Oncology Research最新文献

{"title":"Developing a prognostic signature and characterizing the tumor microenvironment based on centrosome-related genes in lung adenocarcinoma.","authors":"Lingjie Xu, Yiqin Xia, Qin Qin, Guiqun Wang, Kai Tao, Wei Wei","doi":"10.32604/or.2025.056176","DOIUrl":"10.32604/or.2025.056176","url":null,"abstract":"<p><strong>Background: </strong>The centrosome, a crucial cellular structure involved in the mitotic process of eukaryotic cells, plays a significant role in tumor progression by regulating the growth and differentiation of neoplastic cells. This makes the centrosome a promising target for therapeutic strategies in cancer treatment.</p><p><strong>Methods: </strong>Utilizing data from the TCGA database, we identified centrosome-related genes and constructed a prognostic model for 518 lung adenocarcinoma patients. Prognosis-associated genes were initially screened using univariate Cox regression, with overfitting minimized by applying LASSO regression to remove collinearity. Finally, a set of 12 genes was selected through multivariable Cox regression for inclusion in the prognostic model.</p><p><strong>Results: </strong>The model's performance was assessed using ROC curve analysis, demonstrating a robust predictive ability with an AUC of 0.728 in the training group and 0.695 in the validation group. Differential expression analysis between high-risk (HRLAs) and low-risk (LRLAs) individuals was performed, followed by enrichment analyses using KEGG, GO, Progeny, GSVA, and GSEA. These analyses revealed significant differences in immune-related pathways between the two groups. Immune microenvironment assessment through ssGSEA and ESTIMATE indicated that individuals with poor prognosis exhibited lower immune, stromal, and ESTIMATE scores, along with higher tumor purity, suggesting an impaired immune microenvironment in HRLAs patients. Drug susceptibility analysis and molecular docking showed that HRLAs individuals were more responsive to docetaxel, emphasizing the therapeutic relevance of paclitaxel in this cohort.</p><p><strong>Conclusion: </strong>We successfully developed and validated a centrosome-associated gene-based prognostic model, offering clinicians valuable insights for improved decision-making and personalized treatment strategies. This model may facilitate the identification of high-risk patients and guide therapeutic interventions in lung adenocarcinoma.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 7","pages":"1649-1666"},"PeriodicalIF":2.0,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12215551/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560720","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":"Tumor-expressing PD-L1 regulates NT5E expression through MAPK/ERK pathway in triple-negative breast cancer.","authors":"Cheng Cheng, Chao Shi, Shang Wu, Weixing Wu, Jingping Li, Sinuo Gao, Meng Han, Yimin Wang, Xiangmei Zhang, Yunjiang Liu","doi":"10.32604/or.2025.061637","DOIUrl":"10.32604/or.2025.061637","url":null,"abstract":"<p><strong>Objectives: </strong>While programmed cell death 1 (PD-1) inhibitors have improved cancer treatment, the function and mechanisms of programmed cell death ligand 1 (PD-L1), particularly when expressed by cancer cells, remain unclear. This study aims to explore the role of PD-L1 within breast cancer cells and identify key targets for future immunotherapy.</p><p><strong>Methods: </strong>RNA-seq was performed on breast cancer cells with silenced PD-L1 to screen for differentially expressed genes, followed by bioinformatics analysis. Clinical specimens from breast cancer patients undergoing primary surgery without preoperative treatment were collected, along with <i>in vitro</i> analysis to validate the potential mechanism.</p><p><strong>Results: </strong>RNA-seq data revealed a significant positive correlation between Ecto-5'-nucleotidase (NT5E) expression and PD-L1. Bioinformatics analysis corroborated this positive correlation. Immunohistochemistry staining demonstrated higher NT5E expression associated with increased lymph node metastasis. High expression of the NT5E gene was associated with poor overall survival (OS) in breast cancer patients, as determined by KM plotter analysis. Following PD-L1 gene silencing by siRNA in breast cancer cells, NT5E mRNA and protein expression significantly decreased. Conversely, no significant changes were observed in PD-L1 expression after NT5E gene silencing. <i>In vitro</i> experiments confirmed that cancer cell proliferation and metastasis abilities were significantly reduced by either PD-L1 or NT5E gene down-regulation. Western blotting demonstrated that PD-L1 expressed by cancer cells regulates NT5E expression through the MAPK/ERK signaling pathway.