Intriguingly, the FeFe-hydrogenase used for generating H2 has a unique domain structure among eukaryotes and appears to have been present, potentially through a single lateral gene transfer from an unknown donor, in the common aerobic ancestor of all three lineages. The early acquisition and retention of FeFe-hydrogenase helps to explain the facility whereby mitochondrial function can be so radically modified within this diverse and ecologically important group of microbial eukaryotes.
Nuclear miR-320 Mediates Diabetes-Induced Cardiac Dysfunction by Activating Transcription of Fatty Acid Metabolic Genes to Cause Lipotoxicity in the Heart
Authors: Huaping Li, Jiahui Fan, Yanru Zhao, Xiaorong Zhang, Beibei Dai, Jiabing Zhan, Zhongwei Yin, Xiang Nie, Xiang-Dong Fu, Chen Chen, Dao Wen Wang
Journal: Circulation Research (2019)

Rationale: Diabetes mellitus is often associated with cardiovascular complications, which is the leading cause of morbidity and mortality among patients with diabetes mellitus, but little is known about the mechanism that connects diabetes mellitus to the development of cardiovascular dysfunction. Objective: We aim to elucidate the mechanism underlying hyperglycemia-induced cardiac dysfunction on a well-established db/db mouse model for diabetes mellitus and diabetic complications that lead to heart failure. Methods and Results: We first profiled the expression of microRNAs (miRNAs) by microarray and quantitative reverse transcription polymerase chain reaction on db/db mice and identified miR-320 as a key miRNA associated with the disease phenotype. We next established the clinical relevance of this finding by showing the upregulation of the same miRNA in the failing heart of patients with diabetes mellitus. We demonstrated the causal role of miR-320 in inducing diabetic cardiomyopathy, showing that miR-320 overexpression exacerbated while its inhibition improved the cardiac phenotype in db/db mice. Unexpectedly, we found that miR-320 acts as a small activating RNA in the nucleus at the level of transcription. By chromatin immunoprecipitation sequencing and chromatin immunoprecipitation quantitive polymerase chain reaction analysis of Ago2 (argonaute RISC catalytic component 2) and RNA polymerase II in response to miR-320 induction, we identified CD36 (fatty acid translocase) as a key target gene for this miRNA and showed that the induced expression of CD36 is responsible for increased fatty acid uptake, thereby causing lipotoxicity in the heart. Conclusions: These findings uncover a novel mechanism for diabetes mellitus–triggered cardiac dysfunction, provide an endogenous case for small activating RNA that has been demonstrated to date only with synthetic RNAs in transfected cells, and suggest a potential strategy to develop a miRNA-based therapy to treat diabetes mellitus–associated cardiovascular complications.
P1.03-23 Delta-Like 1 Homolog (DLK1) Expression in Non-Small-Cell Lung Cancer and the Development of Radioimmunotherapy Targeting DLK1
Authors: H. Takagi, S. Zhao, S. Muto, H. Mine, M. Watanabe, Y. Ozaki, N. Okabe, T. Hasegawa, Y. Shio, M. Aoki, C. Tan, S. Shimoyama, K. Nakamura, A. Inano, H. Suzuki
Journal: Journal of Thoracic Oncology (2019)
Bilateral Ovarian Metastases From Gastric Carcinoma on FDG PET/CT
Authors: Linh Ho, Heidi Wassef, Andrew Nakla, Robert Henderson
Journal: Clinical Nuclear Medicine (2012)

We report PET/CT appearance of bilateral ovarian metastases in a 63-year-old female patient with newly diagnosed poorly differentiated adenocarcinoma of the stomach. She was also found to have peritoneal metastasis on an outside CT study. Staging PET/CT demonstrates not only the hypermetabolic gastric primary tumor and peritoneal disease but also bilateral enlarged, moderately active ovaries. The patient subsequently underwent biopsies of bilateral ovaries which revealed metastatic disease from primary gastric carcinoma. It is important to consider this form of neoplasm in the differential diagnosis because the treatment and prognosis will be different from a dyssynchronous primary tumor.
