Cancer Genetics最新文献

{"title":"ENPP1 promotes immune suppression, drug resistance, and adverse outcomes in bladder cancer: Potential for targeted therapy","authors":"Chengyu You ,&nbsp;Qixiang Fang ,&nbsp;Xi Xiao ,&nbsp;Yang Liu ,&nbsp;Weiguang Yang ,&nbsp;Liangliang Qing ,&nbsp;Qingchao Li ,&nbsp;Rongxin Li ,&nbsp;Yanan Wang ,&nbsp;Zhilong Dong","doi":"10.1016/j.cancergen.2025.03.001","DOIUrl":"10.1016/j.cancergen.2025.03.001","url":null,"abstract":"<div><h3>Background</h3><div>ENPP1 (Ectonucleotide Pyrophosphatase/Phosphodiesterase 1) plays a critical role in multiple cancers; however, its role in bladder cancer (BC) remains largely unexplored. This study investigates the impact of ENPP1 on tumor progression, apoptosis, and the immune microenvironment through bioinformatics and experimental validation.</div></div><div><h3>Materials and methods</h3><div>ENPP1 expression and clinical significance were analyzed using TCGA-BLCA, GEO datasets, and a local clinical cohort of 36 BC patients. Immune infiltration and functional enrichment were assessed using ESTIMATE, CIBERSORT, and clusterProfiler. Single-cell RNA sequencing (scRNA-seq) data examined ENPP1 expression in BC tissues. Stable ENPP1-overexpressing (UMUC3) and ENPP1-knockdown (J82) cell lines were established. Functional assays, including proliferation, migration, and apoptosis marker analysis, were performed.</div></div><div><h3>Results</h3><div>RT-qPCR, Western blotting, and immunohistochemistry confirmed differential ENPP1 expression between BC tissues and adjacent normal tissues. High ENPP1 expression was associated with worse overall survival (OS), advanced T and N stages, and poor pathological grades. Functional assays demonstrated that ENPP1 overexpression enhanced proliferation, migration, and apoptosis resistance, while knockdown suppressed these processes. Mechanistically, ENPP1 overexpression reduced pro-apoptotic markers BAX and Caspase-3 while increasing anti-apoptotic Bcl-2. Immune infiltration analysis revealed a positive correlation between ENPP1 expression and M2 macrophage infiltration, alongside decreased CD8+ <em>T</em> cell infiltration. scRNA-seq identified high ENPP1 expression in cancer-associated fibroblasts and epithelial cells. Drug sensitivity analysis linked elevated ENPP1 expression to resistance against chemotherapies like gemcitabine and cytarabine.</div></div><div><h3>Conclusion</h3><div>ENPP1 drives tumor progression, modulates immune infiltration, and contributes to chemotherapy resistance in BC, underscoring its potential as a therapeutic target.</div></div>","PeriodicalId":49225,"journal":{"name":"Cancer Genetics","volume":"294 ","pages":"Pages 1-14"},"PeriodicalIF":1.4,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143580189","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Composite mantle cell lymphoma with cryptic ins(11;2)(q13;p11.2p11.2)/IGK::CCND1 and lymphoplasmacytic lymphoma with MYD88 L265P mutation","authors":"Fumiyo Maekawa ,&nbsp;Masahiko Hayashida ,&nbsp;Kayo Takeoka ,&nbsp;Yoshinari Chagi ,&nbsp;Riku Takahashi ,&nbsp;Chiyuki Kishimori ,&nbsp;Shinichi Kotani ,&nbsp;Takashi Akasaka ,&nbsp;Shinichi Sakamoto ,&nbsp;Shinji Sumiyoshi ,&nbsp;Hitoshi Ohno","doi":"10.1016/j.cancergen.2025.02.012","DOIUrl":"10.1016/j.cancergen.2025.02.012","url":null,"abstract":"<div><div>A woman in her 80 s presented with generalized lymphadenopathy, bone marrow (BM) involvement, and leukemic manifestation. Lymph node biopsy revealed typical histopathology of mantle cell lymphoma (MCL) and the CD5⁺ and immunoglobulin μ⁺δ⁺/λ⁺ immunophenotype, with unmutated <em>IGHV</em>. BM was infiltrated with not only MCL but also another B-cell tumor that was CD5⁻ and μ^bright+δ⁺/κ⁺, being consistent with M proteins in the serum and urine, with mutated <em>IGHV</em>. As the latter lymphoma component carried the <em>MYD88</em> L265P mutation, this case represented a composite of MCL and lymphoplasmacytic lymphoma. Next-generation sequencing revealed a cryptic insertion of <em>IGK</em> enhancer sequences into the <em>CCND1</em>-major translocation cluster, accounting for CCND1 expression in MCL cells recognized by immunohistochemistry. Composite lymphoma is rare, but a correct diagnosis is required because effective treatments for each component are now available.