JCO Precision OncologyJCO精准肿瘤学
JCO Precision Oncology(英文缩写 JCO PRECIS ONCOL),ISSN 2473-4284,eISSN 2473-4284,中文译名:JCO精准肿瘤学 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：2025-11-01 至 2026-10-31，按本站收录文献的发表日期统计。
期刊介绍
JCO Precision Oncology 最新收录文献
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1. {"_":"Type II RAF Inhibitor Tovorafenib in Recurrent/Refractory Melanoma or Other Solid Tumors With Fusions or Fusions or Amplification: Phase II FIRELIGHT-1 Substudy.","i":["BRAF","CRAF/RAF1"]}
1. {"_":"II型RAF抑制剂Tovorafenib治疗复发/难治性黑色素瘤或其他伴有融合或扩增的实体瘤：II期FIRELIGHT-1子研究。","i":["BRAF","CRAF/RAF1"]}PMID:日期:2026-10-02Tovorafenib is an oral, selective, CNS-penetrant, type II inhibitor of BRAF and CRAF. fusions and fusions and amplifications are rare oncogenic drivers in many solid tumors. The phase II DAY101-102a substudy of FIRELIGHT-1 (ClinicalTrials.gov identifier: NCT04985604) investigated the efficacy and safety of tovorafenib monotherapy in recurrent/refractory solid tumors with structural alterations in or . Patients ≥12 years of age with a recurrent/refractory solid tumor with a fusion or fusion or amplification were enrolled into a melanoma cohort or tumor-agnostic cohort. The primary end point was overall response rate (ORR), as assessed by investigators. Tovorafenib was administered at 600 mg once weekly (adult dose), continuously, in 28-day cycles. Twenty-three patients were enrolled; eight in the melanoma cohort and 15 in the tumor-agnostic cohort. The median age was 53 years (range, 21-71), and 57% of patients had ≥2 lines of prior therapy. Fourteen patients had tumors with fusion, six fusion, two amplification, and one fusions and amplification. The median duration of tovorafenib treatment was 5.3 months (range, 0.8-22.5). The ORR was 43% (10/23 patients), including 50% (4/8) in patients with melanoma and 40% (6/15) in patients with other tumors. The median time to response was 1.8 months. The median duration of response was 9.2 months. The most common treatment-related adverse events (any grade) were anemia (39%), pruritus (30%), increased creatine phosphokinase (26%), and rash (26%). Tovorafenib demonstrated single-agent clinical activity in solid tumors with fusions or fusions or amplification and had a manageable safety profile. Tovorafenib may offer a new targeted treatment option for adult patients with tumors harboring these rare genomic driver alterations.
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2. Tumor-Free Circulating Tumor DNA in Node-Negative Rectal Cancers Undergoing Neoadjuvant Chemotherapy, Excision, and Observation in the Phase II NEO Trial (CO.28).
2. 在II期NEO试验（CO.28）中接受新辅助化疗、切除术和观察的淋巴结阴性直肠癌患者中的无肿瘤循环肿瘤DNAPMID:日期:2026-10-02Organ preservation is a priority in early-stage rectal cancer as total mesorectal excision (TME) can reduce quality of life. The Canadian Cancer Trials Group CO.28 trial demonstrated that neoadjuvant chemotherapy followed by transanal excision was effective in patients with cT1-3, node-negative (N0) rectal cancer. Here, we explored circulating tumor DNA (ctDNA) from the trial as a potential future decision aid to guide TME. Fifty-three of 58 patients (91.4%) from CO.28 had at least one sample available for ctDNA analysis using the Guardant Reveal epigenomic assay from the following time points: prechemotherapy, postchemotherapy, pretransanal endoscopic surgery (TES), and on follow-up at months 12, 24, and 36. ctDNA was detected in 45.8% of patients before neoadjuvant chemotherapy. Detection was similar by T-stage ( = .18). The rate of detectable ctDNA significantly decreased after chemotherapy (and pre-TES) to 8.7% ( < .0001), with 41.4% of evaluable patients moving from detectable ctDNA to completely undetectable following chemotherapy. ctDNA detection postchemotherapy and pre-TES was associated with poor response and persistent cancer ( = .03), with recommended TME for 100% (n = 4 of 4) of patients with ctDNA detected versus 38.1% (n = 16 of 42) of patients with undetectable ctDNA. Five patients had recurrence during follow-up (two local, three distant), 50% of whom (1 of 2, both local) had longitudinal plasma collected had detectable ctDNA at progression. ctDNA testing identified cancers with inadequate response to chemotherapy in patients for whom TME was recommended. A tissue-free assay may enable faster turnaround times compared with tumor-informed assays and provide a tool to support organ preservation. Further exploration of these assays in early-stage rectal cancers is warranted.
