Genes, Chromosomes & Cancer最新文献

{"title":"Undifferentiated Round Cell Sarcoma With KDM2B::CREBBP Gene Fusion in an Infant.","authors":"Karen R Arispe Angulo, Zonggao Shi, Fouzia Latif, Patrick R Blackburn, Faizan Malik","doi":"10.1002/gcc.70131","DOIUrl":"https://doi.org/10.1002/gcc.70131","url":null,"abstract":"","PeriodicalId":12700,"journal":{"name":"Genes, Chromosomes & Cancer","volume":"65 5","pages":"e70131"},"PeriodicalIF":2.8,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147814222","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Synovial Sarcoma With BRAF V600E Mutation: A Case Report and Literature Review.","authors":"Tian Gao, Tao Deng, Yunfei Shi, Fan Yang, Sheng Xiao, Zhengfu Fan","doi":"10.1002/gcc.70128","DOIUrl":"https://doi.org/10.1002/gcc.70128","url":null,"abstract":"<p><p>Synovial sarcoma (SS) is a genetically defined soft tissue sarcoma driven by the pathognomonic SS18::SSX fusion and is generally characterized by a low burden of secondary genomic alterations. We report a 42-year-old man with metastatic SS harboring both the SS18::SSX1 rearrangement and the BRAF V600E mutation. The patient developed metastatic disease following standard multimodal therapy. Comprehensive genomic profiling using DNA and RNA based next-generation sequencing identified the SS18::SSX1 fusion and the activating BRAF V600E mutation. The SS18 rearrangement was further confirmed by fluorescence in situ hybridization (FISH), and immunohistochemistry supported the histologic diagnosis. Treatment with combined BRAF and MEK inhibition (dabrafenib and trametinib) resulted in a clinical response. In addition to this index case, a literature review identified multiple additional SS harboring BRAF V600E, supporting its role as a recurrent, potentially targetable alteration in a small subset of SS. These findings highlight the value of comprehensive genomic profiling in SS, particularly in advanced or refractory cases, to identify rare but actionable molecular events that may expand therapeutic options.</p>","PeriodicalId":12700,"journal":{"name":"Genes, Chromosomes & Cancer","volume":"65 5","pages":"e70128"},"PeriodicalIF":2.8,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147837154","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Novel SMARCA4::VEZF1 Rearrangement in Pediatric Sarcomas.","authors":"Libing Fu, Rongjun Mao, Changliang Zhang, Fan Yang, Si Chen, Dan Zhou, Sheng Xiao","doi":"10.1002/gcc.70132","DOIUrl":"https://doi.org/10.1002/gcc.70132","url":null,"abstract":"<p><p>The SMARCA4 gene encodes a key ATPase subunit of the SWI/SNF (BAF) chromatin-remodeling complex, which plays an essential role in regulating transcription and cellular differentiation. Loss-of-function alterations of SMARCA4 are common in various human cancers, including sarcomas; however, rare SMARCA4 fusion events, presumably resulting in gain of function, have also been reported. We present two pediatric soft-tissue sarcomas harboring a novel, recurrent in-frame fusion between SMARCA4 and VEZF1 (Vascular Endothelial Zinc Finger 1), a transcription factor important for vascular development and angiogenesis. The predicted fusion protein contains the N-terminal QLQ protein interaction domain of SMARCA4 and preserves most of VEZF1's C2H2 zinc-finger DNA-binding domains. Interestingly, another component of the BAF complex, SS18, has also been reported to be fused to VEZF1 in uterine sarcoma. We propose that fusion of BAF complex components to VEZF1 leads to aberrant recruitment of chromatin-remodeling activity to VEZF1 target loci, resulting in altered chromatin architecture, dysregulated VEZF1-dependent transcription, and tumorigenesis.</p>","PeriodicalId":12700,"journal":{"name":"Genes, Chromosomes & Cancer","volume":"65 5","pages":"e70132"},"PeriodicalIF":2.8,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147837210","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clear Cell Chondrosarcoma With Somatic VHL Inactivation: A Case Report With Integrated Genomic and Transcriptomic Analysis.","authors":"Lalit R Patel, Philip Wong, Shervin Oskouei, Armita Bahrami","doi":"10.1002/gcc.70130","DOIUrl":"https://doi.org/10.1002/gcc.70130","url":null,"abstract":"<p><strong>Background: </strong>Clear cell chondrosarcoma (CCC) is a rare, low-grade malignant bone tumor and a specific subtype of chondrosarcoma. In contrast to conventional central chondrosarcoma, which often exhibits recurrent IDH1/2 mutations, CCC is IDH-wildtype, and its genomic profile remains uncharacterized. Sporadic cases have been described in association with von Hippel-Lindau (VHL) disease, but somatic VHL alterations have not been demonstrated in this tumor.</p><p><strong>Methods: </strong>A 35-year-old man presented with local recurrence of a distal femoral tumor 5 years after curettage and allograft reconstruction for a tumor that was initially diagnosed as clear cell chondrosarcoma. The recurrent tumor was resected and analyzed using a comprehensive DNA/RNA next-generation sequencing assay with matched germline testing to distinguish somatic from germline alterations.