Molecular Oncology最新文献_第10页

TRPM4 contributes to cell death in prostate cancer tumor spheroids, and to extravasation and metastasis in a zebrafish xenograft model system. 在斑马鱼异种移植模型系统中，TRPM4参与前列腺癌肿瘤球体的细胞死亡以及外渗和转移。

IF 6.6 2区医学

Molecular Oncology Pub Date : 2025-05-01 Epub Date: 2025-01-16 DOI: 10.1002/1878-0261.13795

Florian Bochen, Saurav Subedi, Federico La Manna, Sofia Jarrin, Irida Papapostolou, Marianna Kruithof-de Julio, Christine Peinelt

{"title":"TRPM4 contributes to cell death in prostate cancer tumor spheroids, and to extravasation and metastasis in a zebrafish xenograft model system.","authors":"Florian Bochen, Saurav Subedi, Federico La Manna, Sofia Jarrin, Irida Papapostolou, Marianna Kruithof-de Julio, Christine Peinelt","doi":"10.1002/1878-0261.13795","DOIUrl":"10.1002/1878-0261.13795","url":null,"abstract":"Transient receptor potential melastatin-4 (TRPM4) ion channel expression is upregulated in prostate cancer (PCa), contributing to increased cell proliferation, migration, adhesion, epithelial-to-mesenchymal transition, cell cycle shift, and alterations of intracellular Ca2+ signaling. GEO2R platform analysis of messenger RNA (mRNA) expression of ~ 6350 genes in normal and malignant prostate tissue samples from 15 PCa patients demonstrates that TRPM4 expression is upregulated sixfold and is among the most significantly upregulated genes in PCa. We find that absence of TRPM4 reduced PCa tumor spheroid size and decreased PCa tumor spheroid outgrowth. In addition, lack of TRPM4 increased cell death in PCa tumor spheroids, a phenotype that is absent in two-dimensional (2D) cancer cell systems. Lastly, absence of TRPM4 in PCa cells reduced extravasation and metastatic burden in a preclinical zebrafish cancer model. Taken together, our findings show that TRPM4 is an attractive therapeutic target in PCa and highlights the need for future development of pharmacological tools.","PeriodicalId":18764,"journal":{"name":"Molecular Oncology","volume":" ","pages":"1299-1309"},"PeriodicalIF":6.6,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12077273/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143007939","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}

引用次数: 0

Chemoresistome mapping in individual breast cancer patients unravels diversity in dynamic transcriptional adaptation. 个体乳腺癌患者的化疗抵抗体定位揭示了动态转录适应的多样性。

IF 6.6 2区医学

Molecular Oncology Pub Date : 2025-04-28 DOI: 10.1002/1878-0261.70030

Maya Dadiani, Gilgi Friedlander, Gili Perry, Nora Balint-Lahat, Shlomit Gilad, Dana Morzaev-Sulzbach, Anjana Shenoy, Noa Bossel Ben-Moshe, Anya Pavlovsky, Rinat Bernstein-Molho, Eytan Domany, Iris Barshack, Tamar Geiger, Bella Kaufman, Einav Nili Gal-Yam

{"title":"Chemoresistome mapping in individual breast cancer patients unravels diversity in dynamic transcriptional adaptation.","authors":"Maya Dadiani, Gilgi Friedlander, Gili Perry, Nora Balint-Lahat, Shlomit Gilad, Dana Morzaev-Sulzbach, Anjana Shenoy, Noa Bossel Ben-Moshe, Anya Pavlovsky, Rinat Bernstein-Molho, Eytan Domany, Iris Barshack, Tamar Geiger, Bella Kaufman, Einav Nili Gal-Yam","doi":"10.1002/1878-0261.70030","DOIUrl":"https://doi.org/10.1002/1878-0261.70030","url":null,"abstract":"Nongenetic adaptive resistance to chemotherapy, driven by transcriptional rewiring, is emerging as a significant mechanism in tumor survival. In this study we combined longitudinal transcriptomics with temporal pattern analysis to investigate patient-specific mechanisms underlying acquired resistance in breast cancer. Matched tumor biopsies (pretreatment, posttreatment, and adjacent normal) were collected from breast cancer patients who received neoadjuvant chemotherapy. Transcriptomes were analyzed by longitudinal gene-pattern classification to track patient-specific gene expression alterations that occur during treatment. Our findings reveal that resistance-associated genes were already dysregulated in primary tumors, suggesting the presence of a preexisting drug-tolerant state. While each patient displayed unique resistance-associated gene rewiring, these alterations converged into a limited number of dysregulated functional modules. Notably, patients receiving the same treatment exhibited distinct rewiring of genes and pathways, revealing parallel, individualized routes to resistance. In conclusion, we propose that tumor cells survive chemotherapy by sustaining or amplifying a preexisting drug-tolerant state that circumvents drug action. We suggest that individualized \"chemoresistome maps\" could identify cancer vulnerabilities and inform personalized therapeutic strategies to overcome or prevent resistance.","PeriodicalId":18764,"journal":{"name":"Molecular Oncology","volume":" ","pages":""},"PeriodicalIF":6.6,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144030030","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}