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3. {"_":"Decoding Treatment Response and Prognosis in Unresectable Locally Advanced Non-Small Cell Lung Cancer by Integrating Spatiotemporal Heterogeneity From F-FDG Positron Emission Tomography-Computed Tomography: A Multicenter Study.","sup":["18"]}
3. {"_":"通过整合18F-FDG正电子发射断层扫描-计算机断层扫描的时空异质性解读不可切除局部晚期非小细胞肺癌的治疗反应与预后：一项多中心研究。","sup":["18"]}PMID:日期:2026-10-02Treatment response in unresectable locally advanced non-small cell lung cancer (LA-NSCLC) is highly variable due to marked intratumoral heterogeneity, while existing predictive biomarkers lack accuracy. We aimed to develop and validate a pretreatment F-FDG positron emission tomography (PET)-computed tomography (CT)-derived spatiotemporal heterogeneity model to predict treatment response and prognosis in unresectable LA-NSCLC, and to explore its biological underpinnings. In a multicenter cohort of 434 patients with unresectable LA-NSCLC (training: n = 215; internal validation: n = 93; external validation: n = 126), treatment response was classified as responsive or nonresponsive based on initial assessment. Four distinct habitats (PEThigh-CThigh, PETlow-CTlow, PETlow-CThigh, and PEThigh-CTlow) were generated via the Otsu algorithm. Temporal heterogeneity was quantified using metabolic hotspot displacement (normalized distance from the hotspot to the tumor centroid and normalized distance from the hotspot to the tumor periphery) and integrated with spatial radiomics to build a multidimensional spatiotemporal model. Model performance was evaluated against conventional metrics, with interpretability enhanced via nomogram and SHapley Additive exPlanations analysis. Survival outcomes were assessed using Kaplan-Meier curves, and public transcriptomic data were analyzed to characterize underlying pathways. The spatiotemporal model accurately predicted treatment response with AUCs of 0.822 (training), 0.821 (internal validation), and 0.810 (external validation), significantly outperforming conventional whole-tumor PET-CT models. It maintained robust generalizability across treatment subgroups and effectively stratified patients by progression-free survival and overall survival ( < .01). PEThigh-CThigh habitat volume fraction correlated with treatment resistance, whereas PETlow-CTlow habitat correlated with better response. Exploratory pathway analysis highlighted key pathways involving drug metabolism, glycolytic reprogramming, and immune microenvironment remodeling. This study establishes a noninvasive spatiotemporal heterogeneity biomarker based on F-FDG PET-CT that reliably predicts treatment response and prognostic outcomes in unresectable LA-NSCLC. It offers valuable insights for personalized clinical decision making and supports precision oncology.
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4. Latent Class Analysis-Derived Classification and Cancer-Specific Death in Endometrial Carcinoma: A Population-Based Cohort Study.