</div></div>","PeriodicalId":49225,"journal":{"name":"Cancer Genetics","volume":"294 ","pages":"Pages 15-20"},"PeriodicalIF":1.4,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143580290","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RECQL4-related Rothmund-Thomson syndrome: A case series and literature review","authors":"Stephanie Ka Lun Ho ,&nbsp;Grace Pui Yung Tong ,&nbsp;Lai-Ting Leung ,&nbsp;Shirley Sze Wing Cheng ,&nbsp;Eric Chun Ho Fu ,&nbsp;Ivan Fai Man Lo ,&nbsp;Anthony Pak Yin Liu ,&nbsp;Ho-ming Luk","doi":"10.1016/j.cancergen.2025.02.013","DOIUrl":"10.1016/j.cancergen.2025.02.013","url":null,"abstract":"<div><div>Rothmund-Thomson syndrome (RTS) is a multisystemic tumour-predisposing genodermatosis caused by biallelic pathogenic alterations in the <em>ANAPC1</em> gene or <em>RECQL4</em> gene. Herein we describe the clinical and genetic findings in three individuals with molecularly substantiated <em>RECQL4</em>-related RTS. Based on the disease course of two patients with osteosarcoma, we highlight the critical importance of early diagnosis.</div></div>","PeriodicalId":49225,"journal":{"name":"Cancer Genetics","volume":"292 ","pages":"Pages 131-136"},"PeriodicalIF":1.4,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143527507","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ultra-sensitive detection of melanoma NRAS mutant ctDNA based on programmable endonucleases","authors":"Zuoying Zhang ,&nbsp;Qing Ji ,&nbsp;Zhanfang Zhang ,&nbsp;Bao Lyu ,&nbsp;Pei Li ,&nbsp;Liyi Zhang ,&nbsp;Kaifei Chen ,&nbsp;Meiyu Fang ,&nbsp;Jinzhao Song","doi":"10.1016/j.cancergen.2025.02.008","DOIUrl":"10.1016/j.cancergen.2025.02.008","url":null,"abstract":"<div><h3>Background</h3><div>Melanoma is a complex and often fatal disease, with NRAS being one of the most frequently mutated genes in this type of cancer. Liquid biopsies, specifically tests for circulating tumor DNA (ctDNA), represent a promising and less invasive approach to diagnosis. This study aims to develop an ultra-sensitive assay for detecting melanoma NRAS mutant ctDNA.</div></div><div><h3>Methods</h3><div>To detect rare NRAS mutant ctDNA, we developed the NRAS PASEA assay by screening CRISPR-Cas proteins that recognize the PAM sequence 5′-TTN-3′. This method employs CRISPR-Cas proteins to continuously shear wild-type alleles during isothermal amplification, resulting in exponential amplification of mutant alleles to a detectable level by Sanger sequencing.</div></div><div><h3>Results</h3><div>The developed NRAS Q61R/L/K mutation detection method can detect simulated ctDNA samples with mutant allele fractions (MAF) as low as 0.01 % with 30 mins of PASEA treatment. Notably, the NRAS Q61 K mutation was accurately identified by FnCas12a-based NRAS PASEA, even with the nucleotide at the \"N\" position in the PAM site \"TTN.\" The method successfully detected ctDNA in patients with malignant melanoma. All patients (5/5) from 15 melanoma blood samples with NRAS Q61R (4/4) and NRAS Q61 K (1/1) mutations were accurately identified, with no false positives among patients with wildtype NRAS Q61.</div></div><div><h3>Conclusion</h3><div>Detecting ctDNA from peripheral blood samples is highly significant for melanomas in areas where imaging evaluation is challenging. Our assay demonstrated 100 % consistency with tumor tissue NGS, providing a new analytical strategy for companion diagnosis and dynamic assessment of therapeutic efficacy and disease progression in melanoma.