Translational Cancer Research转化癌症研究
Translational Cancer Research(英文缩写 TRANSL CANCER RES),ISSN 2218-676X,eISSN 2219-6803,中文译名:转化癌症研究 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-10-01 至 2026-09-30，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 0.496 | Q4 |
| 2022 | 0.900 | Q4 |
| 2023 | 1.500 | Q4 |
| 2024 | 1.700 | Q4 |
| 2025 | 2.100 | Q3 |
Translational Cancer Research 最新收录文献
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1. {"_":"The prognostic value and molecular mechanisms of infection-associated differentially expressed genes in oral squamous cell carcinoma.","i":["Porphyromonas gingivalis"]}
PMID:日期:2026-08-27Increasing evidence suggests that Porphyromonas gingivalis (Pg) is associated with oral squamous cell carcinoma (OSCC) development and progression. This study aimed to identify Pg-associated genes with prognostic relevance in OSCC through integrated bioinformatics analysis. OSCC-related differentially expressed genes (DEGs) were identified from the The Cancer Genome Atlas (TCGA)-OSCC cohort and intersected with Pg supernatant-associated DEGs from GSE192887. Raw count data were analyzed with DESeq2, whereas transcripts per million (TPM)-transformed expression values were used for downstream visualization and model construction. Weighted gene co-expression network analysis (WGCNA), univariate Cox regression, least absolute shrinkage and selection operator (LASSO) regression, and multivariable Cox modeling were used to develop a seven-gene prognostic signature, which was externally evaluated in GSE41613. Additional analyses examined treatment-associated expression changes in the seven model genes, pairwise correlations among the model genes, and correlations between Pg supernatant-associated differentially expressed gene (PgSDEG)-derived module eigengenes and immune-cell fractions. Quantitative reverse-transcription polymerase chain reaction (qRT-PCR) was performed in eight paired OSCC and adjacent non-tumor tissues and in supplemented-brain heart infusion (BHI) vehicle-control and Pg culture-supernatant-treated HOK, HSC-3, and CAL-27 cells. A prognostic signature comprising , , , , , , and was established. The signature showed limited-to-moderate discrimination in the TCGA training cohort, with 1-, 3-, and 5-year areas under the curve (AUCs) of 0.68, 0.69, and 0.69, respectively, and limited discrimination in the GSE41613 external cohort (AUCs: 0.66, 0.67, and 0.61). Kaplan-Meier analysis showed poorer survival in the high-risk group in both cohorts. The GSE192887 analysis showed significant treatment-associated expression changes in all seven genes after Pg culture-supernatant exposure. In paired tissues, CXCL8 and TMEM92 were significantly higher in OSCC tissues, whereas STC1 was not significant after Holm correction. In CAL-27 cells, CXCL8, STC1, and TMEM92 increased significantly after culture-supernatant treatment, whereas the corresponding comparisons were not significant in HOK or HSC-3 cells after adjustment. This study developed a seven-gene Pg-associated prognostic signature for OSCC and provided complementary transcriptomic, immune-correlation, tissue, and cell-based evidence that placed the signature in biological context. The model showed limited-to-moderate discrimination and is not ready for clinical use. The enrichment, gene-correlation, and immune-correlation findings are hypothesis-generating rather than mechanistic evidence. Further independent validation and dedicated functional studies are required.
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2. Drug-tolerant persister cells use conserved adaptive transcriptional programs.
PMID:日期:2026-08-27该文献暂无摘要。
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3. Combined multi-omics profiling and machine learning analysis reveals that Bregs and RPS2 promote bone metastasis in nasopharyngeal carcinoma.
