Endocrine-related cancer最新文献

{"title":"Larotrectinib in TRK fusion differentiated thyroid carcinoma: updated trial data.","authors":"Steven G Waguespack, Marcia S Brose, Jessica J Lin, Ray McDermott, Mohammed Almubarak, Jessica Bauman, Michela Casanova, Shivaani Kummar, Se-Hoon Lee, Damian T Rieke, Do-Youn Oh, Changsong Qi, Natascha Neu, Domnita-Ileana Burcoveanu, Chiara E Mussi, Alexander Drilon, David S Hong, Maria E Cabanillas","doi":"10.1530/ERC-25-0531","DOIUrl":"10.1530/ERC-25-0531","url":null,"abstract":"<p><p>Larotrectinib is a first-in-class, highly selective, central nervous system-active tropomyosin receptor kinase (TRK) inhibitor approved for tumour-agnostic use in TRK fusion cancer. It has previously demonstrated rapid and durable disease control and favourable safety in patients with advanced TRK fusion thyroid carcinoma (TC). After an additional 4 years of follow-up with the inclusion of two additional patients, and utilising an independent review committee (IRC) to assess overall response rate (ORR), we report updated pooled analyses from three phase 1-2 larotrectinib clinical trials, focusing only on patients with TRK fusion differentiated TC (DTC). The primary endpoint was the IRC-determined ORR per RECIST v1.1. Duration of response (DoR), progression-free survival (PFS), overall survival (OS) and safety were also assessed. Twenty-four patients (papillary TC, n = 21; follicular TC, n = 2; poorly DTC, n = 1) were included (data cut-off: 20 July 2024). ORR was 79% (95% confidence interval (CI): 58-93); best responses were complete response in 3 (13%) patients, partial response in 16 (67%), stable disease in 3 (13%), progressive disease in 1 (4%) and not evaluable in 1 (4%). Median DoR and PFS were 35 (95% CI: 22-not estimable (NE)) and 44 (95% CI: 35-NE) months, respectively; 6-year OS rate was 71% (95% CI: 50-91). Six patients remained on treatment. Treatment-related adverse events (TRAEs) were mainly grade 1/2; no patients permanently discontinued treatment due to TRAEs. Larotrectinib continues to demonstrate durable disease control, extended survival and a favourable long-term safety profile in patients with advanced TRK fusion DTC requiring systemic therapy.</p>","PeriodicalId":93989,"journal":{"name":"Endocrine-related cancer","volume":" ","pages":""},"PeriodicalIF":4.6,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13452024/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148451006","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Epidemiology and overall survival of de novo and transformed neuroendocrine prostate cancer: a two-nation population-based study of 1,465 patients from the United States and England.","authors":"Sunyoung Choi, Mohamed Mortagy, Ker Shiong Tan, Benjamin E White, Sangeeta Paisey, Aya Abdelhameed, Brian Rous, John Ramage","doi":"10.1530/ERC-26-0268","DOIUrl":"10.1530/ERC-26-0268","url":null,"abstract":"<p><p>Neuroendocrine prostate cancer (NEPC) is a rare and aggressive variant of prostate cancer (PC) that can be de novo (d-NEPC) or transform from prior prostate adenocarcinoma (PCa) as treatment-emergent NEPC (t-NEPC). This study aimed to study the clinical characteristics and overall survival (OS) of NEPC using data from the SEER and NCRAS registries and to compare OS of d-NEPC and t-NEPC. A total of 1,465 patients with NEPC were extracted from SEER (n = 990, 2010-2022) and NCRAS (n = 475, 2010-2021). Patients were classified as t-NEPC if preceded by a documented PCa. The primary outcome was OS measured from the date of NEPC diagnosis. Kaplan-Meier analysis, the log-rank test, and Cox regression were performed for SEER, NCRAS, and pooled cohorts. t-NEPC represented 9.9% in NCRAS and 15.2% in SEER. Small cell carcinoma was the most common subtype (80.2% NCRAS, 74.7% SEER). Median time to transformation was 4.63 years in NCRAS and 5 years in SEER. In the pooled cohort, median OS was 9 months for d-NEPC and 7 months for t-NEPC (log-rank P < 0.001). The 60-month OS was 7.9% for d-NEPC and 4.0% for t-NEPC. In the pooled multivariable Cox regression, t-NEPC was independently associated with worse OS (aHR: 1.30, 95% CI: 1.11-1.53, P = 0.001). Data source was not associated with OS (aHR: 1.08, P = 0.206), indicating comparable OS between the USA and England. In this bi-national, population-based study, t-NEPC was associated with worse OS than d-NEPC. OS for NEPC was comparable between the USA and England. These findings support distinguishing d-NEPC from t-NEPC.