American journal of cancer research最新文献

Erratum: cAMP induces cell apoptosis in multiple myeloma and overcomes bortezomib resistance. 勘误：cAMP诱导多发性骨髓瘤细胞凋亡并克服硼替佐米耐药性。

IF 3.6 3区医学

American journal of cancer research Pub Date : 2025-04-25 eCollection Date: 2025-01-01 DOI: 10.62347/WYNP4109

Yingying Wang, Yong Tang, Haifang Hang, Mingming Wang, Yuyang Pang, Yehua Yu, Yingli Wu, Qi Zhu

引用次数: 0

New advances in the treatment of EGFR exon20ins mutant advanced NSCLC. EGFR外显子20ins突变晚期NSCLC治疗的新进展。

IF 3.6 3区医学

American journal of cancer research Pub Date : 2025-04-25 eCollection Date: 2025-01-01 DOI: 10.62347/WTMU5537

Chun Yuan, Jun-Yan Yu, Chuan-Xiu Zeng, Meng-Chao Wang, Shao Zhang, Yan-Bo Huang, Xue-Song Yu, Fan-Ming Kong, Li-Wei Chen

{"title":"New advances in the treatment of EGFR exon20ins mutant advanced NSCLC.","authors":"Chun Yuan, Jun-Yan Yu, Chuan-Xiu Zeng, Meng-Chao Wang, Shao Zhang, Yan-Bo Huang, Xue-Song Yu, Fan-Ming Kong, Li-Wei Chen","doi":"10.62347/WTMU5537","DOIUrl":"https://doi.org/10.62347/WTMU5537","url":null,"abstract":"The epidermal growth factor receptor (EGFR) exon 20 insertion (ex20ins) mutations, albeit less frequent, are a clinically significant subset within the EGFR mutation landscape of non-small cell lung cancer (NSCLC), accounting for roughly 4%-12% of all EGFR-altered cases. Ranking as the third most prevalent EGFR mutation type, these ex20ins mutations trail the widely recognized EGFR exon 19 deletion (19-Del) and exon 21 L858R substitution. In advanced-stage NSCLC patients with EGFR exon 20 insertion mutations, conventional treatments such as EGFR tyrosine kinase inhibitors (TKIs), chemotherapy, and immunotherapies often yield suboptimal responses, resulting in unfavorable clinical outcomes. This unmet clinical need underscores the urgency to explore innovative targeted therapies. In the realm of precision medicine, targeted agents specifically tailored for EGFR ex20ins mutations have emerged as promising candidates. This review examines the latest research on targeted therapies for EGFR ex20ins mutations, dissecting the mechanisms of action of these agents, evaluating the results of relevant clinical trials, and integrating the evidence in a systematic manner. The aim is to uncover novel therapeutic insights and strategies to optimize the clinical management of patients with EGFR ex20ins mutation-positive NSCLC.","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"15 4","pages":"1852-1873"},"PeriodicalIF":3.6,"publicationDate":"2025-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12070093/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144075042","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

PSPH promotes the proliferation and metastasis of esophageal squamous cell carcinoma through MAPK signaling pathways. PSPH通过MAPK信号通路促进食管鳞癌的增殖和转移。

IF 3.6 3区医学

American journal of cancer research Pub Date : 2025-04-25 eCollection Date: 2025-01-01 DOI: 10.62347/OGMW9514

Mengchu Yao, Yu Xie, Mingde Huang, Xiao Han, Yu Zhou, Mingyue Tao, Chang Liu, Yongxin Zhao, Chengwan Zhang, Yong Gao

