Pathology, research and practice最新文献

{"title":"A subgroup of anaplastic thyroid carcinomas harbors MET alterations with potential therapeutic options","authors":"Sarah Theurer ,&nbsp;Hans-Ulrich Schildhaus ,&nbsp;Thomas Herold ,&nbsp;Tim Brandenburg ,&nbsp;Dagmar Führer-Sakel ,&nbsp;Hideo Andreas Baba ,&nbsp;Marc Ingenwerth ,&nbsp;Sabrina Borchert","doi":"10.1016/j.prp.2025.156240","DOIUrl":"10.1016/j.prp.2025.156240","url":null,"abstract":"<div><div>Anaplastic thyroid carcinoma (ATC) is a rare but biologically aggressive thyroid cancer with fatal clinical outcome and limited therapeutic options. Molecular studies of ATCs have described several genetic alterations leading to FDA approval of inhibitor therapy targeting <em>BRAFV600E</em>, <em>NTRK</em>, <em>ALK</em> and <em>RET</em>. <em>MET</em> alterations have been described in single cases, which have not yet led to approval for inhibitor therapy, although approval for these alterations in other tumors, such as lung cancer, already exist. Aim of this study was to provide an overview of MET alterations in ATC, highlighting their potential therapeutic relevance. In this study, a total of 28 ATCs were examined using <em>MET</em> immunohistochemistry (IHC), fluorescence in situ hybridization (FISH), and both RNA- and DNA-based next-generation sequencing. Molecular findings were correlated with tumor morphology as well as clinical follow-up data. Three ATC samples (10 %) revealed <em>MET</em> alterations, namely top-level gene amplification (defined by an average gene count ≥10.0) and <em>ETV6-MET</em> fusion. Concomitant <em>MET</em> protein overexpression was demonstrated by IHC. One case without a detectable <em>MET</em> alteration showed IHC-positivity in &gt; 50 % of the tumor cells with strong staining intensity. Two top-level amplified samples expressed the same chimeric <em>CAPZA2–MET</em> fusion transcript, which we interpret as a biological byproduct rather than a true molecular driver. DNA sequencing did not reveal any activating <em>MET</em> mutations including exon 14 skipping. <em>MET</em> alterations were here mutually exclusive with driver mutations in <em>BRAF</em>, <em>RAS</em>, and <em>PIK3CA</em>, but co-occurred with <em>TP53</em> mutations and <em>TERT</em> promoter mutations. <em>MET</em> alterations in ATC have been poorly described to date. Herein, we present the first structured evaluation of a series of ATCs focusing on <em>MET</em> gene alterations, including gene amplification, immunohistochemical expression, and gene fusions. Our results confirm that <em>MET</em> top-level amplifications (detected by fluorescence in situ hybridization, FISH) and <em>MET</em> gene fusions (detected by RNA-based NGS) occur in a subgroup of ATCs. As these alterations are druggable in other cancers, early molecular testing may identify <em>MET</em>-positive ATCs eligible for anti-<em>MET</em> therapies in clinical trials. We recommend RNA-based sequencing and FISH as biomarker assays to identify <em>MET</em> alterations.</div></div>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":"275 ","pages":"Article 156240"},"PeriodicalIF":3.2,"publicationDate":"2025-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145158496","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Phosphaturic mesenchymal tumors: A pathological perspective","authors":"Xianglin Mei ,&nbsp;Meiying Li","doi":"10.1016/j.prp.2025.156242","DOIUrl":"10.1016/j.prp.2025.156242","url":null,"abstract":"<div><div>Phosphaturic mesenchymal tumors (PMTs) are a rare group of neoplasms most commonly associated with tumor-induced osteocalcin (TIO), a paraneoplastic syndrome that profoundly impairs quality of life. Because the clinical manifestations are nonspecific, diagnosis is often delayed. PMTs are characterized by recurrent molecular alterations, most notably <em>FN1::FGFR1</em> and <em>KL</em> (Klotho/α-Klotho) rearrangements. Tumor cells secrete fibroblast growth factor 23 (FGF23), which disrupts phosphate homeostasis and results in hypophosphatemia, thereby causing bone pain, fragility fractures, and skeletal deformities. Advanced imaging