引用次数: 0

Determination of ADP/ATP translocase isoform ratios in malignancy and cellular senescence. 恶性肿瘤和细胞衰老中ADP/ATP转位酶异构体比值的测定。

IF 6.6 2区医学

Molecular Oncology Pub Date : 2025-04-27 DOI: 10.1002/1878-0261.70039

Zuzana Liblova, Dominika Maurencova, Barbora Salovska, Marek Kratky, Tomas Mracek, Zuzana Korandova, Alena Pecinova, Pavla Vasicova, David Rysanek, Ladislav Andera, Ivo Fabrik, Rudolf Kupcik, Pavel Kashmel, Pinky Sultana, Vojtech Tambor, Jiri Bartek, Josef Novak, Marie Vajrychova, Zdenek Hodny

{"title":"Determination of ADP/ATP translocase isoform ratios in malignancy and cellular senescence.","authors":"Zuzana Liblova, Dominika Maurencova, Barbora Salovska, Marek Kratky, Tomas Mracek, Zuzana Korandova, Alena Pecinova, Pavla Vasicova, David Rysanek, Ladislav Andera, Ivo Fabrik, Rudolf Kupcik, Pavel Kashmel, Pinky Sultana, Vojtech Tambor, Jiri Bartek, Josef Novak, Marie Vajrychova, Zdenek Hodny","doi":"10.1002/1878-0261.70039","DOIUrl":"https://doi.org/10.1002/1878-0261.70039","url":null,"abstract":"Cellular senescence has recently been recognized as a significant contributor to the poor prognosis of glioblastoma, one of the most aggressive brain tumors. Consequently, effectively eliminating senescent glioblastoma cells could benefit patients. Human ADP/ATP translocases (ANTs) play a role in oxidative phosphorylation in both normal and tumor cells. Previous research has shown that the sensitivity of senescent cells to mitochondria-targeted senolytics depends on the level of ANT2. Here, we systematically mapped the transcript and protein levels of ANT isoforms in various types of senescence and glioblastoma tumorigenesis. We employed bioinformatics analysis, targeted mass spectrometry, RT-PCR, immunoblotting, and assessment of cellular energy state to elucidate how individual ANT isoforms are expressed during the development of senescence in noncancerous and glioblastoma cells. We observed a consistent elevation of ANT1 protein levels across all tested senescence types, while ANT2 and ANT3 exhibited variable changes. Alterations in ANT protein isoform levels correlated with shifts in the cellular oxygen consumption rate. Our findings suggest that ANT isoforms are mutually interchangeable for oxidative phosphorylation and manipulating individual ANT isoforms could have potential for senolytic therapy.","PeriodicalId":18764,"journal":{"name":"Molecular Oncology","volume":" ","pages":""},"PeriodicalIF":6.6,"publicationDate":"2025-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144033525","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}

引用次数: 0

Does Porphyromonas gingivalis truly inhibit the oral carcinogenesis? 牙龈卟啉单胞菌真的能抑制口腔癌变吗？

IF 6.6 2区医学

Molecular Oncology Pub Date : 2025-04-25 DOI: 10.1002/1878-0261.70037

Chen-Xi Li, Zhong-Cheng Gong

引用次数: 0

Targeted protein degradation in oncology: novel therapeutic opportunity for solid tumours? 肿瘤靶向蛋白降解：实体瘤的新治疗机会？

