American journal of cancer research最新文献

{"title":"Systemic immunoinflammatory index and prognostic nutrition index for predicting pathologic responses of patients with advanced gastric cancer after neoadjuvant therapy for advanced gastric cancer.","authors":"Meng Fan, Jin Tang, Wei Du, Yang-Feng Du, Hai-Jun Liu","doi":"10.62347/PAYM2267","DOIUrl":"https://doi.org/10.62347/PAYM2267","url":null,"abstract":"<p><p>To investigate the value of prognostic nutrition index (PNI) and systemic immunoinflammatory index (SII) for predicting pathological responses of patients with advanced gastric cancer (GC) after neo-adjuvant chemotherapy (NACT). The clinicopathological data of 326 patients with advanced GC who received NACT in Xiangya School of Medicine, Central South University (The First People's Hospital of Changde City) from January 2017 to December 2021 were retrospectively collected. The SII and PNI of patients were calculated. The receiver operating characteristics (ROC) curve was leveraged for getting the optimal cutoff values of SII and PNI. The pathological response of patients after NACT, as obtained from their postoperative pathological examinations, was evaluated based on the tumor regression grade (TRG) criteria. Multivariate regression analysis was employed for identifying factors that led to various pathological responses after NACT in advanced GC patients. The log-rank test was utilized for between-group comparison of patients' survival curves. The SII and PNI were 507.45 and 48.48 respectively, and their levels were divided into high and low groups. Pathological response (TRG 0-1) was observed in 66 cases (20.25%), while non-pathological response (TRG 2-3) was observed in 260 cases (79.75%). The results of multivariate logistic regression analysis showed that tumor diameter < 5 cm, ypT T0-T2, ypN N0, chemotherapy regimen XELOX (capecitabine combined with oxaliplatin), SII < 507.45 (P=0.002), PNI > 48.48 were all independent factors affecting the pathological responses of advanced GC patients after NACT (all P < 0.05). With SII and PNI being included, the AUC was 0.821 (95% CI: 0.765-0.876), and the specificity was 87.90% and the sensitivity was 64.20%. The Kaplan-Meier survival curve analysis showed that NACT patients with tumor diameter < 5 cm, ypT T0-T2, ypN N0, XELOX chemotherapy regimen, SII < 507.45 and SII ≥ 507.45 had a higher survival rate. (P < 0.001). Before treatment, tumor diameter < 5 cm, ypT T0-T2, ypN N0, chemotherapy regimen XELOX, SII < 507.45, PNI > 48.48 were all independent factors affecting the pathological response of advanced GC patients after NACT. Moreover, the inclusion of SII and PNI increased the accuracy of predicting the pathological response of patients after NACT.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"14 8","pages":"3922-3934"},"PeriodicalIF":3.6,"publicationDate":"2024-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11387872/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142278981","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 significance of the FSTL1-DIP2A axis in early-stage tongue cancer.","authors":"Chie Kudo-Saito, Satoko Matsumura, Taisuke Mori, Yoshitaka Honma, Seiichi Yoshimoto","doi":"10.62347/RZAO3562","DOIUrl":"https://doi.org/10.62347/RZAO3562","url":null,"abstract":"<p><p>In tongue cancer, many patients already have metastasis at the time of diagnosis, and such cases are usually unresponsive to treatment, resulting in a poor prognosis. Therefore, there is an urgent need to develop more effective diagnostic and therapeutic methods to cure tongue cancer at the earliest possible stage in clinical practice. Follistatin-like 1 (FSTL1) is known as a negative effector molecule that induces and enhances the refractoriness of cancer cells directly and indirectly via suppressing anti-tumor immunity in various types of cancer. However, the molecular expression, functions, and clinical significance of FSTL1 and its receptor DIP2A in tongue cancer remains to be elucidated. In this study, we revealed that FSTL1, which is highly expressed in tongue cancer cells, plays a key role in its malignancy and is a significant risk factor for recurrence of early-stage tongue cancer. Basic study shows that FSTL1 is abundantly produced from human tongue cancer cell lines, and blocking FSTL1 with specific siRNAs or mAb significantly suppresses cellular functions. Clinical study shows that both FSTL1 and its receptor DIP2A are highly and correlatively expressed in tumor tissues of tongue cancer patients, and high expression levels of both in stage I tumors are significantly associated with shorter relapse-free survival. These suggest that targeting the FSTL1-DIP2A axis may be useful as a biomarker for early prediction of prognosis in tongue cancer patients, and as a therapeutic target for developing new drugs to treat tongue cancer more effectively. This strategy will contribute to improving clinical outcomes in tongue cancer.