</div></div>","PeriodicalId":49225,"journal":{"name":"Cancer Genetics","volume":"294 ","pages":"Pages 47-56"},"PeriodicalIF":1.4,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143704633","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MicroRNA dysregulation and target genes in common spinal tumors","authors":"Razieh Tavakoli Oliaee ,&nbsp;Majid Reza Farrokhi ,&nbsp;Hamid Moeeni ,&nbsp;Rahele Tavakoly ,&nbsp;Morteza Jafarinia ,&nbsp;Farideh Iravanpour","doi":"10.1016/j.cancergen.2025.02.011","DOIUrl":"10.1016/j.cancergen.2025.02.011","url":null,"abstract":"<div><div>Spinal tumors, although rare, pose significant challenges in diagnosis and treatment due to their complex biological behavior and the variety of tumor types involved. MicroRNAs (miRNAs), small non-coding RNA molecules, have emerged as critical regulators of gene expression and play dual roles as oncogenes or tumor suppressors, depending on their target genes. This review comprehensively examines the role of miRNAs in the pathogenesis and progression of common spinal tumors, including ependymoma, astrocytoma, meningioma, and metastasis, based on existing studies using both human and in vitro models. Several miRNAs have been identified as dysregulated in these tumor types, influencing key cellular processes such as proliferation, migration, and apoptosis. The potential of miRNAs as diagnostic, prognostic, and therapeutic biomarkers is explored, highlighting their value in guiding personalized treatment approaches. Although promising, these findings require further validation to fully understand miRNA-mediated mechanisms and translate these insights into clinical applications. MiRNA-targeted therapies offer a promising avenue for improving patient outcomes in spinal tumor management.</div></div>","PeriodicalId":49225,"journal":{"name":"Cancer Genetics","volume":"292 ","pages":"Pages 124-130"},"PeriodicalIF":1.4,"publicationDate":"2025-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143519752","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinical management of three JMML siblings with germline CBL variation","authors":"Nihat Bugra Agaoglu ,&nbsp;Koray Yalcın ,&nbsp;Busra Unal ,&nbsp;Gizem Onder ,&nbsp;Safiye Suna Celen ,&nbsp;Suleimen Zhumatayev ,&nbsp;Ugur Ozbek ,&nbsp;Ozden Hatirnaz Ng","doi":"10.1016/j.cancergen.2025.02.007","DOIUrl":"10.1016/j.cancergen.2025.02.007","url":null,"abstract":"<div><div>Germline pathogenic variants (PVs) in <em>CBL</em> are found in 15 % of juvenile myelomonocytic leukemia (JMML) cases. Here we report three siblings with <em>CBL</em>(NM_005188):c.1111T&gt;C variation presenting a heterogenous JMML clinic and outcome. The index case was diagnosed at the age of seven, whereas the younger brother was 10 months old and the youngest was one month old. The hematopoietic stem cell transplantation was successful for the index and the youngest brother with event-free survival, but the middle brother showed severe graft versus host disease. This study shows the heterogeneity of JMML and how the outcome might differ even within the family.</div></div>","PeriodicalId":49225,"journal":{"name":"Cancer Genetics","volume":"292 ","pages":"Pages 120-123"},"PeriodicalIF":1.4,"publicationDate":"2025-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143510164","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A case of T-cell acute lymphoblastic leukemia with co-occurrence of NUP214-ABL1 fusion and tetraploidy","authors":"Lijuan Zhu,&nbsp;Wei Zha,&nbsp;Jiajia Zhuo,&nbsp;Xia Yu","doi":"10.1016/j.cancergen.2025.02.009","DOIUrl":"10.1016/j.cancergen.2025.02.009","url":null,"abstract":"<div><div>Although testing and treatment of blood malignancies have been standardized, additional unidentified genetic abnormalities often complicate the diagnosis and therapeutic