IF 6.6 2区医学

Molecular Oncology Pub Date : 2025-04-23 DOI: 10.1002/1878-0261.70034

Noé Herbel, Sophie Postel-Vinay

引用次数: 0

Early metastasis is characterized by Gr1+ cell dysregulation and is inhibited by immunomodulatory nanoparticles. 早期转移的特点是Gr1+细胞失调，并被免疫调节纳米颗粒抑制。

IF 6.6 2区医学

Molecular Oncology Pub Date : 2025-04-23 DOI: 10.1002/1878-0261.70040

Jeffrey A Ma, Sophia M Orbach, Kate V Griffin, Kathryn Kang, Yining Zhang, Rebecca S Pereles, Ian A Schrack, Guillermo Escalona, Jacqueline S Jeruss, Lonnie D Shea

{"title":"Early metastasis is characterized by Gr1+ cell dysregulation and is inhibited by immunomodulatory nanoparticles.","authors":"Jeffrey A Ma, Sophia M Orbach, Kate V Griffin, Kathryn Kang, Yining Zhang, Rebecca S Pereles, Ian A Schrack, Guillermo Escalona, Jacqueline S Jeruss, Lonnie D Shea","doi":"10.1002/1878-0261.70040","DOIUrl":"https://doi.org/10.1002/1878-0261.70040","url":null,"abstract":"Cancer metastasis is supported by dysregulated myeloid-derived suppressor cells, but myeloid cells are highly heterogeneous populations with distinct subsets that may support or inhibit tumor cell colonization. We hypothesize that Gr1+ myeloid cells transform in phenotype to support tumor cell colonization at the metastatic niche. In the 4T1 model of metastatic breast cancer, we investigate changes in the composition and phenotype of Gr1+ cells between premetastatic disease and early metastasis. Gr1+ cells in the lung were found to transition towards immunosuppressive and tumor-supportive phenotypes with disease progression. While the composition of myeloid cells becomes dysregulated systemically, cells in the blood do not develop tumor-supportive phenotypes, indicating that protumor functions are specific to the lung. In vitro assays demonstrate that Gr1+ cells from early metastatic lungs support tumor cell survival, migration, and proliferation, which is linked to chitinase-3-like protein 1 (CHI3L1) signaling. The intravenous injection of polymeric nanoparticles reprograms Gr1+ cell phenotypes, reduces the secretion of CHI3L1, and inhibits metastasis. These findings indicate that dysregulated Gr1+ cells are a therapeutic target for early metastasis and can be targeted with polymeric nanoparticles.","PeriodicalId":18764,"journal":{"name":"Molecular Oncology","volume":" ","pages":""},"PeriodicalIF":6.6,"publicationDate":"2025-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144030031","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}

引用次数: 0

Detecting homologous recombination deficiency for breast cancer through integrative analysis of genomic data. 通过基因组数据的综合分析检测乳腺癌同源重组缺陷。

IF 6.6 2区医学

Molecular Oncology Pub Date : 2025-04-22 DOI: 10.1002/1878-0261.70041

Rong Zhu, Katherine Eason, Suet-Feung Chin, Paul A W Edwards, Raquel Manzano Garcia, Richard Moulange, Jia Wern Pan, Soo Hwang Teo, Sach Mukherjee, Maurizio Callari, Carlos Caldas, Stephen-John Sammut, Oscar M Rueda

{"title":"Detecting homologous recombination deficiency for breast cancer through integrative analysis of genomic data.","authors":"Rong Zhu, Katherine Eason, Suet-Feung Chin, Paul A W Edwards, Raquel Manzano Garcia, Richard Moulange, Jia Wern Pan, Soo Hwang Teo, Sach Mukherjee, Maurizio Callari, Carlos Caldas, Stephen-John Sammut, Oscar M Rueda","doi":"10.1002/1878-0261.70041","DOIUrl":"https://doi.org/10.1002/1878-0261.70041","url":null,"abstract":"Homologous recombination deficiency (HRD) leads to genomic instability, and patients with HRD can benefit from HRD-targeting therapies. Previous studies have primarily focused on identifying HRD biomarkers using data from a single technology. Here we integrated features from different genomic data types, including total copy number (CN), allele-specific copy number (ASCN) and single nucleotide variants (SNV). Using a semi-supervised method, we developed HRD classifiers from 1404 breast tumours across two datasets based on their BRCA1/2 status, demonstrating improved HRD identification when aggregating different data types. Notably, HRD-positive tumours in ER-negative disease showed improved survival post-adjuvant chemotherapy, while HRD status strongly correlated with neoadjuvant treatment response. Furthermore, our analysis of cell lines highlighted a sensitivity to PARP inhibitors, particularly rucaparib, among predicted HRD-positive lines. Exploring somatic mutations outside BRCA1/2, we confirmed variants in several genes associated with HRD. Our method for HRD classification can adapt to different data types or resolutions and can be used in various scenarios to help refine patient selection for HRD-targeting therapies that might lead to better clinical outcomes.","PeriodicalId":18764,"journal":{"name":"Molecular Oncology","volume":" ","pages":""},"PeriodicalIF":6.6,"publicationDate":"2025-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144034235","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}