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"14 8","pages":"3816-3825"},"PeriodicalIF":3.6,"publicationDate":"2024-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11387867/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142278977","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":"Insights into autotaxin- and lysophosphatidate-mediated signaling in the pancreatic ductal adenocarcinoma tumor microenvironment: a survey of pathway gene expression.","authors":"Matthew Gk Benesch, Rongrong Wu, Colin J Rog, David N Brindley, Takashi Ishikawa, Kazuaki Takabe","doi":"10.62347/KQNW1871","DOIUrl":"https://doi.org/10.62347/KQNW1871","url":null,"abstract":"<p><p>Lysophosphatidate (LPA)-mediated signaling is a vital component of physiological wound healing, but the pathway is subverted to mediate chronic inflammatory signaling in many pathologies, including cancers. LPA, as an extracellular signaling molecule, is produced by the enzyme autotaxin (ATX, gene name <i>ENPP2</i>) and signals through six LPA receptors (LPARs). Its signaling is terminated by turnover via the ecto-activity of three lipid phosphate phosphatases (LPPs, gene names <i>PLPP1-3</i>). Many pharmacological developments against the LPA-signaling axis are underway, primarily against ATX. An ATX inhibitor against pancreatic ductal adenocarcinoma (PDAC), a very aggressive disease with limited systemic therapeutic options, is currently in clinical trials, and represents the first in-class drug against LPA signaling in cancers. In the present study, we surveyed the expression of ATX, LPARs, and LPPs in human PDACs and their clinical outcomes in two large independent cohorts, the Cancer Genome Atlas (TCGA) and GSE21501. Correlation among gene expressions, biological function and the cell composition of the tumor microenvironment were analysed using gene set enrichment analysis and cell cyber-sorting with <i>xCell. ENPP2, LPAR1, LPAR4, LPAR5, LPAR6, PLPP1</i>, and <i>PLPP2</i> were significantly elevated in PDACs compared to normal pancreatic tissue, whereas <i>LPAR2, LPAR3</i>, and <i>PLPP3</i> where downregulated (all P≤0.003). Only <i>ENPP2</i> demonstrated survival differences, with overall survival favoring <i>ENPP2</i>-high patients (hazard ration 0.5-0.9). <i>ENPP2</i> was also the only gene with enriched gene patterns for inflammatory and tissue repair gene sets. Epithelial (cancer) cells had increased <i>LPAR2, LPAR5</i> and <i>PLPP2</i> expression, and decreased <i>ENPP2, LPAR1, PLPP1</i>, and <i>PLPP3</i> gene expression (all P<0.02). Tumor fibroblasts had increased <i>ENPP2, LPAR2, LPAR4, PLPP1</i>, and <i>PLPP3</i> expression and decreased <i>LPAR2, LPAR5</i>, and <i>PLPP2</i> expression in both cohorts (all P≤0.01). Immune cell populations were not well correlated to gene expression in PDACs, but across both cohorts, cytolytic scores were increased in high-expressing <i>ENPP2, LPAR1, LPAR6, PLPP1</i>, and <i>PLPP3</i> tumors (P<0.01). Overall, in PDACs, <i>ENPP2</i> may switch from an anti-to-pro tumor promoting gene with disease progression. <i>LPAR2</i> and <i>PLPP2</i> inhibition are also predicted to have potential therapeutic utility. Future multi-omics investigations are necessarily to validate which LPA signaling components are high-value candidates for pharmacological manipulation in PDAC treatment.