techniques play a central role in localizing the tumor, while complete surgical resection remains the most effective curative approach. Pathological evaluation provides the diagnostic gold standard; however, both clinical and histological features are heterogeneous, and the criteria for malignancy are not yet well defined. Furthermore, the biological significance of tumor margins remains an open question. This review summarizes the clinical presentation, molecular pathogenesis, pathological features, diagnostic strategies, therapeutic options, and prognostic implications of PMTs, highlighting current challenges and areas for future investigation.</div></div>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":"275 ","pages":"Article 156242"},"PeriodicalIF":3.2,"publicationDate":"2025-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145200742","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The microbiota–gut–brain axis theory: A new perspective to unlock the pathological mechanism of constipation","authors":"Meiyu Wan,&nbsp;Weijie Liu,&nbsp;Ying Liu,&nbsp;Xiaohan Jiang,&nbsp;Shu Jiang,&nbsp;Jinao Duan","doi":"10.1016/j.prp.2025.156236","DOIUrl":"10.1016/j.prp.2025.156236","url":null,"abstract":"<div><div>Constipation, a common gastrointestinal system disease, has a variety of side effects, but its pathogenesis is diverse and complex. Thus, its treatment is affected by a variety of factors, such as intestinal flora imbalance, nervous system problems (cerebrovascular disease, cognitive impairment or dementia, Parkinson’s disease) and other pathological diseases (hypothyroidism, hypercalcemia and others). With the rise of the microbiota-gut-brain (MGB) axis theory, people's understanding and treatment methods for gastrointestinal diseases such as constipation have also undergone significant changes. Therefore, this paper focuses on the MGB axis and constipation, including the 3 main regulatory pathways of this axis, the gut microbial metabolites and the regulation of neurotransmitters, and the methods and applications of treating constipation and other diseases on the basis of this axis. Further clarification of the pathways and influencing factors related to the MGB axis will help elucidate the pathophysiological mechanisms of constipation and play a key role in the rational treatment of human gastrointestinal diseases.</div></div>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":"275 ","pages":"Article 156236"},"PeriodicalIF":3.2,"publicationDate":"2025-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145200673","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to 'Implication of biosignatures in the progression of endometriosis' [Pathol.-Res. Pract. 254 (2024) 155103].","authors":"Anuja Pant, Kareena Moar, Taruna K Arora, Pawan Kumar Maurya","doi":"10.1016/j.prp.2025.156238","DOIUrl":"https://doi.org/10.1016/j.prp.2025.156238","url":null,"abstract":"","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":" ","pages":"156238"},"PeriodicalIF":3.2,"publicationDate":"2025-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145114016","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Triazolo-indazole-trione-mediated disruption of Wnt/β-catenin pathway drives both autophagic and paraptotic cell deaths in colorectal cancer cells","authors":"Kachigere B. Harsha ,&nbsp;Min Hee Yang ,&nbsp;Darshini Gowda ,&nbsp;Chakrabhavi Dhananjaya Mohan ,&nbsp;Kanchugarakoppal S. Rangappa ,&nbsp;Kwang Seok Ahn","doi":"10.1016/j.prp.2025.156237","DOIUrl":"10.1016/j.prp.2025.156237","url":null,"abstract":"<div><div>Aberrant activation of the Wnt/β-catenin signaling pathway is a hallmark of numerous human cancers, including colorectal carcinoma. Targeting this pathway has been shown to effectively induce cancer cell death and inhibit tumor progression. In this study, we investigated the anti-tumor effects of HR10, a novel synthetic compound, in colorectal carcinoma cells. HR10 significantly suppressed cell viability in HCT-116, HCT-15, HT-29, and SNU-C2A cells while having minimal impact on normal colon cells. Mechanistically, HR10 induced autophagy by