</p><p><strong>Conclusion: </strong>This study proposes a potential mechanism wherein tumor-expressing PD-L1 regulates NT5E through the MAPK/ERK pathway. Down-regulation of PD-L1 or NT5E can significantly inhibit the proliferation and metastatic ability of cancer cells, potentially providing practical therapeutic targets and prognostic markers for combined PD-L1 immunotherapy in breast cancer.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 7","pages":"1633-1648"},"PeriodicalIF":2.0,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12215589/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560656","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":"Immune landscape of neoadjuvant chemoradiotherapy: involvement of MAL, a T-cell differentiation protein.","authors":"Kosei Nakajima, Yoshinori Ino","doi":"10.32604/or.2025.063419","DOIUrl":"10.32604/or.2025.063419","url":null,"abstract":"<p><strong>Background: </strong>Neoadjuvant/preoperative therapy (NAT) involves the administration of chemotherapy, with or without radiation, prior to surgical resection. This approach is commonly used for locally advanced tumors to reduce tumor volume, improve resectability, and minimize the need for extensive surgical procedures. While NAT has been shown to be effective in inducing local anti-tumor immunity in potentially resectable solid tumors, the underlying molecular mechanisms remain poorly understood.</p><p><strong>Methods: </strong>Cohort samples from pancreatic cancer patients who underwent NAT (n = 26) and those who did not (n = 20) were analyzed. Changes in the immune microenvironment induced by NAT were assessed using stratified bioinformatic approaches, including heatmap analysis of immune-related genes selected via Gene Ontology, Gene Set Enrichment Analysis (GSEA) with the immunologic signature database, and Ingenuity Pathway Analysis (IPA). Findings were further validated through immunohistochemical analysis.</p><p><strong>Results: </strong>A comprehensive, stratified evaluation integrating pathological and bioinformatic approaches revealed that NAT induced the upregulation of 212 genes, including DC-SIGN (CD209), and activated 13 immune-associated pathways, such as T-cell receptor (TCR) signaling. Additionally, NAT promoted an increased shift toward CD8 (+) T-cell populations through the upregulation of MAL (T-cell differentiation protein). Immunohistochemical analysis further confirmed a significant accumulation of DC-SIGN (+) dendritic cells and MAL (+) lymphocytes in NAT-treated patients.</p><p><strong>Conclusions: </strong>NAT enhances anti-tumor immunity by promoting CD8 (+) T-cell generation through the activation of DC-SIGN (+) dendritic cells and MAL (+) lymphocytes. This study is the first to report an increase in MAL (+) lymphocytes following NAT. Given its potential significance, further investigation in other solid tumors treated with NAT is warranted.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 7","pages":"1769-1779"},"PeriodicalIF":2.0,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12215608/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560724","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":"CORRECTION: MiR-150-5p Inhibits Cell Proliferation and Metastasis by Targeting FTO in Osteosarcoma.","authors":"Lichen Xu, Pan Zhang, Guiqi Zhang, Zhaoliang Shen, Xizhuang Bai","doi":"10.32604/or.2024.061279","DOIUrl":"10.32604/or.2024.061279","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.32604/or.2024.047704),.].