Cancer Genomics & Proteomics最新文献

{"title":"Elevated <i>Stanniocalcin-1</i> Expression in Uveal Melanoma Predicts Poor Patient Prognosis.","authors":"Shin-Nosuke Yamashita, Yoshiatsu Tanaka, Shajedul Islam, Honoka Kotake, Maki Tanaka, Takao Kitagawa, Kazuhiro Tokuda, Durga Paudel, Sarita Giri, Tohru Ohta, Fumiya Harada, Hiroki Nagayasu, Yasuhiro Kuramitsu","doi":"10.21873/cgp.20526","DOIUrl":"https://doi.org/10.21873/cgp.20526","url":null,"abstract":"<p><strong>Background/aim: </strong>Uveal melanoma (UVM) is the most prevalent primary intraocular malignancy, accounting for 3-5% of all melanomas. Despite its rarity, particularly in Japan (~2 cases per 100,000 individuals annually), UVM exhibits highly aggressive behavior, with nearly 50% of patients developing distant metastases. Once metastasized, the prognosis remains dismal, with a median survival of only 4-5 months. Identifying prognostic biomarkers and potential therapeutic targets is imperative to improve clinical outcomes. Stanniocalcin-1 (STC-1) is a glycoprotein hormone implicated in calcium and phosphate homeostasis. Recent studies have linked <i>STC-1</i> overexpression to tumor progression, poor prognosis, and increased metastatic potential in various malignancies. However, the prognostic significance and mechanistic role of STC-1 in UVM remain unexplored.</p><p><strong>Materials and methods: </strong>To elucidate the clinical relevance of <i>STC-1</i> in UVM, we analyzed publicly available transcriptomic datasets using GEPIA2 and UALCAN, assessing <i>STC-1</i> mRNA expression across disease stages and its correlation with patient survival. In parallel, single-cell RNA sequencing (scRNA-seq) datasets were utilized to identify the cellular sources of <i>STC-1</i> within the UVM tumor microenvironment and to investigate its association with specific functional cellular states.</p><p><strong>Results: </strong><i>STC-1</i> expression was significantly up-regulated in stage IV UVM tumors compared to stage III (<i>n</i>=4 and 36, respectively). Moreover, elevated <i>STC-1</i> expression was inversely correlated with overall survival, suggesting its potential role in disease progression. scRNA-seq analysis revealed that <i>STC-1</i> is expressed by both tumor cells and fibroblasts, indicating a possible cooperative mechanism that may drive tumor progression.</p><p><strong>Conclusion: </strong>These findings suggest that <i>STC-1</i> serves as a potential prognostic biomarker in UVM, providing novel insights into its role in tumor biology. Further investigation is warranted to explore its therapeutic implications and mechanistic contributions to UVM progression.</p>","PeriodicalId":9516,"journal":{"name":"Cancer Genomics & Proteomics","volume":"22 4","pages":"624-631"},"PeriodicalIF":2.6,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144504902","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":"Serum Proteomic Signatures of Pregnancy-associated Breast Cancer.","authors":"Anna-Maria Korakiti, Eleni Zografos, Stavros C Proikakis, Alkistis-Maria Papatheodoridi, Kleoniki Apostolidou, Constantinos G Zografos, Dimitrios Maniatis, Christos Stefanou, Spyridon Marinopoulos, Constantine Dimitrakakis, Grigorios Xepapadakis, George T Tsangaris, Meletios-Athanasios Dimopoulos, Flora Zagouri","doi":"10.21873/cgp.20524","DOIUrl":"https://doi.org/10.21873/cgp.20524","url":null,"abstract":"<p><strong>Background/aim: </strong>Pregnancy-associated breast cancer (PABC) is one of the most frequently diagnosed pregnancy-related malignancies, characterized by a notably rising incidence. Data remain scarce in the literature regarding the molecular nature and pathophysiology of PABC. Proteomic analyses are known to reflect cellular functions more accurately when compared to genomic or transcriptomic studies.