Pathology, research and practice最新文献

{"title":"ALK-rearranged papillary thyroid carcinoma with a germline MEN1 mutation","authors":"Chao Li ,&nbsp;Hongjuan Zhang ,&nbsp;Yingmei Wang ,&nbsp;Ligang Chen ,&nbsp;Qingge Jia ,&nbsp;Mingyang Li","doi":"10.1016/j.prp.2025.156093","DOIUrl":"10.1016/j.prp.2025.156093","url":null,"abstract":"<div><h3>Background</h3><div>Papillary thyroid carcinoma (PTC) is the most common type of thyroid cancer. The 5th edition of the World Health Organization (WHO) Classification of Thyroid Tumors divides PTC into 13 distinct morphological subtypes based on its morphological characteristics. According to molecular features, thyroid cancer is classified into RAS-like and BRAF-like tumors.</div></div><div><h3>Case presentation</h3><div>Here, we present a case of ALK-rearranged papillary thyroid carcinoma (ALK-PTC) with a germline mutation in the MEN1 gene. Next-generation sequencing (NGS) detected an EML4-ALK fusion gene and a germline MEN1 mutation in this case, accompanied by a rare intragenic inversion of the ALK gene.</div></div><div><h3>Conclusion</h3><div>Here we report the first case in the world of PTC with EML4-ALK fusion, accompanied by intragenic inversion of the ALK gene and germline mutation of the MEN1 gene.</div></div>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":"272 ","pages":"Article 156093"},"PeriodicalIF":2.9,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144502418","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":"Exploring alkaloids and flavonoids from natural sources: Emerging natural agents for inhibiting cervical cancer progression through apoptosis induction, anti-inflammatory effects, and oxidative stress reduction","authors":"Yumei Chen ,&nbsp;Denghua Yu ,&nbsp;Dongwei Zhu ,&nbsp;Selvaraj Muthusamy ,&nbsp;Mangirish Deshpande ,&nbsp;Natarajan Kiruthiga ,&nbsp;Panneerselvam Theivendren ,&nbsp;Kanagaraj Rajalakshmi ,&nbsp;Siyi Wu ,&nbsp;Chengdong Zhu","doi":"10.1016/j.prp.2025.156092","DOIUrl":"10.1016/j.prp.2025.156092","url":null,"abstract":"<div><div>Cervical cancer stands as one of the major causes which result in death due to cancer in female patients all over the world. The treatment measures such as chemotherapy and radiations are still producing unfavourable side effects that are also limiting their efficacies in treatment. The capability of alkaloids and flavonoid to target cellular mechanisms that lead to the development of cancer cells has been investigated through research studies. This review study evaluates the mechanism of action of alkaloids in combination with flavonoids derived in various plant species to prevent the progression of cervical cancer. The bioactive constituents exhibit appealing therapeutic effects as they induce apoptosis and reduce inflammation and neutralize oxidative stress. Berberine and sanguinarine alkaloids as well as quercetin and kaempferol flavonoid exhibit cervical cancer cells-damaging apoptotic effects and inhibit inflammation by regulating inflammatory cytokines and strengthening antioxidant defense. The capability of these compounds to modulate PI3K/Akt and NF-kB and MAPK and p53 signaling pathways implies that they can be developed into non-toxic therapeutic options to be used in cases of cervical cancer. Mechanistic insights and clinical evidence of the use of alkaloids and flavonoids in the management of cervical cancer are reviewed and their suitability as natural products in cancer therapeutic intervention considered.</div></div>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":"272 ","pages":"Article 156092"},"PeriodicalIF":2.9,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144513495","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":"Adenoid cystic carcinoma of the breast: Molecular profiling updates and multidimensional detection of MYB","authors":"Yingyue Wu,&nbsp;Jia Luo,&nbsp;Xiangfei Zeng,&nbsp;Wendie Yu,&nbsp;Zhang Zhang,&nbsp;Bing Wei","doi":"10.1016/j.prp.2025.156091","DOIUrl":"10.1016/j.prp.2025.156091","url":null,"abstract":"<div><div>Adenoid cystic carcinoma (AdCC) of the breast is a rare and distinctive subset of breast cancer that presents significant diagnostic challenges due to its histological diversity and poorly defined molecular traits. AdCC is characterized by the <em>MYB-NFIB</em> fusion, which leads to MYB overexpression and activation of oncogenic downstream pathways, constituting a key disease mechanism. Fluorescence in situ hybridization (FISH) to detect <em>MYB</em> rearrangement has become a critical tool for diagnosing this tumor. However, emerging evidence suggests <em>MYB</em> activation in breast AdCC occurs through multiple mechanisms beyond <em>MYB</em> rearrangements, with several recurrently mutated genes contributing to tumorigenesis. This molecular heterogeneity challenges the diagnostic reliability of FISH-based MYB testing alone. For clinical researchers and practitioners dealing with breast AdCC, a current and thorough understanding of its molecular attributes and diagnostic approaches is essential. This review synthesizes recent advances in breast AdCC molecular genetics, encompassing <em>MYB/MYBL1</em> rearrangements or amplifications, NOTCH pathway gene mutations, and chromatin remodeling gene alterations. We critically evaluate contemporary methodologies for MYB assessment and discuss their clinical implications.</div></div>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":"272 ","pages":"Article 156091"},"PeriodicalIF":2.9,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144502420","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":"Clinical insights into the mechanisms of infectious microbes and microbiota in chronic neurologic and psychiatric diseases","authors":"Md. Faysal ,&nbsp;Mehrukh Zehravi ,&nbsp;Md Al Amin ,&nbsp;Safia Obaidur Rab ,&nbsp;Patibandla Jahnavi ,&nbsp;Uppuluri Varuna Naga Venkata Arjun ,&nbsp;Jeetendra Kumar Gupta ,&nbsp;Abdul Ajeed Mohathasim Billah ,&nbsp;Rajeshwar Vodeti ,&nbsp;P. Dharani Prasad ,&nbsp;Sultan Saeed Sultan Aseri ,&nbsp;Falak A. Siddiqui ,&nbsp;Talha Bin Emran","doi":"10.1016/j.prp.2025.156090","DOIUrl":"10.1016/j.prp.2025.156090","url":null,"abstract":"<div><div>Chronic neurologic and psychiatric diseases such as schizophrenia, depression, Parkinson's, and Alzheimer's are increasingly linked to infectious microorganisms and gut microbiota. This review explores how pathogenic microorganisms and microbial communities impact neuropsychiatric, neurodegenerative, and neuroinflammatory processes, highlighting the gut-brain axis' crucial communication network in influencing behavior and brain function. Infectious agents like bacteria, viruses, and fungi cause disease by causing neurotoxic reactions, disrupting the blood-brain barrier, and activating neuroinflammatory cascades. Gut dysbiosis impacts immunological homeostasis and neural transmission by altering the synthesis of metabolites from microorganisms, such as short-chain fatty acids and neurotransmitter precursors. Neurodegeneration and psychiatric diseases are influenced by molecular mechanisms such as toll-like receptor signaling, microglial activation, and mitochondrial dysfunction. This review highlights the potential of microbiota-targeted treatments such as probiotics, prebiotics, and microbiome transplantation as novel treatments for chronic diseases. Understanding the intricate interactions between infectious microorganisms, microbiota, and the central nervous system enables the formation of precision medicine strategies to challenge the rising incidence of neurologic and psychiatric diseases. Future research should explore causal relationships and identify specific microbial biomarkers to enhance early diagnosis, prevention, and personalized treatment plans.</div></div>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":"272 ","pages":"Article 156090"},"PeriodicalIF":2.9,"publicationDate":"2025-06-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144364523","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":"Clinicopathological significance of identifying glypican 3 -positive gastric cancer","authors":"Hai-fen Ma ,&nbsp;Zi-ning Li ,&nbsp;Jun-qiang Li ,&nbsp;Min Wang ,&nbsp;Wei-hua Xiao ,&nbsp;Peng Shu ,&nbsp;Xiao-hai Shi","doi":"10.1016/j.prp.2025.156089","DOIUrl":"10.1016/j.prp.2025.156089","url":null,"abstract":"<div><h3>Objective</h3><div>The aim of this study was to investigate the expression of Glypican 3 (GPC3) in gastric cancer and to identify clinicopathological prognostic factors associated with GPC3-positive gastric cancer (GPC3-GC).