Journal of Cancer Research and Clinical Oncology最新文献

{"title":"Dual targeting of Aurora Kinase A and poly (ADP-ribose) polymerase as a therapeutic option for patients with ovarian cancer: preclinical evaluations.","authors":"Soumya M Turaga, Stacey L Hembruff, Masha G Savelieff, Arnab Ghosh, Rajni V Puri, Harsh B Pathak, Linda J Paradiso, Thomas J Myers, Ao Li, Andrew K Godwin","doi":"10.1007/s00432-025-06152-7","DOIUrl":"10.1007/s00432-025-06152-7","url":null,"abstract":"<p><strong>Purpose: </strong>Epithelial ovarian cancers (EOCs) are often diagnosed at an advanced stage, leading to poor survival outcomes despite chemotherapeutic and surgical advances. Precision oncology strategies have been developed to treat EOCs characterized by BRCA1 and BRCA2 inactivation with consequent homologous recombination (HR) repair defects. HR deficiency enhances tumor sensitivity to poly (ADP-ribose) polymerase (PARP) inhibitors (PARPis), approved for EOCs as maintenance therapy, although they have been discontinued as recurrent EOC monotherapy. However, combination treatment with PARPis may be a viable alternate strategy for EOCs. Moreover, EOC patients with wild-type BRCA are ineligible for PARPs, necessitating novel approaches. We previously discovered that inhibiting Aurora kinase A (AURKA) downregulates PARP and BRCA1/2 expression in EOCs and may constitute a viable approach for EOCs.</p><p><strong>Methods: </strong>Herein, we evaluated combined PARPi olaparib with the selective AURKA inhibitor (AURKAi) VIC-1911 in six different patient-derived xenograft (PDX) EOC models, including two with mutant BRCA1, two with mutant BRCA2, one with mutant BRCA1/2, and one with wild-type BRCA1/2.</p><p><strong>Results: </strong>We found that combined olaparib + VIC-1911 treatment reduced tumor volumes and weights by up 90% in some PDX models, with synergistic effect compared to olaparib and VIC-1911 monotherapy. Additionally, combined olaparib + VIC-1911 treatment improved survival of mice harboring both mutant BRCA1 and wild-type BRCA1/2 PDXs. Generally, mice tolerated the drug combinations well during treatment, though loss of body weight was observed at higher drug dosages and with intensive treatment regimens.</p><p><strong>Conclusion: </strong>Our studies indicate a synergistic benefit from combined PARPi and AURKAi in mutant and wild-type BRCA EOC tumors.</p>","PeriodicalId":15118,"journal":{"name":"Journal of Cancer Research and Clinical Oncology","volume":"151 3","pages":"124"},"PeriodicalIF":2.7,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11946953/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143730197","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":"Does anxiety influence the use of complementary or alternative medicine among cancer patients?","authors":"Caroline Heyder, Judith Büntzel, Hristo Boyadzhiev, Petra Stegmaier, Bijan Zomorodbakhsch, Klaus Heißner, Christoph Stoll, Ludwig Fischer von Weikersthal, Jana Czekay, Ivonne Rudolph, Jutta Hübner","doi":"10.1007/s00432-025-06173-2","DOIUrl":"10.1007/s00432-025-06173-2","url":null,"abstract":"<p><strong>Purpose: </strong>The aim of this study was to investigate the extent to which patients' anxiety due to their cancerous disease has an influence on the use of complementary and alternative medicine (CAM) methods.</p><p><strong>Methods: </strong>230 patients completed an anonymous voluntary questionnaire that was sent to outpatient oncological facilities participating in the survey. This questionnaire included standardised tests such as the Allgemeine Selbstwirksamkeit Kurzskala (ASKU, self-efficacy short scale) and the State-Trait-Anxiety-Inventory (STAI) as well as socio-demographic information and a section on CAM use. Statistical analyses and regression models were used to identify correlations.</p><p><strong>Results: </strong>Female gender, high level of education (high school diploma or university degree) and increased trait anxiety were related to CAM use. All other variables analysed showed no significant results.</p><p><strong>Conclusion: </strong>This study demonstrates that trait anxiety and sociodemographic factors significantly influence CAM usage among cancer patients. Physicians and health care providers should consider this in consultations to guarantee the best possible care for patients.