Cancer research最新文献_第6页

Longitudinal Profiling of Circulating Tumor DNA Reveals the Evolutionary Dynamics of Metastatic Prostate Cancer During Serial Therapy.

IF 12.5 1区医学

Cancer research Pub Date : 2025-02-24 DOI: 10.1158/0008-5472.CAN-24-1943

Yuehui Zhao, Naveen Ramesh, Ping Xu, Emi Sei, Min Hu, Shanshan Bai, Patricia Troncoso, Ana M Aparicio, Christopher J Logothetis, Paul G Corn, Nicholas E Navin, Amado J Zurita

{"title":"Longitudinal Profiling of Circulating Tumor DNA Reveals the Evolutionary Dynamics of Metastatic Prostate Cancer During Serial Therapy.","authors":"Yuehui Zhao, Naveen Ramesh, Ping Xu, Emi Sei, Min Hu, Shanshan Bai, Patricia Troncoso, Ana M Aparicio, Christopher J Logothetis, Paul G Corn, Nicholas E Navin, Amado J Zurita","doi":"10.1158/0008-5472.CAN-24-1943","DOIUrl":"10.1158/0008-5472.CAN-24-1943","url":null,"abstract":"Treatment decisions in metastatic castration-resistant prostate cancer (mCRPC) are mostly guided by clinical variables, but efforts to molecularly monitor the disease remain hampered by challenges in acquiring tumor tissue repeatedly. Here, we simultaneously profiled the genome copy number and exome in longitudinal plasma circulating tumor DNA (ctDNA) acquired before, during, and upon progression to serial treatments with androgen signaling inhibitors (ASI) and taxane chemotherapy from 60 mCRPC patients (2-10 samples per patient). The genomic data was used to delineate the clonal substructure and evolutionary dynamics of each patient, and an evolutionary dynamic index (EDI) was developed to measure the longitudinal changes of the tumor subclones. Treatment with ASI resulted in greater subclonal selection and population structure changes than taxane treatment. The subclones that emerged in association with serial therapy resistance harbored recurrent aberrations in previously identified and new candidate genes, with particular enrichment in genes related to PI3K-AKT signaling. These findings indicate that the integration of detailed clinical and genomics data can provide a framework for future unbiased genomic applications for ctDNA in the clinic to enable precision medicine.","PeriodicalId":9441,"journal":{"name":"Cancer research","volume":" ","pages":""},"PeriodicalIF":12.5,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143482301","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Circulating Tumor Microenvironment in Metastasis.

IF 12.5 1区医学

Cancer research Pub Date : 2025-02-24 DOI: 10.1158/0008-5472.CAN-24-1241

Rui Tang, Shujuan Luo, Hui Liu, Yan Sun, Manran Liu, Lu Li, Haoyu Ren, Martin K Angele, Nikolaus Börner, Keda Yu, Zufeng Guo, Guobing Yin, Haojun Luo

{"title":"Circulating Tumor Microenvironment in Metastasis.","authors":"Rui Tang, Shujuan Luo, Hui Liu, Yan Sun, Manran Liu, Lu Li, Haoyu Ren, Martin K Angele, Nikolaus Börner, Keda Yu, Zufeng Guo, Guobing Yin, Haojun Luo","doi":"10.1158/0008-5472.CAN-24-1241","DOIUrl":"https://doi.org/10.1158/0008-5472.CAN-24-1241","url":null,"abstract":"Activation of invasion and metastasis is a central hallmark of cancer, contributing to the primary cause of death for cancer patients. In the multistep metastatic process, cancer cells must infiltrate the circulation, survive, arrest at capillary beds, extravasate, and form metastatic clones in distant organs. However, only a small proportion of circulating tumor cells (CTCs) successfully form metastases, with transit of CTCs in the circulation being the rate-limiting step. The fate of CTCs is influenced by the circulating tumor microenvironment (cTME), which encompasses factors affecting their biological behaviors in the circulation. This liquid and flowing microenvironment differs significantly from the primary tumor microenvironment or the pre-metastatic niche. This review summarizes the latest advancements in identifying the biophysical cues, key components, and biological roles of the cTME, highlighting the network among biophysical attributes, blood cells, and non-blood factors in cancer metastasis. In addition to the potential of the cTME as a therapeutic target for inhibiting metastasis, the cTME could also represent as a biomarker for predicting patient outcomes and developing strategies for treating cancer.","PeriodicalId":9441,"journal":{"name":"Cancer research","volume":" ","pages":""},"PeriodicalIF":12.5,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143482288","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Targeting PRC2 Enhances the Cytotoxic Capacity of Anti-CD19 CAR-T Cells Against Hematological Malignancies

