Cancer Biomarkers最新文献

{"title":"Long noncoding RNA LINC00885 upregulates NCK1 to promote cell viability and migration of triple-negative breast cancer cells through sponging miR-654-3p.","authors":"Peina He, Zhi Liu, Jinxu Qi, Junrao Shan, Jianyun Sheng","doi":"10.3233/CBM-230143","DOIUrl":"10.3233/CBM-230143","url":null,"abstract":"<p><strong>Background: </strong>LINC00885 is a novel oncogenic long noncoding RNA (LncRNA) which is upregulated in various types of cancer, but its function in triple-negative breast cancer (TNBC) remains unknown.</p><p><strong>Objective: </strong>This study aimed to determine the role of LINC00885 on TNBC development.</p><p><strong>Methods: </strong>Clinical interrelation and survival analysis were determined using online database. The CCK-8 and Transwell assays were used to detect the proliferation and migration behaviors in TNBC cell lines. The interaction among genes was detected by RNA pull down assay.</p><p><strong>Results: </strong>LncRNA LINC00885 was highly expressed in TNBC compared to normal breast like. Low levels of LINC00885 was related to good prognosis in TNBC patients compared to TNBC patients with high LINC00885. LINC00885-downregulation inhibited, whereas LINC00885-overexpression promoted the proliferation and migration capability of TNBC cell lines. In TNBC cell lines, noncatalytic region of tyrosine kinase 1 (NCK1) expression was positively associated with LINC00885 expression, and shRNA-mediated the depletion of NCK1 significantly abolished LINC00885 upregulation-mediated pro-tumor effects. Combined with online databases, miR-654-3p was screened as the direct target gene of LINC00885, which could directly bind to 3'-untranslated regions (3'-UTR) of NCK1, resulting in the decreased expression of NCK1 in TNBC cell lines. LINC00885 overexpression-mediated the upregulation of NCK1 was abrogated by miR-654-3p mimics. MiR-654-3p mimics significantly rescued the tumor promotive role caused by LINC00885-overexpression. However, exogenous NCK1 notably eliminated the anti-tumor effects caused by miR-654-3p mimics in LINC00885-overexpressed cells.</p><p><strong>Conclusions: </strong>LINC00885 is expressed at a high level in TNBC. LINC00885 promoted proliferation and migration by regulating the miR-654-3p/NCK1 axis in TNBC cell lines. Possibly, LINC00885 can be served as a potential therapeutic target for TNBC.</p>","PeriodicalId":56320,"journal":{"name":"Cancer Biomarkers","volume":" ","pages":"63-78"},"PeriodicalIF":3.1,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10977424/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10554360","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The combined detection of hematological indicators is used for the differential diagnosis of colorectal cancer and benign-colorectal lesions.","authors":"Xuan Zhang, Yang-Yang Wu, Yuan-Yuan Qin, Fa-Quan Lin","doi":"10.3233/CBM-230157","DOIUrl":"10.3233/CBM-230157","url":null,"abstract":"<p><strong>Objective: </strong>This article aims to investigate the clinical value of hemoglobin/red cell distribution width ratio (Hb/RDW), C-reactive protein/albumin ratio (CAR) and plateletcrit (PCT) combined with carcinoembryonic antigen (CEA) in colorectal cancer (CRC) auxiliary diagnosis.</p><p><strong>Methods: </strong>We retrospectively analyzed in 718 subjects (212 with CRC, 209 with benign colorectal lesions (BCL), 111 with other cancers, and 186 healthy controls).</p><p><strong>Results: </strong>The CAR, PCT, and CEA in the CRC group were higher than those in the BCL, other cancers, and the healthy control group. However, Hb/RDW in the CRC group was lower than the other three groups. Moreover, there were significant differences in Hb/RDW and CEA among different T-N-M stages (all P< 0.05). Multivariate logistic regression showed that low level of Hb/RDW and high level of CAR, CEA, PCT were risk factors for CRC, and are correlated with CRC stage. Additionally, the area under the receiver operating characteristic curve (AUC) of Hb/RDW+CEA (AUC: 0.735), CAR+CEA (AUC: 0.748), PCT+CEA (AUC: 0.807) was larger than that of Hb/RDW (AUC: 0.503), CAR (AUC: 0.614), or PCT (AUC: 0.713) alone (all P< 0.001) in distinguishing CRC from BCL.