</p><p><strong>Materials and methods: </strong>In the present study, two-dimensional gel electrophoresis and matrix-assisted laser desorption ionization time-of-flight mass spectrometry were employed to identify differentially expressed serum proteins among five patients with PABC, five matched (according to age, histological type and stage) non-pregnant patients diagnosed with BC, and five healthy pregnant controls.</p><p><strong>Results: </strong>A panel of 53 differentially expressed (>1.5-fold) proteins with diverse biological roles and various functional interactions was identified among the three groups examined in our study. Of the 53 differentially expressed proteins, 23 proteins were identified in the PABC group, 8 proteins in the non-PABC group, and 22 proteins in healthy pregnant controls. Many of the proteins differentially expressed in patients with PABC were involved in biological processes known to be deregulated in carcinogenesis, such as metabolism (<i>e.g</i>., apolipoprotein-E, and apolipoprotein-A1) and immune system regulation (<i>e.g</i>., complement factor B, and defensin-5).</p><p><strong>Conclusion: </strong>Differential proteomic expression was detected in PABC-derived serum samples, implying distinct PABC molecular features that require further investigation. The identification of PABC proteomic signatures provides significant insight into PABC pathophysiology and offers novel targets for early diagnosis and optimal treatment.</p>","PeriodicalId":9516,"journal":{"name":"Cancer Genomics & Proteomics","volume":"22 4","pages":"592-610"},"PeriodicalIF":2.6,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144504907","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":"Noggin Promotes Cell Proliferation Through Up-regulating EGFR/HER2 in Pancreatic Cancer Cells.","authors":"Ming Liu, Karl Chan, Amy Bancroft, Fiona Ruge, Chunyi Hao, Wen G Jiang, Lin Ye","doi":"10.21873/cgp.20522","DOIUrl":"https://doi.org/10.21873/cgp.20522","url":null,"abstract":"<p><strong>Background/aim: </strong>Noggin is a secreted antagonist of bone morphogenetic proteins (BMPs) and plays a key role in regulating various developmental and homeostatic biological processes. BMPs have been linked to the development of several types of cancers. However, the impact of Noggin on cellular functions and its role in pancreatic cancer remain unclear. This study aimed to investigate the role of Noggin in pancreatic cancer and its underlying molecular mechanisms.</p><p><strong>Materials and methods: </strong>Noggin expression in both normal and cancerous pancreatic tissues was assessed using both quantitative and conventional PCR methods, alongside an analysis of publicly available gene expression array datasets. Correlations between Noggin expression and patient survival, TNM staging, tumor/stroma subtypes, and the expression of other cancer-related genes were examined. The influence of Noggin on cellular functions was evaluated in pancreatic cancer cell lines Mia PaCa-2 and PANC-1, which were genetically modified to overexpress Noggin.</p><p><strong>Results: </strong>Noggin expression was found to be significantly higher in tumor tissues compared to normal pancreatic tissues. Elevated Noggin expression was associated with shorter overall survival in patients. Overexpression of Noggin led to increased proliferation of pancreatic cancer cells. Furthermore, elevated levels of EGFR and HER2 proteins were observed in the PANC-1 and Mia PaCa-2 cell lines, respectively. Treatment with EGFR and HER2 inhibitors reduced Noggin-induced proliferation in these cell lines.</p><p><strong>Conclusion: </strong>Noggin is overexpressed in pancreatic cancer tissues and is linked to poor patient survival. Noggin promotes the proliferation of pancreatic cancer cells by up-regulating EGFR and HER2.