</p>","PeriodicalId":93989,"journal":{"name":"Endocrine-related cancer","volume":" ","pages":""},"PeriodicalIF":4.6,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148703067","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Whole genome and exome sequencing of pancreatic neuroendocrine tumour to investigate PRRT response.","authors":"Emma Boehm, Aidan Flynn, Alex Caneborg, Athena Hatzimihalis, Annette Hogg, Kelly Waldeck, Louise Jackett, Owen W J Prall, Catherine Mitchell, Grace Kong, Michael Michael, Tim Akhurst, Benjamin N J Thomson, William K Murray, Kwang Chin, Ben Lawrence, Cristin G Print, Joseph H A Vissers, Sean M Grimmond, Richard W Tothill, Rodney J Hicks","doi":"10.1530/ERC-26-0207","DOIUrl":"10.1530/ERC-26-0207","url":null,"abstract":"<p><p>Patients with pancreatic neuroendocrine tumours (PNETs) often have similar baseline clinical characteristics, including grade and molecular imaging phenotype, yet have highly variable responses to peptide receptor radionuclide therapy (PRRT). To identify genomic alterations and mutational patterns associated with PRRT treatment response and acquired somatic changes following PRRT exposure, whole genome or exome sequencing was applied to 40 PNET samples from 32 patients, including eight paired pre- or post-PRRT samples. The genomic profile of tumours reflected the known mutational landscape of PNET with MEN1 (34%), ATRX/DAXX (47%) alterations and a recurrent pattern of aneuploidy (38%) detected. A recurrent PSIP1::TBL1X fusion of unknown function was also identified in four tumours. The disease control rate following PRRT using RECIST1.1 and molecular imaging criteria was 88% (28/32). No mutational features were found to be statistically associated with progression-free survival. There was no significant increase in tumour mutational burden in the post-PRRT tumours, nor recurrent emergent mutational changes in cancer driver genes to explain progression to higher-grade disease, when observed. However, a small indel signature (ID8) previously associated with DNA damage repair by non-homologous end joining (NHEJ) was higher in PRRT-exposed compared with PRRT-naive samples (23.8 vs 4.8%, respectively; P < 0.001). Thus, comprehensive DNA analysis of pancreatic NETs did not identify biomarkers predictive of PRRT response nor evidence for high-level PRRT-induced genomic instability or hypermutation, yet mutation signature analysis supports NHEJ as being important for DNA repair and survival of neuroendocrine cells following exposure to beta-particle radiation.</p>","PeriodicalId":93989,"journal":{"name":"Endocrine-related cancer","volume":" ","pages":""},"PeriodicalIF":4.6,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13452026/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148521712","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Associations of TILs and genomic alterations in HER2+ early breast cancer.","authors":"Shuangshuang Lu, Jiahui Huang, Yijin Gu, Chaofu Wang, Kunwei Shen, Xiaochun Fei, Xiaosong Chen","doi":"10.1530/ERC-25-0411","DOIUrl":"10.1530/ERC-25-0411","url":null,"abstract":"<p><p>This study investigated the associations between tumor-infiltrating lymphocytes (TILs), genomic features, and prognosis in HER2+ early breast cancer (EBC) patients receiving adjuvant trastuzumab. We retrospectively analyzed 864 HER2+ EBC patients from Shanghai Ruijin Hospital (2009-2017). The optimal threshold of TILs for predicting disease-free survival (DFS) and overall survival (OS) was explored. Whole-exome sequencing (WES) on 261 tumors assessed the