Carcinogenesis最新文献

{"title":"Role of the nucleotide excision repair function of CETN2 in the inhibition of the sensitivity of hepatocellular carcinoma cells to oxaliplatin.","authors":"Hengcheng Tang, Huaduan Zi, Donghu Zhou, Yanmeng Li, Xiaojin Li, Zhibin Chen, Qianyu Zhu, Qin Ouyang, Pingping He, Sisi Chen, Yanling Li, Jiang Long, Jian Huang","doi":"10.1093/carcin/bgaf003","DOIUrl":"10.1093/carcin/bgaf003","url":null,"abstract":"<p><p>Resistance to platinum-based chemotherapy agents like oxaliplatin (OXA) poses significant challenges in the treatment of cancers such as hepatocellular carcinoma (HCC). Centrin 2 (CETN2), which functions in nucleotide excision repair (NER) of DNA damage, is overexpressed in HCC. We investigated the potential role of CETN2 in modulating the sensitivity of HCC cells to OXA. CETN2 expression correlated with decreased OXA sensitivity in Huh7 and Hep3B HCC cell lines. CETN2 forms a complex with XPC, which is crucial for the initial DNA damage recognition in NER, thereby enhancing NER and reducing the efficacy of OXA. siRNA-mediated knockdown of CETN2 increased OXA-induced cytotoxicity and apoptosis, confirming its role in chemoresistance. Moreover, overexpression of CETN2 inhibited OXA-induced DNA damage, an effect partially reversed by XPC knockdown. Our findings highlight CETN2 as a potential biomarker and therapeutic target in overcoming OXA resistance in HCC and suggest the possibility for CETN2 inhibitors in enhancing chemotherapeutic efficacy in the treatment of HCC.</p>","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143405744","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Olfactomedin 4 promotes gastric cancer cell G2/M progression and serves as a therapeutic target in gastric adenocarcinoma.","authors":"Wenli Liu, Hongzhen Li, Istvan Botos, Chutima Kumkhaek, Jianqiong Zhu, Griffin P Rodgers","doi":"10.1093/carcin/bgaf010","DOIUrl":"10.1093/carcin/bgaf010","url":null,"abstract":"<p><p>Olfactomedin 4 (OLFM4) is a member of the olfactomedin domain-containing olfactomedin glycoprotein family and plays important roles in innate immunity, inflammation, and cancer. It exhibits increased expression in gastric cancer patient tissues and has been shown to regulate proliferation and apoptosis in gastric cancer cells. However, the molecular mechanism(s) underlying OLFM4's role in gastric cancer remain unknown. In this study, we found that OLFM4 knockdown significantly inhibited YCC3 gastric cancer cell proliferation and induced G2/M cell cycle arrest. Yeast two-hybridization screening revealed that OLFM4 directly interacts with cyclin B1 interacting protein 1 (CCNB1IP1), an E3 ubiquitin protein ligase. In YCC3 cells, OLFM4 co-immunoprecipitated and colocalized with CCNB1IP1 and underwent cell cycle phase-specific nucleo-cytoplasmic shuttling. OLFM4 knockdown decreased both cyclin B1 protein levels and CDK1 activity in YCC3 cells. Screening of a cohort of OLFM4-targeted microRNAs (miRNAs) for their impact on cell proliferation identified several that significantly downregulated OLFM4 protein levels and inhibited YCC3 cell proliferation in vitro. Rescue experiments demonstrated that these miRNAs' inhibitory effect on cell proliferation was partially related to their downregulation of OLFM4. When three of these miRNAs were individually administered intratumorally to nude mice bearing YCC3 cell xenografts, tumor growth was significantly inhibited when compared with tumors treated with a negative control miRNA. These results suggest that OLFM4 promotes cell cycle progression and cell proliferation in gastric cancer cells and may have utility as a therapeutic target in gastric adenocarcinoma.</p>","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12013284/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143582186","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":"NUF2 and NEK2 promote malignant progression of gallbladder cancer by remodeling the extracellular matrix.","authors":"Ming Gao, Peng Ye, Yutong Zhang, Yarong Guo, Jun Xu","doi":"10.1093/carcin/bgaf019","DOIUrl":"10.1093/carcin/bgaf019","url":null,"abstract":"<p><p>Gallbladder cancer (GBC) ranks as the most common malignant tumor of the biliary tract, which has been characterized by late diagnosis, low excisional rate, and poor prognosis. Recent studies exploring the roles of malignant progression-associated genes in GBC remain limited. Our study aims to identify significant hub genes involved in its pathogenesis, which may serve as novel potential therapeutic targets for GBC. Here, we employed RNA-seq analysis to identify differentially expressed genes (DEGs) of seven GBC samples and five matched adjacent samples. After screening the DEGs in clinical sequencing data and GSE139682, we further obtained 549 genes with consistent expression trends in two datasets, including 155 upregulated and 394 downregulated genes. Gene Ontology (GO) enrichment analysis revealed that these genes were