Translational Oncology最新文献

{"title":"Machine learning-derived natural killer cell signature predicts prognosis and therapeutic response in clear cell renal cell carcinoma","authors":"Jinchen Luo ,&nbsp;Mingjie Lin ,&nbsp;Minyu Chen ,&nbsp;Jinwei Chen ,&nbsp;Xinwei Zhou ,&nbsp;Kezhi Liu ,&nbsp;Yanping Liang ,&nbsp;Jiajie Chen ,&nbsp;Hui Liang ,&nbsp;Zhu Wang ,&nbsp;Qiong Deng ,&nbsp;Jieyan Wang ,&nbsp;Meiyu Jin ,&nbsp;Junhang Luo ,&nbsp;Wei Chen ,&nbsp;Junjie Cen","doi":"10.1016/j.tranon.2024.102180","DOIUrl":"10.1016/j.tranon.2024.102180","url":null,"abstract":"<div><h3>Background</h3><div>Natural killer cells, interconnected with patient prognosis and treatment response, play a pivotal role in the tumor immune microenvironment and may serve as potential novel predictive biomarkers for renal cell carcinoma.</div></div><div><h3>Methods</h3><div>Clear cell renal cell carcinoma transcriptome data and the corresponding clinical data were obtained from the Cancer Genome Atlas (TCGA) database. Single-cell sequencing data were sourced from the Gene Expression Omnibus (GEO) database. A risk model was established by integrating ten different machine learning algorithms, which resulted in 101 combined models. The model with the highest average C-index was selected for further analysis, and was assessed using nomogram, time-dependent receiver operating characteristics (ROC) and Kaplan–Meier survival analysis. The differences in immune infiltration fractions, clinicopathological features, and response to various targeted therapies and immunotherapy between high- and low-risk groups were investigated. Furthermore, qRT-PCR, IHC, colony formation test, CCK8 assay and flow cytometry were conducted to explore the expression pattern and function of ARHGAP9 in our own patient samples and renal cancer cell lines.</div></div><div><h3>Results</h3><div>Totally, 156 NK cell-related genes and 5189 prognosis-related genes were identified, and 36 genes of their intersection demonstrated prognostic value. A risk model with 18 genes was established by Coxboost plus plsRcox, which can accurately predict the prognosis of ccRCC patients. Significant correlations were determined between risk score and tumor malignancy and immune cell infiltration. Meanwhile, a combination of tumor mutation burden plus risk score could have higher accuracy of predicting clinical outcomes. Moreover, high-risk group patients were more likely to be responsive to targeted therapy but show no response to immunotherapy.</div></div><div><h3>Conclusions</h3><div>Intricate signaling interactions between NK cells and various cellular subgroups were depicted and the developmental trajectory of NK cells was elucidated. A NK cells-related risk model was established, which can provide reliable prognostic information and identified patients with more probability of benefiting from therapy.</div></div>","PeriodicalId":48975,"journal":{"name":"Translational Oncology","volume":"51 ","pages":"Article 102180"},"PeriodicalIF":5.0,"publicationDate":"2024-11-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142628980","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A conventional radiomics model for predicting disease-free survival in colorectal cancer patients with liver metastasis","authors":"Xiping Shen,&nbsp;Ji Wu","doi":"10.1016/j.tranon.2024.102191","DOIUrl":"10.1016/j.tranon.2024.102191","url":null,"abstract":"","PeriodicalId":48975,"journal":{"name":"Translational Oncology","volume":"51 ","pages":"Article 102191"},"PeriodicalIF":5.0,"publicationDate":"2024-11-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142628958","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Starting points for the development of new targeted therapies for glioblastoma multiforme","authors":"Agnieszka Rusak ,&nbsp;Benita Wiatrak ,&nbsp;Klaudia Krawczyńska ,&nbsp;Tomasz Górnicki ,&nbsp;Karol Zagórski ,&nbsp;Łukasz Zadka ,&nbsp;Wojciech Fortuna","doi":"10.1016/j.tranon.2024.102187","DOIUrl":"10.1016/j.tranon.2024.102187","url":null,"abstract":"<div><div>Glioblastoma multiforme (GBM) is one of the most aggressive and lethal brain tumors, characterized by rapid growth, invasiveness, and resistance to standard therapies, including surgery, chemotherapy, and radiotherapy. Despite