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"14 8","pages":"4004-4027"},"PeriodicalIF":3.6,"publicationDate":"2024-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11387861/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142278954","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":"Machine learning models for prediction of lymph node metastasis in patients with T1b gastric cancer.","authors":"Ji Won Seo, Ki Bum Park, Seung Taek Lim, Kyong Hwa Jun, Hyung Min Chin","doi":"10.62347/KREL8138","DOIUrl":"https://doi.org/10.62347/KREL8138","url":null,"abstract":"<p><p>The prognosis of early gastric cancer (EGC) patients is associated with lymph node metastasis (LNM). Considering the relatively high rate of LNM in T1b EGC patients, it is crucial to determine the factors associated with LNM. In this study, we constructed and validated predictive models based on machine learning (ML) algorithms for LNM in patients with T1b EGC. Data from patients with T1b gastric cancer were extracted from the Korean Gastric Cancer Association database. ML algorithms such as logistic regression (LR), random forest (RF), extreme gradient boosting (XGBoost), and support vector machine (SVM) were applied for model construction utilizing five-fold cross-validation. The performances of these models were assessed in terms of discrimination, calibration, and clinical applicability. Moreover, external validation of XGBoost models was performed using the T1b gastric cancer database of The Catholic University Medical Center. In total, 3,468 T1b EGC patients were included in the analysis, whom 550 (15.9%) had LNM. Eleven variables were selected to construct the models. The LR, RF, XGBoost, and SVM models were established, revealing area under the receiver operating characteristic curve values of 0.8284, 0.7921, 0.8776, and 0.8323, respectively. Among the models, the XGBoost model exhibited the best predictive performance in terms of discrimination, calibration, and clinical applicability. ML models are reliable for predicting LNM in T1b EGC patients. The XGBoost model exhibited the best predictive performance and can be used by surgeons for the identification of EGC patients with a high-risk of LNM, thereby facilitating treatment selection.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"14 8","pages":"3842-3851"},"PeriodicalIF":3.6,"publicationDate":"2024-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11387857/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142278956","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":"Nrf2 in human cancers: biological significance and therapeutic potential.","authors":"Yu Tian, Lixin Tang, Xin Wang, Yanqin Ji, Yanyang Tu","doi":"10.62347/LZVO6743","DOIUrl":"https://doi.org/10.62347/LZVO6743","url":null,"abstract":"<p><p>The nuclear factor-erythroid 2-related factor 2 (Nrf2) is able to control the redox balance in the cells responding to oxidative damage and other stress signals. The Nrf2 upregulation can elevate the levels of antioxidant enzymes to support against damage and death. In spite of protective function of Nrf2 in the physiological conditions, the stimulation of Nrf2 in the cancer has been in favour of tumorigenesis. Since the dysregulation of molecular pathways and mutations/deletions are common in tumors, Nrf2 can be a promising therapeutic target. The Nrf2 overexpression can prevent cell death in tumor and by increasing the survival rate of cancer cells, ensures the carcinogenesis. Moreover, the induction of Nrf2 can promote the invasion and metastasis of tumor cells. The Nrf2 upregulation stimulates EMT to increase cancer metastasis. Furthermore, regarding the protective function of Nrf2, its stimulation triggers chemoresistance. The natural products can regulate Nrf2 in the cancer therapy and reverse drug resistance. Moreover, nanostructures can specifically target Nrf2 signaling in cancer therapy. The current review discusses the potential function of Nrf2 in the proliferation, metastasis and drug resistance. Then, the capacity of natural products and nanostructures for suppressing Nrf2-mediated cancer progression is discussed.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"14 8","pages":"3935-3961"},"PeriodicalIF":3.6,"publicationDate":"2024-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11387866/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142278958","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":"m⁶A modification of CDC5L promotes lung adenocarcinoma progression through transcriptionally regulating WNT7B expression.","authors":"Nanding Yu, Yingxiao Wu, Qiongying Wei, Xiaoping Li, Mengling Li, Weidong Wu","doi":"10.62347/QHFA9669","DOIUrl":"10.62347/QHFA9669","url":null,"abstract":"<p><p>Cell division cycle 5-like (CDC5L) protein is implicated in the development of various cancers. However, its role in the progression of lung adenocarcinoma (LUAD) remains uncertain. Our findings revealed frequent upregulation of CDC5L in LUAD, which correlated with poorer overall survival rates and advanced