</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 7","pages":"1797-1798"},"PeriodicalIF":2.0,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12215563/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560718","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":"Synergistic anticancer and antibacterial effects of novel regimens of phytopolyphenols and repurposing drugs on cultured cells.","authors":"Ya-Ling Yeh, Ying-Jan Wang, Shoei-Yn Lin-Shiau","doi":"10.32604/or.2025.063717","DOIUrl":"10.32604/or.2025.063717","url":null,"abstract":"<p><strong>Background: </strong>The increasing incidence of cancers and infectious diseases worldwide presents a significant public health challenge that requires immediate intervention. Our strategy to tackle this issue involves the development of pharmaceutical formulations that combine phytopolyphenols (P), targeted drugs (T), and metal ions (M), collectively referred to as PTM regimens. The diverse pharmacological properties of PTM regimens are hypothesized to effectively reduce the risk factors associated with both cancers and infectious diseases.</p><p><strong>Methods: </strong>The effects of the pharmaceutical agents on the proliferation of cultured cancer cells and pathogens were assessed after 72 h and 48 h, respectively, using the MTT (3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide) assay and optical density at 600 nm (OD600). The synergistic effects of drug combinations were evaluated by combination index (CI), where CI < 1 indicates synergism, CI = 1 indicates addition, and CI > 1 indicates antagonism. Efficacy index (EI) was also calculated. Assays of efflux pump ATPase activities were conducted using a colorimetric method.</p><p><strong>Results: </strong>This study evaluated the anticancer and antibacterial efficacy of PTM regimens that included phytopolyphenols (specifically curcumin (C) and green tea polyphenols (G)), repurposed drugs (memantine (Mem), thioridazine (TRZ), cisplatin (Cis), and 5-fluorouracil (5FU)), and ZnSO₄ (Zn) across three cultured cancer cell lines and four cultured pathogens. The most effective regimens, GC•Mem•Zn and GC•TRZ•Zn, significantly enhanced the anticancer efficacy (EI) of cisplatin across the three cancer lines (OECM-1, A549 and DLD-1) by 7, 11 and 21; 7, 9, and 17 fold, respectively, while the enhancements for 5-fluorouracil were 5, 6 and 12; 5, 5 and 9 fold, respectively. Furthermore, these PTM regimens demonstrated substantial synergistic inhibition of Na⁺-K⁺-Mg²⁺-ATPase and Mg²⁺-ATPase in the cultured cancer cells, as well as a reduction in biofilm formation by the four cultured pathogens, suggesting their potential to address the challenges of multidrug resistance in cancers and infectious diseases.</p><p><strong>Conclusion: </strong>Given that all drugs incorporated in the PTM regimens have been clinically validated for safety and efficacy, particularly regarding their synergistic selective anticancer efficacy, inhibition of efflux pump ATPase, and antibiofilm formation of pathogens, these regimens may offer a promising therapeutic strategy to alleviate the severe side effects and drug resistance typically associated with chemotherapeutic agents. Further preclinical and clinical investigations are warranted.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 7","pages":"1781-1796"},"PeriodicalIF":2.0,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12215547/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560655","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":"circACTN4 promotes breast cancer cell cycle progression and oncogenesis via c-MYC induced histone H4 acetylation.","authors":"Kefan Liu, Xiaosong Wang, Xin Yang, Bowen Shi, Lei Xing, Junxia Chen","doi":"10.32604/or.2025.061721","DOIUrl":"10.32604/or.2025.061721","url":null,"abstract":"<p><strong>Background: </strong>Accumulating studies have shown the important role of circular RNAs (circRNAs) in the oncogenesis and metastasis of various cancers. We previously reported that circACTN4 could bind with FUBP1 to promote tumorigenesis and the development of breast cancer (BC) by increasing the expression of MYC. However, its exact molecular mechanism and biological function have not been fully elucidated.</p><p><strong>Methods: </strong>Here, Circular RNA microarray analysis was conducted in 3 pairs of BC and paracancerous tissues. The expression of circACTN4 in BC cells and tissues was detected via reverse transcription‒quantitative PCR (RT‒qPCR). Cell Counting Kit-8 (CCK-8), 5-ethynyl-2-deoxyuridine (EdU), transwell migration, and invasion assays were performed to further detect the biological functions of circACTN4 in BC cells. Xenograft models were used to investigate the <i>in vivo</i> role of circACTN4. Fluorescence <i>in situ</i> hybridization, Chromatin immunoprecipitation (ChIP)‒qPCR, coimmunoprecipitation, fluorometric, western blot, and rescue experiments were performed to explore the mechanism of circACTN4.