Molecular Oncology最新文献

{"title":"Analysis of comprehensive genomic profiling of solid tumors with a novel assay for broad analysis in clinical diagnostics.","authors":"Guy Froyen, Pieter-Jan Volders, Ellen Geerdens, Severine Berden, Joni Van der Meulen, Aaron De Cock, Stefanie Vermeire, Jacques Van Huysse, Marie de Barsy, Gabriela Beniuga, Wendy W J de Leng, Anne M L Jansen, Imke Demers, Zeliha Ozgur, Hendrikus Jan Dubbink, Ernst-Jan M Speel, Wilfred F J van IJcken, Brigitte Maes","doi":"10.1002/1878-0261.13812","DOIUrl":"10.1002/1878-0261.13812","url":null,"abstract":"<p><p>Somatic multigene analysis by next-generation sequencing (NGS) is routinely integrated in medical oncology for clinical decision-making. However, with the fast-growing number of recommended and required genes as well as pan-cancer biomarkers, small panels have become vastly insufficient. Comprehensive genomic profiling (CGP) is, thus, required to screen for clinically relevant markers. In this multicentric study, we report on an extensive analysis across seven centers comparing the results of the novel OncoDEEP CGP assay with the diagnostically validated TruSight Oncology 500 (TSO500) kit on 250 samples. Overall concordance was 90% for clinically relevant gene variants and >96% for more complex biomarkers. Agreement for fusion detection was 94% for the 11 overlapping clinically actionable driver genes. The higher coverage uniformity of OncoDEEP compared to TSO500 allows users to pool more samples per sequencing run. Tertiary data analysis, including reporting, is integrated in the OncoDEEP solution, whereas this is an add-on for TSO500. Finally, we showed that, analytically, the OncoDEEP panel performs well, thereby advocating its use for CGP of solid tumors in diagnostic laboratories, providing an all-in-one solution for optimal patient management.</p>","PeriodicalId":18764,"journal":{"name":"Molecular Oncology","volume":" ","pages":"1797-1810"},"PeriodicalIF":6.6,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12161465/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143066755","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":"Interplay of integrins and selectins in metastasis.","authors":"Diana Maltseva, Ashot Nersisyan, Alexander Tonevitsky","doi":"10.1002/1878-0261.70026","DOIUrl":"10.1002/1878-0261.70026","url":null,"abstract":"<p><p>Metastasis is a hallmark of malignancy and poses a formidable challenge for oncologists. This complex process begins when the primary malignant cells start to proliferate unlimitedly. Once the tumor reaches a certain size, cancer cells detach from the primary tumor mass and the basal lamina to which they are anchored, eventually invading nearby blood vessels. Within the bloodstream, these tumor cells have to survive and attach to the endothelium at distant sites. Cell-to-cell and cell-to-matrix interactions play an important role during these stages, in which integrins-a family of cell adhesion molecules (CAMs)-stand out as functionally centrally involved. Their expression on the tumor cell surface needs to be dynamically regulated throughout the process of metastasis. During the attachment phase to the endothelium, another group of CAMs, such as E-/P-selectins-primarily expressed on endothelial cells-may also play a critical role in certain malignancies. Additionally, the interplay between integrins and selectins may influence the tumor microenvironment. This review focuses on the role of integrins and their interplay with selectins in metastasis, emphasizing findings from in vivo studies.</p>","PeriodicalId":18764,"journal":{"name":"Molecular Oncology","volume":" ","pages":"1582-1611"},"PeriodicalIF":6.6,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12161467/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144004591","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":"Integrative systems-level analysis reveals a contextual crosstalk between hypoxia and global metabolism in human breast tumors.","authors":"Raefa Abou Khouzam, Salem Chouaib, Mohammad Askandar Iqbal","doi":"10.1002/1878-0261.13762","DOIUrl":"10.1002/1878-0261.13762","url":null,"abstract":"<p><p>Hypoxia is known to induce reprogramming