clinical stages. <i>In vitro</i> experiments demonstrated that CDC5L overexpression stimulated the proliferation, migration, and invasion of LUAD cells, whereas CDC5L knockdown exerted suppressive effects on these cellular processes. Furthermore, silencing CDC5L significantly inhibited tumor growth and metastasis in a xenograft mouse model. Mechanistically, CDC5L activates the Wnt/β-catenin signaling pathway by transcriptionally regulating WNT7B, thereby promoting LUAD progression. Besides, METTL14-mediated m⁶A modification contributed to CDC5L upregulation in an IGF2BP2-dependent manner. Collectively, our study uncovers a novel molecular mechanism by which the m⁶A-induced CDC5L functions as an oncogene in LUAD by activating the Wnt/β-catenin pathway through transcriptional regulation of WNT7B, suggesting that CDC5L may serve as a promising prognostic marker and therapeutic target for LUAD.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"14 7","pages":"3565-3583"},"PeriodicalIF":3.6,"publicationDate":"2024-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11301290/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141900566","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":"Cancer-associated adipocytes in the ovarian cancer microenvironment.","authors":"Qiuling Cai, Jing Yang, Huiling Shen, Wenlin Xu","doi":"10.62347/XZRI9189","DOIUrl":"10.62347/XZRI9189","url":null,"abstract":"<p><p>The tumor microenvironment (TME) plays a critical role in high energy metabolism during tumorigenesis, progression and metastasis. Among them, adipocytes, as an important component of the TME, can transform into cancer-associated adipocytes (CAAs) through dedifferentiation via interactions with tumor cells. These CAAs provide nutrients, growth factors, cytokines and metabolites to the tumor and later transdifferentiate into other stromal cells at a later stage to alter tumor growth, metastasis and the drug response and ultimately influence the treatment and prognosis of ovarian cancer. This review outlines the physiological functions of CAAs and discusses the progress in the use of CAAs as therapeutic targets in ovarian cancer.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"14 7","pages":"3259-3279"},"PeriodicalIF":3.6,"publicationDate":"2024-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11301307/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141900602","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":"ASB1 inhibits prostate cancer progression by destabilizing CHCHD3 via K48-linked ubiquitination.","authors":"Chunchun Zhao, Zhen Xu, Hongliang Que, Ke Zhang, Fei Wang, Ruoyun Tan, Caibin Fan","doi":"10.62347/FEIZ7492","DOIUrl":"10.62347/FEIZ7492","url":null,"abstract":"<p><p>Prostate cancer is a major contributor to male mortality worldwide. In this study, we revealed that Ankyrin Repeat and SOCS Box Containing 1 (ASB1) expression was significantly decreased in prostate cancer tissues, correlating strongly with poor patient prognosis. Notably, the group with low ASB1 expression exhibited an increased proportion of M2 macrophages and showed resistance to immune checkpoint inhibitors and cisplatin, but remained sensitive to androgen-receptor-targeting drug bicalutamide. Silencing ASB1 enhanced prostate cancer cell proliferation, clonogenicity, and migration, whereas its overexpression exerted the opposite effects. Through quantitative mass spectrometry interactome analysis, we identified 37 novel proteins interacting with ASB1, including CHCHD3. Subsequent experiments including co-immunoprecipitation, cycloheximide treatment, and ubiquitination assays, revealed that ASB1 interacts with CHCHD3, promoting its degradation via K48-linked ubiquitination. Cell rescue experiments further demonstrated that ASB1 inhibits prostate cancer cell through the CHCHD3/reactive oxygen species (ROS) pathway. Taken together, our study indicated that ASB1 functions as a tumor suppressor by inhibiting CHCHD3/ROS signaling, thereby playing a vital part in prevention of prostate cancer proliferation, clonogenicity, and migration.