</p><p><strong>Results: </strong>Our results revealed that circACTN4 was highly expressed in BC cells and tissues. The upregulated expression of circACTN4 was significantly related to the T stage and TNM stage and poor prognosis of patients with BC. circACTN4 was located primarily in the nucleus of BC cells. Upregulation of circACTN4 significantly increased the proliferation, invasion, and growth of BC cells, whereas the downregulation of circACTN4 exerted the opposite effects and induced G1/S cell cycle arrest. Mechanistically, we showed that circACTN4 could upregulate the expression of MYC and that MYC might interact with TIP60 histone acetyltransferase to increase the recruitment of TIP60 to MYC target genes and histone H4 acetylation (AcH4), thus promoting the progression of the breast cancer cell cycle and tumorigenesis.</p><p><strong>Conclusion: </strong>Taken together, our findings reveal for the first time a new mechanism by which circACTN4 could promote oncogenesis and the development of BC by increasing the AcH4 of MYC target genes via TIP60. Therefore, circACTN4 could be a novel target for BC diagnosis and remedy.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 7","pages":"1709-1722"},"PeriodicalIF":2.0,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12215574/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560715","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":"Drug discovery in advanced and recurrent endometrial cancer: Recent advances.","authors":"Alex A Francoeur, Natalie Ayoub, Danielle Greenberg, Krishnansu S Tewari","doi":"10.32604/or.2025.061120","DOIUrl":"10.32604/or.2025.061120","url":null,"abstract":"<p><p>Endometrial cancer is the most common gynecologic cancer diagnosed in the United States and mortality is on the rise. Advanced and recurrent endometrial cancer represents a treatment challenge as historically there have been limited therapeutic options for patients. In the last several years, multiple practice-changing clinical trials have led to significant improvements in the treatment landscape. This review will cover updates in the treatment and management of advanced and recurrent endometrial cancer with a focus on novel therapeutics, such as anti-PD-L1 and PD-1 inhibitors, poly ADP-ribose polymerase (PARP) inhibitors, antibody-drug conjugates, and hormonal therapy.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 7","pages":"1511-1530"},"PeriodicalIF":2.0,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12215578/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560721","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":"N6-Methyladenosine Promotes the Transcription of c-Src Kinase via IRF1 to Facilitate the Proliferation of Liver Cancer.","authors":"Yanxi Peng, Honggen Yuan, Zhanjie Jiang, Xiaoqing Ou, Qian Zhang, Kexin Yi, Yanbin Meng, Qun Xie","doi":"10.32604/or.2025.062747","DOIUrl":"10.32604/or.2025.062747","url":null,"abstract":"<p><strong>Background: </strong>Expression of mRNA is widely regulated by N6-methyladenosine (m⁶A). An increasing number of studies have shown that m⁶A methylation, facilitated by methyltransferase 3 (METTL3), is crucial in the progression of tumors. Previous reports have indicated the involvement of both METTL3 and c-Src kinase in the evolution of liver cancer. However, the potential connection between c-Src and the METTL3-mediated mechanism in liver cancer progression remains elusive.</p><p><strong>Methods: </strong>The correlation expression between c-Src and METTL3 between liver cancer patients and the control group was analyzed using the TCGA database, and was further demonstrated by Western blot and RT-qPCR. The functional roles of c-Src in METTL3-regulated liver cancer progression were investigated by cell proliferation assays and colony formation assays. The regulatory mechanism of METTL3 in c-Src expression was accessed by RNA-immunoprecipitation (RIP)-qPCR.