{"title":"PSPH promotes the proliferation and metastasis of esophageal squamous cell carcinoma through MAPK signaling pathways.","authors":"Mengchu Yao, Yu Xie, Mingde Huang, Xiao Han, Yu Zhou, Mingyue Tao, Chang Liu, Yongxin Zhao, Chengwan Zhang, Yong Gao","doi":"10.62347/OGMW9514","DOIUrl":"https://doi.org/10.62347/OGMW9514","url":null,"abstract":"Esophageal squamous cell carcinoma (ESCC) is an aggressive malignancy with limited therapeutic options and poor prognosis, underscoring the urgent need for novel molecular targets. Here, we identify phosphoserine phosphatase (PSPH) as a key oncogenic driver in ESCC. This study systematically investigated the oncogenic functions of PSPH in ESCC progression and the associated molecular mechanisms. Functional studies revealed that PSPH overexpression markedly enhanced ESCC cell proliferation, migration, and invasion in vitro, while PSPH knockdown exerted opposing effects. Mechanistically, transcriptomic and phosphoproteomic analyses identified the mitogen-activated protein kinase (MAPK) pathway as the key downstream effector of PSPH. In vivo xenograft studies corroborated these findings, demonstrating that PSPH overexpression markedly promoted tumor growth. Notably, the pharmacological inhibitor of c-Jun N-terminal kinase (JNK) effectively abrogated PSPH-induced tumor progression, unequivocally establishing the MAPK pathway as the dominant mediator of PSPH oncogenic functions. Our findings establish PSPH as a key driver of ESCC progression, promoting migration, proliferation, and invasion via MAPK signaling activation. These results position PSPH as a promising therapeutic target for improving outcomes in patients with ESCC.","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"15 4","pages":"1919-1931"},"PeriodicalIF":3.6,"publicationDate":"2025-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12070109/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144075304","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Effects of the carcinogen TCDD on δ-catenin stability and tumorigenic potential in prostate cancer cells. 致癌物TCDD对前列腺癌细胞δ-连环蛋白稳定性和致瘤潜能的影响。

IF 3.6 3区医学

American journal of cancer research Pub Date : 2025-04-25 eCollection Date: 2025-01-01 DOI: 10.62347/WRBD9281

Yue Niu, Hyoung Jae Lee, Zhiwei Chen, Hangun Kim, Kwonseop Kim

{"title":"Effects of the carcinogen TCDD on δ-catenin stability and tumorigenic potential in prostate cancer cells.","authors":"Yue Niu, Hyoung Jae Lee, Zhiwei Chen, Hangun Kim, Kwonseop Kim","doi":"10.62347/WRBD9281","DOIUrl":"https://doi.org/10.62347/WRBD9281","url":null,"abstract":"δ-Catenin is a member of the p120-catenin subfamily of armadillo proteins and is known to be upregulated in prostate cancer, promoting tumorigenesis. Unfortunately, the molecular mechanism underlying this effect remains unclear. The carcinogen 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) has been linked to an increased risk of prostate cancer. In this study, we explored the effect of TCDD on δ-catenin in prostate cancer cells. TCDD increased the protein levels of δ-catenin in a dose-dependent manner by enhancing its stability. Moreover, TCDD led to an increase in β-catenin expression but a decrease in E-cadherin levels. Further experiments revealed that TCDD stabilized the expression of δ-catenin by inhibiting its ubiquitination-mediated degradation. Finally, TCDD enhanced the motility and migration ability of prostate cancer cells through δ-catenin. These findings suggest that TCDD plays a role in stabilizing δ-catenin in prostate cancer cells, offering a new perspective on preventing δ-catenin degradation and potentially increasing the predictive value of δ-catenin for prostate cancer.","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"15 4","pages":"1939-1954"},"PeriodicalIF":3.6,"publicationDate":"2025-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12070107/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144075401","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Predictive value of baseline CT imaging features combined with serum biomarkers for neoadjuvant chemotherapy response in adenocarcinoma of the gastroesophageal junction. 基线CT影像特征结合血清生物标志物对胃食管交界区腺癌新辅助化疗反应的预测价值。

IF 3.6 3区医学

American journal of cancer research Pub Date : 2025-04-25 eCollection Date: 2025-01-01 DOI: 10.62347/XLSV6197