</p>","PeriodicalId":15118,"journal":{"name":"Journal of Cancer Research and Clinical Oncology","volume":"151 3","pages":"123"},"PeriodicalIF":2.7,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11937123/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143709849","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":"Identification of an appropriate reference gene for normalization of qRT-PCR expression analyses in human breast cancer cell lines: application to L-arginine depletion studies.","authors":"Antonia Röglin, Rainer Böger, Fiona Kleinsang, Juliane Hannemann","doi":"10.1007/s00432-025-06165-2","DOIUrl":"10.1007/s00432-025-06165-2","url":null,"abstract":"<p><strong>Purpose: </strong>Quantitative real-time PCR (qRT-PCR) represents a robust methodology to investigate alterations in gene expression patterns during tumorigenesis. The quantification of target gene expression is conventionally standardized through normalization against a stably expressed reference gene. However, the expression profile of a specific reference gene can exhibit variability across different tissue types and diverse physiological conditions. This study aimed to identify a suitable reference gene from a pool of ten potential candidates for the comparison of gene expression profiles between six human breast cell lines, comprising both normal breast (MCF-12A) and breast cancer cells (MCF-7, BT-474, SK-BR-3, MDA-MB-468, MDA-MB-231).</p><p><strong>Methods: </strong>Four different mathematical approaches were used to calculate the stability of reference gene expression (comparative ΔCt method, NormFinder, coefficient of variation and RefFinder).</p><p><strong>Results: </strong>Stability analysis identified ACTB as a suitable reference gene across all cell lines. As we are specifically interested in studying metabolic adaptation of breast cancer, we applied the same approach to identify a suitable reference gene also after maintaining the cell lines in L-arginine-deficient medium for up to 72 h. The stability ranking of reference genes fluctuated after L-arginine was depleted.</p><p><strong>Conclusion: </strong>In the context of investigating specific cell lines under certain conditions, we propose the identification of reference genes that exhibit optimal stability and suitability.</p>","PeriodicalId":15118,"journal":{"name":"Journal of Cancer Research and Clinical Oncology","volume":"151 3","pages":"122"},"PeriodicalIF":2.7,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11937119/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143709850","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":"Correction: Comparison of robotic-assisted and laparoscopic partial nephrectomy based on the PADUA score and the predictive value of the PADUA score and the Mayo Adhesive Probability score for postoperative complications: a single-center retrospective study.","authors":"Shuo Liu, Bowen Zhang, Bowen Weng, Xiangqiang Liu, Sichuan Hou","doi":"10.1007/s00432-025-06170-5","DOIUrl":"10.1007/s00432-025-06170-5","url":null,"abstract":"","PeriodicalId":15118,"journal":{"name":"Journal of Cancer Research and Clinical Oncology","volume":"151 3","pages":"120"},"PeriodicalIF":2.7,"publicationDate":"2025-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11937157/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143709847","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":"Retraction Note: Significances of contactin‑1 expression in human gastric cancer and knockdown of contactin‑1 expression inhibits invasion and metastasis of MKN45 gastric cancer cells.","authors":"De-Hu Chen, Ji-Wei Yu, Ju-Gang Wu, Shou-Lian Wang, Bo-Jian Jiang","doi":"10.1007/s00432-025-06166-1","DOIUrl":"10.1007/s00432-025-06166-1","url":null,"abstract":"","PeriodicalId":15118,"journal":{"name":"Journal of Cancer Research and Clinical Oncology","volume":"151 3","pages":"119"},"PeriodicalIF":2.7,"publicationDate":"2025-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11937210/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143709851","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":"Genomic