</p>","PeriodicalId":9516,"journal":{"name":"Cancer Genomics & Proteomics","volume":"22 4","pages":"564-574"},"PeriodicalIF":2.6,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144504904","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":"CRISPR/Cas9-mediated Knockout of <i>LYVE1</i> In Human Tongue Cancer Cells Reveals Transcriptomic Changes in Metastasis-associated Pathways.","authors":"Sini Karinen, Johanna Forero-Rodríguez, Annika Järvinen, Kari K Eklund, Goncalo Barreto, Abdelhakim Salem","doi":"10.21873/cgp.20519","DOIUrl":"https://doi.org/10.21873/cgp.20519","url":null,"abstract":"<p><strong>Background/aim: </strong>Tongue squamous cell carcinoma (TSCC), a highly aggressive subtype of head and neck cancers, is characterized by frequent lymphatic metastasis and poor prognosis. Recently, we showed that lymphatic vessel endothelial hyaluronan receptor 1 (LYVE-1) is involved in TSCC progression, yet the underlying molecular mechanisms remain unclear.</p><p><strong>Materials and methods: </strong>CRISPR/Cas9 gene editing was employed to generate <i>LYVE1</i> knockout (KO) TSCC cell lines. Single-cell clones were isolated, screened, and validated through sequencing and Inference of CRISPR Edits (ICE) analysis and qRT-PCR. RNA sequencing was performed on <i>LYVE1</i> KO and wild-type (WT) cells to identify differentially expressed genes (DEGs). Bioinformatic analyses, including Gene Ontology (GO) enrichment and protein-protein interaction (PPI) network mapping, were conducted to explore affected pathways. Finally, network topology was examined using NetworkAnalyzer and cytoHubba plugins.</p><p><strong>Results: </strong>Transcriptomic analysis revealed significant down-regulation of pro-metastatic pathways, including epithelial-mesenchymal transition (EMT), extracellular matrix remodeling, and immune modulation. DEG analysis identified 263 genes, with key down-regulated targets such as <i>WNT5A</i>, <i>TGFB2</i>, and <i>MMP2</i>, and up-regulation of tumor-suppressive genes including <i>PTGS2</i>. GO and PPI analyses highlighted <i>LYVE1</i>'s pivotal role in regulating cell adhesion, migration, and immune response.</p><p><strong>Conclusion: </strong><i>LYVE1</i> KO reduces TSCC invasive potential by disrupting EMT and tumor-stroma interactions, aligning with previous experimental findings. These results suggest <i>LYVE1</i> as a critical driver of metastasis, highlighting its potential as a therapeutic target.</p>","PeriodicalId":9516,"journal":{"name":"Cancer Genomics & Proteomics","volume":"22 4","pages":"525-537"},"PeriodicalIF":2.6,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144504901","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":"Particulate Matter 2.5 Induces FGFR1-mediated Integrin Switch to Promote Non-small Cell Lung Cancer Metastasis.","authors":"Nithikoon Aksorn, Zin Zin Ei, Korrakod Petsri, Narumon Phaonakrop, Chalermpong Saenjum, Sittiruk Roytrakul, Pithi Chanvorachote","doi":"10.21873/cgp.20527","DOIUrl":"https://doi.org/10.21873/cgp.20527","url":null,"abstract":"<p><strong>Background/aim: </strong>Particulate matter 2.5 (PM2.5) is known to adversely affect human health. While its involvement in lung cancer pathogenesis is recognized, its specific impact on metastasis-related behaviors of lung cancer cells remains largely unexplored.</p><p><strong>Materials and methods: </strong>In this study, we employed cell culture models, proteomic analysis, and bioinformatic analysis. Target proteins and signaling pathways were validated using western blotting and immunofluorescence assay. Wound healing, transwell migration and phalloidin-rhodamine assays were used to determine the migratory activity.</p><p><strong>Results: </strong>Proteomic analysis identified 3,795 proteins in both control and PM2.5-treated groups. Among these, proteins associated with metastasis, particularly those related to \"cell migration\" (GO: 0016477), were highlighted, identifying six key proteins involved in cancer metastasis. Protein-protein interaction analysis pinpointed fibroblast growth factor receptor 1 (FGFR1) as a central target influenced by PM2.5, which promoted cell migration <i>via</i> the Rap1 signaling pathway through integrin signaling. The enhanced migratory behavior of PM2.5-treated cells aligned with proteomic findings, demonstrating that PM2.5 exposure increases the motility of lung cancer cells. Western blotting and immunofluorescence confirmed that PM2.5 exposure led to up-regulation of FGFR1, integrin αV, β1, and activated p-Akt. Notably, PM2.5-treated cells exhibited significantly increased motility and a higher number of filopodia per cell.