PMID:日期:2026-08-27The bone is the primary site of distant metastasis in patients with nasopharyngeal carcinoma (NPC), and bone metastasis (BM) significantly increases mortality. Deciphering the complex crosstalk between cancer cells and their tumor microenvironment (TME) is crucial for identifying therapeutic targets aimed at eliminating metastasis-initiating cells and preventing the establishment of overt metastases. Regulatory B cells (Bregs), a specialized B-cell subset endowed with potent immunosuppressive functions, play a pivotal regulatory role within the TME. However, their specific contributions, phenotypic characteristics, and underlying molecular mechanisms within the BM niche of NPC remain incompletely characterized and await full elucidation. This study aims to investigate the infiltration dynamics, functional impact, and molecular underpinnings of Bregs in the context of NPC BM. The single-cell sequencing data and RNA sequencing (RNA-seq) microarray matrices from public databases were utilized for the analysis in this study. Subsequently, three machine learning methods, least absolute shrinkage and selection operator (LASSO) regression analysis, random forest algorithm, and Boruta algorithm were combined to identify prognostic genes. The high infiltration of Bregs and high expression of RPS2 in the primary lesions of BM patients were confirmed, and relevant prognostic signatures were constructed. Flow cytometry, cell counting kit-8 (CCK-8) assay, migration assay, Transwell assay, and co-culture system were used to evaluate the effects of Bregs on cell proliferation and metastasis. An animal model of intracardiac injection-induced tumor transplantation was established, and bioluminescence imaging (BLI), digital radiography (DR), and micro computed tomography (Micro-CT) were utilized to assess the impact of Bregs on BM of tumor cells. Finally, clinical cohort analysis was conducted to determine the correlation between Bregs and BM in NPC. Bregs exhibit high infiltration in the primary lesions of NPC with BM, and the high expression of RPS2 in Bregs is highly correlated with prognosis. Mechanistically, RPS2 upregulates the secretion of interleukin-10 (IL-10) by Bregs. IL-10 then activates the PI3K/AKT pathway, which in turn upregulates the expression of the CXCR6 on the surface of tumor cells. These tumor cells, under the attraction of CXCL16 secreted by macrophages in bone, show an increased tendency to undergo BM. In the primary lesions of NPC patients, Bregs expressing RPS2 within tertiary lymphoid structures are highly associated with BM. Bregs and RPS2 can be utilized for the prognostic evaluation of BM in NPC. Pharmacological inhibition targeting Bregs or IL-10 may be a feasible approach to delay and treat BM in NPC.
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4. Sacituzumab-govitecan plus pembrolizumab: redefining first-line therapy in PD-L1-positive advanced triple-negative breast cancer.
4. 戈沙妥珠单抗联合帕博利珠单抗：重新定义PD-L1阳性晚期三阴性乳腺癌的一线治疗PMID:日期:2026-08-25该文献暂无摘要。
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5. Development and internal validation of dual overall and cancer-specific survival nomograms for primary spinal and sacropelvic Ewing sarcoma: a population-based study of 346 patients.
PMID:日期:2026-08-25Primary spinal Ewing sarcoma (ES) is exceptionally rare, and existing prognostic evidence is largely derived from mixed-site cohorts that fail to capture the spine-specific clinical and biological profile. Accurate, site-specific prognostication remains unavailable, limiting consistency in clinical decision-making. This study aimed to define independent prognostic determinants for spinal ES and to develop and internally validate dedicated nomograms and a risk-stratification system for both overall survival (OS) and cancer-specific survival (CSS). Patients diagnosed with primary spinal ES between 1995 and 2015 were identified from the Surveillance, Epidemiology, and End Results (SEER) database. Prognostic variables for OS and CSS were assessed using Cox proportional hazards regression with backward stepwise selection optimized by the Akaike information criterion (AIC). Independent predictors were integrated into separate OS and CSS nomograms. Discrimination, calibration, and clinical utility were evaluated using Harrell's concordance index (C-index), time-dependent area under the receiver operating characteristic curve (AUC), calibration curves with bootstrap resampling, and decision curve analysis (DCA). A three-tier risk classification system was constructed based on total nomogram scores. A total of 346 eligible patients were included and randomly allocated to a training cohort (n=262) and a validation cohort (n=84) in a 3:1 ratio; 158 deaths from any cause and 142 ES-specific deaths were observed. Chemotherapy omission, distant disease and Black race/ethnicity were independent predictors of worse OS and CSS, larger tumor size was an independent predictor of worse OS, and married status was associated with lower mortality risk; the racial association, based on 10 Black patients and none in validation, is hypothesis-generating. The OS and CSS nomograms showed moderate discrimination in the training [OS C-index 0.726, 95% confidence interval (CI): 0.696-0.756; CSS 0.727, 0.697-0.757] and validation cohorts (OS 0.699, 0.640-0.758; CSS 0.680, 0.622-0.738); after 1,000-resample bootstrap internal validation the optimism-corrected C-index was 0.695 (OS) and 0.702 (CSS), with calibration slopes of 0.917 and 0.938, respectively. Calibration curves showed close agreement between predicted and observed survival. The three-tier risk classification produced well-separated survival curves for both OS and CSS, with median CSS of 197 months, 37 months, and 13 months in the low-, intermediate-, and high-risk groups, respectively. This study provides the first dual-endpoint, site-specific prognostic framework for primary spinal and sacropelvic ES. Discrimination was moderate and validation internal only; the nomograms should be regarded as hypothesis-generating, and external validation in independent contemporary cohorts is required before clinical use.