Lei Li, Fei Luo, Xiansheng Cao, Chao Zhang, Qi Liu, Shanqiang Liu, Libo Yu

{"title":"Predictive value of baseline CT imaging features combined with serum biomarkers for neoadjuvant chemotherapy response in adenocarcinoma of the gastroesophageal junction.","authors":"Lei Li, Fei Luo, Xiansheng Cao, Chao Zhang, Qi Liu, Shanqiang Liu, Libo Yu","doi":"10.62347/XLSV6197","DOIUrl":"https://doi.org/10.62347/XLSV6197","url":null,"abstract":"Background: Gastroesophageal junction (GEJ) adenocarcinoma, located at the esophagus-stomach junction, poses significant clinical challenges due to its complex physiological structure. Neoadjuvant chemotherapy (NAC) is standard for tumor downstaging, but response variability necessitates reliable predictive markers. This study evaluates baseline computed tomography (CT) imaging parameters and serum markers as predictors for chemotherapy response in GEJ adenocarcinoma.Methods: A retrospective study included 304 GEJ adenocarcinoma patients treated with the SOX regimen (S-1 + Oxaliplatin) between January 2020 and December 2024. Patients were categorized based on Tumor Regression Grade (TRG) into effective (TRG 0-1) and poor response (TRG 2-3) groups. Baseline CT characteristics were assessed alongside serum markers, including carcinoembryonic antigen (CEA), alpha-fetoprotein (AFP), carbohydrate antigen 19-9 (CA 19-9), and carbohydrate antigen 72-4 (CA 72-4). Multivariate logistic regression identified independent predictors, and a combined predictive model was developed and validated using an external cohort.Results: The effective treatment group showed significantly lower serum markers (CEA, AFP, CA 19-9, CA 72-4) and distinct CT parameters, including decreased maximum tumor thickness and area, and lower CT enhancement values. Extramural vascular invasion (EMVI) and tumor surface ulceration were associated with poor response. The combined predictive model demonstrated high accuracy, with an area under the curve (AUC) of 0.813 in the training set and 0.846 in the validation cohort.Conclusion: Baseline CT characteristics, when combined with serum markers, effectively predict NAC response in GEJ adenocarcinoma.","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"15 4","pages":"1955-1971"},"PeriodicalIF":3.6,"publicationDate":"2025-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12070103/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144075130","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Treatment mechanism and research progress of bevacizumab for glioblastoma. 贝伐单抗治疗胶质母细胞瘤的机制及研究进展。

IF 3.6 3区医学

American journal of cancer research Pub Date : 2025-04-25 eCollection Date: 2025-01-01 DOI: 10.62347/RNUE7193

Xinliang Liu, Zhigang Chen, Pengwei Yan, Tao Yang, Dan Zong, Wenjie Guo, Xia He

{"title":"Treatment mechanism and research progress of bevacizumab for glioblastoma.","authors":"Xinliang Liu, Zhigang Chen, Pengwei Yan, Tao Yang, Dan Zong, Wenjie Guo, Xia He","doi":"10.62347/RNUE7193","DOIUrl":"https://doi.org/10.62347/RNUE7193","url":null,"abstract":"Hypervascularization is a notable pathological hallmark of glioblastoma (GBM). Bevacizumab (Bev) remains the sole antiangiogenic agent approved by the U.S. Food and Drug Administration (FDA) for GBM treatment. The approval for this indication was supported by several phase II studies demonstrating that Bev significantly improved progression-free survival and the best imaging response in patients with recurrent GBM. Three large phase III randomized controlled trials reported that Bev did not significantly extend overall survival (OS). Nevertheless, Bev has been shown to delay the deterioration of patients' quality of life by postponing tumor progression. This review synthesizes findings from recent investigations exploring Bev in combination with targeted therapies, immunotherapy, or reirradiation. Additionally, this review discusses dosing regimens, administration, treatment failure patterns, third-line therapeutic applications, and prognostic markers of Bev. By synthesizing current evidence, this review aims to inform clinical decision-making for neuro-oncology clinicians.","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"15 4","pages":"1874-1901"},"PeriodicalIF":3.6,"publicationDate":"2025-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12070100/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144075343","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Effect of sevoflurane combined with intercostal block on postoperative pulmonary function, opioid consumption, and stress response in lung cancer surgery patients. 七氟醚联合肋间阻滞对肺癌手术患者术后肺功能、阿片类药物消耗及应激反应的影响