IF 11.2 1区医学

Cancer research Pub Date : 2025-02-19 DOI: 10.1158/0008-5472.can-24-1643

Maria Leticia R. Carvalho, Clara O. Andrade, Mariela P. Cabral-Piccin, Gabriela S. Kinker, Glauco A. F. Vitiello, Raylane A. G. Cambui, Luiza Abdo, Eduardo Mannarino, Bruno D. S. Elias, Emmanuel Vinicius O. Araujo, Alexandre S. Chaves, Pedro Henrique B. Pereira, Karina Hajdu, Amanda Rondinelli, Arianne Gusmao, Maria Luisa M. Pierre, Igor Brasil-Costa, Caroline P. Zanella, Marta Maria M. Lemos, Marjorie V. Batista, Jayr S. Filho, Cheryl Arrowsmith, Vladmir Cordeiro de Lima, Martin Bonamino, Tiago da Silva Medina

{"title":"Targeting PRC2 Enhances the Cytotoxic Capacity of Anti-CD19 CAR-T Cells Against Hematological Malignancies","authors":"Maria Leticia R. Carvalho, Clara O. Andrade, Mariela P. Cabral-Piccin, Gabriela S. Kinker, Glauco A. F. Vitiello, Raylane A. G. Cambui, Luiza Abdo, Eduardo Mannarino, Bruno D. S. Elias, Emmanuel Vinicius O. Araujo, Alexandre S. Chaves, Pedro Henrique B. Pereira, Karina Hajdu, Amanda Rondinelli, Arianne Gusmao, Maria Luisa M. Pierre, Igor Brasil-Costa, Caroline P. Zanella, Marta Maria M. Lemos, Marjorie V. Batista, Jayr S. Filho, Cheryl Arrowsmith, Vladmir Cordeiro de Lima, Martin Bonamino, Tiago da Silva Medina","doi":"10.1158/0008-5472.can-24-1643","DOIUrl":"https://doi.org/10.1158/0008-5472.can-24-1643","url":null,"abstract":"Chimeric antigen receptor (CAR) T cell therapy is increasingly being adopted as a clinical modality for patients with relapsed/refractory hematological malignancies. Despite the clinical efficacy of CAR-T cell therapy, a considerable fraction of patients still relapses during the first months following CAR-T cell infusion. The limited CAR-T cell efficiency is thought to relate to epigenetic mechanisms involved in T cell suppression and dysfunction. Here, screening of multiple epigenetic inhibitors revealed that targeting PRC2 consistently induced the development of granzyme B+ effector memory CD8+ T cells. Notably, PRC2 inhibition also promoted the long-term persistence of granzyme B+ effector memory 19BBζ CAR-T cells and sustainably enhanced their antitumor activity both in vitro and in vivo. Consistent with their long-lasting antitumor activity, PRC2-inhibited 19BBζ CAR-T cells did not exhibit signs of exhaustion over time. Furthermore, TCR restimulation along with PRC2 inhibition promoted the differentiation of patient-derived anti-CD19 CAR-T cells to a granzyme B+ effector memory phenotype with enhanced cytotoxic features that elicited potent antitumor responses. A gene signature derived from in-house PRC2-inhibited 19BBζ CAR-T cells was enriched in tisagenlecleucel (tisa-cel) BBζ CAR-T cell therapy responders with large B-cell lymphoma. Collectively, these results demonstrate that targeting PRC2 may be a promising approach to enhance a functional effector program in CAR-T cells to improve the efficacy in treating hematological malignancies.","PeriodicalId":9441,"journal":{"name":"Cancer research","volume":"29 1","pages":""},"PeriodicalIF":11.2,"publicationDate":"2025-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143452337","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Gli2 Facilitates Tumor Immune Evasion and Immunotherapeutic Resistance by Coordinating Wnt Ligand and Prostaglandin Signaling