</p><p><strong>Conclusions: </strong>Hb/RDW, CAR, PCT, and CEA are independent risk factors for CRC. Hb/RDW, CAR, and PCT combined with CEA have significant value for auxiliary differential diagnosis of CRC and BCL.</p>","PeriodicalId":56320,"journal":{"name":"Cancer Biomarkers","volume":" ","pages":"223-230"},"PeriodicalIF":3.1,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11091605/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139466763","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Rho GTPase-activating protein 4 is upregulated in Kidney Renal Clear Cell Carcinoma and associated with poor prognosis and immune infiltration.","authors":"Xuesong Xiao, Xiaofei Lv, Tianyu Lin, Jianqiao Li, Rui Wang, Shaoping Tian, Xinyu Liu, Shiming Liu, Huamao Jiang, Dan Yue, Yong Wang","doi":"10.3233/CBM-230388","DOIUrl":"10.3233/CBM-230388","url":null,"abstract":"<p><strong>Background: </strong>Kidney Renal Clear Cell Carcinoma (KIRC) is a malignant tumor that seriously threatens human health. Rho GTPase-activating protein 4 (ARHGAP4) plays an important role in the occurrence and development of tumors.</p><p><strong>Objective: </strong>The purpose of this study was to explore the role of ARHGAP4 in the progression of KIRC and its diagnostic and prognostic value.</p><p><strong>Methods: </strong>Multiple analytical methods and in vitro cell assays were used to explore the expression of ARHGAP4 and its value in the progression, diagnosis and prognosis of KIRC. The biological function of ARHGAP4 was studied by GO analysis and KEGG pathway analysis, and then the relationship between ARHGAP4 and immune infiltration was analyzed.</p><p><strong>Results: </strong>The expression of ARHGAP4 was significantly up-regulated in KIRC. We found that the high expression of ARHGAP4 was related to the progression of KIRC and suggested a poor prognosis. Compared with normal tissues, ARHGAP4 had a better diagnostic value in KIRC. The biological function of ARHGAP4 was related to immunity, and its expression was also closely related to tumor immune infiltration and immune checkpoints.</p><p><strong>Conclusions: </strong>Our study demonstrated that ARHGAP4 may be a biomarker, which is related to the progression, diagnosis and prognosis of KIRC. Its biological functions are related to tumor immune infiltration.</p>","PeriodicalId":56320,"journal":{"name":"Cancer Biomarkers","volume":" ","pages":"205-223"},"PeriodicalIF":2.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11307029/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141437861","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hypermethylation of the BRCA2 gene promoter and its co-hypermethylation with the BRCA1 gene promoter in patients with breast cancer.","authors":"Liliia Fishchuk, Zoia Rossokha, Olga Lobanova, Valeriy Cheshuk, Roman Vereshchako, Viktoriia Vershyhora, Nataliia Medvedieva, Olha Dubitskaa, Natalia Gorovenko","doi":"10.3233/CBM-230458","DOIUrl":"10.3233/CBM-230458","url":null,"abstract":"<p><strong>Background: </strong>The BRCA2 gene is an important tumour suppressor in breast cancer, and alterations in BRCA2 may lead to cancer progression. The aim of the study was to investigate the association of hypermethylation of the BRCA2 gene promoter and its co-hypermethylation with the BRCA1 gene promoter with the development and course of breast cancer in women.</p><p><strong>Methods: </strong>This study included 74 women with breast cancer (tumour tissue samples and peripheral blood) and 62 women without oncological pathology (peripheral blood) - control group.