upregulating Atg7, p-Beclin-1, and Beclin-1, and triggered paraptosis through the downregulation of Alix, a key inhibitor of this process. Additionally, HR10 increased reactive oxygen species (ROS) levels, disrupted mitochondrial membrane potential, and activated ER stress by elevating ATF4 and CHOP expression. Moreover, HR10 inhibited the Wnt/β-catenin pathway by downregulating β-catenin, Wnt3a, and FZD-1, while enhancing β-TrCP and p-GSK3β (Tyr216). Knockdown of β-catenin further confirmed that HR10-mediated autophagy and paraptosis were directly associated with the suppression of the Wnt/β-catenin signaling cascade. These results highlight the dual mechanisms of autophagy and paraptosis induction, positioning HR10 as a promising therapeutic candidate for colorectal cancer. Overall, our findings demonstrate that HR10 effectively targets the Wnt/β-catenin signaling pathway, inducing autophagic and paraptotic cell death, and providing a potential therapeutic strategy for colorectal carcinoma.</div></div>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":"275 ","pages":"Article 156237"},"PeriodicalIF":3.2,"publicationDate":"2025-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145096138","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Microbiota in cancer care: Clinical prospects","authors":"Peng Li-Hua ,&nbsp;Ousman Bajinka","doi":"10.1016/j.prp.2025.156235","DOIUrl":"10.1016/j.prp.2025.156235","url":null,"abstract":"<div><h3>Background</h3><div>Probiotics and microbial metabolites exhibit dual roles in cancer biology, serving as both therapeutic agents and biomarkers. <em>Lactobacillus</em> species inhibit pathogen-driven tumorigenesis and predict immunotherapy efficacy, yet their depletion correlates with polycystic ovary syndrome (PCOS) and gastrointestinal cancers. Conversely, expansion of specific strains, such as <em>L. plantarum</em> 299 v, enhances iron absorption and mitigates mucositis. Similarly, <em>Bifidobacterium</em> modulates gut microbiota (GM) toward tumor suppression in colorectal cancer (CRC) and improves pediatric outcomes, though paradoxically rising in refractory multiple myeloma. Short-chain fatty acids (SCFAs) acetate, propionate, and butyrate protect against CRC via anti-inflammatory and epigenetic mechanisms, while <em>Akkermansia muciniphila</em> enhances immunotherapy responses in CRC and NSCLC through GM–tumor microenvironment crosstalk.</div></div><div><h3>Objective</h3><div>This mini review aimed to decipher the prospects of macromolecules in their role as anti cancer based on human clinical trials.</div></div><div><h3>Interventions</h3><div>Interventions include multi-strain probiotics, synbiotics, and dietary strategies (Mediterranean diets, fermented foods) that restore GM balance and boost SCFA production.</div></div><div><h3>Limitations</h3><div>Limitations persist on strain-specific variability, biomarker ambiguity, and inconsistent efficacy of probiotics in radiotherapy-induced diarrhea.</div></div><div><h3>Recommendation</h3><div>To address these, precision medicine approaches prioritizing strain-specific formulations, validated biomarkers, and combination therapies are advocated. Personalized nutrition and clinical tools further optimize outcomes.</div></div><div><h3>Conclusion</h3><div>Future research must clarify <em>Akkermansia</em>-TMAO interactions, SCFA epigenetic dynamics, and combinatorial regimens to harness microbiota–host crosstalk. By integrating advanced analytics and population-tailored strategies, microbiota-targeted interventions hold transformative potential in cancer prevention, therapy, and diagnostics.