Journal of Cancer最新文献

{"title":"A CRM-Integrated ypT Staging System Improves Prognostic Stratification Following Neoadjuvant Therapy in Rectal Cancer.","authors":"Wan-Hsuan Chow, Chung-Han Ho, Yi-Chen Chen, Hsuan-Yi Huang, Ching-Chieh Yang","doi":"10.7150/jca.129779","DOIUrl":"10.7150/jca.129779","url":null,"abstract":"<p><strong>Introduction: </strong>The ypT staging system has limited prognostic value after neoadjuvant therapy, as it primarily reflects only tumor characteristics alone. This study proposes a novel staging system that integrates circumferential resection margin (CRM) status with the ypT category to enhance prognostic accuracy following neoadjuvant chemoradiotherapy (nCRT) for rectal cancer.</p><p><strong>Methods: </strong>We analyzed data from 4,308 rectal adenocarcinoma patients treated with nCRT followed by surgery, using the Taiwan Cancer Registry and National Health Insurance Research Database (2011-2021). CRM involvement was defined as a margin ≤1 mm. Overall survival was assessed using multivariable Cox regression, and prognostic performance of the proposed CRM-integrated ypT staging system was compared with the American Joint Committee on Cancer (AJCC) TNM system using Harrell's c-statistic.</p><p><strong>Results: </strong>CRM involvement (≤1 mm) was significantly associated with worse 5-year survival (adjusted odds ratio, 0.44; 95% CI, 0.31-0.61). Due to the low rate of CRM positivity in ypT0-2 patients, a modified ypT classification was established: new ypT3 (ypT3 and CRM-), new ypT4A (ypT4A and CRM-), new ypT4B (ypT3 and CRM+ or ypT4B and CRM-), and new ypT4C (ypT4A and CRM+ or ypT4B and CRM+). This system demonstrated better prognostic discrimination than the current AJCC classification (Harrell's c-statistic: 0.756 vs. 0.752, P = 0.034).</p><p><strong>Conclusions: </strong>Incorporating CRM into the ypT stage offers survival stratification and may guide more individualized postoperative treatment strategies for rectal cancer patients after nCRT.</p>","PeriodicalId":15183,"journal":{"name":"Journal of Cancer","volume":"17 3","pages":"679-687"},"PeriodicalIF":3.2,"publicationDate":"2026-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13003605/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147498975","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prognostic Impact of UBA1 Expression in Breast Cancer.","authors":"Jana Koch, Lea Vatter, Jannis Heyer, Maximilian Klar, Ingolf Juhasz-Böss, Martin Werner, Konrad Kurowski, Peter Bronsert","doi":"10.7150/jca.129539","DOIUrl":"https://doi.org/10.7150/jca.129539","url":null,"abstract":"<p><strong>Background: </strong>The use of established prognostic markers has improved the diagnostic stratification and therapeutic approaches of breast cancer. Ubiquitin-like modifier activating enzyme 1 (UBA1), a key enzyme in the ubiquitin-proteasome pathway, has been reported to play a role in the pathogenesis of various malignant tumors. However, its functional impact on breast cancer progression, especially across intrinsic subtypes, remains poorly understood. This study aimed to evaluate the prognostic relevance of UBA1 protein expression in patients with breast cancer.</p><p><strong>Methods: </strong>Formalin-fixed, paraffin-embedded (FFPE) tissue samples from 413 chemotherapy-naïve patients with invasive breast cancer were obtained from the Institute of Surgical Pathology (ISP) at the University Medical Centre Freiburg in Germany. Haematoxylin and eosin (H&E)-stained slides were digitised and annotated to define regions of interest (ROIs) for tissue microarray (TMA) construction. TMA sections were immunohistochemically stained for UBA1 expression and intrinsic subtype markers, including oestrogen receptor (ER), progesterone receptor (PgR), human epidermal growth factor receptor 2 (HER2), and Ki-67. All slides were digitised. UBA1 and intrinsic markers were evaluated and analysed using AI-assisted image analysis software (HALO AI). Furthermore, UBA1 expression was analysed separately in both tumor cells and tumor-associated stroma. All results were statistically correlated with clinicopathological data parameters.