IF 3.6 3区医学

American journal of cancer research Pub Date : 2025-04-25 eCollection Date: 2025-01-01 DOI: 10.62347/DESK9796

Yixin Wang, Lang Jin, Hongmei Shen, Chuanjie Zong, Jie Zhang

{"title":"Effect of sevoflurane combined with intercostal block on postoperative pulmonary function, opioid consumption, and stress response in lung cancer surgery patients.","authors":"Yixin Wang, Lang Jin, Hongmei Shen, Chuanjie Zong, Jie Zhang","doi":"10.62347/DESK9796","DOIUrl":"https://doi.org/10.62347/DESK9796","url":null,"abstract":"Objective: To investigate the efficacy of sevoflurane combined with intercostal block in lung cancer surgery.Methods: A retrospective analysis was conducted on 252 patients who underwent lung cancer surgery between January 2020 and December 2023. Patients were divided into two groups: the sevoflurane with intercostal block group (Group S, n = 108) and the propofol group (Group P, n = 144). Anesthesia protocols involved sevoflurane and intercostal nerve block or propofol. Postoperative pulmonary function, opioid consumption, stress response, and cognitive effects were compared between the two groups.Results: The VAS scores were significantly lower in Group S at postoperative 2 h (1.96 ± 0.52 vs 2.15 ± 0.56, P = 0.005) and 24 h (3.84 ± 0.95 vs 4.14 ± 0.98, P = 0.015), indicating superior pain management. Group S also showed better preservation of lung function, with higher FEV1 values at postoperative 2 hours (1.49 ± 0.29 L vs 1.36 ± 0.65 L, P = 0.033) and 24 hours (1.59 ± 0.39 L vs 1.45 ± 0.45 L, P = 0.012). Opioid consumption was lower in Group S at both postoperative 24 h (1307.52 ± 259.41 µg vs 1742.26 ± 253.12 µg, P < 0.001) and 48 h. Cognitive function was better preserved immediately post-surgery in Group S (26.03 ± 4.42 vs 24.14 ± 5.28, P = 0.003). However, adverse reactions like nausea were more common in Group S (9.26% vs 2.78%, P = 0.026).Conclusion: Sevoflurane combined with intercostal block outperforms propofol in enhancing postoperative pulmonary function, reducing opioid reliance, and modulating stress responses in lung cancer surgery patients.","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"15 4","pages":"1972-1985"},"PeriodicalIF":3.6,"publicationDate":"2025-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12070098/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144075398","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Endoplasmic reticulum stress in non-small cell lung cancer. 非小细胞肺癌的内质网应激。

IF 3.6 3区医学

American journal of cancer research Pub Date : 2025-04-25 eCollection Date: 2025-01-01 DOI: 10.62347/RGRQ7608

Xiaodong Li, Fangning Hu, Tong Lu, Shuo Wu, Guanqiang Ma, Yani Lin, Hua Zhang

引用次数: 0

Identification of novel NUP98::RARA fusion transcripts in acute promyelocytic leukemia with i(17)(q10) abnormality. 新型NUP98::RARA融合转录物在i(17)（q10）异常的急性早幼粒细胞白血病中的鉴定

IF 3.6 3区医学

American journal of cancer research Pub Date : 2025-04-25 eCollection Date: 2025-01-01 DOI: 10.62347/UKFC7557