</p><p><strong>Results: </strong>Hypermethylation of the BRCA2 gene was significantly more frequently detected in the tumour tissue of women with breast cancer compared to their peripheral blood and peripheral blood of control subjects (p= 0.0006 and p= 0.00001, respectively). Hypermethylation of BRCA2 was more frequently detected in patients with breast cancer over the age of 50 and in patients with higher Ki67 expression levels (p= 0.045 and p= 0.045, respectively). There was a high frequency of unmethylated BRCA1 and BRCA2 gene combination in women of the control group compared to women with breast cancer, both in blood samples and tumour tissue samples (p= 0.014 and p= 0.00001, respectively).</p><p><strong>Conclusion: </strong>Our study confirms the hypothesis that BRCA2 hypermethylation plays an important role in the pathogenesis of breast cancer and the importance of assessing its co-hypermethylation with BRCA1 in predicting the course of the disease.</p>","PeriodicalId":56320,"journal":{"name":"Cancer Biomarkers","volume":" ","pages":"275-283"},"PeriodicalIF":2.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11380246/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142037853","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The paradoxical role of transforming growth factor-β in controlling oral squamous cell carcinoma development.","authors":"Ruiting Peng, Yun Huang, Ping Huang, Linyi Liu, Lei Cheng, Xian Peng","doi":"10.3233/CBM-230354","DOIUrl":"10.3233/CBM-230354","url":null,"abstract":"<p><p>Transforming growth factor-β (TGF-β) is a multifunctional cytokine that plays a vital role in regulating cell growth, differentiation and survival in various tissues. It participates in a variety of cellular processes, including cell apoptosis, cell migration and evasion, and plays a paradoxical role in tumor genesis and development. In the early stage of tumor, TGF-β inhibits the occurrence of tumor by inhibiting cell proliferation and regulating cell apoptosis. In the advanced stage of tumor, TGF-β promotes tumor development and affects prognosis by promoting cell survival and proliferation, cell migration and invasion, participates in immune escape, etc. In this article, we will review the paradoxical role of TGF-β on the occurrence and development of oral squamous cell carcinoma.</p>","PeriodicalId":56320,"journal":{"name":"Cancer Biomarkers","volume":"40 3-4","pages":"241-250"},"PeriodicalIF":2.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11380267/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142115486","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Circ_0049271 targets the miR-1197/PTRF axis to attenuate the malignancy of osteosarcoma.","authors":"Yixin Wen, Feng Xu, Hui Zhang","doi":"10.3233/CBM-230191","DOIUrl":"10.3233/CBM-230191","url":null,"abstract":"<p><strong>Background: </strong>Circular RNAs (circRNAs) perform key regulatory functions in osteosarcoma (OS) tumorigenesis. In this study, we aimed to explore the detailed action mechanisms of circ_0049271 in OS progression.</p><p><strong>Methods: </strong>Cell colony formation, cell counting kit-8, and transwell assays were performed to assess the proliferation and invasion of OS cells. Quantitative reverse transcription-polymerase chain reaction and western blotting were used to determine the expression levels of polymerase 1 and transcript release factor (PTRF), microRNA (miR)-1197, and circ_0049271 in OS cells. Furthermore, RNA immunoprecipitation and dual luciferase assays were conducted to explore the targeted relationships among PTRF, miR-1197, and circ_0049271. Finally, a tumor formation assay was conducted to determine the effects of circ_0049271 on in vivo tumor growth in mice.</p><p><strong>Results: </strong>High expression levels of miR-1197 and low levels of circ_0049271 and PTRF were observed in OS cells. circ _0049271 targeted miR-1197 to mediate PTRF expression. Moreover, the proliferation and invasion of OS cells were repressed by circ_0049271 or PTRF overexpression and increased by miR-1197 upregulation. Enforced circ_0049271 also impeded tumor growth in vivo. Upregulation of miR-1197 reversed the antitumor effects of circ_0049271 on OS progression in vitro; however, PTRF overexpression attenuated the cancer-promoting effects of miR-1197 on OS in vitro.