</p><p><strong>Conclusion: </strong>These results indicate that FGFR1 is a crucial target in PM2.5-induced metastasis in lung cancer cells, operating through an FGFR1/integrin/Akt signaling axis. This study advances our understanding of the role of PM2.5 in lung cancer metastasis and suggests potential therapeutic strategies to mitigate cancer progression.</p>","PeriodicalId":9516,"journal":{"name":"Cancer Genomics & Proteomics","volume":"22 4","pages":"632-653"},"PeriodicalIF":2.6,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144504905","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":"Prognostic Significance of <i>EZH2</i>-Related Gene Variants in Patients With Prostate Cancer Undergoing Androgen Deprivation Therapy.","authors":"Shu-Pin Huang, Bo-Ying Bao, Ta-Hsien Chuang, Chao-Yuan Huang, Chia-Cheng Yu, Victor C Lin, Te-Ling Lu, Yei-Tsung Chen","doi":"10.21873/cgp.20525","DOIUrl":"https://doi.org/10.21873/cgp.20525","url":null,"abstract":"<p><strong>Background/aim: </strong>Prostate cancer remains a major global health burden, with treatment resistance posing a significant challenge. Enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2), a histone methyltransferase, is frequently overexpressed in prostate cancer, contributing to tumor progression and castration resistance. Clinical trials of EZH2 inhibitors may have therapeutic benefits. This study aimed to evaluate the impact of genetic variants in <i>EZH2</i>-related genes on survival outcomes in prostate cancer.</p><p><strong>Patients and methods: </strong>We conducted a genetic association study evaluating 76 single nucleotide polymorphisms (SNPs) across 10 <i>EZH2</i>-related genes in 630 patients with prostate cancer undergoing androgen deprivation therapy (ADT). Functional analyses, including gene ontology and pathway enrichment assessments, were performed to elucidate the biological significance of key genes across multiple datasets.</p><p><strong>Results: </strong><i>DNMT3A</i> rs77993651 was significantly associated with both cancer-specific survival [hazard ratio (HR)=0.82, <i>p</i>=0.042] and overall survival (HR=0.80, <i>p</i>=0.011). Functional annotation indicated that rs77993651 resides within enhancer histone marks, potentially regulating <i>DNMT3A</i> expression. Elevated <i>DNMT3A</i> expression was observed in prostate tumor tissues and correlated with more aggressive features and shorter progression-free survival. Gene set enrichment analysis revealed that <i>DNMT3A</i> expression was strongly associated with cell cycle G₂/M checkpoint regulation, implicating a role in prostate cancer progression.</p><p><strong>Conclusion: </strong>The prognostic significance of <i>DNMT3A</i> and its genetic variant rs77993651 in prostate cancer is herein highlighted. Targeting <i>DNMT3A</i>-mediated pathways may offer novel therapeutic strategies for prostate cancer management.</p>","PeriodicalId":9516,"journal":{"name":"Cancer Genomics & Proteomics","volume":"22 4","pages":"611-623"},"PeriodicalIF":2.6,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144504906","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":"C1orf50 Drives Malignant Melanoma Progression Through the Regulation of Stemness.","authors":"Yusuke Otani, Masaki Maekawa, Atsushi Tanaka, Tirso Peña, Vanessa D Chin, Anna Rogachevskaya, Shinichi Toyooka, Michael H Roehrl, Atsushi Fujimura","doi":"10.21873/cgp.20518","DOIUrl":"https://doi.org/10.21873/cgp.20518","url":null,"abstract":"<p><strong>Background/aim: </strong>Recent advancements in omics analysis have significantly enhanced our understanding of the molecular pathology of malignant melanoma, leading to the development of novel therapeutic strategies that target specific vulnerabilities within the disease. Despite these improvements, the factors contributing to the poor prognosis of patients with malignant melanoma remain incompletely understood. The aim of this study was to investigate the role of <i>C1orf50</i> (Chromosome 1 open reading frame 50), a gene previously of unknown function, as a prognostic biomarker in melanoma.