</div></div>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":"275 ","pages":"Article 156235"},"PeriodicalIF":3.2,"publicationDate":"2025-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145096102","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mutational landscape of glomus tumor and clinical application of genomic profiling based on next-generation sequencing technology","authors":"Minying Deng ,&nbsp;Huimei Wang ,&nbsp;Weiyu Pan ,&nbsp;Rongkui Luo ,&nbsp;Xing Li ,&nbsp;Ayizimugu Abuduwaili ,&nbsp;Lei Xu ,&nbsp;Xiaolei Zhang ,&nbsp;Jieakesu Su ,&nbsp;Jie Huang ,&nbsp;Chen Xu ,&nbsp;Yingyong Hou","doi":"10.1016/j.prp.2025.156230","DOIUrl":"10.1016/j.prp.2025.156230","url":null,"abstract":"<div><div>Glomus tumor (GT) is a rare tumor with incompletely understood biological behavior and molecular genetic characteristics. This study aimed to comprehensively detect genetic mutations in GT using next-generation sequencing (NGS) and correlate these findings with clinical and pathological features to provide new insights into the pathogenesis and precision diagnosis of GT. A total of 171 somatic single nucleotide variants (SNVs) were identified in 44 GT samples, including 114 nonSynonymous_Substitution, 36 Intronic, 11 FrameShift_Duplication, 4 FrameShift_Deletion, 3 Splicing, and 3 Nonsense_Mutation events. The most frequent mutation type was G-A transition. Commonly mutated genes included <em>BCL2L11</em>, <em>MUC16</em>, <em>KRAS</em>, and <em>BCR</em>. Most copy number variations (CNVs) were losses; gains were observed only in <em>CDK4</em> (4/44, 9.1 %) and <em>CDK6</em> (3/44, 6.8 %) and were limited to benign and atypical GT. There is a significant correlation between high TMB and <em>KRAS</em>, <em>TP53</em> mutations. Pathway enrichment analysis revealed <em>KRAS</em> mutations were predominant in distal GT, while <em>BRAF V600E</em> mutations were more prevalent in proximal locations. Atypical/malignant GTs may be associated with the epithelial-mesenchymal transition pathway. Tumor microenvironment gene typing in 51 GTs suggested a tendency for cold tumors to occur more frequently in male patients (<em>P</em> = 0.0686). This study represents the first comprehensive exploration of the molecular genetic characteristics of GT using NGS technology, which provides an initial overview of the genetic mutation landscape in GT.</div></div>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":"275 ","pages":"Article 156230"},"PeriodicalIF":3.2,"publicationDate":"2025-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145096140","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of WNT signaling in papillary thyroid cancer: Mechanisms, epigenetic regulation, therapeutic resistance, and emerging clinical strategies","authors":"Zhongqiang Li ,&nbsp;Dongxia Lv ,&nbsp;Lingjuan Niu ,&nbsp;Yacun Wan ,&nbsp;Junli Li","doi":"10.1016/j.prp.2025.156231","DOIUrl":"10.1016/j.prp.2025.156231","url":null,"abstract":"<div><div>WNT signaling is a key pathway that regulates cell growth, differentiation, and tissue balance. In papillary thyroid cancer (PTC), abnormal activation of both canonical (β-catenin-dependent) and non-canonical pathways contributes to tumor progression and therapy resistance. These mechanisms include reduced response to radioactive iodine (RAI), kinase inhibitors, and immunotherapies. This review outlines how WNT dysregulation drives processes such as epithelial–mesenchymal transition (EMT), cancer stem cell (CSC) plasticity, and crosstalk with major oncogenic pathways, including mitogen-activated protein kinase (MAPK), phosphoinositide 3-kinase/protein kinase B (PI3K/AKT), and transforming growth factor-β (TGF-β). We also examine the role of the tumor microenvironment (TME), where factors like fibroblast-derived cytokines and hypoxia reinforce WNT-driven resistance. Epigenetic modifiers, exosomal WNT ligands, and noncoding RNAs emerge as additional regulators. Finally, we discuss clinical implications, highlighting the value of WNT biomarkers in trials and the potential of combining WNT inhibition with RAI sensitization, MAPK blockade, or immune checkpoint therapy.