American journal of cancer research最新文献

Background: The principal established therapeutic option for localized prostate cancer is the robotic-assisted radical prostatectomy (RARP) over the laparoscopic radical prostatectomy (LRP). Robust data from Chinese hospitals is limited, and the effect of surgeon experience is often overlooked.

Objective: This study retrospectively compares outcomes between RARP and LRP, evaluating the impact of surgeon experience.

Methods: The clinical information of 252 patients who underwent RARP or LRP between 2019 and 2023 was retrospectively analysed. Multivariable regression models, for both patient characteristics and surgeon volume, were employed to evaluate perioperative metrics, complications, positive surgical margins (PSM), continence, and patient-reported outcomes.

Results: RARP demonstrated superior advantages, including a shorter operative time (154.9±28.3 vs. 169.2±23.9 minutes, P<0.001), less blood loss (172.5±56.8 vs. 306.8±82.2 mL, P<0.001), and a shorter hospital stay (2.3 vs. 3.9 days, P<0.001). Multivariable analysis revealed that both surgical approaches and surgeon volume were predictors of outcomes: 66% lower odds of PSM (OR: 0.34, P=0.009) in the RARP group, while high-volume surgeons demonstrated 96% lower odds of PSM compared to low-volume surgeons (OR: 0.039, P<0.001). RARP patients experienced fewer complications (25.4% vs. 39.7%, P=0.016) and a higher continence recovery at 12 months (95.2% vs. 80.2%, P=0.001). Regarding patient-reported outcomes, RARP was consistently favored across all domains (P<0.01).

Conclusion: While preserving comparable functional and short-period cancer-related outcomes, RARP outperformed LRP in perioperative outcomes and patients' quality of life. These findings demonstrate that both surgical technology and surgeon volume are critical, independent determinants of surgical quality. The optimal outcomes are achieved by pairing advanced robotic technology with high-volume surgical expertise.

Interleukin enhancer binding factor 2 (ILF2) has been confirmed to drive the progression and proliferation of multiple malignancies, but the expression and function of ILF2 in colorectal cancer (CRC) remain to be elucidated. In this study, the expression of ILF2 in CRC tissues was evaluated by the public tumor databases, quantitative reverse transcription PCR (qRT-PCR) and tissue array analyses. ILF2 was found to be elevated in CRC, and was predicted to serve as a negative index for patients. Subsequently, cell proliferation was detected by Cell Counting Kit-8 (CCK-8) assay and colony formation, and tumor growth was evaluated by establishing xenografted mouse models. Our results showed that knockout of ILF2 markedly inhibited cell proliferation and tumor growth of CRC. Moreover, we found ILF2 was ubiquitinated, and further co-immunoprecipitation (Co-IP) coupled with liquid chromatography-tandem mass spectrometry analysis indicated that ILF2 may be a novel substrate of the deubiquitinating enzyme ubiquitin specific peptidase 5 (USP5). Further reciprocal Co-IP assays confirmed that ILF2 interacted with USP5. Enforced expression of USP5 reduced ubiquitinated ILF2 and increased ILF2 level, whereas catalytic inactive USP5 did not. While USP5 inhibitor WP1130 downregulated ILF2 and inhibited CRC cell growth, the effects were markedly abolished by ILF2 overexpression. These data demonstrate that the USP5/ILF2 axis mediates the tumorigenesis of CRC, which highlights the USP5/ILF2 axis as a promising therapeutic target for CRC treatment.

[This retracts the article on p. 2209 in vol. 7, PMID: 29218245.].

Background: Information asymmetry between healthcare providers and patients undergoing lung cancer surgery can result in reduced treatment engagement, lower admission satisfaction, and a greater risk of medical disputes, particularly regarding the transition to the intensive care unit (ICU). This study aims to map the ICU pre-experience pattern by first identifying, along a timeline of key ICU stages, the specific information that patients awaiting lung-cancer surgery and their families require during the peri-ICU period.

Methods: A qualitative study was conducted by purposive sampling at the Lung Cancer Center of West China Hospital, Sichuan University. Semistructured interviews were held with 36 participants (17 patients and 19 families). The interview transcripts were analyzed by content analysis with NVivo 12.0 software.