analysis of small renal masses reveals mutations linked with renal cell carcinoma and fast-growing tumors.","authors":"Ieva Vaicekauskaitė, Algirdas Žalimas, Rasa Sabaliauskaitė, Kristina Žukauskaitė, Mantas Trakymas, Jurgita Ušinskienė, Albertas Ulys, Sonata Jarmalaitė","doi":"10.1007/s00432-025-06162-5","DOIUrl":"10.1007/s00432-025-06162-5","url":null,"abstract":"<p><strong>Purpose: </strong>Small renal masses (SRMs) SRMs are a heterogeneous group of small kidney lesions. Currently, the genomic landscape of SRMs is understudied, and clinically relevant tools for malignancy detection and fast tumor growth prediction are lacking. The aim of the study was to evaluate whether mutations in SRMs are associated with increased risk of renal cell carcinoma (RCC) or aggressive tumors.</p><p><strong>Methods: </strong>In this pilot study, 52 patients with SRMs were divided based on tumor histology into RCC and benign tumors, while RCC cases were divided into fast-growing and slow-growing tumor groups. Tissue biopsy samples evaluated for mutations in 51 cancer hotspot genes using next generation sequencing and qPCR. Non-benign mutations were tested for associations with RCC and clinical features. Receiver operating curve analysis used for evaluation of mutation biomarker models prediction of RCC and fast-growing tumors.</p><p><strong>Results: </strong>75% of SRMs harbored non-synonymous alterations in 16/51 genes. 38.5% of detected mutations were listed in ClinVar and correlated with smaller SRM volume (p = 0.023). KRAS, VHL, HNF1A, TP53, and ATM mutations were predominantly detected in RCC rather than benign SRMs (p = 0.046). SRMs with pathogenic mutations were at three times higher risk of being RCC and four times higher risk of fast growth.</p><p><strong>Conclusion: </strong>Genomic biomarkers may improve risk stratification and management of patients with SRMs, however a more extensive genomic analysis of SRMs is still needed.</p>","PeriodicalId":15118,"journal":{"name":"Journal of Cancer Research and Clinical Oncology","volume":"151 3","pages":"118"},"PeriodicalIF":2.7,"publicationDate":"2025-03-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11928375/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143676969","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":"Elevated VRK1 levels after androgen deprivation therapy promote prostate cancer progression by upregulating YAP1 expression.","authors":"Yibo Meng, Jianchao Ge, Cheng Zhou, Hangbin Ma, Chenchen Chen, Yinghao Zhou, Xuetao Hu, Yaozong Xu, Xilong Wang, Guowei Shi, Wandong Yu, Jun Zhang","doi":"10.1007/s00432-025-06168-z","DOIUrl":"10.1007/s00432-025-06168-z","url":null,"abstract":"<p><strong>Purpose: </strong>Vaccinia-related kinase 1 (VRK1) is a serine-threonine kinase involved in the proliferation and migration of various cancer cells. However, its role in prostate cancer (PCa), particularly in the development of therapeutic resistance, remains unclear.</p><p><strong>Methods: </strong>We established an androgen-independent PCa cell line derived from LNCaP prostate cancer cells and conducted transcriptome and proteome sequencing together with bioinformatic analyses of large clinical sample databases to investigate the potential role of VRK1 in PCa progression. The correlation between VRK1 and androgen receptor (AR) signaling was evaluated under simulated clinical treatment conditions. The effects of VRK1 on cell proliferation were assessed in vitro and in vivo using Cell Counting Kit-8 and colony formation assays. Additionally, proteome and transcriptome sequencing, combined with rescue experiments were performed to explore VRK1-regulated signaling pathways related to cell proliferation and therapeutic resistance.</p><p><strong>Results: </strong>VRK1 expression was elevated during the progression of androgen-dependent prostate cancer to castration-resistant prostate cancer under therapeutic conditions, and high VRK1 expression was associated with a poor prognosis in patients with PCa. VRK1 was regulated by AR signaling, and its silencing suppressed PCa cell proliferation both in vitro and in vivo. VRK1 drove cell proliferation and therapeutic resistance in PCa by modulating yes-associated protein 1 (YAP1).