IF 11.2 1区医学

Cancer research Pub Date : 2025-02-19 DOI: 10.1158/0008-5472.can-24-1130

Nicholas C. DeVito, Y-Van Nguyen, Michael Sturdivant, Michael P. Plebanek, Kaylee A. Villarreal, Nagendra Yarla, Vaibhav Jain, Michael Aksu, Georgia M. Beasley, Balamayooran Theivanthiran, Brent A. Hanks

{"title":"Gli2 Facilitates Tumor Immune Evasion and Immunotherapeutic Resistance by Coordinating Wnt Ligand and Prostaglandin Signaling","authors":"Nicholas C. DeVito, Y-Van Nguyen, Michael Sturdivant, Michael P. Plebanek, Kaylee A. Villarreal, Nagendra Yarla, Vaibhav Jain, Michael Aksu, Georgia M. Beasley, Balamayooran Theivanthiran, Brent A. Hanks","doi":"10.1158/0008-5472.can-24-1130","DOIUrl":"https://doi.org/10.1158/0008-5472.can-24-1130","url":null,"abstract":"Therapeutic resistance to immune checkpoint blockade has been commonly linked to the process of mesenchymal transformation (MT) and remains a prevalent obstacle across many cancer types. An improved mechanistic understanding for MT-mediated immune evasion promises to lead to more effective combination therapeutic regimens. Herein, we identified the Hedgehog transcription factor, GLI2, as a key node of tumor-mediated immune evasion and immunotherapy resistance during MT. GLI2 generated an immunotolerant tumor microenvironment through the upregulation of WNT ligand production and increased prostaglandin synthesis. This pathway drove the recruitment, viability, and function of granulocytic myeloid-derived suppressor cells while also impairing type I conventional dendritic cell, CD8+ T cell, and natural killer cell functionality. Pharmacologic inhibition of EP2/EP4 prostaglandin receptor signaling or WNT ligand secretion each reversed a subset of the immunomodulatory effects of GLI2 and prevented primary and adaptive resistance to anti-PD-1 immunotherapy, respectively. A transcriptional GLI2 signature correlated with resistance to anti-PD-1 immunotherapy in stage IV melanoma patients. Together, these findings provide a translational roadmap to direct combination immunotherapies in the clinic.","PeriodicalId":9441,"journal":{"name":"Cancer research","volume":"50 1","pages":""},"PeriodicalIF":11.2,"publicationDate":"2025-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143451477","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Chromatin Helicase CHD6 Establishes Proinflammatory Enhancers and Is a Synthetic Lethal Target in FH-Deficient Renal Cell Carcinoma. 染色质螺旋酶 CHD6 在 FH 缺失的肾细胞癌中建立促炎增强子并成为合成致命靶点

IF 12.5 1区医学

Cancer research Pub Date : 2025-02-17 DOI: 10.1158/0008-5472.CAN-24-0787

Juan Jin, Jun Luo, Xiaodong Jin, Kiat Shenq Lim, Yang He, Jiawei Ding, Yan Shen, Yuchen Hou, Hanqing Liu, Xiaoyu Zhu, Jing Zhao, Wenjie Zhou, Hai Huang, Yi Gao, Jun Xiao, Hongchao He, Qunyi Li, Lianxin Liu, Li Chen, Qiang He, Chuanjie Zhang

{"title":"Chromatin Helicase CHD6 Establishes Proinflammatory Enhancers and Is a Synthetic Lethal Target in FH-Deficient Renal Cell Carcinoma.","authors":"Juan Jin, Jun Luo, Xiaodong Jin, Kiat Shenq Lim, Yang He, Jiawei Ding, Yan Shen, Yuchen Hou, Hanqing Liu, Xiaoyu Zhu, Jing Zhao, Wenjie Zhou, Hai Huang, Yi Gao, Jun Xiao, Hongchao He, Qunyi Li, Lianxin Liu, Li Chen, Qiang He, Chuanjie Zhang","doi":"10.1158/0008-5472.CAN-24-0787","DOIUrl":"10.1158/0008-5472.CAN-24-0787","url":null,"abstract":"Fumarate hydratase (FH) deficiency causes hereditary leiomyomatosis and renal cell carcinoma (RCC). FH-deficient tumors lack effective therapeutic options. Here, we utilized an epigenetic-focused single-guide RNA library to elucidate potential drug targets in FH-deficient tumors. The screen identified chromodomain helicase DNA-binding protein 6 (CHD6) as an essential regulator of the growth of FH-mutated RCC. Mechanically, FH loss induced fumarate-mediated succinylation and inactivation of KEAP1, blocking subsequent ubiquitin-proteasome degradation of CHD6. Stabilized CHD6 formed a complex with p65 to establish proinflammatory enhancers and thereby regulate NF-κB-mediated transcription. Moreover, CHD6 recruited mSWI/SNF ATPases to maintain chromatin accessibility at CHD6-bound enhancers. The PROTAC degrader of SMARCA2/4 AU-15330 effectively abolished structures of cis-regulatory elements bound by CHD6 and suppressed the growth of FH-mutated, but not FH-intact, RCC in vivo. Collectively, these data indicate that CHD6 is a molecular bridge between FH deficiency and proinflammatory enhancer assembly that endows FH-deficient tumors with epigenetic vulnerabilities. Significance: CHD6 links FH deficiency to aberrant NF-κB activity in renal cell carcinoma, highlighting an epigenetic vulnerability for this rare tumor subtype.","PeriodicalId":9441,"journal":{"name":"Cancer research","volume":" ","pages":"675-691"},"PeriodicalIF":12.5,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142715406","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Correction: p38γ MAPK Is Essential for Aerobic Glycolysis and Pancreatic Tumorigenesis.