</p><p><strong>Conclusions: </strong>Our findings revealed that circ_0049271 targeted the miR-1197/PTRF axis to attenuate the malignancy of OS, suggesting a potential target for its clinical treatment.</p>","PeriodicalId":56320,"journal":{"name":"Cancer Biomarkers","volume":" ","pages":"141-153"},"PeriodicalIF":2.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11321495/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140869425","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"GINS2 promotes the progression of human HNSCC by altering RRM2 expression.","authors":"Tianxiang Wang, Luxi Qian, Pingchuan Zhang, Mingyu Du, Jing Wu, Fanyu Peng, Chengyun Yao, Rong Yin, Li Yin, Xia He","doi":"10.3233/CBM-230337","DOIUrl":"10.3233/CBM-230337","url":null,"abstract":"<p><strong>Introduction: </strong>GINS2 exerts a carcinogenic effect in multiple human malignancies, while it is still unclear that the potential roles and underlying mechanisms of GINS2 in HNSCC.</p><p><strong>Methods: </strong>TCGA database was used to screen out genes with significant differences in expression in HNSCC. Immunohistochemistry and qRT-PCR were used to measure the expression of GINS2 in HNSCC tissues and cells. GINS2 was detected by qRT-PCR or western blot after knockdown or overexpression. Celigo cell counting, MTT, colony formation, and flow cytometric assay were used to check the ability of proliferation and apoptosis. Bioinformatics and microarray were used to screen out the downstream genes of GINS2.</p><p><strong>Results: </strong>GINS2 in HNSCC tissues and cells was up-regulated, which was correlated with poor prognosis. GINS2 gene expression was successfully inhibited and overexpressed in HNSCC cells. Knockdown of GINS2 could inhibit proliferation and increase apoptosis of cells. Meanwhile, overexpression of GINS2 could enhance cell proliferation and colony formation. Knockdown of RRM2 may inhibit HNSCC cell proliferation, while overexpression of RRM2 rescued the effect of reducing GINS2 expression.</p><p><strong>Conclusion: </strong>Our study reported the role of GINS2 in HNSCC for the first time. The results demonstrated that in HNSCC cells, GINS2 promoted proliferation and inhibited apoptosis via altering RRM2 expression. Therefore, GINS2 might play a carcinogen in HNSCC, and become a specific promising therapeutic target.</p>","PeriodicalId":56320,"journal":{"name":"Cancer Biomarkers","volume":" ","pages":"171-184"},"PeriodicalIF":2.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11307040/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140190468","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Serum aspartate aminotransferase, a novel potential biomarker of prognosis in extranodal natural killer/T cell lymphoma, nasal type.","authors":"Ningning Yao, Qing Hou, Yu Liang, Xin Cao, Bochen Sun, Lijuan Wei, Ruifang Sun, Jianzhong Cao","doi":"10.3233/CBM-230068","DOIUrl":"10.3233/CBM-230068","url":null,"abstract":"<p><strong>Background: </strong>Aspartate aminotransferase (AST), an indicator of liver cell damage, was related to the prognosis of certain malignant tumors.</p><p><strong>Objective: </strong>This study examined the predictive value of AST in patients with extranodal natural killer/T cell lymphoma (ENKTL).</p><p><strong>Methods: </strong>We reviewed 183 cases diagnosed with ENKTL and selected 26 U/L as the optimum cut-off value of AST. We used the univariate and multivariate Cox regression to compare the different AST groups' overall survival (OS) and progression-free survival (PFS).</p><p><strong>Results: </strong>Prior to propensity score matching (PSM), Kaplan-Meier analysis showed that patients in the low AST subgroup had better OS and PFS than the high AST subgroup. Multivariate analysis revealed that AST was an independent indicator for prognosis. After PSM, the low AST subgroup maintained a significantly better OS and PFS than the high AST subgroup.</p><p><strong>Conclusion: </strong>AST might represent a significant prognostic marker for ENKTL patients.