</p><p><strong>Conclusions: </strong>VRK1 serves as a prognostic marker in PCa, regulated by AR signaling. VRK1 depletion inhibited cell proliferation both in vitro and in vivo, while elevated VRK1 upregulated YAP1, promoting cell proliferation and therapeutic resistance.</p>","PeriodicalId":15118,"journal":{"name":"Journal of Cancer Research and Clinical Oncology","volume":"151 3","pages":"116"},"PeriodicalIF":2.7,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11926012/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143669957","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":"NSUN5 promotes cholangiocarcinoma progression by enhancing GLS mRNA stabilization.","authors":"Ming Shu, Kunpeng Guo, Yikai Huang, Weishan Wang","doi":"10.1007/s00432-025-06163-4","DOIUrl":"10.1007/s00432-025-06163-4","url":null,"abstract":"<p><strong>Background: </strong>NSUN5, also known as NOP2/Sun domain 5, is a pivotal RNA methyltransferase that catalyzes the formation of 5-methylcytosine (m5C). Cuproptosis, induced by elevated copper concentrations, is under investigation as a potential therapeutic strategy for cancer treatment. Despite this, the specific roles and the molecular mechanisms underlying Cuproptosis and NSUN5-mediated m5C modification in cholangiocarcinoma (CCA) remain to be fully elucidated.</p><p><strong>Methods: </strong>Human tissue samples were collected to assess the expression levels of NSUN5 in CCA. In vitro functional assays were conducted to evaluate the biological function of NSUN5. The functional mechanism of NSUN5 on glutaminase (GLS) was investigated using RNA pull-down, RNA immunoprecipitation, molecular docking, and RNA stability assays.</p><p><strong>Results: </strong>This study identified an upregulation of NSUN5 in CCA tissues. The knockdown of NSUN5 diminished the proliferation, migration, and invasion capabilities of CCA cells in vitro. In contrast, the overexpression of NSUN5 enhanced the growth and metastasis of CCA cells. Additionally, an increased copper content was detected in CCA tissues, which correlated with aggressive clinical features. CCA cells exhibited resistance to cuproptosis by upregulating GLS expression. Functionally, NSUN5 was found to positively modulate GLS expression. The NSUN5-mediated m5C modification at site 137 C on the GLS mRNA sequence stabilizes the GLS mRNA, leading to an accumulation of GLS within cells.</p><p><strong>Conclusions: </strong>Our findings highlight the critical role of NSUN5 in CCA progression through m5C-dependent stabilization of the GLS transcript, suggesting a potential targeted therapeutic strategy for CCA.</p>","PeriodicalId":15118,"journal":{"name":"Journal of Cancer Research and Clinical Oncology","volume":"151 3","pages":"117"},"PeriodicalIF":2.7,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11926023/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143669958","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":"Extracellular NAD⁺ levels are associated with CD203a expression on Th17 cells and predict long-term recurrence-free survival in hepatocellular carcinoma.","authors":"Julia Babigian, Philipp Brunnbauer, Can Kamali, Sebastian Knitter, Eriselda Keshi, Matthäus Felsenstein, Philipp Haber, Isis Lozzi, Wenzel Schöning, Johann Pratschke, Felix Krenzien","doi":"10.1007/s00432-025-06155-4","DOIUrl":"10.1007/s00432-025-06155-4","url":null,"abstract":"<p><strong>Background and aims: </strong>Mortality rates for hepatocellular carcinoma (HCC) remain high, while multimodal treatment approaches offer new perspectives. Here, we investigated the association of extracellular nicotinamide adenine dinucleotide (eNAD⁺) on ecto-nucleotide pyrophosphatase/phosphodiesterase 1 (CD203a, ENPP1 or PC-1) on Th17 cells in relation to the likelihood of HCC recurrence following liver resection.</p><p><strong>Method: </strong>The study compared heparinized blood plasma samples from 95 patients who underwent liver resection, including 25 patients with HCC and 24 control patients without liver disease. Plasma eNAD⁺ concentrations were determined using a heat-based dichotomous pH extraction method, followed by enzymatic cycling and a colorimetric assay for quantification. Fibrosis was graded histologically using the Desmet score (F0-F4). Surface expression analysis was performed using flow cytometry.