MA03.11 Chemotherapy After PD-1 Inhibitors Versus Chemotherapy Alone in Patients with Non–Small Cell Lung Cancer (WJOG10217L)
Authors: E. Miyawaki, R. Kato, H. Hayashi, Y. Chiba, J. Shimizu, T. Ozaki, D. Fujimoto, R. Toyozawa, Y. Akazawa, M. Okuno, S. Morikawa, T. Ohira, T. Harada, R. Ushio, A. Kubo, T. Harada, N. Kimura, H. Yamaguchi, K. Nishikawa, N. Yamamoto, K. Nakagawa
Journal: Journal of Thoracic Oncology (2019)
EP1.04-44 Exploration of Factors Relating to Paradoxical Immune Response in Patients Treated with Immune Checkpoint Inhibitors for NSCLC
Authors: A.F. Cardona, O.G. Arrieta, A. Ruiz-Patiño, Z.L. Zatarain Barrón, L.L. Rojas, L. Corrales, C. Martin, F. Barrón, C. Sotelo, J. Rodriguez, L. Ricaurte, H. Freitas, V. Cordeiro De Lima, L. Mas, J. Ávila, M. Bravo, D. Mayorga, P. Archila, J. Otero, H. Carranza, C. Vargas, R. Rosell
Journal: Journal of Thoracic Oncology (2019)
P2.18-15 Surgical Outcomes of Pneumonectomy After Induction Therapy for Non-Small-Cell Lung Cancer
Authors: N. Okumura, Y. Otsuki, H. Kayawake, A. Takahashi, T. Nakashima, T. Matsuoka, T. Yokoyama, S. Itasaka, Y. Yamamoto
Journal: Journal of Thoracic Oncology (2019)
P2.03-19 Co-Targeting PIM Kinase to Overcome MET Amplified Resistance to EGFR TKIs in NSCLC
Authors: A. Tranberg Madsen, G. Moore, N. Simon, A. Mahon, S. Cuffe, S. Finn, M. O'Neill, B. Sorensen, K. Gately
Journal: Journal of Thoracic Oncology (2019)
MA25.01 Pembrolizumab Plus Chemotherapy for Advanced NSCLC Without Tumor PD-L1 Expression: Pooled Analysis of KN021G, KN189 and KN407
Authors: H. Borghaei, C. Langer, L. Paz-Ares, D. Rodriguez Abreu, B. Halmos, V. Papadimitrakopoulou, M. Garassino, B. Houghton, T. Kurata, Y. Cheng, J. Lin, M.C. Pietanza, B. Piperdi, S. Gadgeel
Journal: Journal of Thoracic Oncology (2019)
P1.14-45 Surgical Outcome of Non-Small Cell Lung Cancer with Clinical Single Zone N2 in Aortopulmonary Zone (LN#5 and LN#6)
Authors: K. Lee, H.R. Kim, J. Ryu, Y. Kim, S. Park, D.K. Kim, Y. Kim, S. Choi, G.D. Lee, Y.H. Jeong, J.K. Yun, Y. Chong
Journal: Journal of Thoracic Oncology (2019)
EP1.17-24 Biologically Effective Dose Was Associated with Overall Survival in Stereotactic Body Radiotherapy for Lung Tumors
Authors: O. Tanaka, N. Funaguchi, S. Toyoshi, T. Taniguchi, K. Ono, Y. Kunishima, Y. Masui, M. Matsuo
Journal: Journal of Thoracic Oncology (2019)
P2.15-02 Primary Salivary Gland-Type Lung Tumours, Surgically Treatable Rare Entity Lung Cancer: A Sixteen-Year Experience of a Single Centre
Authors: S. Ricciardi, G. Alì, D. Bacchin, M. Ambrogi, G. Fontanini, F. Melfi, M. Lucchi
Journal: Journal of Thoracic Oncology (2019)
P1.01-107 KEYNOTE-495/KeyImPaCT: Phase 2 Biomarker-Directed Study of Pembrolizumab-Based Therapy for Non–Small Cell Lung Cancer
Authors: M. Gutierrez, M. Hellmann, M. Gubens, C. Aggarwal, D. Tan, E. Felip, W. Lam, J.W.Y. Chiu, J. Lee, J. Yang, E. Garon, A. Basso, H. Ma, L. Fong, A. Snyder, J. Yuan, R. Herbst
Journal: Journal of Thoracic Oncology (2019)
P1.01-08 Randomized Phase II Trial of CBDCA+nab-PTX vs CDDP+GEM in Patients with Chemo-Naïve Squamous Cell Lung Cancer: NJLCG1302
Authors: T. Harada, Y. Kawashima, Y. Fujita, T. Nakagawa, K. Watanabe, N. Morikawa, K. Takamura, K. Kanazawa, K. Tomoya, K. Usui, A. Inoue, A. Sekine, S. Sugawara
Journal: Journal of Thoracic Oncology (2019)
Mitochondrial Protein Poldip2 (Polymerase Delta Interacting Protein 2) Controls Vascular Smooth Muscle Differentiated Phenotype by O-Linked GlcNAc (N-Acetylglucosamine) Transferase–Dependent Inhibition of a Ubiquitin Proteasome System
Authors: Felipe Paredes, Holly C. Williams, Raymundo A. Quintana, Alejandra San Martin
Journal: Circulation Research (2019)

