American journal of cancer research最新文献

{"title":"Efficacy of chemotherapy combined with immune checkpoint inhibitors for advanced non-small cell lung cancer and construction and validation of a prognostic model: a multicenter retrospective cohort study.","authors":"Chunmei Gong, Fenghong Lv, Beibei Xiong, Lilan Li, Mingming Wu, Lu Luo","doi":"10.62347/NAPG2526","DOIUrl":"https://doi.org/10.62347/NAPG2526","url":null,"abstract":"<p><p>The goal of this multicenter retrospective cohort study was to determine the efficacy of chemotherapy in combination with immune checkpoint inhibitors (ICIs) as compared to chemotherapy alone in patients with advanced non-small cell lung cancer (NSCLC). Further, the study will assess the efficacy between the PD-1 inhibitors, evaluate independent prognostic factors and build nomogram models for predicting progression free survival (PFS) and overall survival (OS). Clinical data were retrospectively collected from patients of two centers who received first-line treatment between January 2019 and December 2023 (training cohort n=286, external validation cohort n=124). To balance baseline characteristics, propensity score matching (PSM) was adopted. Cox regression analyses were then performed to find the independent prognostic factors. After PSM (propensity score matching), a significantly higher objective response rate and disease control rate were found in the combination therapy group as compared with a single-agent therapy group (both P<0.05). The combination therapy group also exhibited a significantly longer median PFS of 10 months as compared with 6 months of single-agent therapy group; HR=1.92, P<0.001. Similarly, the combination therapy group exhibited significantly longer median OS of 21 months as compared with 12 months of single-agent therapy group; HR=2.07, P<0.001. The effectiveness of tislelizumab was similar to sintilimab in treating multiple cancers, which was further confirmed by network meta-analysis. Based on the multivariate analysis, treatment regimen, serum albumin, age, smoking status, Charlson Comorbidity Index, ECOG performance status, organ metastasis status and number of organ metastasis were independent prognostic factors for PFS, while first six variables (except smoking status and CCI) for OS. The area under the curve (AUC) values for both nomograms in internal and external validation were greater than 0.75, and they showed good calibration, good clinical utility and good risk stratification performances or capabilities. In conclusion, chemotherapy plus ICIs significantly improves short-term efficacy and long-term survival in advanced NSCLC, tislelizumab and sintilimab showed comparable efficacy, and the constructed nomograms could provide some significance for individualized clinical decision-making.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"16 3","pages":"985-1012"},"PeriodicalIF":2.9,"publicationDate":"2026-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13090500/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147721483","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":"Carbon-ion beam irradiation combined with miR-17-5p/miR-17-3p inhibitors effectively kill osteosarcoma cells.","authors":"Eun Ho Kim, Won Seok Lee, Sei Sai","doi":"10.62347/AAMD9401","DOIUrl":"10.62347/AAMD9401","url":null,"abstract":"<p><p>Osteosarcoma (OS) is the most common type of bone cancer and is highly resistant to conventional photon beam radiotherapy; however, carbon-ion radiotherapy (CIRT) is effective in treating OS. In this study, to investigate whether miR-17-5p/miR-17-3p inhibitors act as radiosensitizers for CIRT, U2OS and MG63 OS cells were treated with carbon-ion beam irradiation (IR) alone, X-ray IR alone, or with one of the IR treatments in combination with miR-17-3p inhibitors. Cell death and invasive and migratory abilities were analyzed using cell viability and cell Transwell migration and invasion assays. Apoptosis and autophagy-related protein expression and DNA double-strand break (DSB) induction was determined using western blotting and immunofluorescence staining. We found that carbon-ion beam IR combined with miR-17-5p/miR-17-3p inhibitors significantly inhibited OS cell proliferation, migration, and invasion and markedly increased apoptosis-related cleaved-caspase 3, cleaved-PARP expression compared to carbon-ion beam IR and X-ray IR alone. Furthermore, carbon-ion beam IR combined with miR-17-5p/miR-17-3p inhibitors markedly promoted autophagy induction. In addition, combination treatment with miR-17-5p/miR-17-3p inhibitors and carbon-ion beam IR significantly increased the number of γH2AX foci as well as its phosphorylation. Taken together, miR-17-5p/miR-17-3p inhibitors enhanced the carbon-ion beam radiosensitivity of OS cells, presenting a novel strategy for the development of carbon-ion beam combination therapy.