advances in treatment, GBM remains highly resistant due to its complex molecular mechanisms, including angiogenesis, invasion, immune modulation, and lipid metabolism dysregulation. This review explores recent breakthroughs in targeted therapies, focusing on innovative drug carriers such as nanoparticles and liposomes, and their potential to overcome GBM's chemo- and radioresistant phenotypes. We also discuss the molecular pathways involved in GBM progression and the latest therapeutic strategies, including immunotherapy and precision medicine approaches, which hold promise for improving clinical outcomes. The review highlights the importance of understanding GBM's genetic and molecular heterogeneity to develop more effective, personalized treatment protocols aimed at increasing survival rates and enhancing the quality of life for GBM patients.</div></div>","PeriodicalId":48975,"journal":{"name":"Translational Oncology","volume":"51 ","pages":"Article 102187"},"PeriodicalIF":5.0,"publicationDate":"2024-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142628992","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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 combined PCPE-1 and α-fetoprotein for hepatocellular carcinoma","authors":"Ruhua Zhang ,&nbsp;Wanqi Chen ,&nbsp;Xuelan Peng ,&nbsp;Zhiguang Zhang ,&nbsp;Shangjiu Yang ,&nbsp;Li Zhong","doi":"10.1016/j.tranon.2024.102185","DOIUrl":"10.1016/j.tranon.2024.102185","url":null,"abstract":"<div><h3>Purpose</h3><div>Procollagen C-proteinase enhancer 1 (PCPE-1) is associated with liver fibrosis, a major risk factor of hepatocellular carcinoma (HCC). However, its role in HCC remains unclear.</div></div><div><h3>Materials and Methods</h3><div>The mRNA and protein expression levels of PCPE-1 were analyzed using publicly available datasets of HCC tissues and matched normal tissues. Western blotting was performed to determine PCPE-1 levels in 7 paired HCC tumor and normal tissues. Immunohistochemistry was used to detect PCPE-1 levels in 155 HCC patients. The ROC curve was employed to determine the optimal cutoff value of PCPE-1. Univariate and multivariate analyses identified independent risk factors associated with overall survival (OS) of HCC patients. Kaplan-Meier analysis assessed the relationship between PCPE-1 expression and OS, and a prognostic model was constructed.</div></div><div><h3>Results</h3><div>PCPE-1 protein was upregulated in HCC tissues compared to normal tissues and positively correlated with the expression of several procollagens. 78 out of 155 HCC patients exhibited elevated PCPE-1 expression with cytoplasmic staining. High PCPE-1 expression significantly correlated with tumor necrosis (<em>P</em> = 0.045), poorer histologic grade (G3-G4, <em>P</em> = 0.008), and higher α-fetoprotein (AFP) level (&gt;20 ng/ml, <em>P</em> = 0.043). Both univariate and multivariate analyses showed a significant association between elevated PCPE-1 and poorer overall survival (<em>P</em> &lt; 0.001 in both analyses). Remarkably, combined prognostic model with PCPE-1 and AFP effectively stratified the risk for OS in HCC.</div></div><div><h3>Conclusion</h3><div>Our results demonstrate for the first time that PCPE-1 serves as an independent prognostic marker for HCC, and the combined prognostic model involving PCPE-1 and AFP emerges as a valuable tool for predicting patient outcomes.</div></div>","PeriodicalId":48975,"journal":{"name":"Translational Oncology","volume":"51 ","pages":"Article 102185"},"PeriodicalIF":5.0,"publicationDate":"2024-11-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142628990","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Histone-acetyl epigenome regulates TGF-β pathway-associated chemoresistance in colorectal cancer","authors":"Xianglong Tian ,&nbsp;Guihua Liu ,&nbsp;Linhua Ji ,&nbsp;Yi Shen ,&nbsp;Junjun Gu ,&nbsp;Lili Wang ,&nbsp;Jiali Ma ,&nbsp;Zuguang Xia ,&nbsp;Xinghua Li","doi":"10.1016/j.tranon.2024.102166","DOIUrl":"10.1016/j.tranon.2024.102166","url":null,"abstract":"<div><div>TGF-β signaling pathway has been demonstrated to be closely related to chemoresistance, which is the major cause of recurrence and poor outcome in colorectal cancer (CRC), however, the comprehensive epigenetic