</p><p><strong>Results: </strong>The recurrent tumor measured 5.0 cm and showed classic CCC morphology with focal areas of conventional chondrosarcoma-like differentiation. No IDH1/2 mutations were identified. Two pathogenic loss-of-function variants were detected: COL2A1 c.1262_1266+2delinsTCC (variant allele frequency [VAF], 34%) and VHL c.341-2A>C (VAF, 45%). The tumor had a low tumor mutational burden, low loss of heterozygosity, and a complex karyotype with monosomy of chromosome 3. Gene expression profiling revealed decreased VHL mRNA expression. Germline testing showed no germline VHL alteration, confirming somatic VHL inactivation.</p><p><strong>Conclusion: </strong>To our knowledge, this report is the first to describe a molecularly profiled CCC with somatic VHL inactivation. These results expand the evolving genomic spectrum of CCC beyond its previously known IDH-wildtype status and suggest that VHL pathway dysregulation may contribute to tumorigenesis in a subset of cases.</p>","PeriodicalId":12700,"journal":{"name":"Genes, Chromosomes & Cancer","volume":"65 5","pages":"e70130"},"PeriodicalIF":2.8,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147837213","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Complex Karyotype in CLL-How to Count Cytogenetic Aberrations Consistently and Efficiently.","authors":"Alessandro Baldi, Anna Stengel, Martha-Lena Müller, Gregor Hoermann, Wolfgang Kern, Isolde Summerer","doi":"10.1002/gcc.70129","DOIUrl":"https://doi.org/10.1002/gcc.70129","url":null,"abstract":"<p><p>Complex karyotype (CK) in chronic lymphocytic leukemia (CLL), defined by ≥ 3 or ≥ 5 (high-CK) chromosomal aberrations, is an established adverse prognostic marker. However, different methods for counting aberrations are used in the literature and clinical trials, potentially affecting CK classification and risk stratification. We systematically compared two established counting methods: the approach by Jondreville et al., which counts one aberration per item separated by commas, and the International System for Human Cytogenomic Nomenclature (ISCN) method, which counts unbalanced aberrations involving multiple chromosomes as two aberrations. Chromosome banding analyses from 1605 CLL patients were evaluated using both counting methods. This revealed that CK classification by the two methods disagreed in 7.5% of all cases. However, both methods performed similarly in prognostic stratification of these ambiguous cases. This suggests that the method proposed by Jondreville et al. should be adopted, as it is simpler to perform and less ambiguous. Furthermore, we compared how cases were stratified if aberrations are counted across all (sub)clones (as suggested both by Jondreville et al. and the ISCN) or only in the clone with the most aberrations. In total, 3.5% of all cases were differentially classified depending on whether aberrations were counted across all clones or only in the most complex clone. Importantly, these ambiguous cases were better stratified by counting aberrations in the most complex clone only. We therefore suggest the method proposed by Jondreville et al. to determine CK status in CLL and to count aberrations only in the clone with the most aberrations.</p>","PeriodicalId":12700,"journal":{"name":"Genes, Chromosomes & Cancer","volume":"65 5","pages":"e70129"},"PeriodicalIF":2.8,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147837186","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Causative Role for a BRCA2 Germline Pathogenic Variant in External Auditory Canal Squamous Cell Carcinoma","authors":"José Camacho-Valenzuela,&nbsp;Dylan Pelletier,&nbsp;Paz Polak,&nbsp;Lili Fu,&nbsp;Nancy Hamel,&nbsp;Carla Daniela Robles-Espinoza,&nbsp;William D. Foulkes","doi":"10.1002/gcc.70123","DOIUrl":"10.1002/gcc.70123","url":null,"abstract":"<p>External auditory canal squamous cell carcinoma (EACSCC) is rare, affecting 1.6 in a million individuals. We report a case of EACSCC in a 66-year-old woman carrying a heterozygous <i>BRCA2</i> germline pathogenic variant (GPV) (c.8537_8538del), with prior history of breast cancer. Tumor copy-number analysis showed loss of heterozygosity at the <i>BRCA2</i> locus. Genomic scar analysis supported homologous recombination repair deficiency (HRD), with mutational signatures showing the predominance of APOBEC activity and lower contributions of HRD-associated single base (SBS3, SBS8) and INDEL (ID6) signatures. A somatic <i>TP53</i> pathogenic variant was also identified. These findings suggest a contributory role for <i>BRCA2</i> in EACSCC development.