significantly enriched in extracellular matrix (ECM)-related processes, such as organization, structure, and composition, which hint to us that remodeling of ECM may be the main driving factor for the malignant progression of GBC. In addition, we screened 17 candidate hub genes through protein-protein interaction (PPI) network analysis and Cytoscape, subsequent GO and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses showed that the remodeled ECM mainly functions by affecting cell division. Moreover, we found that NEK2 and NUF2 were overexpressed in GBC tumor tissues and validated their function in the pro-proliferation of GBC cells. Our results highlight that NEK2 and NUF2 may be hub genes promoting the malignant progression of GBC and are expected to be reliable new therapeutic targets for GBC.</p>","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12137899/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143977441","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":"Current challenges and potential opportunities for interception and prevention of head and neck cancer.","authors":"Karam El-Bayoumy, Neil Christensen, James Broach, Craig Meyers, Douglas Stairs, Mitchell Machtay, Jiafen Hu, Zachary T Bitzer, Todd D Schell, Kun-Ming Chen, Yuan-Wan Sun, Dhimant Desai, Vonn Walter, Junjia Zhu","doi":"10.1093/carcin/bgaf025","DOIUrl":"10.1093/carcin/bgaf025","url":null,"abstract":"<p><p>Globally, the incidence of head and neck squamous cell carcinoma (HNSCC) has increased over recent decades and is projected to continue to rise, largely driven by increases in oropharyngeal squamous cell carcinoma (OPSCC), which is linked to HPV infection. HPV infection is also involved in the development of other cancers (anogenital and cervical), and almost 100% of cervical cancer patients are positive for HPV. OPSCC is the most common HPV-associated cancer in men and has exceeded the incidence of cervical cancer cases in women in the USA. Our knowledge of the carcinogenesis process from HPV infection to OPSCC development has been primarily extrapolated from cervical cancer models. While the cooperation of tobacco smoking and HPV infection is documented in cervical cancer, mechanistic studies to address this interaction in management and control of HNSCC are scarce and are also extrapolated from cervical cancer models. The molecular heterogeneity of HNSCC constitutes a tremendous challenge, and despite advances in several fronts in the management and control of HNSCC, short- and long-term treatment-associated morbidities remain substantial. In addition to deaths directly caused by this disease, survivors of this cancer have the second-highest rate of suicide compared with other cancers survivors. Given the existing gaps in our knowledge and the current clinical challenges, future studies including a number of new conceptual and methodological elements discussed in this review can lead to the discovery of biomarkers for early detection of the disease and novel strategies that will advance our knowledge to intercept and prevent HNSCC.</p>","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12163314/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144092900","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":"Smoking behavior-related genetic variants and lung cancer risk in Japanese: an assessment by mediation analysis.","authors":"Sayaka Yamamoto, Yuriko N Koyanagi, Yuji Iwashita, Tomohiro Shinozaki, Yutaka Fujiwara, Noriaki Sakakura, Megumi Hara, Yuichiro Nishida, Jun Otonari, Hiroaki Ikezaki, Shiroh Tanoue, Chihaya Koriyama, Yumiko Kasugai, Isao Oze, Teruhide Koyama, Satomi Tomida, Nobuaki Michihata, Yohko Nakamura, Sadao Suzuki, Hiroko Nakagawa-Senda, Mako Nagayoshi, Yoko Kubo, Yasufumi Kato, Kenji Wakai, Takeshi Watanabe, Masashi Ishizu, Naoyuki Takashima, Aya Kadota, Yukihide Momozawa, Masahiro Nakatochi, Takashi Tamura, Akio Niimi, Hidemi Ito, Keitaro Matsuo","doi":"10.1093/carcin/bgaf011","DOIUrl":"10.1093/carcin/bgaf011","url":null,"abstract":"<p><p>Cigarette smoking is one of the most important risk factors for lung cancer. Genetic studies have shown that smoking behavior-related genetic variants are directly associated with lung cancer, independent of smoking behavior, mainly in European populations. A recent genome-wide association study in Japan identified five loci associated with the number of cigarettes smoked per day. This study aimed to evaluate whether these loci are associated with lung cancer risk directly or indirectly through changing smoking behavior. Here, we conducted a case-control study (1427 cases and 5595 controls) and a prospective cohort study (128 incident cases in 10 520 subjects). Using mediation analysis, we decomposed the total effect of the lead single nucleotide polymorphism (SNP) at each locus on lung cancer risk into direct and indirect effects. The results of the two studies were pooled using a random-effects model to estimate summary relative risks (RRs) and their 95% confidence intervals (CIs). Two studies showed that: (i) rs78277894 (EPHX2-CLU, G > A) had a protective direct effect (RR: 0.84; 95% CI: 0.77-0.93) on lung cancer risk; and (ii) rs56129017 (CYP2A6, C > T) had carcinogenic direct and indirect effects on lung cancer risk (RR: 1.26; 95% CI: 1.15-1.39 and RR: 1.01; 95% CI: 1.00-1.01, respectively). This mediation analysis revealed that two smoking behavior-related SNPs, EPHX2-CLU rs78277894 and CYP2A6 rs56129017, were associated with lung cancer risk through pathways independent of changing smoking behavior. Our findings may contribute to our understanding of lung carcinogenesis pathways that cannot be addressed by changes in smoking behavior.