引用次数: 0

Aberrant expression of nuclear prothymosin α contributes to epithelial-mesenchymal transition in lung cancer. 核原胸腺酶α的异常表达参与肺癌的上皮-间质转化。

IF 6.6 2区医学

Molecular Oncology Pub Date : 2025-04-21 DOI: 10.1002/1878-0261.70035

Liyun Chen, Chung-Teng Wang, Jia-Ming Chang, Ai-Li Shiau, Gia-Shing Shieh, Yau-Lin Tseng, Yi-Ting Yen, Tang-Hsiu Huang, Li-Hsin Cheng, Yu-Chih Wu, Chao-Liang Wu, Bing-Hua Su, Pensee Wu

{"title":"Aberrant expression of nuclear prothymosin α contributes to epithelial-mesenchymal transition in lung cancer.","authors":"Liyun Chen, Chung-Teng Wang, Jia-Ming Chang, Ai-Li Shiau, Gia-Shing Shieh, Yau-Lin Tseng, Yi-Ting Yen, Tang-Hsiu Huang, Li-Hsin Cheng, Yu-Chih Wu, Chao-Liang Wu, Bing-Hua Su, Pensee Wu","doi":"10.1002/1878-0261.70035","DOIUrl":"https://doi.org/10.1002/1878-0261.70035","url":null,"abstract":"Elevated expression of prothymosin α (ProT) is frequently observed in cancers, but the underlying molecular mechanism remains poorly understood. Here, we report the clinical relevance of ProT expression and its correlation with lung cancer progression. We have shown that ProT was highly expressed in early-stage lung cancer, exhibiting nuclear localization; on the contrary, a loss of nuclear ProT expression was detected in late-stage tumor specimens. Furthermore, the expression of nuclear ProT impaired lung cancer cell migration, suppressed TGF-β-induced epithelial-to-mesenchymal transition (EMT)-associated transcription factor expression, and inhibited in vivo tumor metastasis. The suppressive effect of ProT was further found to trigger Smad7 acetylation-dependent deregulation of TGF-β signaling. ProT enhanced Smad7 stability by promoting its lysine acetylation, thereby competing with the binding of Smad2 to the SNAI1, TWIST1, and ZEB1 promoters. Eventually, the binding of Smad7 in the presence of ProT resulted in reduced expression of the EMT transcription factors, leading to the inhibition of TGF-β-induced EMT and tumor metastasis. Collectively, this study unravels the role of ProT in lung cancer progression and highlights the potential of nuclear ProT as an indicator for monitoring tumor development.","PeriodicalId":18764,"journal":{"name":"Molecular Oncology","volume":" ","pages":""},"PeriodicalIF":6.6,"publicationDate":"2025-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144032991","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}

引用次数: 0

A large-scale retrospective study in metastatic breast cancer patients using circulating tumour DNA and machine learning to predict treatment outcome and progression-free survival. 一项使用循环肿瘤DNA和机器学习预测治疗结果和无进展生存期的转移性乳腺癌患者的大规模回顾性研究。

IF 6.6 2区医学

Molecular Oncology Pub Date : 2025-04-15 DOI: 10.1002/1878-0261.70015

Emma J Beddowes, Mario Ortega Duran, Solon Karapanagiotis, Alistair Martin, Meiling Gao, Riccardo Masina, Ramona Woitek, James Tanner, Fleur Tippin, Justine Kane, Jonathan Lay, Anja Brouwer, Stephen-John Sammut, Suet-Feung Chin, Davina Gale, Dana W Y Tsui, Sarah-Jane Dawson, Nitzan Rosenfeld, Maurizio Callari, Oscar M Rueda, Carlos Caldas