Results: The analysis identified a structured hierarchy of information needs, comprising 2 first-level themes, 4 second-level themes, and 13 third-level themes. The core finding was that patients' information needs were greater than those of their families. Patients were predominantly concerned about postoperative care and their physical perceptions. In contrast, families focused more on process-oriented information, such as the ICU transfer process and required signatures before admission, as well as the patient's surgical outcomes and treatment process after admission.

Conclusion: Patients and their families have comprehensive yet distinct information needs prior to ICU admission. Healthcare providers are their primary information source, underscoring the necessity for a structured, proactive, and patient-centered approach to information delivery. These findings provide a foundational framework for developing an "ICU pre-experience" pattern to mitigate uncertainty and improve nursing quality.

Gliomas, particularly glioblastoma multiforme (GBM), represent the most prevalent primary intracranial malignancies, characterized by high invasiveness, aggressive proliferation, and poor clinical outcomes. Recent studies have highlighted the critical role of tumor microenvironment interactions and cellular stress responses, including endoplasmic reticulum (ER) stress, in modulating glioma progression. While ER stress can induce autophagy and apoptosis, glioma cells exhibit remarkable plasticity, adapting to stress conditions and exploiting them to promote survival and self-renewal, thereby contributing to therapeutic resistance. In this study, we established an individualized ER stress risk score using glioma transcriptomic data, demonstrating its association with adverse prognosis, aggressive molecular subtypes, and pro-tumorigenic biological functions. Through systematic screening, we identified DERL3 as a core effector gene mediating ER stress adaptation. Functional validation revealed that DERL3 drove glioma proliferation and invasion by binding to and stabilizing Heterogeneous nuclear ribonucleoprotein A2/B1 (HNRNPA2B1), consequently activating the NF-κB signaling pathway. These findings elucidate the DERL3-HNRNPA2B1-NF-κB axis as a critical mechanistic link between ER stress adaptation and glioma malignancy. Targeting this axis may offer novel therapeutic strategies to overcome treatment resistance, providing significant translational potential for improving glioma management. This study advances our understanding of stress response mechanisms in tumorigenesis and underscores the clinical relevance of ER stress-related pathways in precision oncology.

[This corrects the article on p. 1751 in vol. 5, PMID: 26175943.].

Relapsed or refractory diffuse large B-cell lymphoma (R/R DLBCL) remains a therapeutic challenge with poor prognosis. Selinexor, a selective inhibitor of nuclear export (XPO1), has shown activity in this setting. We retrospectively evaluated the efficacy and safety of selinexor combined with R-GDP (rituximab, gemcitabine, dexamethasone, and cisplatin) as second-line therapy in 22 patients with R/R DLBCL treated at Fudan University Shanghai Cancer Center between January 2023 and August 2023. Patients were scheduled to receive 3 cycles of selinexor plus R-GDP, and subsequently followed by high-dose chemotherapy and autologous stem cell transplantation (ASCT), anti-CD19 chimeric antigen receptor T-cell (CAR-T) therapy, or alternative regimens, as appropriate. At a median follow-up of 25.5 months, the selinexor plus R-GDP regimen yielded an overall response rate of 52.4% in patients with R/R DLBCL. The median overall survival (OS) was 26.9 months (95% CI, 12.1-not reached), with 1- and 2-year OS rates of 67.6% and 52.3%. The median progression-free survival (PFS) was 7.7 months (95% CI, 2.27-not reached). Survival outcomes were significantly influenced by subsequent therapy: patients bridged to ASCT or CAR-T therapy had significantly longer OS (P=0.0217) and PFS (P=0.0029) than those receiving other treatments. The median OS was not reached in the ASCT group, 26.9 months (95% CI, 15.9-not reached) in the CAR-T group, and 11.2 months (95% CI, 10.2-not reached) in patients receiving other therapies. The median PFS was not reached for ASCT or CAR-T group, compared with 2.2 months (95% CI, 2.1-not reached) in patients receiving other therapies. Additionally, patients with relapsed disease exhibited a significantly longer median PFS than those with primary refractory disease (not reached vs 2.82 months, [95% CI, 2.17-not reached]; P=0.0072). No significant difference in OS was observed between these two groups (P=0.2323). Common adverse events included thrombocytopenia (100%), fatigue (59%), neutropenia (45%), anemia (45%), and pneumonia (23%), while were manageable through supportive care or temporary dose interruption. In this real-world analysis, selinexor combined with R-GDP demonstrated modest efficacy in R/R DLBCL, while highlighting the importance of optimizing subsequent sequencing with ASCT or CAR-T therapy.