of glucose metabolism in cancer. However, the impact of hypoxia on global metabolism remains poorly understood. Here, using the systems approach, we evaluated the potential crosstalk between hypoxia and global metabolism using data from > 2000 breast tumors. Tumor samples were scored for hypoxia and 90 metabolic pathways, and these metrics were subjected to an analysis pipeline. Hypoxia showed a very strong association with metabolic aggression and an overall contextual relationship with metabolism. Out of three (M1, M2, and M3) metabolic types in breast cancer, M3 exhibited the strongest relationship with hypoxia; that is, high hypoxic tumors were also metabolically deregulated. Further, the overall correlation pattern between hypoxia and metabolic pathway scores was specific to each type, with M1 showing maximal sensitivity to hypoxia, followed by M2 and then M3. Experimental validation using metabolic inhibitors on cell lines with high or low hypoxia scores further confirmed the metabolic type-dependence of hypoxia. In addition, evaluation of the impact of hypoxia on cancer pathways other than metabolic ones revealed a potential role of hypoxia in immune evasive characteristic of M3 tumors. Overall, the results suggest a complex interplay between hypoxia and metabolism in the context of human breast tumors, with potential implications for both basic cancer biology and breast cancer therapy.</p>","PeriodicalId":18764,"journal":{"name":"Molecular Oncology","volume":" ","pages":"1725-1736"},"PeriodicalIF":6.6,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12161489/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142894910","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":"Molecular and functional profiling unravels targetable vulnerabilities in colorectal cancer.","authors":"Efstathios-Iason Vlachavas, Konstantinos Voutetakis, Vivian Kosmidou, Spyridon Tsikalakis, Spyridon Roditis, Konstantinos Pateas, Ryangguk Kim, Kymberleigh Pagel, Stephan Wolf, Gregor Warsow, Antonia Dimitrakopoulou-Strauss, Georgios N Zografos, Alexander Pintzas, Johannes Betge, Olga Papadodima, Stefan Wiemann","doi":"10.1002/1878-0261.13814","DOIUrl":"10.1002/1878-0261.13814","url":null,"abstract":"<p><p>Colorectal cancer (CRC) patients with microsatellite-stable (MSS) tumors are mostly treated with chemotherapy. Clinical benefits of targeted therapies depend on mutational states and tumor location. Many tumors carry mutations in KRAS proto-oncogene, GTPase (KRAS) or B-Raf proto-oncogene, serine/threonine kinase (BRAF), rendering them more resistant to therapies. We performed whole-exome sequencing and RNA-Sequencing of 28 tumors of the Athens Comprehensive Cancer Center CRC cohort, and molecularly characterized CRC patients based on their microsatellite instability (MSI) status, single-nucleotide variations (SNVs)/copy number alterations (CNAs), and pathway/transcription factor activities at the individual patient level. Variants were classified using a computational score for integrative cancer variant annotation and prioritization. Complementing this with public multi-omics datasets, we identified activation of transforming growth factor beta (TGFβ) signaling to be more strongly activated in MSS patients, whereas Janus kinase (JAK)-signal transducer and activator of transcription (STAT) and mitogen-activated protein kinase (MAPK) molecular cascades were activated specifically in MSI tumors. We unraveled mechanisms consistently perturbed in the transcriptional and mutational circuits and identified Runt-related transcription factors (RUNX transcription factors) as putative biomarkers in CRC, given their role in the regulation of pathways involved in tumor progression and immune evasion. Assessing the immunogenicity of CRC tumors in the context of RAS/RAF mutations and MSI/MSS status revealed a critical impact that KRAS mutations have on immunogenicity, particularly in the MSS patient subgroup, with implications for diagnosis and treatment.