{"title":"A large-scale retrospective study in metastatic breast cancer patients using circulating tumour DNA and machine learning to predict treatment outcome and progression-free survival.","authors":"Emma J Beddowes, Mario Ortega Duran, Solon Karapanagiotis, Alistair Martin, Meiling Gao, Riccardo Masina, Ramona Woitek, James Tanner, Fleur Tippin, Justine Kane, Jonathan Lay, Anja Brouwer, Stephen-John Sammut, Suet-Feung Chin, Davina Gale, Dana W Y Tsui, Sarah-Jane Dawson, Nitzan Rosenfeld, Maurizio Callari, Oscar M Rueda, Carlos Caldas","doi":"10.1002/1878-0261.70015","DOIUrl":"https://doi.org/10.1002/1878-0261.70015","url":null,"abstract":"Monitoring levels of circulating tumour-derived DNA (ctDNA) provides both a noninvasive snapshot of tumour burden and also potentially clonal evolution. Here, we describe how applying a novel statistical model to serial ctDNA measurements from shallow whole genome sequencing (sWGS) in metastatic breast cancer patients produces a rapid and inexpensive predictive assessment of treatment response and progression-free survival. A cohort of 149 patients had DNA extracted from serial plasma samples (total 1013, mean samples per patient = 6.80). Plasma DNA was assessed using sWGS and the tumour fraction in total cell-free DNA estimated using ichorCNA. This approach was compared with ctDNA targeted sequencing and serial CA15-3 measurements. We identified a transition point of 7% estimated tumour fraction to stratify patients into different categories of progression risk using ichorCNA estimates and a time-dependent Cox Proportional Hazards model and validated it across different breast cancer subtypes and treatments, outperforming the alternative methods. We used the longitudinal ichorCNA values to develop a Bayesian learning model to predict subsequent treatment response with a sensitivity of 0.75 and a specificity of 0.66. In patients with metastatic breast cancer, a strategy of sWGS of ctDNA with longitudinal tracking of tumour fraction provides real-time information on treatment response. These results encourage a prospective large-scale clinical trial to evaluate the clinical benefit of early treatment changes based on ctDNA levels.","PeriodicalId":18764,"journal":{"name":"Molecular Oncology","volume":" ","pages":""},"PeriodicalIF":6.6,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143993462","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}

引用次数: 0

Ubiquitination of transcription factors in cancer: unveiling therapeutic potential. 癌症中转录因子的泛素化：揭示治疗潜力。

IF 6.6 2区医学

Molecular Oncology Pub Date : 2025-04-14 DOI: 10.1002/1878-0261.70033

Dongha Kim, Hye Jin Nam, Sung Hee Baek

{"title":"Ubiquitination of transcription factors in cancer: unveiling therapeutic potential.","authors":"Dongha Kim, Hye Jin Nam, Sung Hee Baek","doi":"10.1002/1878-0261.70033","DOIUrl":"https://doi.org/10.1002/1878-0261.70033","url":null,"abstract":"Transcription factors, pivotal in gene expression regulation, are essential in cancer progression. Their function is meticulously regulated by post-translational modifications, including ubiquitination. This process, which marks proteins for degradation, can either enhance or inhibit the function of transcription factors, contingent on the context. In cancers, dysregulated ubiquitination of transcription factors contributes to the hallmark of uncontrolled growth and survival of tumors. For example, tumor suppressors such as p53 might be degraded prematurely due to abnormal ubiquitination, causing genomic instability. On the other hand, oncogenic transcription factors may gain stability via ubiquitination, thus facilitating tumorigenesis. Targeting the ubiquitin-proteasome system (UPS) therefore could be a viable therapeutic approach in cancer. Emerging treatments aim to block the ubiquitination of oncogenic transcription factors or to stabilize tumor suppressors. This review underscores the critical impact of transcription factor-altered ubiquitination on cancer progression. Additionally, it outlines innovative therapeutic approaches that involve inhibitors or drugs directed at specific ubiquitin E3 ligases and deubiquitinases (DUBs) that regulate transcription factor activity.","PeriodicalId":18764,"journal":{"name":"Molecular Oncology","volume":" ","pages":""},"PeriodicalIF":6.6,"publicationDate":"2025-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143971669","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}

引用次数: 0