</p><p><strong>Results: </strong>High UBA1 expression in both the tumor and stromal compartments was significantly associated with reduced overall survival (OS). Subtype-specific analyses revealed that elevated stromal UBA1 expression, particularly in the cytoplasm, was associated with poorer survival in luminal A and luminal B subtypes. Conversely, increased nuclear UBA1 expression in tumor cells was associated with worse outcomes in the luminal B subtype. Multivariable Cox regression analyses revealed that UBA1 expression in tumor cells was an independent prognostic marker. Furthermore, bivariate analyses revealed that high stromal UBA1 expression was associated with a broader range of adverse clinicopathological parameters, most notably at the cytoplasmic level.</p><p><strong>Conclusion: </strong>This study highlights the prognostic significance of UBA1 protein expression in breast cancer, thereby demonstrating its potential utility as a diagnostic and therapeutic target.</p>","PeriodicalId":15183,"journal":{"name":"Journal of Cancer","volume":"17 4","pages":"688-702"},"PeriodicalIF":3.2,"publicationDate":"2026-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13104717/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147772440","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Overexpression of Myelin and Lymphocyte Protein (MAL) Downregulates MUC1 and Enhances Cisplatin Sensitivity in Non-Small Cell Lung Cancer Cells.","authors":"Ana Karina Saldaña-Villa, Bismarck Vázquez-Almazán, Catalina Flores-Maldonado, Juan Carlos Vizuet-de-Rueda, Elisa Natalia Oropeza-Durán, José Bonilla-Delgado, Enoc Mariano Cortés-Malagón, Rubén Gerardo Contreras, Luis Manuel Teran, Blanca Ortiz-Quintero, Roberto Lara-Lemus","doi":"10.7150/jca.129125","DOIUrl":"https://doi.org/10.7150/jca.129125","url":null,"abstract":"<p><p>The epigenetic repression of myelin and lymphocyte protein gene (<i>MAL</i>) and over-expression of MUC1 protein are two well-documented hallmarks of various carcinomas including lung cancer. The purpose of this work was to investigate whether ectopic expression of MAL could modify the proliferative activity of MUC1 in human lung adenocarcinoma HCC827 cells. We generated stable HCC827 cell lines, expressing GFP- or myc-MAL constructs, then, followed the expression of MUC1 by RT-qPCR and Western blot, and tested proliferation and sensitivity of those cells to cisplatin. Our results showed that ectopic expression of MAL nearly eliminated cellular levels of MUC1-C. This effect is primarily due to down-regulation of <i>MUC1</i> expression, as confirmed by RT-qPCR. Additionally, lysosomal-associated degradation of MUC1 may also contribute, as observed when the cells were treated with ammonium chloride and chloroquine. The reduced quantity of MUC1-C negatively affected both cyclin D1 and c-Myc, protein levels, which are linked to cell-proliferative signals involving MUC1-C. Furthermore, expression of MAL decreased the viability of HCC827 cells, and increased their sensitivity to cisplatin. MAL and MUC1 showed an antagonistic relationship in cancer cells, and these findings provide new insights with respect to the regulation of MUC1 and a better understanding of MAL as a potential tumor suppressor.</p>","PeriodicalId":15183,"journal":{"name":"Journal of Cancer","volume":"17 4","pages":"703-711"},"PeriodicalIF":3.2,"publicationDate":"2026-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13104723/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147772424","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fluid-Derived Organoids from Pleural Effusion and Ascites: Emerging Models for Drug Resistance and Personalized Oncology.","authors":"Yongyang Chen, Xiaoqing Xu, Jialin Chen, Miao Yin, Jinhui Chen, Zhanghua Qi, Ming Shi, Wenmei Su","doi":"10.7150/jca.127511","DOIUrl":"10.7150/jca.127511","url":null,"abstract":"<p><p>Malignant pleural effusion (MPE) and malignant ascites (MA) are common complications in