mutational profiles, tumor mutational burden (TMB), and copy number alteration (CNA). Associations between these genomic features, TIL levels, and prognosis were further evaluated. TILs showed a right-skewed distribution (median: 15%, IQR: 1-30%), and higher TIL levels were significantly associated with hormone receptor negativity and high histologic grade (P < 0.001). A 15% TIL threshold optimally predicted prognosis, with low-TIL (≤15%, 63.0%) patients showing inferior DFS (HR: 1.63, P = 0.009) and OS (HR: 2.12, P = 0.037). WES identified frequent mutations in TP53 (62.8%), PIK3CA (34.5%), and BRCA2 (9.6%). A higher TIL density was observed in TP53-wild-type, low-TMB or low-CNA tumors (P < 0.05). PIK3CA mutations conferred a significant DFS advantage. Integrating TIL level with PIK3CA or BRCA2 mutational status yielded distinct DFS trajectories (log-rank P = 0.023 and 0.040, respectively); patients with both high TIL levels and either PIK3CA or BRCA2 mutations had the most favorable outcomes. Stromal TILs at a 15% cutoff provide robust prognostic information in trastuzumab-treated HER2+ EBC. Integrating TIL levels with PIK3CA or BRCA2 mutational status enables refined risk stratification, offering a practical framework for personalized treatment decisions.</p>","PeriodicalId":93989,"journal":{"name":"Endocrine-related cancer","volume":" ","pages":""},"PeriodicalIF":4.6,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148681579","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Molecular subtyping of adrenocortical carcinoma reveals distinct subtypes with prognostic and therapeutic implications.","authors":"Luming Wu, Tingwei Su, Cui Zhang, Lei Jiang, Jing Xie, Weiwei Zhou, Yiran Jiang, Xu Zhong, Weiqing Wang","doi":"10.1530/ERC-25-0342","DOIUrl":"10.1530/ERC-25-0342","url":null,"abstract":"<p><p>Adrenocortical carcinoma (ACC) is a rare but aggressive malignancy with poor survival and limited treatment options. To comprehensively characterize its molecular landscape and identify clinically relevant subtypes, we performed an integrated genomic analysis - including whole-exome sequencing, RNA sequencing, and copy number variation profiling - on 61 Chinese patients with ACC. We identified recurrent mutations in TP53 (25%), CTNNB1 (15%), ZNRF3 (10%), and MEN1 (8%). Unsupervised clustering of transcriptomic data revealed four distinct molecular subtypes: cortisol-driven (CD, 14%), immune-suppressed (IS, 40%), cell cycle-altered (CCA, 22%), and immunomodulatory (IM, 24%). The CD subtype exhibited steroidogenic pathway activation; the IS subtype showed T cell receptor downregulation and the worst disease-free survival; the CCA subtype was marked by chromosomal instability and cell cycle gene overexpression; and the IM subtype displayed enriched immune signaling and favorable outcomes. Copy number analysis further uncovered focal amplifications (e.g. TERT, CDK4) and HLA-II deletions. This study establishes a novel molecular classification of ACC, providing a framework for subtype-specific therapeutic strategies, such as CDK4/6 inhibition for CCA and immunotherapy for IM tumors, while highlighting the clinical challenges of immune-cold IS tumors.</p>","PeriodicalId":93989,"journal":{"name":"Endocrine-related cancer","volume":" ","pages":""},"PeriodicalIF":4.6,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13482824/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148671774","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Great Escape: the systems biology of endocrine resistance and lineage plasticity.","authors":"Christo P C Dragnev, Zirui Fu, Sida Huang, Curtis J Perry, Adriana Kahn, Michaela A Dinan, Wei Shen Tan, Michael Leapman, David A Braun, Joshua Warrick, Himisha Beltran, Ping Mu","doi":"10.1530/ERC-26-0130","DOIUrl":"10.1530/ERC-26-0130","url":null,"abstract":"<p><p>Endocrine therapies initially enforce lineage identity in hormone-driven cancers, yet sustained hormonal suppression often triggers a coordinated systems-level rewiring through lineage