Carcinogenesis最新文献_第2页

The evolving role for surgery in pancreatic cancer. 外科手术在胰腺癌中不断演变的角色。

IF 3.3 3区医学

Carcinogenesis Pub Date : 2024-11-22 DOI: 10.1093/carcin/bgae062

David Tuveson, Peter Allen

引用次数: 0

Germline Alteration Analysis Reveals EPHB4R91H Mutation as a Key Player in Multiple Primary Lung Tumors. 种系畸变分析揭示 EPHB4R91H 突变是多种原发性肺肿瘤的关键因素

IF 3.3 3区医学

Carcinogenesis Pub Date : 2024-11-22 DOI: 10.1093/carcin/bgae074

Jing Li, Yanan Li, Xinjuan Wang, Zhigang Zhou, Xiangnan Li, Songwei Yue, Huaqi Wang, Ming Yang, Guojun Zhang

{"title":"Germline Alteration Analysis Reveals EPHB4R91H Mutation as a Key Player in Multiple Primary Lung Tumors.","authors":"Jing Li, Yanan Li, Xinjuan Wang, Zhigang Zhou, Xiangnan Li, Songwei Yue, Huaqi Wang, Ming Yang, Guojun Zhang","doi":"10.1093/carcin/bgae074","DOIUrl":"https://doi.org/10.1093/carcin/bgae074","url":null,"abstract":"Multiple primary lung tumor is garnering attention from clinicians, with adenocarcinoma emerging as the predominant histological type. Because of the heterogeneity and diffuse distribution of lesions in the same patient, the treatment of multiple primary lung adenocarcinoma (MPLA) is a significant challenge. As a kind of variation unaffected by tumor heterogeneity, germline alterations may play a key role in the development of MPLA. Here, whole-exome sequencing (WES) of peripheral blood was employed to obtain germline alteration data. Intergroup comparative analyses on rare and deleterious alterations of MPLA, solitary lung adenocarcinoma, and healthy individuals in a MPLA family were performed to clarify the candidate alterations. WES and targeted Sanger sequencing were performed in 27 disseminated MPLA patients to detect the mutation site that had been screened. A rare and deleterious germline alteration, EPHB4R91H, was found in all of the patients of an MPLA family and a patient with disseminated MPLA. It was revealed that EPHB4R91H was able to enhance the proliferation, migration, and invasion ability of A549 cells through increased binding affinity to ephrinB2, which in turn activated the EPHB4/ERK/JNK/MAPK pathway. Our findings corroborate that germline alterations are involved in the development of MPLA. And it was found for the first time that the EPHB4R91H mutation promotes the development of MPLA by enhancing its affinity for ephrinB2 and thereby active EPHB4/ERK/JNK/MAPK pathway.","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2024-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142686222","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}

引用次数: 0

CAFomics: convergence to translation for precision stroma approaches. CAFomics：精准基质方法的转化。

IF 3.3 3区医学

Carcinogenesis Pub Date : 2024-11-22 DOI: 10.1093/carcin/bgae063

Ian C McCabe, Xianlu L Peng, Joseph F Kearney, Jen Jen Yeh

{"title":"CAFomics: convergence to translation for precision stroma approaches.","authors":"Ian C McCabe, Xianlu L Peng, Joseph F Kearney, Jen Jen Yeh","doi":"10.1093/carcin/bgae063","DOIUrl":"10.1093/carcin/bgae063","url":null,"abstract":"A noticeable characteristic of pancreatic ductal adenocarcinoma (PDAC) tumors is a dense tumor microenvironment with abundant and dense, desmoplastic stroma woven tightly with both cellular and matrix components. The high stromal density is associated with higher intratumor pressures which, until the last decade, was largely assumed to be tumor protective, confirmed by early studies demonstrating that altering the stroma was effective in genetically engineered models of PDAC. However, clinical trials using these approaches have been disappointing. There is increasing recognition that stroma heterogeneity is much greater than initially thought with an explosion of investigation into cancer-associated fibroblast (CAF) subpopulations led by experimental and single-cell transcriptomic studies. This review summarizes and attempts to harmonize the current transcriptomic data of CAF subpopulations. Understanding the heterogeneity of CAFs, the matrix, and other tumor microenvironment features will be critical to developing effective therapeutic approaches. Identifying model systems that best recapitulate the clinical behavior and treatment response of human PDAC will be important. Examining subpopulations as defined by clinical outcome will remain a critical step in defining clinically impactful CAF subtypes in larger clinical cohorts. The future of precision oncology in PDAC will depend on the integration of precision tumor epithelial and precision stroma approaches.","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":"817-822"},"PeriodicalIF":3.3,"publicationDate":"2024-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142602972","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}