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"16 3","pages":"1231-1241"},"PeriodicalIF":2.9,"publicationDate":"2026-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13090501/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147721390","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":"Predictive value of the systemic immune-inflammation index and geriatric nutritional risk index on the efficacy of immunotherapy and survival prognosis in advanced non-small cell lung cancer: a retrospective study.","authors":"Jing Wu, Zhipei Duan, Jing Qian, Chengru Hu, Chao Chen, Yan Li, Tinghua Cao","doi":"10.62347/QMNU5628","DOIUrl":"10.62347/QMNU5628","url":null,"abstract":"<p><strong>Objective: </strong>To investigate the predictive value of the systemic immune-inflammation index (SII) and geriatric nutritional risk index (GNRI) for immunotherapy efficacy and survival prognosis in advanced non-small cell lung cancer (NSCLC).</p><p><strong>Methods: </strong>This retrospective study enrolled 152 patients with advanced NSCLC who received immunotherapy. Patients were divided into effective (n = 106) and ineffective (n = 46) groups based on treatment response. Pretreatment SII, GNRI, and programmed cell death-ligand 1 (PD-L1) levels were compared between groups. Multivariate logistc regression identified factors influencing immunotherapy efficacy. Receiver operating characteristic curve analysis evaluated the predictive value of these indicators. Kaplan-Meier method analyzed the relationship between SII, GNRI, and progression-free survival (PFS)/overall survival (OS). Cox regression analyzed their impact on survival and interaction.</p><p><strong>Results: </strong>The effective group had significantly lower pretreatment SII but higher GNRI and PD-L1 than the ineffective group (all <i>P</i><0.05). All three indicators significantly influenced immunotherapy efficacy (all <i>P</i><0.05). SII combined with GNRI yielded a higher AUC (0.879) for predicting efficacy than SII alone (0.778), GNRI alone (0.699), or PD-L1 alone (0.707). Patients with high SII (≥418.67) had worse 2-year OS and shorter median PFS/OS than those with low SII (all <i>P</i><0.05). Patients with low GNRI (<97.89) had worse outcomes than those with high GNRI (≥97.89) (all <i>P</i><0.05). SII ≥418.67 and GNRI <97.89 were independent risk factors for poor survival (both <i>P</i><0.05), with significant interaction between them.</p><p><strong>Conclusions: </strong>SII and GNRI are closely associated with immunotherapy efficacy in advanced NSCLC, and their interaction influences patient survival.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"16 3","pages":"920-936"},"PeriodicalIF":2.9,"publicationDate":"2026-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13090494/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147721479","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":"Integrated bulk and single-cell transcriptomics with experimental validation to identify calmodulin-related prognostic genes in lung adenocarcinoma.","authors":"Zhouyan Lin, Minshu Ao, Yue Hu, Ziyan Yu, Mengyu Lu, Yuchao Dong, Chong Bai, Meng Guo","doi":"10.62347/SDLR5143","DOIUrl":"10.62347/SDLR5143","url":null,"abstract":"<p><p>Lung adenocarcinoma (LUAD) exhibits poor prognosis partly due to dysregulated calcium signaling. Here, we integrated bulk RNA-seq (TCGA/LUAD, n = 440) and single-cell sequencing (GSE131907) to identify calmodulin-related prognostic genes. Differential expression analysis and LASSO-Cox regression identified SPHK1 and ASPM as independent predictors of overall survival (HR = 1.52/1.47, <i>P</i> < 0.001). A risk model incorporating these genes stratified patients into high/low-risk groups with distinct clinical outcomes (3-year AUC = 0.83). High-risk patients showed elevated γδ T cells and TIDE scores, while SPHK1/ASPM expression correlated with an immunosuppressive myeloid phenotype and M2-like polarization. Single-cell analysis revealed SPHK1⁺-ASPM⁺ myeloid cells dominated in early differentiation stages, with pseudo-time trajectories indicating SPHK1 downregulation and ASPM upregulation during myeloid maturation. Multiplex immunofluorescence validated co-localization of SPHK1/ASPM with MPO⁺ myeloid cells in tumor tissues. Importantly, the MPO⁺SPHK1⁺/ASPM⁺ myeloid compartment was significantly enriched in anti-PD-1 non-responders (<i>P</i> < 0.05). Our study establishes a calcium signaling-based prognostic signature, uncovers myeloid SPHK1/ASPM as drivers of immunosuppression, and provides a potential biomarker for immunotherapy stratification.