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"14 7","pages":"3404-3418"},"PeriodicalIF":3.6,"publicationDate":"2024-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11301297/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141900601","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":"Flavopereirine exerts anti-cancer activities in various human thyroid cancer cells.","authors":"Jung-Ju Wu, Shu-Hsin Chen, Chien-Hsing Lee, Yi-Zhen Li, Yu-Wei Hsu, Ming-Ying Hsieh, Ying-Ray Lee","doi":"10.62347/MINX1330","DOIUrl":"10.62347/MINX1330","url":null,"abstract":"<p><p>Thyroid cancer (TC) stands out as the most prevalent endocrine malignancy globally, with a steadily increasing incidence. Its clinical manifestations include enlarged thyroid nodules, dysphagia, enophthalmos, and various other symptoms. While standard treatments such as thyroidectomy and radioiodine therapy effectively manage most cases of differentiated thyroid cancers (DTC), some recurrent cases of DTC or those involving poorly differentiated thyroid cancers (PDTC) require specialized interventions. However, existing drugs primarily address symptom management without offering a curative solution. Therefore, the development of a new therapeutic agent for these challenging cases is of utmost importance. Flavopereirine, derived from <i>Geissospermum vellosii</i>, has demonstrated promise as a potential anti-cancer agent across various human cancers. However, its specific anti-cancer effects on human thyroid cancer (TC) have remained unclear. Therefore, this study aims to investigate the anti-cancer activity of flavopereirine in human TC. The research findings revealed that flavopereirine effectively hinders the growth of human TC cells, induces cell cycle arrest, promotes apoptosis, and modulates autophagy. Moreover, the study delved into the underlying mechanisms by which flavopereirine influenced signaling pathways. To validate these anti-cancer effects, an <i>in vivo</i> zebrafish model was utilized, confirming the efficacy of flavopereirine against human TC cells. In summary, this study establishes that flavopereirine exhibits notable anti-human TC activities, positioning it as a promising therapeutic candidate for the treatment of human thyroid cancer.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"14 7","pages":"3317-3334"},"PeriodicalIF":3.6,"publicationDate":"2024-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11301305/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141900608","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":"Survival impact of pre-transplant local treatments in liver transplant recipients with BCLC stage A hepatocellular carcinoma.","authors":"Po-Jung Hsu, Szu-Yuan Wu, Wan-Ming Chen, Yu-Cheng Chang, Ta-Chun Chou, Ming-Feng Chiang, Ming-Che Lee, Ruey-Shyang Soong","doi":"10.62347/BXDX8100","DOIUrl":"10.62347/BXDX8100","url":null,"abstract":"<p><p>This study aimed to evaluate the impact of different pre-transplant local treatments on the survival of liver transplantation (LTx) recipients with BCLC Stage A Hepatocellular Carcinoma (HCC). We analyzed data from the Taiwan Cancer Registry and National Health Insurance Research Databases spanning 2012 to 2018. Employing propensity score matching, patients were categorized into three groups: those receiving local treatments (180 patients), hepatectomy (179 patients), and combined treatments (180 patients). The primary outcomes were overall mortality and HCC-specific death, assessed using time-varying Cox regression models and Kaplan-Meier survival analysis. During a median follow-up period of 3.92 years, all-cause mortality rates were observed as 74.44% for local treatments, 42.46% for hepatectomy, and 65.00% for combined treatments. HCC-specific mortality rates followed a similar pattern at 65.00%, 39.11%, and 59.44%, respectively. Adjusted hazard ratios demonstrated significantly elevated mortality risks associated with local and combined treatments compared to hepatectomy. Notably, the 2-year overall and HCC-specific survival rates were highest in the hepatectomy group, surpassing those observed in both the combined treatment and local treatment groups. The findings of our study highlight that for patients with BCLC Stage A HCC, undergoing hepatectomy prior to LTx is associated with superior survival outcomes compared to solely local treatments. This underscores the importance of considering hepatectomy as a vital component of the treatment strategy in this patient population.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"14 7","pages":"3555-3564"},"PeriodicalIF":3.6,"publicationDate":"2024-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11301294/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141900573","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}