plasticity. Previously, lineage plasticity has been characterized as a discrete bypass mechanism, which lacks fluidic identity changes. Here, we describe the process as a progressive, adaptive trajectory of endocrine escape. We describe how the disruption of hormone receptor-anchored identity programs creates permissive conditions for transitions into HR-indifferent or neuroendocrine- or basal-like states. Next, we summarize historical methodologies for investigating lineage plasticity, such as patient-derived organoids, genetically engineered mouse models (GEMMS), lineage tracing, and single-cell multi-omics, and discuss novel systems biology approaches to enable the early detection and modeling of these unstable intermediate states. Finally, we present promising and potential uses for artificial intelligence and machine learning for dissecting therapy-induced identity shifts and resistance mechanisms. Intercepting these trajectories before lineage commitment offers a critical window for precision oncology interventions.</p>","PeriodicalId":93989,"journal":{"name":"Endocrine-related cancer","volume":" ","pages":""},"PeriodicalIF":4.6,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13545732/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148703100","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ERRATUM: The inhibition of Wnt/β-catenin signalling by 1α,25-dihydroxyvitamin D3 is abrogated by Snail1 in human colon cancer cells.","authors":"María Jesús Larriba, Noelia Valle, Héctor G Pálmer, Paloma Ordóñez-Morán, Silvia Álvarez-Díaz, Karl-Friedrich Becker, Carlos Gamallo, Antonio García de Herreros, José Manuel González-Sancho, Alberto Muñoz","doi":"10.1530/ERC-06-0028e","DOIUrl":"https://doi.org/10.1530/ERC-06-0028e","url":null,"abstract":"","PeriodicalId":93989,"journal":{"name":"Endocrine-related cancer","volume":"33 8","pages":""},"PeriodicalIF":4.6,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148868576","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Somatic genetic alterations in pituitary neuroendocrine tumors.","authors":"Yair Schwarz, Reut Halperin, Amit Tirosh","doi":"10.1530/ERC-26-0213","DOIUrl":"10.1530/ERC-26-0213","url":null,"abstract":"<p><p>The molecular characterization of pituitary neuroendocrine tumors (PitNETs) has progressed pronouncedly in recent years, unraveling the molecular pathways driving initiation and progression of different PitNET types and allowing a better understanding of their biology. The most frequent recurring somatic driver alterations were recognized in corticotroph PitNETs (USP8, USP48, BRAF) and somatotroph PitNETs (GNAS) and, much less frequently, in lactotroph PitNETs (SF3B1). Additional well-characterized somatic driver alterations, including TP53, ATRX, and DAXX, are enriched in aggressive corticotroph tumors. Identification of new molecular markers and delineation of their clinical phenotypes are enabling further subclassification of PitNETs based on tumor molecular profiles, with earlier recognition of more aggressive variants. These molecular markers also provide an opportunity for new targeted therapies. Beyond single-gene alterations, epigenetic modifications, such as DNA methylation, histone modifications, and noncoding RNA dysregulation, are emerging as important contributors to PitNET pathogenesis and potential therapeutic targets. Multi-omics approaches encompassing genomics, transcriptomics, epigenomics, and proteomics are transforming PitNET classification. In this review, we provide a comprehensive, data-driven update on somatic driver alterations, epigenetic alterations, converging signaling pathways, and the related emerging therapeutic targets in PitNETs, integrating pooled analyses from published cohorts.