引用次数: 0

BRAF V600E-induced distinct DNA damage response defines the therapeutic potential of p53 activation for TP53 wild-type colorectal cancer. BRAF V600E 诱导的独特 DNA 损伤反应决定了 p53 激活对 TP53 野生型结直肠癌的治疗潜力。

IF 3.3 3区医学

Carcinogenesis Pub Date : 2024-11-22 DOI: 10.1093/carcin/bgae040

Shinji Tokuyama, Hisakazu Kato, Hidekazu Takahashi, Kyoko Ueda, Asami Arita, Ryuta Ueda, Hiroto Seto, Yuki Sekido, Tsuyoshi Hata, Atsushi Hamabe, Takayuki Ogino, Norikatsu Miyoshi, Mamoru Uemura, Ken Matsuoka, Osamu Tsukamoto, Hirofumi Yamamoto, Yuichiro Doki, Hidetoshi Eguchi, Seiji Takashima

{"title":"BRAF V600E-induced distinct DNA damage response defines the therapeutic potential of p53 activation for TP53 wild-type colorectal cancer.","authors":"Shinji Tokuyama, Hisakazu Kato, Hidekazu Takahashi, Kyoko Ueda, Asami Arita, Ryuta Ueda, Hiroto Seto, Yuki Sekido, Tsuyoshi Hata, Atsushi Hamabe, Takayuki Ogino, Norikatsu Miyoshi, Mamoru Uemura, Ken Matsuoka, Osamu Tsukamoto, Hirofumi Yamamoto, Yuichiro Doki, Hidetoshi Eguchi, Seiji Takashima","doi":"10.1093/carcin/bgae040","DOIUrl":"10.1093/carcin/bgae040","url":null,"abstract":"BRAF V600E, one of the most frequent mutations in the MAPK pathway, confers poor prognosis to colorectal cancers (CRCs), partly because of chemotherapeutic resistance. Oncogene-induced DNA damage responses (DDRs) that primarily activate p53 are important mechanistic barriers to the malignant transformation of cells; however, the mechanism underlying this impairment in cancer remains unknown. Here, we evaluated the responses of BRAFV600E-induced DDRs in two CRC cell lines, SW48 and LIM1215, both of which harbor wild-type TP53, KRAS, and BRAF. BRAFV600E transduction exhibited distinct phenotypes in these cells: SW48 cell proliferation markedly decreased, whereas that of LIM1215 increased. BRAFV600E expression induced the activation of oncogene-induced DDR signaling in SW48 cells, but not in LIM1215 cells, whereas chemotherapeutic agents similarly activated DDRs in both cell lines. Knockdown experiments revealed that these responses in SW48 cells were mediated by p53-p21 pathway activation. Comet assay (both alkaline and neutral) revealed that BRAFV600E increased single-strand breaks to the same extent in both cell lines; however, in the case of LIM1215 cells, it only facilitated double-strand breaks. Furthermore, the proliferation of LIM1215 cells, wherein no oncogene-induced DDRs occurred, was synergistically inhibited upon MDM2 inhibitor-mediated p53 activation combined with MEK inhibition. Taken together, these distinct DDR signaling responses highlight the novel characteristics of BRAFV600E-mutated CRC cells and define the therapeutic potential of p53 activation combined with MAPK inhibition against TP53 wild-type CRC harboring a BRAFV600E mutation.","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":"857-867"},"PeriodicalIF":3.3,"publicationDate":"2024-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141310122","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}

引用次数: 0

Prognostic value of circulating tumor DNA in different cancer types detected by ultra-low-pass whole-genome sequencing. A systematic review and patient-level survival data meta-analysis. 通过超低通量全基因组测序检测不同癌症类型中循环肿瘤DNA的预后价值。系统综述和患者生存数据荟萃分析。