</p>","PeriodicalId":18764,"journal":{"name":"Molecular Oncology","volume":" ","pages":"1751-1774"},"PeriodicalIF":6.6,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12161475/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143059603","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":"Addressing persistent challenges in digital image analysis of cancer tissue: resources developed from a hackathon.","authors":"Sandhya Prabhakaran, Clarence Yapp, Gregory J Baker, Johanna Beyer, Young Hwan Chang, Allison L Creason, Robert Krueger, Jeremy Muhlich, Nathan Heath Patterson, Kevin Sidak, Damir Sudar, Adam J Taylor, Luke Ternes, Jakob Troidl, Xie Yubin, Artem Sokolov, Darren R Tyson","doi":"10.1002/1878-0261.13783","DOIUrl":"10.1002/1878-0261.13783","url":null,"abstract":"<p><p>The National Cancer Institute (NCI) supports numerous research consortia that rely on imaging technologies to study cancerous tissues. To foster collaboration and innovation in this field, the Image Analysis Working Group (IAWG) was created in 2019. As multiplexed imaging techniques grow in scale and complexity, more advanced computational methods are required beyond traditional approaches like segmentation and pixel intensity quantification. In 2022, the IAWG held a virtual hackathon focused on addressing challenges in analyzing complex, high-dimensional datasets from fixed cancer tissues. The hackathon addressed key challenges in three areas: (1) cell type classification and assessment, (2) spatial data visualization and translation, and (3) scaling image analysis for large, multi-terabyte datasets. Participants explored the limitations of current automated analysis tools, developed potential solutions, and made significant progress during the hackathon. Here we provide a summary of the efforts and resultant resources and highlight remaining challenges facing the research community as emerging technologies are integrated into diverse imaging modalities and data analysis platforms.</p>","PeriodicalId":18764,"journal":{"name":"Molecular Oncology","volume":" ","pages":"1565-1581"},"PeriodicalIF":6.6,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12161476/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143382669","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":"Inhibition of acyl-CoA synthetase long-chain isozymes decreases multiple myeloma cell proliferation and causes mitochondrial dysfunction.","authors":"Connor S Murphy, Heather Fairfield, Victoria E DeMambro, Samaa Fadel, Carlos A Gartner, Michelle Karam, Christian Potts, Princess Rodriguez, Ya-Wei Qiang, Habib Hamidi, Xiangnan Guan, Calvin P H Vary, Michaela R Reagan","doi":"10.1002/1878-0261.13794","DOIUrl":"10.1002/1878-0261.13794","url":null,"abstract":"<p><p>Multiple myeloma (MM) is an incurable cancer of plasma cells with a 5-year survival rate of 59%. Dysregulation of fatty acid (FA) metabolism is associated with MM development and progression; however, the underlying mechanisms remain unclear. Herein, we explore the roles of long-chain fatty acid coenzyme A ligase (ACSL) family members in MM. ACSLs convert free long-chain fatty acids into fatty acyl-CoA esters and play key roles in catabolic and anabolic fatty acid metabolism. Analysis of the Multiple Myeloma Research Foundation (MMRF) CoMMpass^SM study showed that high ACSL1 and ACSL4 expression in myeloma cells are both associated with worse clinical outcomes for MM patients. Cancer Dependency Map (DepMap) data showed that all five ACSLs have negative Chronos scores, and ACSL3 and ACSL4 were among the top 25% Hallmark Fatty Acid Metabolism genes that support myeloma cell line fitness. Inhibition of ACSLs in myeloma cell lines in vitro, using the pharmacological inhibitor Triacsin C (TriC), increased apoptosis, decreased proliferation, and decreased cell viability, in a dose- and time-dependent manner. RNA-sequencing analysis of MM.1S cells treated with TriC showed a significant enrichment in apoptosis, ferroptosis, and endoplasmic reticulum (ER) stress, and proteomic analysis of these cells revealed enriched pathways for mitochondrial dysfunction and oxidative phosphorylation. TriC also rewired mitochondrial metabolism by decreasing mitochondrial membrane potential, increasing mitochondrial superoxide levels, decreasing mitochondrial ATP production rates, and impairing cellular respiration. Overall, our data support the hypothesis that suppression of ACSLs in myeloma cells is a novel metabolic target in MM that inhibits their viability, implicating this family as a promising therapeutic target in treating myeloma.