outcome. Thus, improvement of contemporary therapy requires further stratification of patients based on detailed genetic information. Here, we describe an extremely rare case of Philadelphia chromosome-like T-cell acute lymphoblastic leukemia (Ph-like T-ALL) with NUP214-ABL1 fusion and presentation of unusually enlarged nuclei in the leukemic cells, which was attributed to tetraploidy. Despite receiving the protocol-guided induction chemotherapy, the patient did not respond favorably. The challenges in treating Ph-like T-ALL with rare genetic abnormalities, highlight the need of further research and personalized medication.</div></div>","PeriodicalId":49225,"journal":{"name":"Cancer Genetics","volume":"292 ","pages":"Pages 116-119"},"PeriodicalIF":1.4,"publicationDate":"2025-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143488758","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Three FGFR4 gene polymorphisms contribute to the susceptibility of urethral cancer in the middle and south of Iraq population","authors":"Zahraa Isam Jameel","doi":"10.1016/j.cancergen.2025.02.006","DOIUrl":"10.1016/j.cancergen.2025.02.006","url":null,"abstract":"<div><h3>Background</h3><div>Urothelial cell carcinoma is quite prevalent, making up close to 90 % of all cases. Men are more likely to suffer from it than women, and it mostly affects the elderly. Fibroblast growth factor receptor 4 (<em>FGFR4</em>) plays an important role in cell proliferation and cancer progression.</div></div><div><h3>Aim</h3><div>this study was conducted to assess the association between <em>FGFR4</em> gene polymorphism and the risk of Urothelial Cell Carcinoma in Iraq.</div></div><div><h3>Methods</h3><div>genomic DNA samples were extracted from a total 200 samples of blood. Three primers were designed to enhance three commonly observed genetic variation, rs2011077, rs351855, and rs1966265. The single strand conformation polymorphisms technique (SSCP) was genotyped and confirmed by further sequencing protocols.</div></div><div><h3>Results</h3><div>The results of this study show that cases with the G/A variant of the rs351855 genotype have a marked increase in risk to Urothelial Cell Carcinoma (<em>P</em> = 0.001, OR 0.32, 95 % CI 0.20 to 0.94). Cases with genotype rs2011077: TC has also associated with the increased the risk of UCC (<em>P</em> = 0.001, OR= 0.50, 95 % CI = 0.33 to 0.76). The Linkage Disequilibrium revealed a significant relationship between the T allele of the rs2011077 locus and the A allele of the rs351855 locus, leading to the formation of the TA haplotype in cases diagnosed with the UCC. Our results show that <em>FGFR</em>4 gene polymorphisms (rs351855 and rs2011077) have significant associations with increased risk of Urothelial Cell Carcinoma.</div></div><div><h3>Conclusion</h3><div>current study indicates that the specific polymorphisms have proven to be promising as a major genetic marker for identifying cases who may be more susceptible to diagnosis and recurrence Urothelial Cell Carcinoma.</div></div>","PeriodicalId":49225,"journal":{"name":"Cancer Genetics","volume":"292 ","pages":"Pages 77-84"},"PeriodicalIF":1.4,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143437307","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Complex genetic structural aberrations revealed by optical genome mapping in a case of APL-like morphology","authors":"Shivaprasad H. Sathyanarayana ,&nbsp;Michelle A. Bickford ,&nbsp;Narcisa A. Smuliac ,&nbsp;Kyle A. Tonseth ,&nbsp;Farzana Murad ,&nbsp;Jing Bao ,&nbsp;Heather B. Steinmetz ,&nbsp;Matthew R. Sullivan ,&nbsp;Prabhjot Kaur ,&nbsp;Jeremiah X. Karrs ,&nbsp;Wahab A. Khan","doi":"10.1016/j.cancergen.2025.02.005","DOIUrl":"10.1016/j.cancergen.2025.02.005","url":null,"abstract":"<div><div>We present a detailed cytogenomic analysis from a patient with suspected acute promyelocytic