Translational cancer research最新文献

{"title":"Erratum: CK1α-targeting inhibits primary and metastatic colorectal cancer <i>in vitro</i>, <i>ex vivo</i>, in cell-line-derived and patient-derived tumor xenograft mice models.","authors":"","doi":"10.21037/tcr-2025b-9","DOIUrl":"10.21037/tcr-2025b-9","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.21037/tcr.2020.02.13.].</p>","PeriodicalId":23216,"journal":{"name":"Translational cancer research","volume":"14 6","pages":"3880-3881"},"PeriodicalIF":1.5,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12268381/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144675751","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Erratum: Impact of apatinib in combination with osimertinib on EGFR T790M-positive lung adenocarcinoma.","authors":"","doi":"10.21037/tcr-2025b-10","DOIUrl":"10.21037/tcr-2025b-10","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.21037/tcr.2019.09.35.].</p>","PeriodicalId":23216,"journal":{"name":"Translational cancer research","volume":"14 6","pages":"3877-3879"},"PeriodicalIF":1.5,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12268876/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144675752","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrated single-cell and bulk RNA sequencing reveals prognostic and immunotherapy-associated myofibroblastic cancer-associated fibroblast subtypes in head and neck squamous cell carcinoma.","authors":"Xiufang Qiu, Yuhao Lin, Qian Li, Ameya A Asarkar, Zhiheng Ke, Yiying Xu, Lisha Chen","doi":"10.21037/tcr-2025-649","DOIUrl":"10.21037/tcr-2025-649","url":null,"abstract":"<p><strong>Background: </strong>Cancer-associated fibroblasts (CAFs) are involved in some critical aspects of the pathogenesis of head and neck squamous cell carcinoma (HNSCC), including the formation of a tumor-permissive extracellular matrix (ECM) structure, angiogenesis, and the immune and metabolic reprogramming of the tumor microenvironment (TME). This study aimed to examine the plasticity and metabolic heterogeneity of CAFs in HNSCC patients before and after immunotherapy.</p><p><strong>Methods: </strong>An integrated single-cell and bulk RNA sequencing (RNA-seq) analysis based on data from the GSE195832, GSE65868, and The Cancer Genome Atlas (TCGA)-HNSCC datasets was conducted. The functional plasticity and transcriptome diversity of the categorized CAF subtypes were analyzed using the DoRothEA tool and scMetabolism package. The relationship between the genes specifically expressed in the myofibroblast-like cancer-associated fibroblast (myCAF) subtype and prognosis was then examined by univariate and multivariate analyses. The influence of myCAF on immune cell modulation within the TME was analyzed using the Seurat and clusterProfiler packages. The therapeutic strategies for HNSCC were explored using the Cancer Therapeutics Response Portal (CTRP) and PRISM Repurposing datasets.</p><p><strong>Results: </strong>In total, seven types of cells were annotated based on 11 clusters. The CAFs were then re-categorized into the following three subtypes: inflammatory cancer-associated fibroblasts (iCAFs), proliferating cancer-associated fibroblasts (pCAFs), and myCAFs. The percentage of myCAFs was reduced in HNSCC following the immunotherapy. The functional plasticity of the CAFs was further confirmed by the diverse enriched pathways. Notably, the myCAFs were closely associated with DNA repair, oxidative phosphorylation, and transcription factor E2F targets. Further, the myCAFs were found to be the subtype most relevant to the prognosis of HNSCC and were found to be involved in modulating the immune cells in the TME of HNSCC. Additionally, a higher myCAF score was related to the higher half-maximal inhibitory concentration (IC50) values of D-4476, GW-583340, spautin-1, and VER-155008, and the lower IC50 values of JTE-607, TG100-115, ML320, and TGX-221. Moreover, patients with lower myCAF scores responded better to immunotherapy.</p><p><strong>Conclusions: </strong>This study, which was based on single-cell and bulk RNA-seq analyses, showed the plasticity and metabolic heterogeneity of CAFs in HNSCC. Our findings may contribute to understandings of the immunotherapy response in HNSCC.