</p>","PeriodicalId":18764,"journal":{"name":"Molecular Oncology","volume":" ","pages":"1687-1706"},"PeriodicalIF":6.6,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12161464/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143033710","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":"Multiplex single-cell profiling of putative cancer stem cell markers ALDH1, SOX9, SOX2, CD44, CD133 and CD15 in endometrial cancer.","authors":"Hilde E Lien, Marta E Hjelmeland, Hege F Berg, Rose M Gold, Kathrine Woie, Lars A Akslen, Ingfrid S Haldorsen, Camilla Krakstad","doi":"10.1002/1878-0261.13815","DOIUrl":"10.1002/1878-0261.13815","url":null,"abstract":"<p><p>The presence of cancer stem cells is linked to aggressive disease and higher risk of recurrence, and multiple markers have been proposed to detect cancer stem cells. However, a detailed evaluation of the expression patterns and the prognostic value of markers relevant for endometrial cancer is lacking. As organoid models are suggested to be enriched in cancer stem cells, such models may prove valuable to define tissue-specific cancer stem cells. To address this, imaging mass cytometry and multiplex single-cell analyses were performed on an endometrial cancer patient series including both tumor biopsies and corresponding patient-derived organoids. An antibody panel focused on cancer stem cell markers was used to identify cancer stem cell phenotypes. Over 70% of epithelial cells in the tumor biopsies expressed at least one putative cancer stem cell marker. We identified distinct cancer cell phenotypes with heterogeneous expression within individual patients and between patient samples. Few differences in the distribution of cancer cell phenotypes were observed between tumor biopsies and corresponding organoids. Cells expressing aldehyde dehydrogenase 1 (ALDH1) were more prevalent in high-grade tumors, while expression of CD44 was more prevalent in grade 1 tumors. Spatial analysis revealed significantly less interaction between ALDH1- and CD44-expressing cells. Gene expression data was used to further investigate selected markers. CD44 gene expression was associated with a favorable prognosis and was further validated using immunohistochemistry. High expression of CD44 was significantly associated with better survival. The general high expression of proposed stem cell markers may indicate alternative roles for these in endometrial cancer.</p>","PeriodicalId":18764,"journal":{"name":"Molecular Oncology","volume":" ","pages":"1651-1667"},"PeriodicalIF":6.6,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12161474/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143066758","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":"Stochastic variation in the FOXM1 transcription program mediates replication stress tolerance.","authors":"Hendrika A Segeren, Kathryn A Wierenga, Frank M Riemers, Elsbeth A van Liere, Bart Westendorp","doi":"10.1002/1878-0261.13819","DOIUrl":"10.1002/1878-0261.13819","url":null,"abstract":"<p><p>Oncogene-induced replication stress (RS) is a vulnerability of cancer cells that forces reliance on the intra-S-phase checkpoint to ensure faithful genome duplication. Inhibitors of the intra-S-phase checkpoint kinases ATR and CHK1 have been developed, but resistance to these drugs remains problematic. Understanding drug tolerance mechanisms is impeded by analysis of bulk samples, which neglect tumor heterogeneity and often fail to accurately interpret cell cycle-mediated resistance. Here, by combining intracellular immunostaining and single-cell RNA-sequencing, we characterized the transcriptomes of oncogenic RAS-expressing cells with variable levels of RS when challenged with a CHK1 inhibitor combined with gemcitabine. We identified 37 genes differentially expressed between tolerant and sensitive cells, including several FOXM1 targets. While complete knockdown of FOXM1 impeded cell proliferation, partial knockdown protected cells against DNA damage, and improved recovery from drug-induced RS. Remarkably, knockdown of individual FOXM1 target genes UBE2C and MKI67 also mitigated DNA damage, uncovering unanticipated roles for these in the replication stress response. Our results suggest that low levels of FOXM1-dependent gene expression during S and G2 phase protects cells against excessive DNA damage during drug-induced replication stress.