IF 12.5 1区医学

Cancer research Pub Date : 2025-02-17 DOI: 10.1158/0008-5472.CAN-24-4956

Fang Wang, Xiao-Mei Qi, Ryan Wertz, Matthew Mortensen, Catherine Hagen, John Evans, Yuri Sheinin, Michael James, Pengyuan Liu, Susan Tsai, James Thomas, Alexander Mackinnon, Michael Dwinell, Charles R Myers, Ramon Bartrons Bach, Liwu Fu, Guan Chen

引用次数: 0

Deterministic Role of FOXF2 in Organ-Specific Macrometastasis Transition

IF 11.2 1区医学

Cancer research Pub Date : 2025-02-17 DOI: 10.1158/0008-5472.can-24-4078

Igor L. Bado

引用次数: 0

Breast Cancer Subtype-Specific Organotropism Is Dictated by FOXF2-Regulated Metastatic Dormancy and Recovery. 乳腺癌亚型特异性器官转移受 FOXF2 调节的转移蛰伏和恢复的支配

IF 12.5 1区医学

Cancer research Pub Date : 2025-02-17 DOI: 10.1158/0008-5472.CAN-24-0479

Wen-Jing Jiang, Tian-Hao Zhou, Huan-Jing Huang, Lin-Sen Li, Hao Tan, Rui Zhang, Qing-Shan Wang, Yu-Mei Feng

{"title":"Breast Cancer Subtype-Specific Organotropism Is Dictated by FOXF2-Regulated Metastatic Dormancy and Recovery.","authors":"Wen-Jing Jiang, Tian-Hao Zhou, Huan-Jing Huang, Lin-Sen Li, Hao Tan, Rui Zhang, Qing-Shan Wang, Yu-Mei Feng","doi":"10.1158/0008-5472.CAN-24-0479","DOIUrl":"10.1158/0008-5472.CAN-24-0479","url":null,"abstract":"Breast cancer subtypes display different metastatic organotropism. Identification of the mechanisms underlying subtype-specific organotropism could help uncover potential approaches to prevent and treat metastasis. In this study, we found that forkhead box F2 (FOXF2) promoted the seeding and proliferative recovery from dormancy of luminal breast cancer (LumBC) and basal-like breast cancer (BLBC) cells in the bone by activating the NF-κB and BMP signaling pathways. FOXF2 promoted LumBC cell seeding but not proliferative recovery in the lung by activating the BMP signaling pathway. Conversely, FOXF2 suppressed the seeding and proliferative recovery of BLBC cells in the lung by repressing the TGFβ signaling pathway. FOXF2 directly upregulated RelA/p65 transcription and expression in LumBC and BLBC cells by binding to the RELA proximal promoter region and RelA/p65 bound to the FOXF2 proximal promoter region to upregulate expression, forming a positive feedback loop. Targeting the NF-κB pathway efficiently prevented the metastasis of FOXF2-overexpressing breast cancer cells to the bone, whereas inhibiting TGFβ signaling blocked the metastasis of BLBC with low FOXF2 expression to the lung. These findings uncover critical mechanisms of breast cancer subtype-specific organotropism and provide insights into precision assessment and treatment strategies. Significance: FOXF2 regulates signaling pathways in a subtype-specific manner to coordinate the fate of disseminated breast cancer cells in distant organs, suggesting that FOXF2 functions could be harnessed to prevent organ-specific metastasis. See related commentary by Bado, p. 639.","PeriodicalId":9441,"journal":{"name":"Cancer research","volume":" ","pages":"644-659"},"PeriodicalIF":12.5,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142715271","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Correction: Long Noncoding RNA MIR17HG Promotes Colorectal Cancer Progression via miR-17-5p.