</p>","PeriodicalId":23216,"journal":{"name":"Translational cancer research","volume":"14 6","pages":"3730-3745"},"PeriodicalIF":1.5,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12268884/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144675760","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Investigation of effects of CFI-400945 and ionizing radiation on DNA damage response in triple-negative breast cancer.","authors":"Harjot Athwal, Vasudeva Bhat, Alison L Allan, Armen Parsyan","doi":"10.21037/tcr-2024-2495","DOIUrl":"10.21037/tcr-2024-2495","url":null,"abstract":"<p><p>Breast cancer is the leading cause of cancer-related morbidity and mortality in women. Triple-negative breast cancer (TNBC) is the most aggressive subtype of breast cancer, often resistant to therapies including radiation treatment (RT). Developing new strategies for TNBC treatment is of paramount importance. In our previous studies, we have shown that a novel drug, Polo-like kinase 4 inhibitor CFI-400945, acts synergistically with RT to enhance antiproliferative effects in TNBC. Since one of the main anticancer mechanisms of RT is deoxyribonucleic acid (DNA) damage with ensuing DNA damage response (DDR) activation, in the current study, we aimed to investigate if and how CFI-400945 modulates DDR in response to RT. Using MDA-MB-231 and MDA-MB-468 TNBC cell lines, we investigated the levels and the foci formation of γ-H2AX, Ku70 and Rad51 proteins-the markers of DNA damage, non-homologous end joining (NHEJ) and homologous recombination (HR) repair pathways, respectively. We demonstrate that RT induces sustained DNA damage that is not further meaningfully enhanced or prolonged by CFI-400945. We also observed cell-line-dependent differences in the timing of activation of NHEJ and HR pathways in response to RT, and that CFI-400945 might lead to impeding RT-induced NHEJ pathway activation or result in earlier activation of the HR pathway. Notably, despite activation of the DDR responses, DNA damage persisted for 24 or more hours after RT. While some of these observations were cell-line dependent (emphasizing known molecular heterogeneity of TNBC), we highlight that canonical DDR pathways activity in response to RT might be inefficient and modulated by drugs, such as CFI-400945-a cancer cell vulnerability that warrants further investigations for better understanding the biology of TNBC, its responses to treatment and novel drug development.</p>","PeriodicalId":23216,"journal":{"name":"Translational cancer research","volume":"14 6","pages":"3822-3832"},"PeriodicalIF":1.5,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12268609/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144675761","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A predictive model based on immune related genes for diffuse large B cell lymphoma (DLBCL).","authors":"Ruixin Sun, Pengcheng Liu, Zizhen Xu","doi":"10.21037/tcr-24-2043","DOIUrl":"10.21037/tcr-24-2043","url":null,"abstract":"<p><strong>Background: </strong>Anti-tumor immunity is the front line of human response to malignancy, which may shed light on early diagnosis of diffuse large B cell lymphoma (DLBCL). We aim at the introduction of immune-related genes to bring new insight in the establishment of a predictive model to facilitate the diagnosis of DLBCL and guide its therapy.</p><p><strong>Methods: </strong>First, we identified immune-related genes in DLBCL via GeneCards. With these genes, we conducted least absolute shrinkage and selection operator (LASSO) regression to select the genes with significant contribution to DLBCL and established a validated risk model to generate risk score. Later, a nomogram combining risk score with other common clinical index (age, gender, stage) was established to comprehensively evaluate the survival probability of patients with DLBCL. To guide the treatment, we implemented drug sensitivity analysis. To further understand the modulation and explore potential biomarkers, we constructed a competing endogenous RNA (ceRNA) network.</p><p><strong>Results: </strong>Hence, we established an immune-related genes-based risk model to predict the survival and progression of DLBCL. Validation of this risk model in internal test dataset and additional external validation datasets confirmed the robust performance of this model. The risk score was also found to be correlated with advanced stages and age over 60 years. We also found four novel second-line chemotherapies that can be used to treat patients with different risk scores.</p><p><strong>Conclusions: </strong>Overall, we established a predictive risk model based on immune-related genes from transcription level. This risk model can be utilized in clinical practice to facilitate physicians in diagnosing patients with DLBCL at an early stage and guide the treatment of DLBCL.</p>","PeriodicalId":23216,"journal":{"name":"Translational cancer research","volume":"14 6","pages":"3611-3626"},"PeriodicalIF":1.5,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12268872/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144675731","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A retrospective study using the Surveillance Epidemiology and End Results (SEER) database to predict risk and prognostic factors for lung metastasis in cervical carcinoma: nomogram development and validation.","authors":"Hao Jin, Hairong Wang, Junting Guo, Nan Gong, Zhengchao Jin","doi":"10.21037/tcr-2025-221","DOIUrl":"10.21037/tcr-2025-221","url":null,"abstract":"<p><strong>Background: </strong>Lung metastasis is commonly observed in patients with cervical carcinoma and is frequently linked to a poor prognosis. Currently, there is a gap in research specifically addressing the diagnostic and prognostic assessment of lung metastasis in cervical carcinoma patients through the use of nomograms. Therefore, developing effective predictive models is crucial for guiding clinical practice and improving patient management. The objective of this study is to develop and validate nomogram-based models for predicting lung metastasis and prognosis in patients with cervical carcinoma.