</p>","PeriodicalId":18764,"journal":{"name":"Molecular Oncology","volume":" ","pages":"1633-1650"},"PeriodicalIF":6.6,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12161472/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143516196","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":"Crosstalk between gut microbiota and tumor: tumors could cause gut dysbiosis and metabolic imbalance.","authors":"Siyuan Zhang, Haimei Wen, Ying Chen, Jingya Ning, Di Hu, Yujiao Dong, Chenyu Yao, Bo Yuan, Shuanying Yang","doi":"10.1002/1878-0261.13763","DOIUrl":"10.1002/1878-0261.13763","url":null,"abstract":"<p><p>Gut microbiota has a proven link with the development and treatment of cancer. However, the causality between gut microbiota and cancer development is still unknown and deserves exploration. In this study, we aimed to explore the alterations in gut microbiota in murine tumor models and the crosstalk between the tumor and the gut microbiota. The subcutaneous and intravenous murine tumor models using both the colorectal cancer cell line MC38 and lung cancer cell line LLC were constructed. Then fecal samples before and after tumor inoculation were collected for whole metagenomics sequencing. Both subcutaneous and metastatic tumors markedly elevated the α-diversity of the gut microbiota. Relative abundance of Ligilactobacillus and Lactobacillus was reduced after subcutaneously inoculating tumor cells, whereas Bacteroides and Duncaniella were reduced in metastatic tumors, regardless of tumor type. At the species level, Lachnospiraceae bacterium was enriched after both subcutaneous and intravenous tumors inoculation, whereas levels of Muribaculaceae bacterium Isolate-110 (HZI), Ligilactobacillus murinus and Bacteroides acidifaciens reduced. Metabolic function analysis showed that the reductive pentose phosphate cycle, urea cycle, ketone body biosynthesis, ectoine biosynthesis, C4-dicarboxylic acid cycle, isoleucine biosynthesis, inosine 5'-monophosphate (IMP), and uridine 5'-monophosphate (UMP) biosynthesis were elevated after tumor inoculation, whereas the cofactor and vitamin biosynthesis were deficient. Principal coordinates analysis (PCoA) showed that subcutaneous and metastatic tumors partially shared the same effect patterns on gut microbiota. Furthermore, fecal microbiota transplantation revealed that this altered microbiota could influence tumor growth. Taken together, this study demonstrated that both colorectal cancer (MC38) and non-colorectal cancer (LLC) can cause gut dysbiosis and metabolic imbalance, regardless of tumor type and process of tumor inoculation, and this dysbiosis influenced the tumor growth. This research gives novel insights into the crosstalk between tumors and the gut microbiota.</p>","PeriodicalId":18764,"journal":{"name":"Molecular Oncology","volume":" ","pages":"1707-1724"},"PeriodicalIF":6.6,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12161466/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142730721","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":"EACR 2025 Congress: Innovative Cancer Science, 16-19 June 2025.","authors":"","doi":"10.1002/1878-0261.70070","DOIUrl":"10.1002/1878-0261.70070","url":null,"abstract":"<p><p>Abstracts submitted to the 'EACR 2025 Congress: Innovative Cancer Science', from 16-19 June 2025 and accepted by the Congress Organising Committee are published in this Supplement of Molecular Oncology, an affiliated journal of the European Association for Cancer Research (EACR).</p>","PeriodicalId":18764,"journal":{"name":"Molecular Oncology","volume":"19 Suppl 1 ","pages":"1-895"},"PeriodicalIF":6.6,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12155586/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144275421","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}