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"16 3","pages":"1171-1197"},"PeriodicalIF":2.9,"publicationDate":"2026-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13090484/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147721470","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":"PIM1 expression is prognostic in clear cell renal cell carcinoma and influenced by an IL-6/JAK/STAT axis.","authors":"Kimberly S Meza, Kimberly Seymour, Elias Ou Eteshola, Natalie Payne, Brianna Rodriguez, Stephanie L Graff, Norm Smith, Andrew Elliott, Wafik S El-Deiry, Sheldon L Holder","doi":"10.62347/LQQL3584","DOIUrl":"10.62347/LQQL3584","url":null,"abstract":"<p><p>Renal cell carcinoma (RCC) is among the top ten most common cancers diagnosed in the United States. The incidence of RCC has continued to increase in recent years, yet our understanding of its etiology is incomplete. Clear cell RCC (ccRCC) is the major subtype, constituting over 75% of all RCC cases. Treatment options for RCC are limited in efficacy, as RCC tumors typically acquire resistance to current therapies, particularly in advanced and metastatic RCC. von Hippel-Lindeau (VHL) status is the only clinically validated biomarker approved for therapeutic intervention in RCC to date. The identification of novel molecular targets is therefore critical for improving therapeutic strategies for RCC. PIM1 is a constitutively active serine/threonine kinase involved in promoting proliferation, invasion, migration, and apoptosis evasion in cancer. <i>PIM1</i> expression is dysregulated in ccRCC, contributing to oncogenesis and tumor progression. Here, we explore the influence of <i>PIM1</i> expression in real-world outcomes of patients with RCC. We identify a link between IL-6 expression and <i>PIM1</i> expression and activity in human ccRCC tumors and cell lines. Our work provides evidence that targeting an IL-6/JAK/STAT/PIM1 axis may be a viable therapeutic strategy for patients with <i>PIM1</i>-high expressing ccRCC.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"16 3","pages":"1027-1041"},"PeriodicalIF":2.9,"publicationDate":"2026-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13090478/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147721508","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":"CBX3 promotes epithelial-mesenchymal transition in synovial sarcoma via the SHH signaling pathway.","authors":"Yachao Sun, Zhibing Dai, Junwei Du, Maierdanjian Maihemuti, Suzhi Ji, Renbing Jiang","doi":"10.62347/YPDZ7241","DOIUrl":"https://doi.org/10.62347/YPDZ7241","url":null,"abstract":"<p><p>Synovial sarcoma (SS) is a malignant mesenchymal tumor of uncertain histogenesis, representing approximately 5% to 10% of all soft tissue sarcomas. It predominantly affects adolescents and young adults. The role of CBX3 (Chromobox homolog 3) in Synovial sarcoma progression, particularly in relation to epithelial mesenchymal transition (EMT), remains unclear. This study aimed to investigate the functional role of CBX3 in synovial sarcoma and to elucidate the underlying molecular mechanisms by which it regulates EMT. Human synovial sarcoma cell lines (SYO-1, HS-SY-II, YaFuSS, and Fuji) and the immortalized human keratinocyte line (HaCaT) were used for <i>in vitro</i> studies. For <i>in vivo</i> modeling, mice were inoculated with Fuji cells. CBX3 expression was significantly upregulated in human synovial sarcoma tumor specimens compared to control tissues. Clinically, patients with high CBX3 expression exhibited significantly shorter overall survival than those with low expression. In vitro, CBX3 promoted cell proliferation, induced EMT, and suppressed mitochondrial oxidative metabolism. Conversely, siRNA-mediated knockdown of CBX3 (si-CBX3) enhanced mitochondrial oxidative activity. Moreover, CBX3 overexpression inhibited ferroptosis in SS cells, whereas its knockdown (sh-CBX3) promoted both ferroptosis and mitochondrial oxidation - effects consistently observed in both in vitro assays and the mouse xenograft model. Mechanistically, CBX3 activated the Sonic Hedgehog (SHH) signaling pathway. Pharmacological inhibition of SHH signaling abrogated CBX3-mediated suppression of ferroptosis and restoration of mitochondrial oxidation. Furthermore, co-immunoprecipitation assays demonstrated that CBX3 physically interacts with SHH protein and stabilizes it by reducing its polyubiquitination. CBX3 drives EMT and tumor progression in SS by activating the SHH/Gli1 signaling axis. Mechanistically, CBX3 binds directly to and SHH and prevents its ubiquitin-mediated degradation, thereby stabilizing the protein. CBX3-SHH subsequently suppresses mitochondrial oxidative metabolism, which in turn inhibits ferroptosis and facilitates EMT - ultimately promoting SS aggressiveness.