The mitochondrial Poldip2 (protein polymerase interacting protein 2) is required for the activity of the tricarboxylic acid cycle. As a consequence, Poldip2 deficiency induces metabolic reprograming with repressed mitochondrial respiration and increased glycolytic activity. Though homozygous deletion of Poldip2 is lethal, heterozygous mice are viable and show protection against aneurysm and injury-induced neointimal hyperplasia, diseases linked to loss of vascular smooth muscle differentiation. Thus, we hypothesize that the metabolic reprograming induced by Poldip2 deficiency controls VSMC differentiation.To determine the role of Poldip2-mediated metabolic reprograming in phenotypic modulation of VSMC.We show that Poldip2 deficiency in vascular smooth muscle in vitro and in vivo induces the expression of the SRF (serum response factor), myocardin, and MRTFA (myocardin-related transcription factor A) and dramatically represses KLF4 (Krüppel-like factor 4). Consequently, Poldip2-deficient VSMC and mouse aorta express high levels of contractile proteins and, more significantly, these cells do not dedifferentiate nor acquire macrophage-like characteristics when exposed to cholesterol or PDGF (platelet-derived growth factor). Regarding the mechanism, we found that Poldip2 deficiency upregulates the hexosamine biosynthetic pathway and OGT (O-linked N-acetylglucosamine transferase)-mediated protein O-GlcNAcylation. Increased protein glycosylation causes the inhibition of a nuclear ubiquitin proteasome system responsible for SRF stabilization and KLF4 repression and is required for the establishment of the differentiated phenotype in Poldip2-deficient cells.Our data show that Poldip2 deficiency induces a highly differentiated phenotype in VSMCs through a mechanism that involves regulation of metabolism and proteostasis. Additionally, our study positions mitochondria-initiated signaling as key element of the VSMC differentiation programs that can be targeted to modulate VSMC phenotype during vascular diseases.
MA13.05 Nab-Paclitaxel Maintenance in Squamous Non-Small Cell Lung Cancer (NSCLC): Updated Results of the Phase III ABOUND.sqm Study
Authors: D. Spigel, R. Jotte, S. Aix, L. Gressot, D. Morgensztern, M. Mccleod, M. Socinski, D. Daniel, O. Juan, K. Mileham, H. West, R. Page, N. Reinmuth, J. Knoble, O. Tian, R. Bhore, M. Wolfsteiner, T. Jin Ong, C. Gridelli, M. Thomas
Journal: Journal of Thoracic Oncology (2019)
P1.16-08 Integration of Durvalumab into the Treatment of Stage III Non-Small Cell Lung Cancer: Real-World Considerations
Authors: S. Gorgens, E. Schreibmann, M. Behera, C. Steuer, R. Pillai, T. Owonikoko, J. Shelton, S. Ramalingam, W. Curran, K. Higgins
Journal: Journal of Thoracic Oncology (2019)
Incidence trends and survival prediction of hepatoblastoma in children: a population‐based study
Authors: Jincheng Feng, Georgios Polychronidis, Ulrike Heger, Giovanni Frongia, Arianeb Mehrabi, Katrin Hoffmann
Journal: Cancer Communications (2019)

Abstract Background Hepatoblastoma is a rare disease that nevertheless accounts for the majority of liver malignancies in children. Due to limited epidemiological data, therapy for hepatoblastoma tends to be individualized. This study aimed to evaluate incidence trends of hepatoblastoma and to develop a nomogram to predict the survival of children with newly diagnosed hepatoblastoma on a population‐based level. Methods Individuals up to 18 years of age with hepatoblastoma recorded in 18 registries of the Surveillance, Epidemiology, and End Results (SEER) database between 2004 and 2015 were examined. Joinpoint regression analyses were applied to assess incidence trends in annual percentage change (APC). Multivariable Cox regression was used to identify factors associated with overall survival (OS). A nomogram was constructed to predict OS in individual cases based on independent predictors. Concordance index (C‐index) and calibration curves were used to evaluate predictive performance. Results Between 2004 and 2015, hepatoblastoma incidence increased significantly (APC, 2.2%; 95% confidence interval [CI] 0.5% to 3.8%, P &lt; 0.05). In particular, this increase was observed among 2‐ to 4‐year‐old patients, males, and African–Americans. The 5‐ and 10‐year OS rates were 81.5% and 81.0%, respectively. Age of 2 to 4 years, African–American ethnicity, and no surgery were independent predictors for short OS. Distant disease at presentation was found not to be an independent factor of survival. The nomogram had a C‐index of 0.79 (95% CI 0.74–0.84) with appropriate calibration curve fitting. Conclusions We constructed a nomogram that integrates common factors associated with survival for hepatoblastoma patients. It provides accurate prognostic prediction for children with hepatoblastoma.