IF 12.5 1区医学

Cancer research Pub Date : 2025-02-17 DOI: 10.1158/0008-5472.CAN-24-4903

Jie Xu, Qingtao Meng, Xiaobo Li, Hongbao Yang, Jin Xu, Na Gao, Hao Sun, Shenshen Wu, Giuseppe Familiari, Michela Relucenti, Haitao Zhu, Jiong Wu, Rui Chen

引用次数: 0

A Potent, Selective, Small-Molecule Inhibitor of DHX9 Abrogates Proliferation of Microsatellite Instable Cancers with Deficient Mismatch Repair. 一种强效、选择性小分子 DHX9 抑制剂可抑制错配修复缺陷的微卫星不稳定性癌症的增殖

IF 12.5 1区医学

Cancer research Pub Date : 2025-02-17 DOI: 10.1158/0008-5472.CAN-24-0397

Jennifer Castro, Matthew H Daniels, David Brennan, Brian Johnston, Deepali Gotur, Young-Tae Lee, Kevin E Knockenhauer, Chuang Lu, Jie Wu, Sunaina Nayak, Cindy Collins, Rishabh Bansal, Shane M Buker, April Case, Julie Liu, Shihua Yao, Brian A Sparling, E Allen Sickmier, Serena J Silver, Stephen J Blakemore, P Ann Boriack-Sjodin, Kenneth W Duncan, Scott Ribich, Robert A Copeland

{"title":"A Potent, Selective, Small-Molecule Inhibitor of DHX9 Abrogates Proliferation of Microsatellite Instable Cancers with Deficient Mismatch Repair.","authors":"Jennifer Castro, Matthew H Daniels, David Brennan, Brian Johnston, Deepali Gotur, Young-Tae Lee, Kevin E Knockenhauer, Chuang Lu, Jie Wu, Sunaina Nayak, Cindy Collins, Rishabh Bansal, Shane M Buker, April Case, Julie Liu, Shihua Yao, Brian A Sparling, E Allen Sickmier, Serena J Silver, Stephen J Blakemore, P Ann Boriack-Sjodin, Kenneth W Duncan, Scott Ribich, Robert A Copeland","doi":"10.1158/0008-5472.CAN-24-0397","DOIUrl":"10.1158/0008-5472.CAN-24-0397","url":null,"abstract":"DHX9 is a multifunctional DExH-box RNA helicase with important roles in the regulation of transcription, translation, and maintenance of genome stability. Elevated expression of DHX9 is evident in multiple cancer types, including colorectal cancer. Microsatellite instable-high (MSI-H) tumors with deficient mismatch repair (dMMR) display a strong dependence on DHX9, making this helicase an attractive target for oncology drug discovery. In this report, we show that DHX9 knockdown increased RNA/DNA secondary structures and replication stress, resulting in cell-cycle arrest and the onset of apoptosis in cancer cells with MSI-H/dMMR. ATX968 was identified as a potent and selective inhibitor of DHX9 helicase activity. Chemical inhibition of DHX9 enzymatic activity elicited similar selective effects on cell proliferation as seen with genetic knockdown. In addition, ATX968 induced robust and durable responses in an MSI-H/dMMR xenograft model but not in a microsatellite stable/proficient MMR model. These preclinical data validate DHX9 as a target for the treatment of patients with MSI-H/dMMR. Additionally, this potent and selective inhibitor of DHX9 provides a valuable tool with which to further explore the effects of inhibition of DHX9 enzymatic activity on the proliferation of cancer cells in vitro and in vivo. Significance: DHX9 is required in cancer cells with deficient mismatch repair and can be inhibited by ATX968, providing a promising strategy for the development of precision cancer therapeutics.","PeriodicalId":9441,"journal":{"name":"Cancer research","volume":" ","pages":"758-776"},"PeriodicalIF":12.5,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11831107/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142715324","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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