advanced-stage cancers, often signifying disease progression and resistance to treatment. Compared to tissue biopsies or surgical specimens, materials derived from effusions offer advantages such as minimal invasiveness, ease of accessibility, and the feasibility of repeated collection during therapeutic interventions. Organoids generated from tumor cells in effusions, termed fluid-derived organoids (FDOs), have demonstrated the ability to maintain genetic heterogeneity and accurately replicate patient-specific tumor phenotypes. These characteristics position FDOs as promising models for investigating drug resistance mechanisms and informing personalized oncology strategies. In the context of lung cancer, organoids derived from pleural effusions have been employed to study acquired resistance to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors and immunotherapy. Similarly, in ovarian and gastrointestinal cancers, organoids derived from ascites have proven to be valuable platforms for examining chemotherapy resistance and conducting drug sensitivity testing. FDOs have shown significant potential for translational applications by effectively correlating <i>ex vivo</i> drug responses with clinical outcomes, thus facilitating real-time monitoring of resistance evolution. However, several challenges remain, such as achieving culture standardization, maintaining the integrity of tumor microenvironment components, and integrating with multi-omics approaches. This review provides a comprehensive overview of recent advancements in the use of pleural effusion- and ascites-derived organoids for drug resistance research, underscores their applications in personalized oncology, and explores future research directions.</p>","PeriodicalId":15183,"journal":{"name":"Journal of Cancer","volume":"17 3","pages":"614-625"},"PeriodicalIF":3.2,"publicationDate":"2026-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13003542/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147499011","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"FAM188B promotes progression of hepatocellular carcinoma by regulating YAP/TAZ via interaction with USP10.","authors":"Siwei Hu, Yuting Wen, Yihong Chen, Yuliang Fang, Mingshan Mu, Linglan Tu, Wenhu Chen, Kangsheng Tu, Xin Liu, Qiuran Xu, Dongsheng Huang, Xiaoyan Li","doi":"10.7150/jca.125659","DOIUrl":"10.7150/jca.125659","url":null,"abstract":"<p><strong>Background: </strong>Hepatocellular carcinoma (HCC) is one of the most common malignancies worldwide and its incidence and mortality rates remain high. Therefore, new diagnostic and therapeutic approaches are urgently required. Family with sequence similarity 188 member B (FAM188B) encodes an evolutionarily conserved protein that is highly expressed in various cancers. While FAM188B has been implicated in the progression of several tumors, its role in HCC progression remains unknown.</p><p><strong>Methods: </strong>We analyzed FAM188B expression in HCC using The Cancer Genome Atlas (TCGA) and The University of Alabama at Birmingham Cancer data analysis Portal (UALCAN) databases. Functional studies included <i>in vitro</i> proliferation, migration, and invasion assays, as well as <i>in vivo</i> xenograft models. Co-immunoprecipitation (Co-IP), Western blotting, and immunofluorescence were used to investigate the FAM188B-Ubiquitin-specific peptidase 10 (USP10)-Yes-associated protein/Transcriptional coactivator with PDZ-binding motif (YAP/TAZ) interaction.</p><p><strong>Results: </strong>FAM188B was found highly expressed in HCC cells and associated with poor prognosis. Both <i>in vitro</i> and <i>in vivo</i>, FAM188B promoted the proliferation, migration, and invasion of HCC. FAM188B directly interacts with and stabilizes USP10 and the downregulation of FAM188B by shRNA led to decreased USP10 and YAP/TAZ protein levels, suggesting that FAM188B may regulate the YAP/TAZ pathway through its interaction with USP10.