</p>","PeriodicalId":12700,"journal":{"name":"Genes, Chromosomes & Cancer","volume":"65 4","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13064416/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147638580","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sibling Osteosarcoma Without Retinoblastoma Associated With a Low Penetrance RB1 Variant: Whole Genome Findings From a Single Family","authors":"Weisong Zhao,&nbsp;Zhuoying Wang,&nbsp;Kai Tian,&nbsp;Xiyu Yang,&nbsp;Yafei Jiang,&nbsp;Zhiwei Cheng,&nbsp;Wei Sun,&nbsp;Gangyang Wang,&nbsp;Zhengdong Cai,&nbsp;Yingqi Hua","doi":"10.1002/gcc.70124","DOIUrl":"10.1002/gcc.70124","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Purpose</h3>\u0000 \u0000 <p>Osteosarcoma is the most common primary malignant bone tumor in children and adolescents, yet its genetic etiology remains poorly understood. In this study, we described a family from the Shanghai General Hospital Osteosarcoma (SGH-OS) cohort in which two siblings developed osteosarcoma as their first primary malignancy, and we investigated the germline and somatic genetic basis underlying this familial presentation.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Whole-genome sequencing (WGS) was performed on tumors and matched germline DNA from the affected siblings, as well as germline DNA from their parents and unaffected sister. Comprehensive somatic and germline analyses were conducted to assess mutational profiles, copy-number alterations, and structural variants.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Both affected siblings carried a paternally inherited RB1 splice-donor variant (NM_000321.3:c.539+1G&gt;A), with biallelic inactivation confirmed by 13q14 loss in both tumors. Tumor WGS revealed additional somatic alterations, suggesting cooperation between germline and acquired mutations in osteosarcoma development. In addition, the carrier father and elder sister remained unaffected, consistent with incomplete penetrance.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>This study further supports the expanding spectrum of RB1-associated cancer predisposition, showing that low-penetrance RB1 variants may present with osteosarcoma without preceding retinoblastoma. In addition, our findings underscore the value of integrated WGS for characterizing inherited susceptibility in familial osteosarcoma.</p>\u0000 </section>\u0000 </div>","PeriodicalId":12700,"journal":{"name":"Genes, Chromosomes & Cancer","volume":"65 4","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147633142","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multimodal Cytogenetic and Molecular Approach for the Detection of a Constitutional Balanced Paracentric Inversion Disrupting RB1 in an Infant With Bilateral Retinoblastoma","authors":"Arti S. Pandey,&nbsp;Alexa Siskar,&nbsp;Alice Moore,&nbsp;Kim E. Nichols,&nbsp;Julieann C. Lee,&nbsp;Matthew W. Wilson,&nbsp;Mohammad K. Eldomery,&nbsp;Jie Liu,&nbsp;Patrick R. Blackburn","doi":"10.1002/gcc.70120","DOIUrl":"10.1002/gcc.70120","url":null,"abstract":"<div>\u0000 \u0000 <p>We report a case of hereditary bilateral retinoblastoma due to a <i>de novo</i> germline inversion on chromosome 13, resulting in disruption of the <i>RB1</i> gene. The patient is a 22-month-old female who initially presented to the emergency room at 11 months of age with an erythematous left eye and leukocoria of the right eye. Computed tomography (CT) of the brain and orbits showed solid internal calcifications arising from the posterior globes concerning for bilateral retinoblastoma. Magnetic resonance imaging (MRI) of the brain and orbits confirmed bilateral retinoblastoma without associated pineal region or suprasellar mass. On initial examination under anesthesia, the right eye showed one tumor in the macula and two tumors in the inferior mid-periphery. Sub-retinal seeding extended to the inferior periphery. The left eye was enucleated and pathology showed leptomeningeal extension along the optic nerve extending to the surgical margin. The patient was treated on a non-protocol treatment plan with five cycles of vincristine, carboplatin, etoposide, cyclophosphamide, and weekly intraventricular topotecan via Ommaya reservoir, followed by autologous stem cell rescue. Tumor analysis showed loss of pRB protein expression by immunohistochemistry and methylation copy number profiling showed several segmental gains and losses, including focal loss of <i>RB1</i> on 13q. A 123-gene cancer predisposition germline panel using genome and exome sequencing initially did not identify any <i>RB1</i> single nucleotide variants or insertion/deletions. Subsequent constitutional chromosome analysis for <i>RB1</i> showed a paracentric inversion between bands 13q14.2 and 13q31. Optical genome mapping (OGM) showed that the proximal breakpoint of the balanced inversion at 13q14.2 was within intron 17 of <i>RB1</i>, while the distal breakpoint at 13q31.3 did not interrupt any known genes of clinical significance. We review the various molecular techniques that aided in diagnosis of this patient and provide a summary of similar <i>RB1</i>-disrupting structural variants reported in the literature.