leukemia (APL), based on morphological and immunophenotypic characteristics. Initial testing with fluorescence in situ hybridization (FISH) and chromosome analysis was negative for the canonical <em>PML::RARA</em> and other <em>RARA</em> partners translocations. Polymerase chain reaction (PCR) did not detect <em>PML::RARA</em> transcripts. However, chromosome analysis results revealed loss of 5q and 17p, as well as the presence of double minutes (dmin). To further assess the involvement of other retinoic acid receptor (RAR) partners, such as <em>RARB</em> and <em>RARG</em>, and to elucidate the origin of the dmin, we conducted genome-wide structural variant analysis (gwSVA) using optical genome mapping (OGM) as part of a research and confirmatory follow-up. Using gwSVA, we identified the double minutes to be of <em>MYC</em> origin, with approximately 44 copies. Additionally, gwSVA revealed a loss of <em>TP53</em>, along with polyploidy showing loss of chromosomes 1, 2, 8, 9 (including <em>CDKN2A</em>), 10, 11, 15 and gains of chromosomes 3, 6, and 7 indicating distinct clonal events in a diagnostic and follow up bone marrow. Next generation sequencing (NGS) with an exome-based heme targeted panel identified a Tier I deleterious <em>TP53</em> single nucleotide variant (p.S241C). The follow-up bone marrow analyzed with gwSVA, four months post-induction therapy, showed a reduction in number of cells exhibiting <em>MYC</em> amplification. This study provides a rare instance of a <em>TP53</em> positive case with APL-like bone marrow morphology, no <em>RARA</em> rearrangement, and <em>MYC</em> amplification. It further lends evidence towards comprehensive cytogenomic and molecular analyses for accurate risk stratification and subsequent disease tracking.</div></div>","PeriodicalId":49225,"journal":{"name":"Cancer Genetics","volume":"292 ","pages":"Pages 111-115"},"PeriodicalIF":1.4,"publicationDate":"2025-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143478793","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MYC-r with a non-IG partner concurrently with a cryptic t(12;21) in B-lymphoblastic leukemia: A case and prognostic significance","authors":"Prasad Koduru ,&nbsp;Weina Chen ,&nbsp;Franklin Fuda ,&nbsp;Martha Pacheco ,&nbsp;Rolando Garcia","doi":"10.1016/j.cancergen.2025.01.008","DOIUrl":"10.1016/j.cancergen.2025.01.008","url":null,"abstract":"<div><div>B-lymphoblastic leukemia (B-ALL) in children is characterized by recurrent chromosomal rearrangements that mostly have prognostic value. <em>MYC</em> rearrangements (<em>MYC</em>-r), typically associated with Burkitt lymphoma or mature B-cell neoplasms are infrequent in B-ALL. We report here a unique case of childhood B-ALL with concurrent <em>MYC</em>-r with a non-<em>IG</em> partner and a cryptic t(12;21). Leukemic cells had lymphoblastic morphology. Immunophenotypically, leukemic blasts were CD10 (+, slightly bright), CD15 (few +), CD19 (+), CD20 (+, partial), CD22 (+), CD34 (-), CD38 (+, slightly variably), CD45 (+, partial), cytoplasmic CD79a (+), HLA-DR (+), surface Ig (-), MPO (-), and TdT (+, partially). This immunophenotype was consistent with B-ALL. Cytogenetically, the karyotype was complex including a t(4;8)(q31;q24), and FISH analysis showed <em>MYC</em>-r, <em>ETV6</em>::<em>RUNX1</em> and loss of <em>ETV6</em> allele. The patient has been in complete remission for 11 years following the diagnosis. We reviewed cases of B-ALL with double leukemogenic alterations and <em>MYC</em>-r with non-<em>IG</em> partners to understand the clinical outcome in these rare patients.</div></div>","PeriodicalId":49225,"journal":{"name":"Cancer Genetics","volume":"292 ","pages":"Pages 85-91"},"PeriodicalIF":1.4,"publicationDate":"2025-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143444995","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}