IF 3.3 3区医学

Carcinogenesis Pub Date : 2024-11-16 DOI: 10.1093/carcin/bgae073

Miguel Sogbe, Daniel Aliseda, Paloma Sangro, Manuel de la Torre-Aláez, Bruno Sangro, Josepmaria Argemi

{"title":"Prognostic value of circulating tumor DNA in different cancer types detected by ultra-low-pass whole-genome sequencing. A systematic review and patient-level survival data meta-analysis.","authors":"Miguel Sogbe, Daniel Aliseda, Paloma Sangro, Manuel de la Torre-Aláez, Bruno Sangro, Josepmaria Argemi","doi":"10.1093/carcin/bgae073","DOIUrl":"https://doi.org/10.1093/carcin/bgae073","url":null,"abstract":"Ultra-low-pass whole-genome sequencing (ULP-WGS) (≤0.5× coverage) of plasma cell-free DNA (cfDNA) has emerged as a low-cost promising tool to assess circulating tumor DNA (ctDNA) fraction. This meta-analysis aims to summarize the current findings and comprehensively investigate the prognostic value of baseline ctDNA detected by ULP-WGS in solid tumors. A systematic review was carried out by searching PubMed/MEDLINE and Scopus databases to identify eligible studies conducted between January 2014 and January 2024. Inclusion criteria comprised studies with reported overall survival (OS) and progression-free survival (PFS) outcomes across therapy-naïve patients with different solid tumors. All patients underwent baseline ULP-WGS of plasma cfDNA and were categorized as ctDNA positive (tumor fraction ≥10%) or negative (tumor fraction <10%). A one-stage meta-analysis was performed using patient-level survival data reconstructed from published articles. A Cox proportional hazards model with shared frailty was used to assess the difference in survival between arms. A total of six studies, comprising 620 patients (367 negative ctDNA and 253 positive ctDNA), were included in the OS analysis, while five studies, involving 349 patients (212 negative ctDNA and 137 positive ctDNA), were included in the PFS analysis. The meta-analysis showed that patients with baseline positive ctDNA had a significantly higher risk of death (HR = 2.60, 95% CI: 2.01-3.36) and disease progression (HR = 2.28, 95% CI: 1.71-3.05) compared to those with negative ctDNA. The presence of a positive ctDNA at baseline is associated with increased risk of death and progression in patients with same stage cancer.","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2024-11-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142643499","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}

引用次数: 0

Correction to: Characterization of microRNA-29 family expression and investigation of their mechanistic roles in gastric cancer. 更正为microRNA-29家族的表达特征及其在胃癌中的作用机制研究。

IF 3.3 3区医学

Carcinogenesis Pub Date : 2024-11-11 DOI: 10.1093/carcin/bgae070

引用次数: 0

Establishing a new-onset diabetes-related metabolism signature for predicting the prognosis and immune landscape in pancreatic cancer. 建立新发糖尿病相关代谢特征，用于预测胰腺癌的预后和免疫状况。

IF 3.3 3区医学

Carcinogenesis Pub Date : 2024-11-11 DOI: 10.1093/carcin/bgae072

Yilei Yang, Luyao Liu, Haochen Cui, Bin Cheng, Wang Peng, Ronghua Wang, Jinlin Wang, Wei Chen, Mengdie Cao, Yanling Li, Jingwen Liang, Shiru Chen, Shuya Bai, Yuchong Zhao

{"title":"Establishing a new-onset diabetes-related metabolism signature for predicting the prognosis and immune landscape in pancreatic cancer.","authors":"Yilei Yang, Luyao Liu, Haochen Cui, Bin Cheng, Wang Peng, Ronghua Wang, Jinlin Wang, Wei Chen, Mengdie Cao, Yanling Li, Jingwen Liang, Shiru Chen, Shuya Bai, Yuchong Zhao","doi":"10.1093/carcin/bgae072","DOIUrl":"https://doi.org/10.1093/carcin/bgae072","url":null,"abstract":"New-onset diabetes (NOD) is a common condition among patients with pancreatic adenocarcinoma (PAAD) and is related to poor clinical outcomes. The potential impact of NOD on PAAD progression and the tumor microenvironment remains unclear. Here, we revealed that NOD in PAAD was associated with metabolic disorders. Utilizing three machine learning algorithms, a new-onset diabetes-related metabolism signature (NRMS) was established. Validated in three independent cohorts, patients with a high NRMS score exhibited worse prognosis. Moreover, an elevated NRMS score was associated with an immunosuppressive microenvironment and diminished response to immunotherapy. Further experiments demonstrated that ALDH3A1, a key feature in NRMS, was significantly up-regulated in tissues from PAAD patients with NOD and played a crucial role in tumor progression and immune suppression. Our findings highlight the potential of NRMS as a prognostic biomarker and an indicator of immunotherapy response for patients with PAAD.","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2024-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142615485","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}