landscape that functionally implicates in the regulation of TGF-β pathway-associated chemoresistance has not yet well established in CRC. In our study, chromatin immunoprecipitation sequencing (ChIP-seq) and Western blot were employed to investigate epigenetic modifications for histones in response to TGF-β1 intervene. We found that the activation of the TGF-β pathway was characterized by genome-wide high levels of H3K9ac and H3K18ac. Mechanistically, the activation of the TGF-β signaling pathway leads to the downregulation of the deacetylase HDAC4, resulting in the upregulation of H3K9ac and H3K18ac. Consequently, this cascade induces oxaliplatin chemoresistance in CRC by triggering the anti-apoptotic PI3K/AKT signaling pathway. Our in vivo experiment results confirmed that overexpression of HDAC4 significantly enhances the sensitivity of CRC to oxaliplatin chemotherapy. Moreover, the expression level of HDAC4 was positively correlated with patients’ prognosis in CRC. Our data suggest that histone-acetyl modification demonstrates a crucial role in modulating TGF-β pathway-associated chemoresistance in CRC, and HDAC4 would be a biomarker for prognostic prediction and potential therapeutic target for treatment in CRC.</div></div>","PeriodicalId":48975,"journal":{"name":"Translational Oncology","volume":"51 ","pages":"Article 102166"},"PeriodicalIF":5.0,"publicationDate":"2024-11-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142628976","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RIPK2 and lysosomal pathway: Unveiling a new mechanism for lung cancer metastasis","authors":"Wei Liu ,&nbsp;Wei Xu ,&nbsp;Hui Hao ,&nbsp;Lin Yang ,&nbsp;Bo Zhang ,&nbsp;Yan Zhang","doi":"10.1016/j.tranon.2024.102182","DOIUrl":"10.1016/j.tranon.2024.102182","url":null,"abstract":"<div><h3>Background</h3><div>This study aims to explore the role of RIPK2 in lung cancer metastasis and its potential mechanisms.</div></div><div><h3>Methods</h3><div>The expression levels of RIPK2 in lung cancer patients and cell lines were detected by immunohistochemistry, qRT-PCR, and Western blot. RIPK2 expression was knocked down using siRNA technology, and its effects on the proliferation, migration, and invasion capabilities of lung cancer cells were assessed through CCK-8, EdU, colony formation, and Transwell assays. Furthermore, by overexpressing RIPK2 and LAMP2, the regulatory effect of RIPK2 on the lysosomal pathway and its mechanism of action in lung cancer metastasis were investigated.</div></div><div><h3>Results</h3><div>The results showed that the expression of RIPK2 was significantly increased in lung cancer patients and cell lines. Knockdown of RIPK2 significantly inhibited the migration, invasion, and proliferation capabilities of lung cancer cells, while overexpression of RIPK2 promoted these malignant behaviors. Further studies found that RIPK2 promoted lung cancer metastasis by inhibiting LAMP2 expression, thereby suppressing the lysosomal pathway and altering the tumor microenvironment. Additionally, overexpression of LAMP2 could reverse the promotive effects of RIPK2 overexpression on the malignant behaviors of lung cancer cells.</div></div><div><h3>Conclusion</h3><div>This study reveals for the first time that RIPK2 promotes lung cancer metastasis by inhibiting LAMP2 expression, thereby suppressing the lysosomal pathway and altering the tumor microenvironment. In the future, targeted therapy against RIPK2 and LAMP2 may become an effective means to inhibit lung cancer metastasis.</div></div>","PeriodicalId":48975,"journal":{"name":"Translational Oncology","volume":"51 ","pages":"Article 102182"},"PeriodicalIF":5.0,"publicationDate":"2024-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142606213","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Artemis and its role in cancer","authors":"Armen Parsyan ,&nbsp;Vasudeva Bhat ,&nbsp;Harjot Athwal ,&nbsp;Emily A. Goebel ,&nbsp;Alison L Allan","doi":"10.1016/j.tranon.2024.102165","DOIUrl":"10.1016/j.tranon.2024.102165","url":null,"abstract":"<div><div>Artemis is a key nuclease involved in the non-homologous end joining repair pathway upon DNA double-stranded breaks and during V(D)J recombination. It participates in various cellular processes and cooperates