4. 潜在类别分析衍生的分类与子宫内膜癌特异性死亡：一项基于人群的队列研究PMID:日期:2026-10-02Molecular classifications have advanced prognostic stratification in endometrial carcinoma (EC), but they do not explicitly account for cause-specific mortality (CSM) and host-clinical context. We aimed to derive a clinically accessible classification that links demographic/clinicopathologic features, CSM, and molecular landscapes and to test whether it refines molecular-based survival stratification. We conducted latent class analysis (LCA) on 46,772 cases of primary EC from the SEER program to identify latent characteristic lineages. The resulting LCA scheme was mapped to The Cancer Genome Atlas (TCGA) data. Cumulative incidence functions and Fine-Gray competing risks regression were used to estimate CSM. The Fisher test was employed to evaluate its association with TCGA subtypes. Transcriptomic differential expression analysis and pathway enrichment analysis were performed where data were accessible. Likelihood ratio tests assessed treatment-LCA interactions. Five clinically interpretable classes emerged. Class 4 had significantly increased subdistribution hazard for CSM (1.34, = .031); classes 3/5 trended higher. Classes were associated with TCGA subtypes ( < .001). Specifically, class 3 was associated with copy number (CN)-high enriched sybtype and class 1 was associated with CN-low subtype. Incorporating LCA labels into molecular survival models increased C-index and robustness of prognostic discrimination. Transcriptomics revealed class specific signatures implicating metabolic reprogramming, DNA repair, and immune pathways. Treatment benefit varied by class: compared with surgery alone, class 3 demonstrated the most significant survival advantage with surgery-radiotherapy-chemotherapy. Class 4 exhibited sensitivity to radiotherapy, while class 5 benefited exclusively from the triple therapy. Conversely, class 1/2 did not benefit from combined treatment. LCA of routine clinical variables identifies subgroups susceptible to CSM and complements TCGA molecular classification, improving survival stratification.
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5. {"_":"Efficacy Study of Vemurafenib in Children With Recurrent or Progressive BRAF- or BRAF-Mutant Brain Tumors: PNOC002.","sup":["V600E","InsT"]}
PMID:日期:2026-09-23Pediatric gliomas constitute the most prevalent central nervous system tumors in children, and aberrations in BRAF signaling contribute to their pathogenesis by disrupting the MAPK pathway. Targeted inhibition of this pathway using agents such as vemurafenib may hold therapeutic promise. PNOC002 was a multicenter trial conducted through the Pediatric Neuro-Oncology Consortium in patients younger than 25 years with recurrent or progressive BRAF-mutant brain tumors. This combined phase 0/1 study aimed to establish the recommended phase II dose (RP2D) and assess preliminary efficacy, including tumor growth trajectories and rebound (defined as ≥25% increase in lesion size within 6 months, usually within 3 months, of stopping therapy). Thirty-patients (range, 3-23 years) were treated at the RP2D of 550 mg/m twice a day: 22 low-grade glioma (LGG) and 8 high-grade glioma (HGG). PFS at 6 months (PFS6) for the entire cohort was 80% (95% CI, 67 to 96). In patients with LGG, PFS6 was higher at 86% (95% CI, 73 to 100), compared with 63% (95% CI, 37 to 100) in patients with HGG. The best responses were stable disease (13 patients) and partial responses (13 patients). Four patients experienced PD, with three patients in the HGG cohort. Responsiveness varied by lesion type, with cystic lesions showing a larger and longer-lasting decrease in tumor size than solid lesions. Of 13 patients with LGG who discontinued treatment and had follow-up imaging, 3 (23%) experienced rebound within 78-97 days. The most common grade 3 adverse event was maculopapular rash (57%). Vemurafenib showed efficacy in children with recurrent or progressive BRAF-mutant brain tumors with acceptable toxicity. However, the rebound rate of 23% warrants further investigation.
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6. Clinical and Proteomic Biomarkers of Trifluridine/Tipiracil in Fluoropyrimidine-Refractory Advanced Pancreatic Adenocarcinoma: A Single-Arm Phase II Trial.