</p><p><strong>Materials and methods: </strong>We performed comprehensive transcriptome data analysis and subsequent functional validation of the human Skin Cutaneous Melanoma project from The Cancer Genome Atlas (TCGA).</p><p><strong>Results: </strong>Elevated expression levels of <i>C1orf50</i> correlated with worse survival outcomes. Mechanistically, we revealed that C1orf50 plays a significant role in the regulation of cell cycle processes and cancer cell stemness, providing a potential avenue for novel therapeutic interventions in melanoma.</p><p><strong>Conclusion: </strong>This study is the first to identify <i>C1orf50</i> as a prognostic biomarker in melanoma. The clinical relevance of our results sheds light on the importance of further investigation into the biological mechanisms underpinning C1orf50's impact on melanoma progression and patient prognosis.</p>","PeriodicalId":9516,"journal":{"name":"Cancer Genomics & Proteomics","volume":"22 4","pages":"510-524"},"PeriodicalIF":2.6,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144504898","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":"High Expression of <i>PKCζ</i> And <i>CTNNBIP1</i> Is Associated With Poor Prognosis in Luminal B Breast Cancer.","authors":"Yuka Nagashima, Kazunori Sasaki, Ryosuke Chiwaki, Hayato Ishii, Kana Nohata, Yuki Maemura, Takahiro Kasai, Ayaka Ozaki, Shoma Tamori, Shigeo Ohno, Kazunori Akimoto","doi":"10.21873/cgp.20520","DOIUrl":"https://doi.org/10.21873/cgp.20520","url":null,"abstract":"<p><strong>Background/aim: </strong>The relationship between protein kinase C zeta (<i>PKCζ</i>) expression and medical treatment resistance in breast cancer subtypes is unclear. Therefore, the present study aimed to analyze this relationship using disease-specific survival.</p><p><strong>Materials and methods: </strong>Open-source datasets with clinical and gene expression information (METABRIC, n=2509; and TCGA Pan-Cancer Atlas, n=1084) were downloaded and Kaplan-Meier survival and Cox proportional hazard analyses were performed.</p><p><strong>Results: </strong>High expression of <i>PKCζ</i> indicated a poor prognosis in patients with luminal B type treated with endocrine therapy and aromatase inhibitor as endocrine therapy. Furthermore, catenin beta interacting protein 1 (<i>CTNNBIP1</i>) was identified as a differentially expressed gene between the <i>PKCζ</i> ^high and <i>PKCζ</i> ^low luminal B breast cancer cohorts treated with endocrine therapy and aromatase inhibitors. <i>PKCζ</i> ^high <i>CTNNBIP1</i> ^high luminal B breast cancer treated with endocrine therapy and aromatase inhibitor indicated a poor prognosis. These results suggest that <i>PKCζ</i> and <i>CTNNBIP1</i> are involved in breast cancer progression and contribute to reduced susceptibility to endocrine therapy in the luminal B breast cancer subtype.</p><p><strong>Conclusion: </strong><i>PKCζ</i> and <i>CTNNBIP1</i> may serve as a prognostic biomarker for predicting the efficacy of endocrine therapy in the luminal B breast cancer.</p>","PeriodicalId":9516,"journal":{"name":"Cancer Genomics & Proteomics","volume":"22 4","pages":"538-556"},"PeriodicalIF":2.6,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144504903","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":"CD84 as a Prognostic Biomarker and Therapeutic Target in Breast Cancer: Interconnections With PDL1, CD74, and Immune Tolerance Mechanisms.","authors":"Umar Wazir, Amber X Li, Carolyn Cai Wang, Henson Han Gao, Tracey A Martin, Wen G Jiang, Kefah Mokbel","doi":"10.21873/cgp.20521","DOIUrl":"https://doi.org/10.21873/cgp.20521","url":null,"abstract":"<p><strong>Background/aim: </strong>Cluster of differentiation 84 (CD84), a member of the signalling lymphocytic activating molecule (SLAM) family, has emerged as a potential prognostic biomarker and therapeutic target in breast cancer. This study explored CD84 expression and its correlation with clinicopathological features in a well-characterised cohort.