</p>","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143584838","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A novel tRNA-derived small RNA 5'-tiRNA-His is a promising biomarker for diagnosis of colorectal cancer.","authors":"Xinliang Gu, Xincheng Yang, Danping Zhu, Xinwei Liu, Junjie Nie, Tao Xu, Yuqin Pan, Huiling Sun, Shukui Wang","doi":"10.1093/carcin/bgaf026","DOIUrl":"10.1093/carcin/bgaf026","url":null,"abstract":"<p><p>Colorectal cancer (CRC) is one of the most serious gastrointestinal tumors. The survival rate of patients with advanced stages is meager, so it is urgent to identify new diagnostic biomarkers with high sensitivity and specificity. tRNA-derived small RNAs (tsRNAs) are an emerging class of small non-coding RNAs that are highly abundant in the blood of cancer patients and are associated with various physiological and pathological processes. Therefore, the clinical value of tsRNAs in diagnosing CRC requires further investigation. In this study, we identified the differential expression profiles of tsRNAs in CRC tissues via Pandora sequencing. We selected 5'-tiRNA-His that were significantly highly expressed in CRC plasma and tissues for further investigation. Interestingly, the expression level of 5'-tiRNA-His was increased dramatically in the plasma of CRC patients and correlated with various clinicopathologic parameters. ROC analysis revealed that 5'-tiRNA-His had good diagnostic value in diagnosing CRC patients, superior to that of CEA, CA199, and CA724, and could significantly differentiate patients with CRC from healthy donors and patients with intestinal polyps. Moreover, 5'-tiRNA-His still had good diagnostic efficacy in the diagnosis of patients with early-stage CRC, and the diagnostic efficacy was further elevated when combined with clinically used tumor markers. In conclusion, our study identified plasma 5'-tiRNA-His as a promising biomarker for diagnosing and screening CRC.</p>","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144118926","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Triple-negative breast cancer molecular subtypes and potential detection targets for biological therapy indications.","authors":"Yanchuan Zhang, Qinghua Li, Jie Lan, Guojing Xie, Guangjie Zhang, Junhao Cui, Ping Leng, Yingshuang Wang","doi":"10.1093/carcin/bgaf006","DOIUrl":"10.1093/carcin/bgaf006","url":null,"abstract":"<p><p>Triple-negative breast cancer (TNBC) is a highly aggressive subtype of breast cancer associated with poor prognosis. While chemotherapy remains the conventional treatment approach, its efficacy is limited and often accompanied by significant toxicity. Advances in precision-targeted therapies have expanded treatment options for TNBC, including immunotherapy, poly (ADP-ribose) polymerase inhibitors, androgen receptor inhibitors, cell cycle-dependent kinase inhibitors, and signaling pathway inhibitors. However, the heterogeneous nature of TNBC contributes to variations in treatment outcomes, underscoring the importance of identifying intrinsic molecular subtypes for personalized therapy. Additionally, due to patient-specific variability, the therapeutic response to targeted treatments is inconsistent. This highlights the need to strategize patients based on potential therapeutic targets for targeted drugs to optimize treatment strategies. This review summarizes the classification strategies and immunohistochemical (IHC) biomarkers for TNBC subtypes, along with potential targets for identifying indications for targeted drug therapy. These insights aim to support the development of personalized treatment approaches for TNBC patients.