Jifang Tu, Huanping Wang, Yungui Wang, Hongyan Tong

{"title":"Identification of novel NUP98::RARA fusion transcripts in acute promyelocytic leukemia with i(17)(q10) abnormality.","authors":"Jifang Tu, Huanping Wang, Yungui Wang, Hongyan Tong","doi":"10.62347/UKFC7557","DOIUrl":"https://doi.org/10.62347/UKFC7557","url":null,"abstract":"Acute promyelocytic leukemia (APL) is one subtype of acute myeloid leukemia (AML) primarily associated with the typical fusion gene PML::RARA/t(15;17). A small percentage of APL cases are caused by atypical gene transcript variants lacking the PML::RARA. We report one case with two novel NUP98::RARA fusion transcripts in APL lacking the fusion gene PML::RARA/t(15;17). These NUP98::RARA fusion transcripts were identified using next-generation sequencing (NGS), which were confirmed by Sanger sequencing. One of the transcripts differs from the previously reported transcript in terms of break sites and transcript length, which identified as subtype of NUP98::RARA fusion transcript. The other one is the same as previously reported, demonstrating reproducible abnormality of this fusion gene. The patient was treated with all-trans retinoic acid (ATRA), realgar-Indigo naturalis formula (RIF) and chemotherapy. According to the published paper, this is the second report of NUP98::RARA fusion transcript in APL. It is also the first variant APL with der(11)(p15)t(11;17)(p15;q21) and i(17)(q10) chromosome abnormalities. Therefore, we compared and summarized these two cases.","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"15 4","pages":"1932-1938"},"PeriodicalIF":3.6,"publicationDate":"2025-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12070106/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144075349","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Autophagy-dependent apoptosis induction by oridonin are mediated by ROS-dependent AMPK-mTOR-ULK1 pathway in colon cancer. oridonin诱导结肠癌细胞自噬依赖性凋亡是通过ros依赖性AMPK-mTOR-ULK1通路介导的。

IF 3.6 3区医学

American journal of cancer research Pub Date : 2025-04-25 eCollection Date: 2025-01-01 DOI: 10.62347/CGIO2604

Bin Shao, Heqi Bu, Ganglei Li, Dapeng Kang, Qi Ju

{"title":"Autophagy-dependent apoptosis induction by oridonin are mediated by ROS-dependent AMPK-mTOR-ULK1 pathway in colon cancer.","authors":"Bin Shao, Heqi Bu, Ganglei Li, Dapeng Kang, Qi Ju","doi":"10.62347/CGIO2604","DOIUrl":"https://doi.org/10.62347/CGIO2604","url":null,"abstract":"Oridonin, a bioactive diterpenoid isolated from Rabdosia species, exhibits broad-spectrum anticancer activity across various tumor types. However, its impact on colon cancer and the underlying molecular mechanisms remains poorly understood. Our study revealed that oridonin significantly suppressed the proliferation of HCT8 and HCT116 colon cancer cells by inducing G2/M phase cell cycle arrest. Moreover, oridonin triggered apoptotic cell death, as indicated by elevated levels of cleaved caspase-3 and PARP. Simultaneously, it activated autophagy, as evidenced by increased expression of Beclin 1 and LC3-II, along with decreased LC3-I and p62 levels. In addition, inhibiting autophagy with 3-methyladenine (3-MA) reduced cell apoptosis, whereas blocking apoptosis using Z-Val-Ala-Asp(OMe)-FMK (Z-VAD-FMK) enhanced autophagy. Furthermore, oridonin also induced the accumulation of reactive oxygen species (ROS), which contributed to apoptosis; this effect was largely reversed by the ROS scavenger N-acetyl-L-cysteine (NAC). Mechanistically, oridonin increased phosphorylation of AMP-activated protein kinase (AMPK) and suppressed phosphorylation of mammalian target of rapamycin (mTOR) and Unc-51-like kinase 1 (ULK1). Silencing AMPK with siRNA blocked oridonin's effects on the AMPK/mTOR pathway, as well as its regulation of autophagy and apoptosis. Moreover, co-treatment with NAC almost completely blocked activation of the AMPK-mTOR-ULK1 signaling pathway. In vivo, oridonin significantly suppressed tumor growth in a xenograft model, accompanied by elevated expression of LC3-II and cleaved caspase-3. Collectively, these findings demonstrated that oridonin could exert potent anti-tumor effects in colon cancer by inducing cell cycle arrest and promoting autophagy-dependent apoptosis via ROS-mediated activation of the AMPK-mTOR-ULK1 signaling pathway.","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"15 4","pages":"1902-1918"},"PeriodicalIF":3.6,"publicationDate":"2025-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12070090/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144075362","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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