引用次数: 0

Inhibition of phospholipase D1 reduces pancreatic carcinogenesis in mice partly through a FAK-dependent mechanism. 抑制磷脂酶 D1 可部分通过 FAK 依赖性机制减少小鼠胰腺癌的发生。

IF 3.3 3区医学

Carcinogenesis Pub Date : 2024-11-02 DOI: 10.1093/carcin/bgae071

Hala A Addassi, Irena Krga, Fernando Villarreal, Joseph F LaComb, Michael A Frohman, Karen Matsukuma, Gerardo G Mackenzie

{"title":"Inhibition of phospholipase D1 reduces pancreatic carcinogenesis in mice partly through a FAK-dependent mechanism.","authors":"Hala A Addassi, Irena Krga, Fernando Villarreal, Joseph F LaComb, Michael A Frohman, Karen Matsukuma, Gerardo G Mackenzie","doi":"10.1093/carcin/bgae071","DOIUrl":"https://doi.org/10.1093/carcin/bgae071","url":null,"abstract":"Phospholipase D (PLD) plays a critical role in cancer progression. However, its role in pancreatic cancer remains unclear. Thus, we evaluated the role of PLD1, one of two classical isoforms of PLD, in pancreatic carcinogenesis in vivo. The role of PLD1 in tumor growth was evaluated by subcutaneously transplanting human MIA PaCa-2 cells expressing endogenous PLD1 levels (Ctr KD cells) or cells in which PLD1 was knocked down (Pld1 KD cells) into immunodeficient mice. Twenty days post-implantation, tumors that arose from Pld1-KD cells were significantly smaller, compared to controls (Ctr KD). Then, we assessed the role of PLD1 in the tumor microenvironment, by subcutaneously implanting mouse LSL-KrasG12D/+;Trp53R172H/+;Pdx-1-Cre (KPC) cells into wild-type (WT) or PLD1 knockout (Pld1-/-) mice. Compared to WT, tumor growth was attenuated in Pld1-/- mice by 39%, whereas treatment of Pld1-/- mice with gemcitabine reduced tumor growth by 79%. When PLD1 was ablated in LSL-KrasG12D;Ptf1Cre/+ (KC) mice, no reduction in acinar cell loss was observed, compared to KC mice. Finally, treatment of KC mice with a small molecule inhibitor of PLD1 and PLD2 (FIPI) significantly reduced acinar cell loss and cell proliferation, compared to vehicle-treated mice. Mechanistically, the effect of PLD on tumor growth is mediated, partly, by the FAK pathway. In conclusion, while PLD1 is a critical regulator of pancreatic xenograft and allograft growth, playing an important role at the tumor and at the microenvironment levels, inhibition of PLD1 and PLD2 are necessary to reduce pancreatic carcinogenesis in KC mice, and might represent a novel therapeutic target.","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2024-11-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142564080","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}

引用次数: 0

Colorectal cancer cells with high metastatic potential drive metastasis by transmitting exosomal miR-20a-3p through modulating NF1/MAPK pathway. 具有高转移潜能的结直肠癌细胞通过调节 NF1/MAPK 通路传递外泌体 miR-20a-3p 推动转移。

IF 3.3 3区医学

Carcinogenesis Pub Date : 2024-10-10 DOI: 10.1093/carcin/bgae036

Yahang Liang, Junyu Li, Tao Li, Mingming Li, Hualin Liao, Yang Liu, Yao Yao, Lingling Yang, Xiong Lei