</div></div><div><h3>Methods</h3><div>Gene expression and survival differences of GPC3 were analyzed by the TCGA-STAD database and immunohistochemical detection in the gastric adenocarcinoma tissues.</div></div><div><h3>Results</h3><div>Bioinformatic analysis revealed that the GPC3 gene was highly expressed in gastric adenocarcinoma tissues (P &lt; 0.05), and Univariate Cox regression analysis further demonstrated that the hazard ratio (HR) for GPC3 was 1.8 (95% CI: 1.3-2.5) (P &lt; 0.001). Among the 218 cases of gastric adenocarcinoma tissue samples in this study, the positive rate of GPC3 was 17.0 % (37/218), increasing to 53.6 % (15/28) in cases with elevated serum AFP. Liver metastasis is more common in GPC3-positive gastric cancer (P &lt; 0.001). GPC3-positive was more prevalent in adenocarcinomas with hepatoid or enteroblastic differentiation, depth of T3 + T4, clinical TNM stage III+IV (all P &lt; 0.05). The Kaplan-Meier results revealed significant differences between the GPC3-negative and GPC3-positive groups (P &lt; 0.001). However, no significant difference was found between GPC3-focal and diffuse tumors (P &gt; 0.05). Cox regression analyses identified GPC3-positive as a risk factor affecting postoperative prognosis in gastric adenocarcinoma (P &lt; 0.001). However, GPC3 can’t serve as a prognostic indicator independent of other indicators (P &gt; 0.05).</div></div><div><h3>Conclusion</h3><div>GPC3 is expressed in some cases of gastric adenocarcinoma, particularly in cancers with elevated serum AFP levels, providing a potential basis for clinical monitoring and exploring new immunotherapy targets. GPC3-GC often exhibits strong invasive and metastatic capabilities and may carry a poor prognosis, especially in cases with enteroblastic differentiation and elevated serum AFP. Therefore, it is crucial to enhance awareness and differentiate GPC3-GC from common adenocarcinoma.</div></div>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":"272 ","pages":"Article 156089"},"PeriodicalIF":2.9,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144329632","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":"TREM-1 as a potential biomarker for malignant transformation risk in oral leukoplakia: Insights from bioinformatics and dual immunofluorescence analysis","authors":"Na Zhao ,&nbsp;Guocheng Mei ,&nbsp;Qiaozhi Jiang ,&nbsp;Yuchen Huang ,&nbsp;Yi Chen ,&nbsp;Ziqing Liu ,&nbsp;Shuai Wang ,&nbsp;Renchuan Tao","doi":"10.1016/j.prp.2025.156088","DOIUrl":"10.1016/j.prp.2025.156088","url":null,"abstract":"<div><h3>Background</h3><div>Oral leukoplakia (OLK) is a precancerous lesion of oral squamous cell carcinoma (OSCC), but its malignant transformation mechanisms remain unclear. This study investigates TREM-1’s role in OLK progression through bioinformatics and pathological validation, highlighting its potential as a prognostic biomarker for malignant transformation</div></div><div><h3>Methods</h3><div>TREM-1 expression in OLK was analyzed using Kaplan–Meier and Cox regression based on public datasets identified it as an independent risk factor Cox regression based on GEO clinical data. Single-cell RNA sequencing identified macrophages as the primary TREM-1-expressing cells. Dual-label immunofluorescence was performed on 69 OLK and 63 control tissues to validate TREM-1 expression and its co-localization with CD68. Statistical analysis included non-parametric tests, chi-square tests, and multivariate Cox regression to assess associations with malignant transformation. Significance was defined as p &lt; 0.05.</div></div><div><h3>Results</h3><div>Kaplan–Meier analysis showed that high TREM-1 expression was significantly associated with OLK malignant transformation (p = 0.007), and Cox regression based on public datasets identified it as an independent risk factor (HR = 2.702, p = 0.032). Single-cell RNA sequencing revealed macrophages as the main TREM-1-expressing cells. Immunofluorescence confirmed elevated TREM-1 expression in OLK macrophages compared to controls. In 69 clinical samples, chi-square analysis supported a significant association with malignant transformation, though this was not confirmed by Cox regression.