</p>\u0000 </div>","PeriodicalId":12700,"journal":{"name":"Genes, Chromosomes & Cancer","volume":"65 4","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147622565","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CRTC1::TRIM11 Cutaneous Tumors With Atypia: Melanoma Mimicry, Aggressive Potential, and Methylation Classifier Limitations.","authors":"Bethany Batson, Arivarasan Karunamurthy, Azfar Neyaz, John M Skaugen, Steven D Billings, Karen Fritchie, Ivy John","doi":"10.1002/gcc.70127","DOIUrl":"https://doi.org/10.1002/gcc.70127","url":null,"abstract":"<p><p>CRTC1::TRIM11 cutaneous tumors are an emerging subset of MITF pathway-activated neoplasms that typically present as dermal nodules and can closely mimic clear cell sarcoma or malignant melanoma. Most reported tumors behave in an indolent manner, yet rare malignant cases have been documented. We report three additional CRTC1::TRIM11 cutaneous tumors with atypical features, including two patients with nodal or visceral disease at presentation. Histologically, all three tumors showed marked cytologic atypia with prominent nucleoli, and the usual nested and short-fascicular architecture was largely replaced by broad sheet-like growth, raising concern for melanoma. The tumors expressed SOX10 (diffuse) and S100 protein (patchy) with focal to absent expression of Melan-A and HMB45. PRAME was negative. CRTC1::TRIM11 was confirmed in all tumors. Two tumors harbored TERT promoter mutations, and one showed additional low-level copy-number gains of 1q, 8q, and 12q with 14q loss. In one case, methylation profiling yielded a clear cell sarcoma score of 0.885, just below the confidence threshold, likely due to shared CREB-MITF pathway activation and the lack of a dedicated CRTC1::TRIM11 reference class. A literature review identified nine previously reported metastatic CRTC1::TRIM11 cutaneous tumors. When combined with our series, extremities were the predominant primary site, and metastases most often involved regional lymph nodes and the lung. Fusion status remains the molecular gold standard, while secondary events such as TERT promoter mutations and 8q gains may contribute to aggressive behavior in a subset of tumors.</p>","PeriodicalId":12700,"journal":{"name":"Genes, Chromosomes & Cancer","volume":"65 4","pages":"e70127"},"PeriodicalIF":2.8,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13100558/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147769239","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Transcript-Specific DNA Methylation Alterations of the RASSF1 Locus in Cancer Cells.","authors":"Litzy Gisella Bermudez, Camila Bernal Forigua, Carmen María Ayala-Roldán, Jesús Manuel Romero, Rafael R Ariza, Teresa Morales-Ruiz, Teresa Roldán-Arjona, Alejandra Cañas, Adriana Rojas","doi":"10.1002/gcc.70125","DOIUrl":"10.1002/gcc.70125","url":null,"abstract":"<p><strong>Background: </strong>The locus encoding Ras association domain family member 1 (RASSF1) encodes multiple transcripts with opposing roles in cancer, such as RASSF1A (tumor suppressor), RASSF1C (oncogene), and the lncRNA RASSF1-AS1 (function undefined). Although DNA methylation-mediated repression of RASSF1A expression has been extensively studied in different cancer types, the epigenetic regulation of RASSF1C and RASSF1-AS1 is unclear. We profiled gene expression and promoter DNA methylation of RASSF1A, RASSF1C, and RASSF1-AS1 across 11 tumor cell lines, quantified RASSF1A methylation in lung cancer tissues and plasma by quantitative methylation-specific PCR (qMSP), and integrated single-CpG methylation (pyrosequencing) with in silico transcription factor binding site (TFBS) prediction.</p><p><strong>Results: </strong>We found that RASSF1A promoter hypermethylation was strongly and inversely associated with its mRNA levels. In contrast, RASSF1C promoter methylation did not correlate with expression. RASSF1-AS1 showed low promoter methylation accompanied by high expression. In clinical samples, RASSF1A methylation was detected in tissue biopsy (54% of cases) and plasma (42% of cases) from lung cancer patients, whereas no methylation was detected in 85% of control individuals, regardless of their smoking history. Finally, the analysis of DNA methylation at specific CpG sites combined with the prediction of TFBS in the evaluated promoter regions allowed the identification of binding domains overlapping differentially methylated regions. Notably, the RASSF1C promoter region exhibited a higher TFBS frequency containing CpG sites with low methylation levels, as determined by pyrosequencing.</p><p><strong>Conclusions: </strong>These findings highlight isoform-specific epigenetic regulation at the RASSF1 locus and suggest that RASSF1A methylation may represent a promising minimally invasive marker in lung cancer.</p>","PeriodicalId":12700,"journal":{"name":"Genes, Chromosomes & Cancer","volume":"65 4","pages":"e70125"},"PeriodicalIF":2.8,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13125737/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147728567","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}