</p><p><strong>Conclusion: </strong>Our findings reveal that FAM188B plays a crucial role in enhancing HCC cell proliferation, migration, and invasion, primarily through regulating the USP10/YAP/TAZ signaling axis, which was validated <i>in vitro</i> and <i>in vivo</i>.</p>","PeriodicalId":15183,"journal":{"name":"Journal of Cancer","volume":"17 3","pages":"626-636"},"PeriodicalIF":3.2,"publicationDate":"2026-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13003555/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147498996","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of Skeletal Muscle-related Parameters on Survival in Patients with Advanced Pancreatic Cancer Treated with Gemcitabine plus Nab-paclitaxel as First-line Chemotherapy.","authors":"Nanako Matsuo, Toshifumi Yamaguchi, Hiroki Yukami, Hiroyuki Kodama, Takako Ikegami, Toru Kadono, Shin Kameisihi, Dai Okemoto, Elham Fakhrejahani, Hiroki Nishikawa","doi":"10.7150/jca.126673","DOIUrl":"10.7150/jca.126673","url":null,"abstract":"<p><strong>Background: </strong>Sarcopenia, defined as a reduction in muscle mass assessed using scales such as the psoas muscle mass index (PMI), is accompanied by decreased muscle strength or physical function. However, sarcopenia's effect in patients with pancreatic cancer (PC) receiving chemotherapy remains unclear. In addition, recent international studies have demonstrated that intramuscular fat infiltration, assessed using parameters such as FRPM, is associated with poor prognosis across various malignancies. However, evidence regarding its prognostic significance in pancreatic cancer remains limited. We aimed to evaluate the relationship between sarcopenia and the prognosis of patients with PC receiving palliative chemotherapy.</p><p><strong>Methods: </strong>We retrospectively reviewed patients diagnosed with unresectable PC who received gemcitabine plus nab-paclitaxel (GnP) as the first-line therapy at our hospital between 2018 and 2021. We calculated PMI, defined as the sum of the bilateral psoas muscle mass at the lumbar three (L3) level and FRPM, defined as the sum of areas within the psoas muscles corresponding to fat at the L3 level from Vincent® on the CT images. We compared the overall survival (OS) between the PMI-high and PMI-low groups and the FRPM-high and FRPM-low groups.</p><p><strong>Results: </strong>Of 46 patients, 37 were eligible. Eighteen (49%) and 19 (51 %) patients were classified into PMI-high and PMI-low groups, respectively. Twenty (54%) and 17 patients (46%) were classified into FRPM-high and FRPM-low groups, respectively. The median OS was 16.4 months in PMI-high and 8.7 months in PMI-low groups (hazard ratio [HR]: 0.45, 95% confidence interval [CI]: 0.23-0.90, P < 0.01). The median OS was 15.6 months in FRPM-low and 8.5 months in FRPM-high groups (HR: 0.36, 95% CI: 0.18-0.76, P < 0.01). In multivariate analysis, the presence of ascites (P < 0.01), PMI-low (P = 0.02), and FRPM-high (P = 0.03) were independent adverse prognostic factors for OS.</p><p><strong>Conclusion: </strong>Muscle-related parameters may be independent indicators of poor prognosis in patients with PC treated with first-line GnPs.</p>","PeriodicalId":15183,"journal":{"name":"Journal of Cancer","volume":"17 3","pages":"604-613"},"PeriodicalIF":3.2,"publicationDate":"2026-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13003557/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147499032","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Molecular Mechanisms of Symptom Fluctuations in Malignant Tumor Patients: Stable by Day and Severe at Night.","authors":"Zhongxuan Xie, Wei Jin, Juezhou Pang, Kangshuo Hu, Lihong Li","doi":"10.7150/jca.128423","DOIUrl":"10.7150/jca.128423","url":null,"abstract":"<p><p>Patients with malignant tumors often experience fluctuations in the severity of their symptoms depending on the time of day. In traditional Chinese medicine, symptoms are said to follow a pattern of \"mild in the morning, stable by day, worsening in the evening, and severe at night.