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"16 3","pages":"966-984"},"PeriodicalIF":2.9,"publicationDate":"2026-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13090498/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147721427","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":"TNFAIP1 suppresses hepatocellular carcinoma progression via the PXR/CYP3A4 signaling axis.","authors":"Qian Nie, Yiping Guo, Haowen Xiao, Dini Zhang, Haiyue Li, Ling Wang","doi":"10.62347/FSIQ3194","DOIUrl":"https://doi.org/10.62347/FSIQ3194","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) is characterized by poor prognosis and limited effective treatment options, necessitating a deeper understanding of its pathogenesis. This study focuses on tumor necrosis factor-α-induced protein 1 (TNFAIP1) and cytochrome P450 3A4 (CYP3A4) in HCC, aiming to investigate their association and functional roles in tumor progression. Bioinformatics analyses and experimental validation revealed that both TNFAIP1 and CYP3A4 are downregulated in HCC, and that TNFAIP1 positively regulates CYP3A4 expression. TNFAIP1 knockout not only decreased CYP3A4 expression but also significantly impaired the ability of rifampicin (RIF), an upstream nuclear receptor-pregnane X receptor (PXR) agonist, to induce CYP3A4, indicating that TNFAIP1 is an essential regulator of PXR/CYP3A4 pathway. Co-immunoprecipitation (Co-IP) experiment further confirmed the direct interaction between TNFAIP1 and PXR. TNFAIP1 knockout promoted HCC cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT), while suppressing apoptosis; these effects were partially attenuated by pharmacological activation of PXR or genetic overexpression of CYP3A4. In vivo experiments demonstrated that overexpression of Tnfaip1 upregulated the Pxr/Cyp3a11 pathway and inhibited tumor growth, whereas Tnfaip1 knockout suppressed this pathway. This study identified TNFAIP1-PXR-CYP3A4 as a novel tumor-suppressive axis in HCC, providing potential molecular targets for HCC diagnosis and treatment.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"16 3","pages":"905-919"},"PeriodicalIF":2.9,"publicationDate":"2026-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13090476/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147721522","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":"27-Hydroxycholesterol in bile duct tissue promotes cholangiocarcinoma progression through estrogen receptor signaling.","authors":"Naoki Konishi, Teruo Miyazaki, Mitsugi Shimoda, Yukio Morishita, Akira Honda, Tadashi Ikegami, Shuji Suzuki","doi":"10.62347/VNCF6546","DOIUrl":"10.62347/VNCF6546","url":null,"abstract":"<p><strong>Background: </strong>The oxysterol 27-hydroxycholesterol (27-HC) is widely produced in human tissues, functions as a selective estrogen receptor modulator (SERM), is implicated in the progression of estrogen receptor (ER)-positive cancers. While 27-HC is abundant in bile, its SERM role in extrahepatic cholangiocarcinoma (eCCA) remains unclear. Therefore, this study aims to test the hypothesis that 27-HC promotes eCCA cell proliferation via ER activation.</p><p><strong>Methods: </strong>Oxysterol levels and the expression of ERs and proliferation-related genes were compared between eCCA tissues (N = 17) and noncancerous extrahepatic bile ducts (N = 6). The effects of 27-HC on cell proliferation were evaluated in two human cholangiocarcinoma cell lines: ERα-expressing intrahepatic CCA-1 and ERβ-expressing extrahepatic TFK-1 cells.</p><p><strong>Results: </strong>27-HC and mRNA expression levels of ERα and ERβ were significantly higher in eCCA tissues than in noncancerous tissues. Expression levels of cMYC, HIF-1α, and VEGFα expression levels were elevated in eCCA tissues with high ERα and/or ERβ expression. In both cell lines, 27-HC (1-1,000 nM) dose-dependently enhanced cell proliferation for 48 h, similar to that of 17β-estradiol; these effects were blocked by ER inhibitors ICI-182,780 and PHTPP.</p><p><strong>Conclusions: </strong>These findings indicate that 27-HC promotes eCCA cell proliferation through ERα- and ERβ-mediated SERM-like effects, highlighting that 27-HC and ERs as potential therapeutic targets in eCCA.