</p><p><strong>Methods: </strong>We selected patients from the Surveillance, Epidemiology, and End Results (SEER) database, covering the period from 2000 to 2021. In order to find independent risk factors for lung metastasis in cervical carcinoma patients, we used both univariate and multivariate logistic regression analyses. We also performed univariate and multivariate Cox proportional hazards regression analyses to determine independent prognostic factors for cervical cancer patients with lung metastasis. From these analyses, we constructed two innovative nomograms. We evaluated their performance using receiver operating characteristic (ROC) curves, calibration curves, and decision curve analysis (DCA).</p><p><strong>Results: </strong>A total of 12,632 cervical carcinoma patients were included in the study, with 379 patients diagnosed with lung metastasis at the time of their initial diagnosis. Age, marital status, histology, grade, primary site, T stage, N stage, surgery, chemotherapy, liver metastasis, and bone metastasis were identified as independent risk factors for lung metastasis in patients with cervical carcinoma. Also, the lack of chemotherapy and radiotherapy, combined with liver metastasis, were recognized as independent prognostic factors affecting the outcomes of patients with cervical carcinoma and lung metastasis. The predictive performance of the two nomograms for lung metastasis and prognosis in cervical carcinoma patients was verified using ROC curves, calibration, DCA curves, and Kaplan-Meier survival curves in both the training and validation groups.</p><p><strong>Conclusions: </strong>The two nomograms accurately predict lung metastasis in cervical carcinoma patients and forecast outcomes for those with lung metastases. Therefore, they are significant tools for enhancing personalized clinical decision-making in future practices.</p>","PeriodicalId":23216,"journal":{"name":"Translational cancer research","volume":"14 6","pages":"3670-3689"},"PeriodicalIF":1.5,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12268780/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144675732","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of radiotherapy, chemotherapy, and chemoradiotherapy on survival outcomes in patients with gallbladder carcinoma: a real population-based study.","authors":"Feng Liu, Yanchao Qin, Linjie Li, Baoping Jiao","doi":"10.21037/tcr-2024-2543","DOIUrl":"10.21037/tcr-2024-2543","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;The clinical value of radiotherapy or chemotherapy in gallbladder carcinoma (GBC) remains controversial, especially for GBCs at different stages. Therefore, this study analyzed the effects of radiotherapy, chemotherapy, and concurrent chemoradiotherapy on overall survival (OS) and cancer-specific survival (CSS) in patients with different stages of GBC based on data from the Surveillance, Epidemiology, and End Results (SEER) database.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;Data on patients diagnosed with GBC from January 1, 2010 to December 31, 2017 were collected from the SEER database, and those involved patients were divided into the following groups according to their treatment regimens: non-therapy group, radiotherapy alone group, chemotherapy alone group, and concurrent chemoradiotherapy group. After adjusting for factors related to demographics, the tumor, and the procedure, Cox regression was performed to analyze the effect of radiotherapy, chemotherapy, and chemoradiotherapy on OS. The relationships between these three therapies and CSS were assessed using the competing risk model.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;This study included 6,275 GBC patients, among whom 3,444 received no therapy, 152 received radiotherapy alone, 1,913 received chemotherapy alone, and 766 received chemoradiotherapy. Of these patients, there were 4,886 (77.86%) all-cause death cases and 4,379 (69.78%) cancer-specific death cases. The multivariate analysis showed that radiotherapy [hazard ratio (HR) =0.700, 95% confidence interval (CI): 0.581, 0.844], chemotherapy (HR =0.500, 95% CI: 0.465, 0.538), and chemoradiotherapy (HR =0.486, 95% CI: 0.439, 0.538) significantly improved OS in all patients (all P&lt;0.001); for stage III and IV GBC patients, radiotherapy, chemotherapy, and chemoradiotherapy significantly improved OS (all P&lt;0.001). Regarding CSS, the competing risk model showed that chemotherapy (HR =0.589, 95% CI: 0.540, 0.635] and chemoradiotherapy (HR =0.577, 95% CI: 0.523, 0.636) improved CSS in all patients (both P&lt;0.001); for patients with stage III GBC, radiotherapy, chemotherapy, and chemoradiotherapy significantly improved CSS (P=0.02, &lt;0.001, &lt;0.001, respectively); and for patients with stage IV GBC, chemotherapy and chemoradiotherapy significantly improved CSS (both P&lt;0.001). The subgroup analyses based on different pathological types showed similar patterns in the effects of radiotherapy, chemotherapy, and chemoradiotherapy on OS and CSS.