\" This article investigates the circadian chronobiology of symptoms and examines their molecular pathophysiology. Evidence suggests that disruptions in core circadian clock genes, such as BMAL1 and PER, along with the dysregulation of cellular metabolic pathways, immune responses, and endocrine functions, synergistically facilitate tumor growth and metastasis during nocturnal periods. These molecular alterations contribute to symptom exacerbation through mechanisms which include direct tumor invasion, neural infiltration, inflammatory processes, dorsal root ganglion (DRG) sensitization, and abnormal melatonin secretion. The article further explores three chronotherapeutic strategies and assesses melatonin's role in targeted oncological therapy, aiming to optimize circadian regulation and symptom management, thereby providing a scientific foundation for personalized anti-tumor interventions that are based on circadian rhythms.</p>","PeriodicalId":15183,"journal":{"name":"Journal of Cancer","volume":"17 3","pages":"571-582"},"PeriodicalIF":3.2,"publicationDate":"2026-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13003552/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147499002","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Proteasome Assembly Chaperone 3 Defines Metabolic-Immune Programs and Poor Prognosis in Breast Cancer via Multi-Omics Approaches.","authors":"Sachin Kumar, Hoang Dang Khoa Ta, Hao-Chien Yang, Chia-Lung Shih, Dahlak Daniel Solomon, Ching-Chung Ko, Do Thi Minh Xuan, Yung-Kuo Lee, Kai-Fu Chang, Hui-Ru Lin, Shu-Huei Kao, Jian-Ying Chuang, Jian-Bin Chen, Chih-Yang Wang, Ngoc Uyen Nhi Nguyen","doi":"10.7150/jca.126116","DOIUrl":"10.7150/jca.126116","url":null,"abstract":"<p><p>The proteasome assembly chaperone (<i>PSMG</i>) gene family (comprised of <i>PSMG1</i>, <i>PSMG2</i>, <i>PSMG3</i>, and <i>PSMG4</i>) plays a critical role in proteasome biogenesis; however, its involvement in breast cancer remains poorly understood. Among these chaperones, <i>PSMG3</i> is uniquely and markedly elevated in breast cancer and is associated with poor clinical outcomes. We systematically investigated the roles of <i>PSMG</i> family genes in breast cancer by integrating multi-cohort genomic and transcriptomic datasets, including TCGA-BRCA, METABRIC, and multiple NCBI GEO cohorts. Comprehensive bioinformatics analyses were performed using bulk RNA sequencing and single-cell RNA sequencing data. A gene set enrichment analysis (GSEA) and immune infiltration analyses (CIBERSORT and TIMER) were applied to characterize dysregulated biological pathways, tumor microenvironmental features, and clinical relevance. In addition, molecular docking analyses were conducted to assess the druggability and binding potential of PSMG family proteins with selected small-molecule inhibitors. Elevated PSMG3 expression was consistently associated with poor survival outcomes across multiple breast cancer cohorts. Functional enrichment analyses revealed that PSMG3-high tumors were characterized by activation of hypoxia-related signaling pathways and dysregulated fatty acid metabolism, suggesting a role for PSMG3 in metabolic reprogramming. Immune deconvolution analyses further demonstrated significant correlations between PSMG3 expression and distinct immune cell populations within the tumor microenvironment. These findings were supported by single-cell transcriptomic profiling, which revealed subtype-specific expression patterns of PSMG3 in malignant epithelial cell populations. This integrative multi-omics analysis identified PSMG3 as a clinically relevant proteasome assembly chaperone associated with aggressive breast cancer phenotypes, metabolic dysregulation, and tumor immune contexture. Collectively, these results highlight PSMG3 as a promising prognostic biomarker and potential therapeutic target in breast cancer.