PMID:日期:2026-09-23Patients with refractory pancreatic cancer have limited therapeutic option and dismal prognoses. This study aimed to evaluate the efficacy and safety of trifluridine/tipiracil (FTD/TPI) in patients with fluoropyrimidine-refractory pancreatic cancer and their predictive biomarkers. In this single-arm phase II clinical trial, patients of refractory pancreatic cancer were enrolled and administered with FTD/TPI on days 1-5 and 8-12 of a 28-day cycle. The primary end point was the 16-week progression-free survival (PFS) rate. Secondary end points included median PFS, median overall survival (OS), disease control rate (DCR), and toxicities. Clinical and proteomic biomarkers were assessed before treatment and correlated with PFS and OS. Between March 2021 and June 2023, a total of 28 patients were enrolled. The median age was 64 years (range, 49-80), and 16 (57.1%) patients were male. All patients (100%) received prior fluoropyrimidine. Twenty-three patients (82.1%) received two or more lines of chemotherapy. After a median follow-up of 4.8 months, the 16-week PFS rate was 35.7% (95% CI, 17.8 to 53.2). The median PFS was 3.3 months (95% CI, 1.8 to 4.8) and the median OS was 4.6 months (95% CI, 3.8 to 5.4). The DCR was 50% (14/28; 95% CI, 30.7 to 69.4). The most common grade 3 or worse adverse events were neutropenia (n = 9, 32.1%) and anemia (n = 4, 14.3%) without new safety signals. Neutrophil-to-lymphocyte ratio (NLR) > 5 and high IL1RL1 level were poor prognostic factors, while high APOA4, MSTN, and LUM levels were associated with better prognoses. To our knowledge, this is the first prospective study to suggest the potential efficacy and acceptable safety of FTD/TPI in patients with pancreatic cancer refractory to fluoropyrimidine. Further randomized trials are needed to validate these findings. NLR, IL1RL1, APOA4, MSTN, and LUM levels are promising biomarkers that warrant further investigation.
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7. Tumor Immune Microenvironment and Response to Preoperative Chemoradiotherapy in Locally Advanced Rectal Cancer: Results From the STAR-01 Study Cohort.
7. 肿瘤免疫微环境与局部晚期直肠癌术前放化疗反应：来自STAR-01研究队列的结果PMID:日期:2026-09-23Preoperative chemoradiotherapy (CRT) can reshape the composition of the tumor immune microenvironment (TIME) in locally advanced rectal cancer (LARC), augmenting T-cell density and activation. As TIME may provide predictive insights, we analyzed the association of immune cell distribution and remodeling after CRT with pathologic response and clinical outcomes in patients with LARC derived from the STAR-01 (fluorouracil-based CRT plus/minus oxaliplatin) trial. Tumor-infiltrating lymphocytes (TILs) were assessed by standard stains and immunostains (CD3, CD20, CD4, CD8, FOXP3, PD-1, and CD68). Immune cell populations in pretreatment biopsies and post-treatment surgical specimens were compared and associated with complete pathological response (ypT0N0) and overall (OS) and event-free (EFS) survival. We retrieved 413 samples from 303 patients from the original cohort, including 110 paired pretreatment biopsies and post-treatment surgical tumor specimens. In pretreatment biopsies, CD20 cell counts were associated with improved EFS ( = .051), independent of other prognostic factors. After therapy, intermediate-high TILs, CD3 cells, low CD4/CD8 ratio, and CD68 macrophage counts significantly increased, whereas FOXP3 and CD20 cells decreased. ypT0N0 was associated with low CD4/CD8 ratio ( < .001), reduced CD68 ( = .001), and absence of eosinophils ( < .001) in post-treatment surgical specimens. In post-treatment specimens, low CD4/CD8 ratio and CD20 cell counts were significantly associated with both improved EFS (CD4/CD8: = .016; CD20 cells: = .002) and OS (CD4/CD8: = .005; CD20 cells: = .014). This prognostic role was confirmed in a multivariable analysis for CD20 cells. In LARC, CRT reshapes the type and amount of immune cell contents, and the effects on certain immune populations are associated with tumor regression and clinical outcome.
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8. Noncontrast Magnetic Resonance Fingerprinting-Habitat Framework for Intratumoral Heterogeneity Decoding and Isocitrate Dehydrogenase Mutation Prediction in Diffuse Gliomas.