</p><p><strong>Materials and methods: </strong>Using quantitative real-time PCR, mRNA expression levels of CD84 and related molecules, including PDL1, CD74, and other immune tolerance markers, were analysed.</p><p><strong>Results: </strong>The findings reveal that elevated CD84 expression predicts poor overall survival, independent of conventional prognostic factors such as the Nottingham Prognostic Index (NPI). Notably, a combined signature of CD84, CD48, VAV1, and CTNNB1 demonstrated stronger prognostic power than individual markers. CD84 exhibited significant correlations with immunosuppressive molecules, including PDL1 and CD74, underscoring its role in fostering immune tolerance within the tumour microenvironment.</p><p><strong>Conclusion: </strong>CD84 may mediate an immunosuppressive phenotype, facilitating immune evasion in breast cancer. This highlights its potential as a therapeutic target, particularly in triple-negative breast cancer, to overcome immune resistance and enhance treatment efficacy.</p>","PeriodicalId":9516,"journal":{"name":"Cancer Genomics & Proteomics","volume":"22 4","pages":"557-563"},"PeriodicalIF":2.6,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144504899","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":"Contribution of MRE11, RAD50, and NBS1 Genotypes to Bladder Cancer Susceptibility.","authors":"Cheng-Hsi Liao, Wen-Shin Chang, Hou-Yu Shih, Yun-Chi Wang, Che-Lun Hsu, Shu-Yu Chang, Chao-Hsiang Chang, Wen-Chi Chen, DA-Tian Bau, Chia-Wen Tsai","doi":"10.21873/cgp.20523","DOIUrl":"https://doi.org/10.21873/cgp.20523","url":null,"abstract":"<p><strong>Background/aim: </strong>Genome instability is a hallmark of cancer, often accelerated by defects in DNA damage responses. MRE11-RAD50-NBS1 (MRN) complex plays a crucial role in sensing and repairing DNA damage; however, there is limited literature on the involvement of <i>MRN</i> genotypes in bladder cancer (BLCA) susceptibility. This study aimed to elucidate the impact of <i>MRN</i> genotypes on the risk of BLCA.</p><p><strong>Materials and methods: </strong>We genotyped 14 single nucleotide polymorphisms (SNPs) in <i>MRN</i> genes, including rs684507, rs2155209, rs10831234, rs13447720, rs601341 in <i>MRE11</i>, rs17166050, rs17772583, rs6871536, rs3798134, rs2244012 in <i>RAD50</i>, and rs1805794, rs2735383, rs1063053, rs1063054 in <i>NBS1</i>, among 375 BLCA cases and 375 controls, and evaluated their contributions to BLCA susceptibility.</p><p><strong>Results: </strong>Among these SNPs, only <i>NBS1</i> rs2735383 was significantly associated with BLCA risk (<i>p</i> for trend=0.0053), with both CG and CC genotypes conferring higher risks (OR=1.48 and 1.95, respectively). Subgroup analysis showed that <i>NBS1</i> rs2735383 was associated with BLCA risk in individuals older than 55 years (OR=2.29, <i>p</i>=0.0053), smokers (OR=2.56, <i>p</i>=0.0026), alcohol drinkers (OR=3.25, <i>p</i>=0.0005), and those with muscle-invasive disease (OR=1.97, <i>p</i>=0.0243), but not in younger individuals, non-smokers, non-drinkers, or non-muscle-invasive cases.</p><p><strong>Conclusion: </strong><i>NBS1</i> rs2735383 genotype may serve as a genetic biomarker for BLCA susceptibility, particularly in high-risk subpopulations, including elders, smokers, drinkers, and those with muscle-invasive disease.</p>","PeriodicalId":9516,"journal":{"name":"Cancer Genomics & Proteomics","volume":"22 4","pages":"575-591"},"PeriodicalIF":2.6,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144504900","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}