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"16 3","pages":"1142-1156"},"PeriodicalIF":2.9,"publicationDate":"2026-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13090489/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147721350","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":"Nomogram outperforms gradient boosting machine for prognostic prediction of laryngeal squamous cell carcinoma: a combined analysis of SEER and single-center data.","authors":"Difeng Guo, Guanghai Ji, Mengru Jian, Kebing Chen, Yan Li","doi":"10.62347/AHUE7844","DOIUrl":"10.62347/AHUE7844","url":null,"abstract":"<p><p>The incidence of laryngeal squamous cell carcinoma (LSCC) remains persistently high, necessitating accurate prognostic prediction for clinical treatment guidance. By comparing the performance of LSCC models based on the Surveillance, Epidemiology, and End Results (SEER) database and those constructed from single-center datasets, this study provides an effective tool for clinical prognosis evaluation. Data from 526 patients with LSCC were extracted from the SEER database. Univariate and multivariate Cox regression analyses were performed to identify independent predictors of overall survival (OS) in LSCC patients. Subsequently, patients were randomly assigned in a 7:3 ratio to the modeling group and the test group. Based on the modeling group data, nomograms and gradient boosting machine (GBM) models were constructed using R software (version 4.4.1) and their performance was evaluated. The testing cohort was utilized to assess the predictive accuracy of the model. In addition, 207 LSCC patients diagnosed at The First Affiliated Hospital of Yangtze University from February 2020 to April 2024 were retrospectively selected as an external validation cohort. Univariate and Multivariate Cox regression analyses determined that age (60-75 years: HR=1.333, P=0.085; >75 years: HR=2.726, P<0.001), tumor size (HR=1.013, P=0.035), radiation (HR=7.555, P<0.001), cause of death (COD, HR=3.996, P<0.001), marital status at diagnosis (HR=1.444, P=0.006), and T stage (HR=1.652, P=0.017) were independent predictive indicators affecting the OS of LSCC patients (<i>P</i><0.05). On this basis, nomogram and GBM models were constructed. The ROC curve showed that the GBM model had an AUC of 0.747, 0.763, and 0.785 at 1-, 2- and 3-years, respectively. For nomogram model, the 1-, 2- and 3-year AUC values reached 0.809, 0.782 and 0.811, respectively. Delong test showed that the AUC values of nomogram were all higher than those of the GBM model (P<0.05). Next, we used nomogram models for verification. AUC values in the verification cohort were 0.783, 0.786, and 0.801, respectively. The AUC values for the external validation cohort were 0.795, 0.760, and 0.783, respectively. The calibration curve shows that the predicted value is basically consistent with the real value. The nomogram model has robust prediction ability and reliable calibration, and its performance is better than that of GBM model.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"16 3","pages":"1198-1214"},"PeriodicalIF":2.9,"publicationDate":"2026-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13090486/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147721486","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":"Rare <i>NUP98::SETBP1</i> fusion transcript in a refractory adult T-cell lymphoblastic lymphoma.","authors":"Xiaoyong Chen, Linlin Wang, Junyan Zou, Jihao Zhou, Yaying Zhou, Min Zuo, Lina Hu, Xiaoying Dong, Peng Ke, Junjie Hou","doi":"10.62347/PPME9616","DOIUrl":"10.62347/PPME9616","url":null,"abstract":"<p><p>T-lymphoblastic lymphoma (T-LBL) is an aggressive malignancy of T-lymphoid precursors, rarely co-occurring with consequent rearrangement of nucleoporin 98 (<i>NUP98</i>) gene. The <i>NUP98::SETBP1</i> fusion gene was first reported in a de novo T-cell acute lymphoblastic leukemia (T-ALL) patient. However, it has not yet been reported in patients with T-LBL. We report a case of T-LBL with the <i>NUP98::SETBP1</i> fusion gene. The <i>NUP98::SETBP1</i> fusion gene was discovered by RNA sequencing (RNA-seq) in the patient's bone marrow cells and verified in various tissues through direct sequencing and reverse transcriptase polymerase chain reaction (RT-PCR). Unfortunately, despite the use of various treatment methods, including traditional chemotherapy, anti-CD7 CAR-T cell therapy, and CD38-targeted therapy, the patient showed no improvement and ultimately died from disease progression. To our knowledge, this is the first report of the translocation involving <i>NUP98</i> and <i>SETBP1</i> genes in T-LBL. It is necessary to collect additional cases and conduct carefully designed experiments to establish the recurrence of this fusion in other T-LBL cohorts and confirm its role as a novel oncogenic rearrangement in T-LBL, providing a basis for managing such patients.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"16 3","pages":"937-946"},"PeriodicalIF":2.9,"publicationDate":"2026-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13090480/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147721503","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}