</p>","PeriodicalId":93989,"journal":{"name":"Endocrine-related cancer","volume":" ","pages":""},"PeriodicalIF":4.6,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148687098","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Peptide receptor radionuclide therapy (PRRT) and the pituitary: safety and efficacy.","authors":"Francesco Ferraù, Elena Sofia Blanca, Carla Paola Costa, Salvatore Cannavò","doi":"10.1530/ERC-26-0109","DOIUrl":"10.1530/ERC-26-0109","url":null,"abstract":"<p><p>Peptide receptor radionuclide therapy (PRRT) is an emerging and promising targeted treatment for aggressive pituitary neuroendocrine tumours (PitNETs) and pituitary carcinomas refractory to conventional therapies. Its use is supported by the frequent expression of somatostatin receptors (SSTRs), predominantly SSTR2, in pituitary tumour cells, enabling selective delivery of β-emitting radionuclides, such as 177Lu-DOTATATE and 90Y-DOTATOC, resulting in targeted antitumour and antisecretory effects. This narrative review summarises current limited evidence on PRRT efficacy and safety in aggressive pituitary tumours. Successful outcomes have been reported in some cases in terms of tumour growth reduction and/or hormonal reduction or relief of mass-effect-related symptoms. PRRT-related adverse events are mostly mild and transient, predominantly haematological, with clinically significant renal toxicity uncommon when amino acid nephroprotection is used. Preserved pituitary function and no clinically significant PRRT-induced hypopituitarism have been reported. Overall, PRRT represents a biologically rational and potentially effective option for selected patients with SSTR-positive aggressive PitNETs after failure of previous therapies.</p>","PeriodicalId":93989,"journal":{"name":"Endocrine-related cancer","volume":" ","pages":""},"PeriodicalIF":4.6,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148714984","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Value of TERT promoter mutations for early outcomes in papillary thyroid cancer.","authors":"Min Jhi Kim, Daham Kim, Hye Sun Lee, Se Hee Park, Eun Jin Kim, Jin Kyong Kim, Sang-Wook Kang, Jandee Lee, Jong Ju Jeong, Woong Youn Chung, Kee-Hyun Nam","doi":"10.1530/ERC-25-0424","DOIUrl":"10.1530/ERC-25-0424","url":null,"abstract":"<p><p>Telomerase reverse transcriptase (TERT) promoter mutations are associated with aggressive clinicopathological features of papillary thyroid cancer (PTC). However, their independent prognostic value remains unclear. This study aimed to evaluate the prognostic significance of TERT promoter mutations (TPMs) in predicting early treatment outcomes and event-free survival (EFS) in patients with PTC. We retrospectively analyzed a prospective cohort; patients underwent surgery at a single tertiary referral center between 2019 and 2022. Patients underwent thyroidectomy, selective postoperative radioactive iodine ablation, and levothyroxine suppression therapy. Propensity score matching (PSM, 1:1) was applied to adjust for baseline clinicopathological differences. Of 10,642 patients with available molecular data, 115 (1.1%) harbored TPMs. After PSM, 90 matched pairs of patients with TERT-wild-type and TERT-mutant tumors were analyzed. Early treatment responses at 1 and 2 years post-treatment and EFS were evaluated. Early treatment responses did not differ significantly between groups at 1 year (P = 0.212) and 2 years (P = 0.571). However, patients with TERT-mutant tumors had fewer excellent responses and higher rates of structural incomplete response. During follow-up, the TERT-mutant group experienced more recurrences and one disease-specific death. Cumulative EFS was significantly poorer in the TERT-mutant group than in the TERT-wild-type group (P = 0.022). Despite their low prevalence, TPMs were independently associated with adverse oncological outcomes, including higher rates of recurrence and mortality. TPMs may serve as valuable prognostic markers for early risk stratification in PTC.</p>","PeriodicalId":93989,"journal":{"name":"Endocrine-related cancer","volume":" ","pages":""},"PeriodicalIF":4.6,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13506541/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147701341","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}