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6. Quantitative magnetic resonance imaging for accurate delineation of radiotherapy: a narrative review.
PMID:日期:2026-08-25Quantitative magnetic resonance imaging (qMRI) can provide quantifiable biological information, such as tissue relaxation times, diffusion coefficients, and perfusion parameters, thereby enabling accurate characterization of tumor heterogeneity, hypoxic status, and microenvironmental features. It holds unique clinical value in the precise delineation of radiotherapy targets. This review aims to systematically evaluate the research progress and clinical application prospects of qMRI in the biological definition of radiotherapy target volumes and to explore its potential in driving the paradigm shift from geometry-guided to biology-guided radiotherapy. This narrative review systematically searched seven databases up to January 2026. Eligible English full-text human studies focusing on qMRI and biology-guided radiotherapy target delineation were included. qMRI enables the acquisition of quantitative parameters, including apparent diffusion coefficient (ADC) values, relaxation times, and perfusion metrics, which accurately reflect tumor cellularity, microvascular perfusion, and metabolic status. It demonstrates unique value in identifying tumor infiltration boundaries, delineating internal subtargets, assessing tumor hypoxia, and predicting early radiotherapy response. Currently, this technique has shown significant advantages in target delineation for tumors of the brain, head and neck, prostate, and other sites. However, key challenges remain regarding standardization of data acquisition, parameter reproducibility, multicenter validation, and deep integration with radiotherapy treatment planning systems. qMRI is driving a critical paradigm shift in radiotherapy from geometry-guided to biology-guided approaches, providing a powerful tool for individualized target delineation and dose "three-dimensional sculpting" based on tumor biology. Future efforts should focus on multi-parameter combined validation, establishing standardized systems covering acquisition, calibration, and post-processing, conducting large-scale prospective clinical trials to generate high-level evidence, and deeply integrating artificial intelligence to mine radiomics features and develop robust predictive models. Through technical optimization, clinical validation, and multidisciplinary collaboration, qMRI is expected to serve as an indispensable biological "eye" in precision radiotherapy systems, laying a solid foundation for individualized, adaptive radiotherapy (ART) and improved oncological outcomes.
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7. Measuring toxicity better: patient-reported outcome-informed calibration for CTCAE assessment.
PMID:日期:2026-08-13该文献暂无摘要。
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9. Cancer associated fibroblasts: heterogenous modifiers of treatment response.
PMID:日期:2026-08-01该文献暂无摘要。
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10. CST2 promotes melanoma malignant phenotypes through the IL-6-STAT3-NF-κB signaling axis.
PMID:日期:2026-07-30Melanoma is a highly aggressive malignancy with increasing incidence and mortality over recent decades. Cystatin SA (CST2) encodes a secreted cysteine protease inhibitor that is overexpressed in various cancers and promotes tumor progression; however, its role in melanoma remains unclear. This study aimed to investigate the expression and clinical significance of CST2 in melanoma as well as its biological functions and underlying molecular mechanisms in melanoma progression. CST2 expression was analyzed in melanoma tissues using The Cancer Genome Atlas (TCGA) dataset. The prognostic value of CST2 was assessed using Kaplan-Meier analysis. In vitro gain- and loss-of-function experiments were performed to evaluate the effect of CST2 on melanoma cell proliferation, colony formation, and migration. Mechanistic studies included protein-protein docking and co-immunoprecipitation to detect the interaction between CST2 and interleukin-6 (IL-6). Western blotting was used to examine the activation status of IL-6 downstream signaling pathways. CST2 was significantly upregulated in melanoma tissues and was correlated with poor patient prognosis. Overexpression of CST2 promoted melanoma cell proliferation, clonogenicity, and migration, whereas CST2 knockdown suppressed these malignant behaviors. CST2 interacted with IL-6, and its knockdown reduced the expression of IL-6, phospho-STAT3, and phospho-NF-κB. These suppressive effects were reversed by IL-6 overexpression, indicating that CST2 exerted its oncogenic effects through the IL-6-STAT3-NF-κB axis. CST2 promotes melanoma progression by activating the IL-6-STAT3-NF-κB signaling pathway, and may serve as a potential prognostic biomarker and therapeutic target in melanoma.