</p>","PeriodicalId":15183,"journal":{"name":"Journal of Cancer","volume":"17 3","pages":"583-603"},"PeriodicalIF":3.2,"publicationDate":"2026-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13003543/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147498970","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Potential influence of omentin-1 genetic variants on the clinicopathological features of patients with hepatocellular carcinoma.","authors":"Sung-Lin Hu, Hsiang-Lin Lee, Ming-Yu Lien, Edie-Rosmin Wu, Shun-Fa Yang, Chih-Hsin Tang","doi":"10.7150/jca.128357","DOIUrl":"10.7150/jca.128357","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) ranks as the fifth supreme prevalent cancer within men globally and the ninth among female, serving as a significant contributor to cancer-associated deaths. The adipokine omentin-1 has been demonstrated to have a defensive effect by decreasing the secretion of proinflammatory cytokines. The connections among lifestyle factors that promote cancer, <i>OMNT1</i> polymorphisms, and HCC are still not well understood. Our investigation focused on the influence of clinicopathological characteristics and four variants of the <i>OMNT1</i> gene (rs2274907, rs35779394, rs4656959, and rs79209815) on healthy controls as well as Taiwanese individuals with HCC. According to our data, individuals with the <i>OMNT1</i> rs79209815 variant (TC or CC genotypes) are at an elevated risk of progressing to stage III/IV disease and larger tumors than those with the TT genotype. Males exhibited these associations more prominently than females. Moreover, <i>OMNT1</i> expression levels were markedly reduced in individuals with the wild-type TT homozygous genotype when compared to those with the TC or CC genotypes of rs79209815. The complexity of genetic influences on HCC is highlighted by our study, which suggests that <i>OMNT1</i> polymorphisms may have an impact on tumor stage and progression.</p>","PeriodicalId":15183,"journal":{"name":"Journal of Cancer","volume":"17 3","pages":"564-570"},"PeriodicalIF":3.2,"publicationDate":"2026-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13003546/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147498980","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MZB1 at the ER-immunity interface: from antibody folding to disease vulnerability in autoimmunity, inflammation, and cancer.","authors":"Yu Zhang, Wei Yang, Xiaofang Yang, Yuqing Pan, Rong Guo, Dong Chen, Shicong Tang, Xi Zhang","doi":"10.7150/jca.125922","DOIUrl":"10.7150/jca.125922","url":null,"abstract":"<p><p>MZB1 (marginal zone B and B1 cell-specific protein 1) is an endoplasmic reticulum-resident molecular chaperone that is predominantly expressed in marginal zone B cells, B1 cells, plasma cells, and pDCs. Functioning as a co-chaperone of GRP94 and BiP, MZB1 selectively facilitates the proper folding and secretion of immunoglobulin M (IgM) and J-chain-containing immunoglobulin A (IgA) dimers, and maintains the homeostasis of highly secretory cells by upregulating the expression of partner proteins such as BiP/GRP94. This review highlights the emerging role of MZB1 across various pathological conditions. In autoimmune diseases such as systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA), MZB1 contributes to aberrant autoantibody and cytokine secretion. MZB1 also modulates inflammatory responses in conditions such as colitis and periodontitis by regulating the B cell-skewed inflammatory microenvironment. In oncology, MZB1 is overexpressed in breast cancer (BC), lymphoma, and multiple myeloma (MM), where it is associated with enhanced tumor cell proliferation and poor prognosis. Conversely, in hepatocellular carcinoma (HCC) and gastric cancer (GC), MZB1 is transcriptionally silenced due to promoter hypermethylation. In summary, the tissue-specific expression pattern of MZB1 endows it with potential as both a diagnostic biomarker and therapeutic target, holding significant implications for the exploration of future cancer prognosis and treatment strategies.</p>","PeriodicalId":15183,"journal":{"name":"Journal of Cancer","volume":"17 3","pages":"542-554"},"PeriodicalIF":3.2,"publicationDate":"2026-02-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13003553/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147498960","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}