Objective: To evaluate clinical, molecular, and immunological predictors of response to immunotherapy among patients with advanced endometrial cancer and to develop a combined biomarker model for predicting treatment outcomes.

Methods: This retrospective case-control study included 590 advanced endometrial cancer patients treated at the Affiliated Hospital of Hebei University of Engineering between December 2024 and May 2025. Eligible women underwent total hysterectomy, pelvic lymph node dissection, and received immune checkpoint inhibitors alongside standard chemotherapy. Patients were stratified into good and poor response groups based on 1-year post-treatment prognosis and response evaluation criteria in solid tumors. Baseline blood biomarkers, gene mutation status (breast cancer gene [BRCA] 1, BRCA2, DNA polymerase epsilon, tumor protein p53 [TP53], mutS homolog 6), and immunophenoscore (IPS) were assessed. Logistic regression and receiver operating characteristic (ROC) analyses were performed. A random forest model was constructed for combined biomarker prediction.

Results: No significant differences in baseline demographic or clinical characteristics were found between response groups. Good responders had significantly lower baseline levels of C-reactive protein (CRP), interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-α), neutrophil-lymphocyte ratio (NLR), cancer antigen 125 (CA125), and IPS, and higher frequencies of gene mutations. Multivariate regression identified elevated CRP, IL-6, TNF-α, NLR, CA125, and IPS as independent predictors of poor response; BRCA2 and TP53 mutations were independently associated with favorable outcomes. The combined biomarker model achieved an area under the ROC curve of 0.812, demonstrating strong predictive accuracy.

Conclusion: Inflammatory and tumor biomarkers, IPS, and specific gene mutations are independently associated with immunotherapy response in advanced endometrial cancer. A combined biomarker model may enhance the prediction of treatment outcomes and guide individualized therapy.

Lung cancer is one of the most common cancers and the leading cause of cancer death worldwide. Opportunistic infections (OI) are increasingly recognized in this population due to disease-related immune dysfunction and treatment-induced immunosuppression. Compared with the chemotherapy era, the use of immune checkpoint inhibitors and targeted agents has shifted the OI profile. Pneumocystis jirovecii pneumonia (PJP) and invasive pulmonary aspergillosis (IPA) are reported more often in older adults and patients with lymphopenia, while tuberculosis (TB) and nontuberculous mycobacteria (NTM) cluster in those with structural lung disease (e.g., bronchiectasis, cavities) and prolonged immunosuppression. High-risk features include absolute lymphocyte count <500/µL, corticosteroids ≥20 mg prednisone-equivalent for ≥4 weeks, airway obstruction, prior TB, chronic obstructive pulmonary disease/interstitial lung disease (ILD), and recent broad-spectrum antibiotics. Diagnosis should integrate high-resolution computed tomography (HRCT) patterns (e.g., diffuse ground-glass for PJP; nodules with halo sign for IPA), microbiology [bronchoalveolar lavage fluid (BALF) culture/microscopy, galactomannan (GM)/β-D-glucan (BDG)], and metagenomic next-generation sequencing, interpreted against host factors and treatment timeline, while carefully distinguishing immune-related pneumonitis and TKI-associated ILD. Prophylaxis with TMP-SMX is recommended for high-risk patients; voriconazole (or isavuconazole) is first-line for IPA with attention to drug-drug interactions; TB/NTM regimens require coordination with anticancer therapy, especially where rifamycins interact with TKIs. Vaccination (influenza, pneumococcus, zoster) and antimicrobial stewardship are essential. Future work should validate risk scores prospectively and clarify microbiome-immunotherapy-infection relationships.

Advances in radiomics and machine learning techniques have facilitated the extraction of quantitative radiomic features that can be correlated with genomic data. Breast MRI-based radiogenomics, which combines MRI radiomics and genomics, is an emerging field that non-invasively reflects tumor heterogeneity and assesses the biological behaviour of breast cancer. Studies have shown that radiogenomics has the potential to replace traditional genetic testing for breast cancer, reducing the need for invasive procedures such as biopsies. In the future, the clinical application of radiogenomics as a tool for molecular subtype identification, treatment response and prognosis prediction, and recurrence risk assessment is both necessary and feasible.