</p>","PeriodicalId":56320,"journal":{"name":"Cancer Biomarkers","volume":" ","pages":"265-275"},"PeriodicalIF":2.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11191476/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138813954","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"KIF18A promotes cervical squamous cell carcinoma progression by activating the PI3K/AKT pathway through upregulation of CENPE.","authors":"Fengyi Sun, Tiantian Zhao","doi":"10.3233/CBM-240074","DOIUrl":"10.3233/CBM-240074","url":null,"abstract":"<p><strong>Background: </strong>Cervical cancer is a prevalent malignancy that significantly contributes to morbidity and mortality rates among women in developing nations. Although the association of KIF18A with various cancers has been established, its role in cervical squamous cell carcinoma (CESC) remains elusive.</p><p><strong>Methods: </strong>The KIF18A impact on the progression of CESC and its underlying mechanism were investigated through comprehensive bioinformatics analysis utilizing publicly available datasets. The levels of KIF18A and CENPE were assessed in clinical CESC samples through western blotting and qRT-PCR. To discover the role and molecular pathways of KIF18A in CESC, a combination of experimental approaches, including wound-healing, flow cytometry, CCK-8, and Transwell assay, were employed.</p><p><strong>Results: </strong>Our results demonstrate a significant KIF18A expression upregulation in CESC tissues in contrast to healthy tissues. In vitro, KIF18A upregulation was found to enhance cell growth, migration, and invasion and activate the PI3K/AKT signaling pathway while concurrently suppressing apoptosis. Conversely, downregulating KIF18A exhibited contrasting effects. Mechanistically, we observed a positive significant connection between KIF18A and CENPE in CESC cells.</p><p><strong>Conclusion: </strong>KIF18A promotes tumor growth in CESC by modulating the PI3K/AKT signaling pathway through regulation of CENPE, making it a potential biomarker for diagnosis and prognosis as well as a therapeutic target.</p>","PeriodicalId":56320,"journal":{"name":"Cancer Biomarkers","volume":" ","pages":"165-178"},"PeriodicalIF":2.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11492023/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142333424","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Glioma stem cells remodel immunotolerant microenvironment in GBM and are associated with therapeutic advancements.","authors":"Xifeng Fei, Jie Wu, Haiyan Tian, Dongyi Jiang, Hanchun Chen, Ke Yan, Yuan Wang, Yaodong Zhao, Hua Chen, Xiangtong Xie, Zhimin Wang, Wenyu Zhu, Qiang Huang","doi":"10.3233/CBM-230486","DOIUrl":"10.3233/CBM-230486","url":null,"abstract":"<p><p>Glioma is the most common primary tumor of the central nervous system (CNS). Glioblastoma (GBM) is incurable with current treatment strategies. Additionally, the treatment of recurrent GBM (rGBM) is often referred to as terminal treatment, necessitating hospice-level care and management. The presence of the blood-brain barrier (BBB) gives GBM a more challenging or \"cold\" tumor microenvironment (TME) than that of other cancers and gloma stem cells (GSCs) play an important role in the TME remodeling, occurrence, development and recurrence of giloma. In this review, our primary focus will be on discussing the following topics: niche-associated GSCs and macrophages, new theories regarding GSC and TME involving pyroptosis and ferroptosis in GBM, metabolic adaptations of GSCs, the influence of the cold environment in GBM on immunotherapy, potential strategies to transform the cold GBM TME into a hot one, and the advancement of GBM immunotherapy and GBM models.</p>","PeriodicalId":56320,"journal":{"name":"Cancer Biomarkers","volume":" ","pages":"1-24"},"PeriodicalIF":2.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11492047/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142141868","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}