with various proteins involved in tumorigenesis. Its hereditary mutations lead to several pathological conditions, such as severe combined immunodeficiency with radiation sensitivity. Recent studies suggest that Artemis deregulation plays an important role in cancer and is associated with poorer oncologic outcomes and resistance to treatment including radiotherapy, chemotherapy and targeted therapeutics. Artemis emerges as an attractive candidate for cancer prognosis and treatment. Its role in modulating sensitivity to ionizing radiation and DNA-damaging agents makes it an appealing target for drug development. Various existing drugs and novel compounds have been described to inhibit Artemis activity. This review synthesizes the up-to-date information regarding Artemis function, its role in different malignancies and its clinical utility as a potential biomarker and therapeutic target in Oncology.</div></div>","PeriodicalId":48975,"journal":{"name":"Translational Oncology","volume":"51 ","pages":"Article 102165"},"PeriodicalIF":5.0,"publicationDate":"2024-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142628960","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"IGF2BP2 orchestrates global expression and alternative splicing profiles associated with glioblastoma development in U251 cells","authors":"Wenqing Liu ,&nbsp;Yan Liu ,&nbsp;Haoyuan Li ,&nbsp;Shixiong Wang ,&nbsp;Pengfei Chen ,&nbsp;Zhongtao Liu ,&nbsp;Xianhao Huo ,&nbsp;Jihui Tian","doi":"10.1016/j.tranon.2024.102177","DOIUrl":"10.1016/j.tranon.2024.102177","url":null,"abstract":"<div><div>Glioblastoma (GBM) is a highly invasive and malignant central nervous system tumor with a median survival duration of 15 months despite multimodal therapy. The insulin-like growth factor 2 mRNA binding protein 2 (IGF2BP2) has been implicated in various cancers and is known to regulate RNA metabolism and alternative splicing (AS). However, its role in GBM remains unclear. Overexpression of IGF2BP2 led to significant alterations in gene expression, with 472 genes upregulated and 99 downregulated. Gene ontology (GO) analysis indicated enrichment in immune-related biological processes. Notably, IGF2BP2 was found to regulate AS events, with 1372 regulated AS genes (RASGs) and 2096 significantly distinct ASEs identified. Furthermore, IGF2BP2 selectively bound to 3′ and 5′ untranslated regions (UTRs) via GG[AU]C motifs, and IFIH1 was identified as a direct binding partner and upregulated gene upon IGF2BP2 overexpression. Functional enrichment analysis suggested that IGF2BP2 influences pathways related to RNA splicing and immune responses. Our findings demonstrate that IGF2BP2 plays a crucial role in GBM by modulating the transcriptome and AS events. The upregulation of immune-related genes and the regulation of AS by IGF2BP2 highlight its potential as a therapeutic target in GBM, particularly for immunotherapy. The study provides a foundation for further investigation into the molecular mechanisms of IGF2BP2 in GBM and its implications for cancer treatment.</div></div>","PeriodicalId":48975,"journal":{"name":"Translational Oncology","volume":"51 ","pages":"Article 102177"},"PeriodicalIF":5.0,"publicationDate":"2024-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142606081","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Res@ZIF-90 suppress gastric cancer progression by disturbing mitochondrial homeostasis","authors":"Guanglin Qiu ,&nbsp;Lindi Cai ,&nbsp;Gan Li ,&nbsp;Yiwei Ren ,&nbsp;Enmeng Li ,&nbsp;Kai Deng ,&nbsp;Mengke Zhu ,&nbsp;Shangning Han ,&nbsp;Xiangming Che ,&nbsp;Xuqi Li ,&nbsp;Lin Fan","doi":"10.1016/j.tranon.2024.102179","DOIUrl":"10.1016/j.tranon.2024.102179","url":null,"abstract":"<div><h3>Background</h3><div>Gastric cancer (GC) is still a serious threat to human health worldwide. As a natural compound, resveratrol has been proven to have anti-tumor activity, and the nano-delivery carrier has shown its excellent ability to retain and control drug release.