</p><p><strong>Results: </strong>We demonstrated that c-Src kinase promoted liver cancer development, and the expression of <i>SRC</i> (encodes c-Src kinase) was positively correlated with METTL3 in liver cancer cases. We showed that <i>SRC</i> mRNA could be m⁶A-modified, and METTL3 regulated the transcription of <i>SRC</i> mRNA through interferon regulatory factor 1 (IRF1). We revealed that IRF1, the expression of which was positively regulated by METTL3, was a novel transcription factor of c-Src. Lastly, The pro-proliferative effect of METTL3 on hepatocellular carcinoma was mechanistically linked to IRF1/c-Src axis activation, as evidenced by our experimental data.</p><p><strong>Conclusion: </strong>Results suggested that the METTL3/IRF1/c-Src axis played potential oncogenic roles in liver cancer development and the axis may be a promising therapeutic target in the disease.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 7","pages":"1679-1693"},"PeriodicalIF":2.0,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12215556/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560649","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":"Oncolytic virus therapy in hepatocellular carcinoma.","authors":"Yuyu Ye, Ying Liu","doi":"10.32604/or.2025.061857","DOIUrl":"10.32604/or.2025.061857","url":null,"abstract":"<p><p>Liver cancer is the fifth most common cancer in the world, with China bearing a disproportionate burden of cases. Typically diagnosed at advanced stages, liver cancer often utilizes surgical treatments such as resection, transcatheter hepatic artery chemoembolization (TACE), and radiofrequency ablation. However, advancements in genetic engineering and tumor immunology have unveiled the distinct potential of targeted oncolytic virus therapy. Oncolytic virus, in particular, can selectively destroy tumor cells without harming normal cells, offering a promising avenue for liver cancer treatment through immune system activation, tumor microenvironment modulation, and other mechanisms. This review describes the mechanism of action of oncolytic viruses, the new development of several common oncolytic viruses, and the combination with traditional therapies, aiming to provide directions for the subsequent therapeutic research on hepatocellular carcinoma (HCC).</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 7","pages":"1593-1610"},"PeriodicalIF":2.0,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12215577/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560650","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":"Lynch syndrome and colorectal cancer: A review of current perspectives in molecular genetics and clinical strategies.","authors":"Raquel Gómez-Molina, Raquel Martínez, Miguel Suárez, Ana Peña-Cabia, MARíA CONCEPCIóN Calderón, Jorge Mateo","doi":"10.32604/or.2025.063951","DOIUrl":"10.32604/or.2025.063951","url":null,"abstract":"<p><p>Lynch syndrome (LS), also known as hereditary non-polyposis colorectal cancer (HNPCC), is an inherited condition associated with a higher risk of colorectal cancer (CRC) and other cancers. It is caused by germline mutations in DNA mismatch repair (MMR) genes, including <i>MLH1, MSH2, MSH6</i> and <i>PMS2</i>. These mutations lead to microsatellite instability (MSI) and defective DNA repair mechanisms, resulting in increased cancer risk. Early detection of LS is crucial for effective management and cancer prevention. Endoscopic surveillance, particularly regular colonoscopy, is recommended for individuals with LS to detect CRC at early stages. Additionally, universal screening of CRC for MMR deficiency can help identify at-risk individuals. Genetic counseling plays a valuable role in LS by guiding patients and their families in understanding the genetic basis, making informed decisions regarding surveillance and prevention, and offering reproductive options to reduce the transmission of pathogenic variants of the offspring. The aim of this review is to outline current strategies for the diagnosis, surveillance, and management of LS, with a focus on the role of genetic counseling, endoscopic screening, and emerging therapeutic approaches to mitigate cancer risk in affected individuals.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 7","pages":"1531-1545"},"PeriodicalIF":2.0,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12215587/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560648","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}