8. 非增强磁共振指纹-生境框架用于弥漫性胶质瘤的瘤内异质性解码及异柠檬酸脱氢酶突变预测PMID:日期:2026-09-23To develop and validate a magnetic resonance fingerprinting (MRF)-based habitat imaging framework for noninvasively decoding intratumoral heterogeneity (ITH) and preoperatively predicting isocitrate dehydrogenase (IDH) mutation status in diffuse gliomas. In this prospective study (January 2024-September 2025), 141 adults with diffuse gliomas (56 IDH-mutant, 85 IDH-wildtype) were enrolled. Tumors were segmented into three habitats via K-means clustering of coregistered MRF-derived T2 and free water maps. A habitat-based radiomic model for IDH status was developed in a training cohort (n = 98) and validated in an independent test cohort (n = 43). Its performance was compared against a conventional whole-tumor model using area under the curve (AUC) and net reclassification improvement (NRI). Pathophysiological validation was performed by correlating habitats with the Ki-67 proliferation index, dynamic contrast-enhanced magnetic resonance imaging (), and apparent diffusion coefficient (ADC). The prognostic value for progression-free survival (PFS) was also assessed. The MRF-habitat model outperformed the whole-tumor model for IDH genotyping (test AUC, 0.819 0.758; NRI, 0.833, = .003). It identified a prognostically significant subregion (Subregion1) where T2 uniformity was an independent predictor of PFS (hazard ratio: 0.008; = .033). Subregion2, a hypoxic-angiogenic niche, correlated with Ki-67 and exhibited higher and lower ADC in IDH-wildtype tumors (both < .05). Patients stratified as high-risk by the model had significantly shorter median PFS (5.8 months not reached, = .043). The MRF-based habitat framework noninvasively decodes ITH, improves preoperative IDH genotyping, and identifies pathophysiologically distinct subregions with prognostic relevance.
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9. Triple-Negative Transformation in Hormone Receptor-Positive/Human Epidermal Growth Factor Receptor 2-Negative Metastatic Breast Cancer: Tissue Versus Liquid Biopsy in Two Cases.
9. 激素受体阳性/人表皮生长因子受体2阴性转移性乳腺癌中的三阴性转化：两例病例中组织活检与液体活检的比较PMID:日期:2026-09-23该文献暂无摘要。
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10. Cross-Ancestry and Phenome-Wide Associations of Cancer-Specific Polygenic Risk Scores.
10. 癌症特异性多基因风险评分的跨 ancestry 与全表型组关联研究PMID:日期:2026-09-17Genome-wide association studies have identified many common variants associated at low effect sizes with various cancers. Summing the effects of these variants into polygenic risk scores (PRS) can improve cancer risk prediction. However, cross-cancer and cross-phenotype pleiotropic associations of cancer-specific PRS are limited. Using logistic regression models, we tested the association of 13 cancer-specific PRS with curated phenotypes representing the same 13 cancers and 340 cancer and cardiometabolic phecodes in 560,287 individuals (114,255 African ancestry [AFR] and 446,032 European ancestry [EUR]) from the Million Veteran Program. Models were stratified by ancestry and used age, principal components, and cancer-specific PRS per standard deviation as independent variables, and correction was applied for multiple comparisons. All 13 cancer-specific PRS were significantly associated with their respective cancers among EUR individuals with odds ratios per standard deviation of PRS (odds ratio [OR]) 1.05-1.70. Among AFR individuals, the effect sizes of the cancer PRS were lower, with OR 1.01-1.48, and cancer-specific PRS were significantly associated with their respective cancers for five of 13 cancers (bladder, breast in female patients, colorectal, prostate, and thyroid). In cancer-cancer pleiotropy studies, only the renal cancer-specific PRS was significantly associated with skin cancer (OR = 1.04, = 4.5 × 10) among EUR individuals. PheWAS demonstrated five positive pleotropic associations with cardiometabolic conditions (thyroid cancer PRS with thyroid goiter, oral cancer PRS with diabetes phenotypes, and hypothyroidism) and two negative associations (oral and lung cancer PRS separately with coronary artery disease). Cancer PRS have stronger associations per cancer among EUR versus AFR individuals. In contrast to PRS of other chronic diseases, the majority of cancer-related PRS are highly specific and pleiotropic associations with other cancers and cardiometabolic traits are uncommon.