</div></div><div><h3>Methods</h3><div>Res@ZIF-90 underwent synthesis via a one-pot method and subsequent characterization encompassing Dynamic Light Scattering, Scanning Electron Microscope, Transmission Electron Microscope, and UV–vis absorption spectroscope. The release of resveratrol from Res@ZIF-90 across varied pH environments were delineated employing High Performance Liquid Chromatography. The mitochondrial targeting of Res@ZIF-90 was scrutinized utilizing Fluorescent Inverted Microscopy. The cytotoxic impact of Res@ZIF-90 on HGC-27 cells was evaluated through CCK-8 assay, Live/Dead staining, scratch test, and JC-1 assay. Furthermore, the HGC-27 tumor-bearing mice model was established to explore the anti-tumor effect of Res@ZIF-90.</div></div><div><h3>Results</h3><div>ZIF-90 can effectively release resveratrol under acidic (pH = 5.5) conditions. In addition, Res@ZIF-90 could be taken up by cells and localized into mitochondria. ZIF-90 has no obvious cytotoxicity at the experimental concentration, while Res@ZIF-90 was more cytotoxic to HGC-27 cells than free resveratrol at the same concentration. Res@ZIF-90 significantly reduced the expressions of PGCS 1α, TFAM, PINK1, and COX IV, which together induced mitochondrial homeostasis disorders and inhibited the tumor growth of HGC-27 tumor-bearing mice in vivo.</div></div><div><h3>Conclusions</h3><div>Res@ZIF-90 can inhibit the progression of gastric cancer by targeting the mitochondria of gastric cancer cells and disrupting mitochondrial homeostasis to produce cytotoxic effects. Res@ZIF-90 may be a promising antitumor drug with potential application value.</div></div>","PeriodicalId":48975,"journal":{"name":"Translational Oncology","volume":"51 ","pages":"Article 102179"},"PeriodicalIF":5.0,"publicationDate":"2024-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142592843","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"An exploration of the optimal combination chemotherapy regimen based on neoadjuvant therapy containing pyrotinib for HER2-positive breast cancer: A multicenter real-world study","authors":"Shan Wang ,&nbsp;Zining Jin ,&nbsp;Zhaohui Li ,&nbsp;Guolian Zhu ,&nbsp;Bin Liu ,&nbsp;Dianlong Zhang ,&nbsp;Shuhong Tang ,&nbsp;Fan Yao ,&nbsp;Jian Wen ,&nbsp;Yi Zhao ,&nbsp;Xiaolan Wang ,&nbsp;Feng Jin ,&nbsp;Jia Wang","doi":"10.1016/j.tranon.2024.102173","DOIUrl":"10.1016/j.tranon.2024.102173","url":null,"abstract":"<div><h3>Background</h3><div>The combination of pyrotinib (Py) with cytotoxic agents proved to be effective in early human epidermal growth factor receptor 2 (HER2)-positive breast cancer (BC). However, the optimal chemotherapy regimen is unknown. This study attempts to explore it from real-world research data.</div></div><div><h3>Methods</h3><div>Information was collected from patients with early-stage HER2-positive BC from 23 centers across the country. They were categorized into the anthracycline group (A group) and non-anthracycline group (non-A group). Patients in the non-A group were further categorized into the platinum group and non-platinum group and the short-cycle (≤4 cycles) taxane group and long-cycle (&gt;4 cycles) taxane group. Total pathological complete response (tpCR, ypT0/is ypN0) and breast pathological complete response (bpCR, ypT0/is) rates were assessed.</div></div><div><h3>Results</h3><div>A total of 107 patients were enrolled. Postoperative pathology indicated a tpCR rate of 36.8 %, a bpCR rate of 42.1 % in the A group, the non-A group had a tpCR rate of 47.8 %, and a bpCR rate of 53.6 %, with <em>P</em>-values of 0.273 and 0.254, respectively. In the long-cycle taxane group, the tpCR and bpCR rates were 60.8 % and 66.7 %, respectively. In the short-cycle taxane group, the tpCR and bpCR rates were 11.1 % and 16.7 %, respectively (both <em>P</em>&lt;0.001). The platinum group had higher tpCR rate (62.9 % vs. 32.4 %, respectively; <em>P</em> = 0.011) and bpCR rate (65.7 % vs. 41.2 %, respectively; <em>P</em> = 0.041).</div></div><div><h3>Conclusion</h3><div>As for a neoadjuvant therapy regimen with Py, an anthracycline-free regimen is feasible. Besides, platinum-containing, long-cycle taxane regimens appear to achieve superior efficacy under anthracycline-removed conditions.</div></div>","PeriodicalId":48975,"journal":{"name":"Translational Oncology","volume":"51 ","pages":"Article 102173"},"PeriodicalIF":5.0,"publicationDate":"2024-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142586265","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}