</div></div><div><h3>Conclusions</h3><div>This study suggests that TREM-1 may be involved in OLK malignant transformation through macrophages. Although its expression is not related to dysplasia severity, it could serve as a biomarker for assessing the cancerous transformation</div></div>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":"272 ","pages":"Article 156088"},"PeriodicalIF":2.9,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144364722","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":"From EGFR mutations to STAT30-driven resistance in NSCLC: Biomarkers and multi-modal treatment approach","authors":"Surya Nath Pandey ,&nbsp;Kavita Goyal ,&nbsp;Mohit Rana ,&nbsp;Soumya V. Menon ,&nbsp;Subhashree Ray ,&nbsp;Mandeep Kaur ,&nbsp;Swati Sharma ,&nbsp;Abida Khan","doi":"10.1016/j.prp.2025.156087","DOIUrl":"10.1016/j.prp.2025.156087","url":null,"abstract":"<div><div>Non–small-cell lung cancer (NSCLC) accounts for approximately 85 % of lung cancer cases and remains the leading cause of cancer mortality worldwide. However, the emergence of drug resistance and tumor immune evasion limits long-term treatment efficacy and reduces overall patient survival. We examine how activating EGFR mutations or overexpression induce STAT3 phosphorylation and regulate transcription factors such as Snail, Twist, and ZEB1. Next, we critically evaluate therapies ranging from first- to third-generation EGFR tyrosine kinase inhibitors and novel STAT3 antagonists to immune checkpoint inhibitors. Although numerous preclinical studies demonstrate synergistic activity when EGFR-TKIs are combined with STAT3 inhibitors or ICIs, clinical trial data remain sparse and preliminary. Preclinical studies of Polyphyllin I and MTI31 illustrate the reversal of epithelial-mesenchymal transition and restoration of sensitivity to EGFR-targeted agents. In contrast to previous reviews, we offer a comparative analysis of monotherapy versus combination regimens, highlight remaining knowledge gaps, and propose an integrated framework for co-targeting EGFR, STAT3, and immune checkpoints. We aim to elucidate EGFR–STAT3 signaling crosstalk in NSCLC and distinguish preclinical findings from clinical data to enhance the translational relevance of combination therapies.</div></div>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":"272 ","pages":"Article 156087"},"PeriodicalIF":2.9,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144313426","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":"Dedifferentiated liposarcoma exhibiting myxoid liposarcoma-like morphology with DDIT3 co-amplifcation and STAT6 nuclear expression","authors":"Bohui Zhang,&nbsp;Hong Li,&nbsp;Zhixing Cao,&nbsp;Huihui Cao","doi":"10.1016/j.prp.2025.156086","DOIUrl":"10.1016/j.prp.2025.156086","url":null,"abstract":"<div><div>Dedifferentiated liposarcoma (DDLPS) arises from atypical lipomatous tumor/well-differentiated liposarcoma (ALT/WDLPS) through progression into non-lipogenic sarcomas of varying histological grades, driven by amplification of the chromosome 12q13-15 region containing <em>MDM2, CDK4, DDIT3, STAT6, GLI1, HMGA2,</em> etc. DDLPS demonstrates marked morphological heterogeneity in its dedifferentiated components. We describe two DDLPS cases featuring a prominent arborizing vascular network, myxoid stroma, and STAT6 nuclear expression—features that complicate differentiation from solitary fibrous tumors (SFT), myxoid liposarcoma (MLPS), myxofibrosarcoma (MFS), <em>GLI1</em>-altered tumors, low-grade fibromyxoid sarcoma (LGFMS), soft tissue angiofibroma (STA), etc. Immunohistochemistry (IHC) confirmed STAT6 overexpression, while fluorescence in situ hybridization (FISH) revealed co-amplification of <em>MDM2</em> and <em>DDIT3</em>. <em>STAT6</em> amplification in DDLPS leads to detectable protein expression by IHC. <em>DDIT3</em> amplification in select WDLPS/DDLPS cases correlates with such unique MLPS-like morphology. These observations imply that analogous mechanisms may involve other genes within the 12q13-15 region, underscoring the genomic and phenotypic heterogeneity of DDLPS. Tumor diagnosis requires integrating morphological assessment, immunohistochemistry, molecular testing, clinical context, and imaging findings rather than relying on isolated genetic or immunohistochemical markers. This represents the first reported instance of DDLPS with MLPS-like morphology accompanied by <em>MDM2</em> and <em>DDIT3</em> co-amplification and concurrent STAT6 nuclear expression.