{"title":"Colorectal cancer cells with high metastatic potential drive metastasis by transmitting exosomal miR-20a-3p through modulating NF1/MAPK pathway.","authors":"Yahang Liang, Junyu Li, Tao Li, Mingming Li, Hualin Liao, Yang Liu, Yao Yao, Lingling Yang, Xiong Lei","doi":"10.1093/carcin/bgae036","DOIUrl":"10.1093/carcin/bgae036","url":null,"abstract":"Cancer cells exhibit heterogeneous metastatic potential, and high metastatic (HM) subclones can enhance the metastatic potential of low metastatic subclones by transmitting some factors. Exosomal miRNAs play a pivotal role in the crosstalk of heterogeneous metastatic subclones. This study discovered that miR-20a-3p was upregulated in colorectal adenocarcinoma (CRA), correlated with metastasis, and potentially served as a prognostic indicator for CRA. miR-20a-3p could promote the proliferation, migration, and invasion of CRA cells. Interestingly, HM CRA cells could promote malignant phenotypes of low metastatic CRA cells by transmitting exosomal miR-20a-3p. Mechanically, miR-20a-3p could inhibit neurofibromin 1(NF1), thereby activate the rat sarcoma viral oncogene (RAS)-mediated mitogen-activated protein kinases (MAPK) signaling pathway to drive the metastasis of CRA. In summary, our study provided evidence that colorectal cancer cells with HM potential drive metastasis by transmitting exosomal miR-20a-3p through modulating the NF1/MAPK pathway.","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":"773-785"},"PeriodicalIF":3.3,"publicationDate":"2024-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141199183","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}

引用次数: 0

Dehydroabietylamine exerts antitumor effects by affecting nucleotide metabolism in gastric cancer. 脱氢阿糖胞苷胺通过影响胃癌核苷酸代谢发挥抗肿瘤作用

IF 3.3 3区医学

Carcinogenesis Pub Date : 2024-10-10 DOI: 10.1093/carcin/bgae037

Jingsong Ma, Jiabao Zhao, Zhengxin Wu, Jinshui Tan, Meijuan Xu, Wenjie Ye, Mengya Zhong, Yubo Xiong, Guangchao Pan, Huiwen Zhou, Shengyi Zhou, Xuehui Hong

{"title":"Dehydroabietylamine exerts antitumor effects by affecting nucleotide metabolism in gastric cancer.","authors":"Jingsong Ma, Jiabao Zhao, Zhengxin Wu, Jinshui Tan, Meijuan Xu, Wenjie Ye, Mengya Zhong, Yubo Xiong, Guangchao Pan, Huiwen Zhou, Shengyi Zhou, Xuehui Hong","doi":"10.1093/carcin/bgae037","DOIUrl":"10.1093/carcin/bgae037","url":null,"abstract":"Nucleotide metabolism is the ultimate and most critical link in the self-replication process of tumors, including gastric cancer (GC). However, in clinical treatment, classic antitumor drugs such as 5-fluorouracil (5-FU) are mostly metabolic analogs of purines or pyrimidines, which lack specificity for tumor cells and therefore have significant side effects. It is unclear whether there are other drugs that can target nucleotide metabolism, except for nucleic acid analogs. Here, we found that a natural compound, dehydroabietylamine (DHAA), significantly reduced the viability and proliferation of GC cells and organoids. DHAA disrupts the purine and pyrimidine metabolism of GC cells, causing DNA damage and further inducing apoptosis. DHAA treatment decreased transcription and protein levels of key enzymes involved in the nucleotide metabolism pathway, with significant reductions in the expression of pyrimidine metabolism key enzymes CAD, DHODH, and purine metabolism key enzymes PAICS. We also found that DHAA directly binds to and reduces the expression of Forkhead box K2 (FOXK2), a common transcription factor for these metabolic enzymes. Ultimately, DHAA was shown to delay tumorigenesis in K19-Wnt1/C2mE transgenic mice model and reduce levels of CAD, DHODH, and PAICS in vivo. We demonstrate that DHAA exerts an anticancer effect on GC by targeting transcription factor FOXK2, reducing transcription of key genes for nucleotide metabolism and impairing nucleotide biosynthesis, thus DHAA is a promising candidate for GC therapy.","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":"759-772"},"PeriodicalIF":3.3,"publicationDate":"2024-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11464700/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141310123","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}

引用次数: 0