</div></div>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":"275 ","pages":"Article 156231"},"PeriodicalIF":3.2,"publicationDate":"2025-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145096113","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Taming hyper-active Cdk5: Disrupting the Cdk5–p25 axis as a therapeutic avenue for neurodegeneration and beyond","authors":"Emadeldin M. Kamel ,&nbsp;Sulaiman A. Alsalamah ,&nbsp;Sally Mostafa Khadrawy ,&nbsp;Noha A. Ahmed ,&nbsp;Faris F. Aba Alkhayl ,&nbsp;Al Mokhtar Lamsabhi","doi":"10.1016/j.prp.2025.156234","DOIUrl":"10.1016/j.prp.2025.156234","url":null,"abstract":"<div><div>Cyclin-dependent kinase 5 (Cdk5) is essential for neuronal development and synaptic function when activated by its physiological cofactors p35 and p39. Pathological calpain cleavage of p35 generates the more stable fragment p25, producing a hyperactive, mislocalized kinase complex that has been implicated in tau hyperphosphorylation, DNA damage, neuroinflammation, and aberrant neuronal cell-cycle re-entry. Three decades of work position the Cdk5–p25 axis as a convergent pathogenic mechanism in Alzheimer’s disease and related dementias, Parkinson’s disease, traumatic brain injury, and in subsets of metabolic and solid-tumor contexts. High-resolution structures of Cdk5–p25 reveal a distinctive activation-loop “cradle” and a tract leading toward catalytic Lys33 that enable structure-guided inhibitor design. Recent advances include (i) small molecules that “vector” toward Lys33 and achieve ∼70–125 × selectivity over closely related CDKs in biochemical assays, (ii) brain-penetrant peptide disruptors that preferentially inhibit Cdk5–p25 while sparing basal Cdk5–p35 signaling in rodent models, and (iii) early-stage degradation or genetic approaches (e.g., dual-target PROTACs; calpain-resistant p35 or Cdk5 knockdown) that reduce p25 signaling or Cdk5 levels in cells. Across inducible mouse models, toxin paradigms, and tumor xenografts, interventions that blunt the p25-driven switch ameliorate cognitive deficits, preserve dopaminergic neurons, improve insulin secretion in β-cell models, and slow tumor growth, respectively. Key translational challenges include achieving durable brain exposure, defining the long-term safety of partial kinase suppression, establishing fluid biomarkers for human studies, and anticipating compensatory signaling. Multiple mechanistic classes are in preclinical development, placing precise disruption of Cdk5–p25 on a credible path toward clinical testing across neurology, oncology, and metabolic disease.</div></div>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":"275 ","pages":"Article 156234"},"PeriodicalIF":3.2,"publicationDate":"2025-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145086105","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Non-coding RNA methylation modifications in ovarian cancer","authors":"Siyun Deng ,&nbsp;Ziyi Guo ,&nbsp;Shaojia Wang ,&nbsp;Siyu Cao ,&nbsp;Jiayuan Huang ,&nbsp;Yanli Li","doi":"10.1016/j.prp.2025.156232","DOIUrl":"10.1016/j.prp.2025.156232","url":null,"abstract":"<div><div>Ovarian cancer (OC) is a highly heterogeneous gynecological cancer with high mortality rates. Non-coding RNA is a class of transcripts which do not encode proteins, but plays important regulatory roles in gene expression and protein function by targeting specific genes or interacting with proteins. RNA methylation, mainly focused on m6A, m1A, m5C, and m7G, is a common post-transcriptional modification that is essential for regulating various biological processes, such as RNA transcription, splicing, structure, stability, and translation, and has been reported to be involved in the regulation of the development of various human malignancies. Recent scholarly inquiries have posited that methylation alterations occur on ncRNAs, implicating their involvement in the etiology of ovarian cancer. In this review, we summarized four common types of RNA methylation modifications and their associated enzymes, as well as methylated ncRNAs involved in regulating ovarian cancer. We briefly introduced the mechanisms of action of ncRNA methylation in the occurrence, proliferation, immune response, and drug resistance of ovarian cancer as reported currently, and the methylation-related lncRNAs that can be further studied.</div></div>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":"275 ","pages":"Article 156232"},"PeriodicalIF":3.2,"publicationDate":"2025-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145118400","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}