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusions: &lt;/strong&gt;Our study shows that advanced gallbladder cancer patients receiving radiotherapy, chemotherapy, or chemoradiotherapy can significantly improve their OS and CSS. Therefore, it is recommended that advanced patients routinely include radiotherapy, chemotherapy, or chemoradiotherapy in comprehensive treatment to improve survival rates. However, for early-stage gallbladder cancer, the improvement effects of radiotherapy, chemotherapy, or chemoradiotherapy on OS a","PeriodicalId":23216,"journal":{"name":"Translational cancer research","volume":"14 6","pages":"3627-3641"},"PeriodicalIF":1.5,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12268753/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144675748","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Erratum: MT-12 inhibits the growth and metastasis of bladder cancer cells via suppressing tumor angiogenesis <i>in vivo</i> and <i>in vitro</i>.","authors":"","doi":"10.21037/tcr-2025b-11","DOIUrl":"10.21037/tcr-2025b-11","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.21037/tcr.2019.01.12.].</p>","PeriodicalId":23216,"journal":{"name":"Translational cancer research","volume":"14 6","pages":"3874-3876"},"PeriodicalIF":1.5,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12268873/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144675753","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Key considerations for interpreting patient-reported outcomes in deep inferior epigastric artery perforator flap reconstruction with post-mastectomy radiotherapy.","authors":"Janhavi Venkataraman, Kefah Mokbel","doi":"10.21037/tcr-2025-423","DOIUrl":"10.21037/tcr-2025-423","url":null,"abstract":"","PeriodicalId":23216,"journal":{"name":"Translational cancer research","volume":"14 6","pages":"3292-3294"},"PeriodicalIF":1.5,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12268471/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144675762","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CNTN1 promotes cell proliferation and metastasis in ovarian cancer through PSEN1.","authors":"Zhiying Qi, Yuqing Ji, Yanying Xu, Ruimeng Guo, Xuewang Guo, Yu Dou, Yingying Yue, Fang Wang","doi":"10.21037/tcr-2024-2234","DOIUrl":"10.21037/tcr-2024-2234","url":null,"abstract":"<p><strong>Background: </strong>Ovarian cancer (OC) is a commonly occurring malignant tumor in women with a high mortality rate. Early detection remains challenging, and therapeutic options for advanced OC are severely limited. Therefore, there is an urgent need to identify novel biomarkers and therapeutic targets to improve outcomes for patients. Contactin-1 (CNTN1), a member of the immunoglobulin superfamily, functions as a modulator of cancer progression, yet its specific role in OC remains undefined. The present study aimed to investigate the clinical significance and regulatory role of CNTN1 in OC proliferation and metastasis.</p><p><strong>Methods: </strong>This study examined CNTN1 expression in 40 paired OC tissue samples and cell lines using real-time quantitative reverse transcription polymerase chain reaction and immunohistochemistry. Colony formation assays assessed proliferative capacity, while transwell assays measured invasive and migratory potential. Additionally, a tumor xenograft model in nude mice was employed to verify in vivo proliferative effects.</p><p><strong>Results: </strong>The results demonstrated that CNTN1 expression was markedly elevated in OC tissues and positively associated with advanced tumor stage, metastasis, and poor prognosis. Silencing CNTN1 significantly inhibited proliferation, migration, and invasion in OC cell lines. Bioinformatics analysis combined with luciferase assays identified a regulatory interaction between CNTN1 and presenilin-1 (PSEN1), with CNTN1 expression positively correlating with PSEN1 levels in patient samples. Notably, PSEN1 overexpression reversed the impaired proliferation, migration, and invasion induced by CNTN1 suppression.</p><p><strong>Conclusions: </strong>These findings suggest that CNTN1 promotes OC progression through PSEN1 regulation and may represent a prognostic biomarker for OC.</p>","PeriodicalId":23216,"journal":{"name":"Translational cancer research","volume":"14 6","pages":"3690-3701"},"PeriodicalIF":1.5,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12268885/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144675710","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}