</p>","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143467166","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genetic variants in glycosylation pathways are associated with colorectal cancer risk.","authors":"Hanchi Wu, Xiaoting He, Hao Wang, Junying Xu, Junli Ding, Dong Hua, Huiyu Wang","doi":"10.1093/carcin/bgae075","DOIUrl":"10.1093/carcin/bgae075","url":null,"abstract":"<p><p>The glycosylation pathway serves as a vital regulatory mechanism in colorectal cancer. However, how genetic variants in these pathways may affect the risk of colorectal cancer is still unknown. To examine the relationships between the risk of colorectal cancer and the presence of selected single-nucleotide polymorphisms (SNPs), 1150 patients and 1342 controls were included in this case-control study. We found that GALNT2 rs76000797 and rs11576324, GALNT6 rs67726586, FUT8 rs117497405, FUT2 rs111311275, and B4GALT5 rs6125695 were strongly correlated with the risk of colorectal cancer. Moreover, rs111311275 exhibited an expression quantitative trait locus effect on FUT2 in colorectal cancer tissues, which could increase the risk of colorectal cancer by influencing FUT2 expression. GEPIA research and microarray data revealed that FUT2 expression was higher in colorectal cancer tissues than in normal tissues and that individuals with colon cancer with high expression of FUT2 had longer overall survival times. Our study highlights the significant impact of genetic variants on glycosylation pathways and offers novel insights into potential biomarkers for colorectal cancer risk.</p>","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143964243","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Regulatory mechanisms of PFKFB2 in glycolysis and tumor metabolism: implications for cancer therapy.","authors":"Qiuwen Lou, Jie Chang, Yi Pan, Yuzhuo Gong, Wenxia Xu, Minfeng Tong, Lude Wang, Fengfeng Jiang","doi":"10.1093/carcin/bgaf022","DOIUrl":"10.1093/carcin/bgaf022","url":null,"abstract":"<p><p>Glycolysis is a crucial metabolic process that facilitates the rapid proliferation of cancer cells. Phosphofructokinase-1 (PFK-1) is the key rate-limiting enzyme in glycolysis, with fructose-2,6-diphosphate (F-2,6-BP) acting as its most effective regulator. The levels of F-2,6-BP are closely correlated with the activity of 6-phosphate fructose-2-kinase/fructose-2,6-diphosphatase (PFK-2/FBPase-2, PFKFB). The PFKFB family consists of four isoenzymes: PFKFB1-4. Most evidence suggests that PFKFB activity is essential for activating glycolytic and oncogenic properties in tumor cells. However, previous studies have focused predominantly on PFKFB3 and PFKFB4, with relatively few investigating PFKFB2. The role of PFKFB2 in cancer is complex and multifaceted, encompassing various aspects of tumor metabolism, cell migration, invasion, and the immune response. Consequently, this review aims to summarize the current understanding of the gene structure and biological function of PFKFB2 and to explore its pathogenic mechanisms in different cancers. Additionally, we highlight the metabolic signaling pathways associated with PFKFB2. This review seeks to provide insights into the current status of PFKFB2 and to assist in identifying new targets for cancer therapy.</p>","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":"46 2","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144332490","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MACC1 is a potential prognostic biomarker for cancer immunotherapy in lung adenocarcinoma.","authors":"Changqie Pan, Zhiyuan Zhou, Jun Cao, Lemeng Zhang, Tianli Cheng, Haitao Li, Zhou Jiang, Danhui Huang, Dongqiang Zeng, Yongzhong Luo, Jianhua Wu","doi":"10.1093/carcin/bgaf015","DOIUrl":"10.1093/carcin/bgaf015","url":null,"abstract":"<p><p>Our team previously reported that MACC1 levels are closely related to a variety of tumors and the efficacy of immune checkpoint blockade (ICB) therapy. However, the predictive value of MACC1 levels for lung adenocarcinoma (LUAD) immunotherapy has not been studied. This study aimed to investigate the predictive effect of the oncogene MACC1 on ICB reactivity in patients with LUAD. First, the expression patterns and clinical features of MACC1 in The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases were comprehensively evaluated using R packages. We subsequently assessed the correlations between MACC1 and immunological characteristics in the LUAD tumor microenvironment (TME) using the CIBERSORT algorithm. The results revealed that MACC1 overexpression was significantly correlated with 3 immune checkpoints, 14 tumor-infiltrating immune cells (TIICs), 9 immunomodulators, 5 anticancer immune process activities, and 3 effector genes of TIICs in LUAD. Additionally, on the basis of the prognostic genes from LASSO analysis, we developed the MACC1-related Risk Score (MRRS), which can accurately predict the prognosis and response to cancer immunotherapy in LUAD patients (HR = 3.50, AUC at 1, 2, and 3 years = 0.737, 0.744, and 0.724, respectively). Finally, in vivo experiments revealed that the combination of MACC1 silencing and PD-L1 inhibitors significantly inhibits tumor progression. These findings increase our understanding of MACC1 as a potential prognostic biomarker and potential therapeutic target for cancer immunotherapy. The MRRS may play a critical role in predicting the response of LUAD patients to ICB therapy.</p>","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143673375","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}