</div></div>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":"272 ","pages":"Article 156086"},"PeriodicalIF":2.9,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144321291","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 the Nrf2 pathway in inhibiting ferroptosis in kidney disease and its future prospects","authors":"Jia-Yuan Huang,&nbsp;Hai-ning Yu","doi":"10.1016/j.prp.2025.156084","DOIUrl":"10.1016/j.prp.2025.156084","url":null,"abstract":"<div><div>Kidney disease (KD) has gradually become a major social and economic burden on the healthcare system. Recent studies highlight ferroptosis as a critical mechanism in the progression of these conditions. Recognized for its essential role in renal pathogenesis, ferroptosis is attracting increasing research attention and emerging as a key focus of investigation. The Nrf2 signaling pathway, known for its regulatory influence on ferroptosis, plays a central role in this context. Activation of the nuclear factor E2-related factor 2 (Nrf2) pathway and the subsequent attenuation of ferroptosis present substantial opportunities as novel therapeutic targets for managing kidney injury (KI). This article summarizes the latest mechanism of action of the Nrf2 pathway in ferroptosis, explores how the Nrf2 pathway affects ferroptosis in KD therapy, and investigates the potential therapeutic effects of natural products targeting the Nrf2 pathway. These natural products have been shown to inhibit ferroptosis through the Nrf2 pathway, providing new insights and therapeutic strategies for the clinical and individualized management of KD.</div></div>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":"272 ","pages":"Article 156084"},"PeriodicalIF":2.9,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144291078","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":"Integration of machine learning in biomarker discovery for esophageal squamous cell carcinoma: Applications and future directions","authors":"Wanli Yang ,&nbsp;Lili Duan ,&nbsp;Xinhui Zhao ,&nbsp;Liaoran Niu ,&nbsp;Chenyang Wang ,&nbsp;Daiming Fan ,&nbsp;Liu Hong","doi":"10.1016/j.prp.2025.156083","DOIUrl":"10.1016/j.prp.2025.156083","url":null,"abstract":"<div><h3>Purpose</h3><div>Recent advancements in sequencing technologies and bioinformatics algorithms have facilitated significant breakthroughs in both fundamental and clinical tumor research. Nevertheless, the processing and utilization of large-scale data continue to pose substantial challenges. Machine learning (ML)-based integrative analysis methods present a novel approach for navigating these complex datasets, thereby enhancing the understanding of tumors from multiple perspectives.</div></div><div><h3>Methods</h3><div>Here, we present a comprehensive overview of ML processes and methodologies that have the potential to advance research and management of esophageal squamous cell carcinoma (ESCC). Specifically, our focus is on their application in key areas such as early detection, prognosis prediction, therapeutic target identification, and drug discovery. Additionally, we examine the challenges and opportunities that ML introduces in the context of ESCC research.</div></div><div><h3>Results</h3><div>Our findings indicate that ML techniques have the capacity to enhance medical decision-making, improve patient care, and drive progress in healthcare. The prospective integration of ML in oncology poses several challenges, highlighting the need for interdisciplinary collaboration. Addressing these challenges will require coordinated efforts from medical professionals, data scientists, information technology specialists, and policymakers.</div></div><div><h3>Conclusions</h3><div>The identification of biomarkers for ESCC via ML significantly enhances the quality of medical care and supports expert diagnostic and therapeutic decision-making, thereby markedly improving diagnostic efficiency and advancing the field of intelligent healthcare.</div></div>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":"272 ","pages":"Article 156083"},"PeriodicalIF":2.9,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144280222","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}