</p><p><strong>Results: </strong>With increasing grades of liver fibrosis predominant in HCC patients, a significant reduction in plasma eNAD⁺ concentrations was measured (p < 0.05). Further, a significant correlation was found between HCC patients and CD203a expression on CD4⁺, CCR4⁺ as well as CCR6⁺ T cells (p < 0.05). Patients who exhibited high proportions of CD203a expressing Th17 cells (CD4⁺, CCR6⁺ CCR4⁺) post surgery were found to be at a sixfold increased risk (HR 6.38, 95% Cl 1.51-27.00) of HCC recurrence and had a median recurrence-free survival of 233 days (p < 0.05), compared to patients with low CD203a expressing Th17 cells (CD4⁺ CCR6⁺ CCR4⁺). Similarly, patients who had a high proportion of CD203a expressing Th17 cells (CD4⁺ CCR6⁺) following surgery had a fivefold increased risk (HR 5.56, 95% Cl 1.58-19.59) of HCC recurrence and a median recurrence-free survival of 334 days (p < 0.05) compared to those with low CD203a expressing Th17 cells (CCR6⁺).</p><p><strong>Conclusion: </strong>The data indicates that eNAD⁺ levels are decreased in patients with liver fibrosis or cirrhosis. Strikingly, patients with high CD203a expression on Th17 cells had a significantly increased likelihood of recurrence, highlighting its potential as a valuable prognostic marker and a possible therapeutic target.</p>","PeriodicalId":15118,"journal":{"name":"Journal of Cancer Research and Clinical Oncology","volume":"151 3","pages":"115"},"PeriodicalIF":2.7,"publicationDate":"2025-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11923025/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143662533","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":"Upstream stimulating factor 1 (USF1) -202 G/A polymorphism and serum levels of USF1 and USF2 are associated with gastric cancer risk: a case control study.","authors":"Ghizlane Bounder, Mohamed Reda Jouimyi, Imane Essaidi, Ilhame Elyounsi, Hasna Boura, Valérie Michel, Wafa Badre, Eliette Touati, Fatima Maachi","doi":"10.1007/s00432-025-06158-1","DOIUrl":"10.1007/s00432-025-06158-1","url":null,"abstract":"<p><strong>Purpose: </strong>Gastric cancer is an inflammation-driven disease often associated with a bad prognosis. Upstream stimulatory factors USF1 and USF2 are pleiotropic transcription factors, with tumor suppressor function. Low expression of USF1 is associated with low survival in gastric cancer patients. USF1 genetic polymorphism -202G > A has been associated with cancer susceptibility. Our aim was to investigate USF1 gene polymorphism and serum level with the risk of gastric cancer.</p><p><strong>Methods: </strong>USF1-202 G/A polymorphism was analyzed by sanger sequencing, with the measure of USF1/USF2 serum levels by ELISA in H. pylori-positive patients with chronic gastritis, gastric precancerous lesions, gastric cancer and in healthy controls.</p><p><strong>Results: </strong>Our results show that the presence of the USF1-202 A allele increased the risk of gastric cancer compared to G (OR = 2; 95% CI 1.07-3.9; P = 0.02). Genotypically and under the dominant mutation model, the combined USF1- GA/AA -202 genotypes corresponded to higher risk of gastric cancer (OR = 3.5; 95% CI 1.4-8.2; p-value = 0.005) than the GG genotype. Moreover, the G/A transition at USF1-202 was associated with lower USF1 serum level, and mostly observed in gastric cancer patients where the average serological level of USF1 were 2.3 and twofold lower for the AA and GA genotypes, respectively, compared to GG.</p><p><strong>Conclusion: </strong>USF1-202 G/A polymorphism constitutes a gastric cancer genetic risk factor. Together with USF1/USF2 serum level, they can be proposed as promising biomarkers for gastric cancer detection/prevention.</p>","PeriodicalId":15118,"journal":{"name":"Journal of Cancer Research and Clinical Oncology","volume":"151 3","pages":"113"},"PeriodicalIF":2.7,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11919976/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143657115","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}