American journal of cancer research最新文献

This study aimed to evaluate the efficacy of transoral endoscopic plasma resection (TEPR) in treating early glottic laryngeal cancer (GLC) and identify prognostic factors. A retrospective analysis was conducted on the medical records of 212 patients with early GLC treated with TEPR between February 2015 and September 2018 at Dongying People's Hospital. Clinical characteristics, objective voice function changes, and clinical outcomes of the patients were analyzed. Meanwhile, Kaplan-Meier curve was plotted to assess the impact of TERP on 3- and 5-year survival in GLC patients. Additionally, univariate and multivariable logistic regression analyses were performed to assess prognostic factors for GLC recurrence, and Receiver Operating Characteristic (ROC) curves were generated to assess their predictive value for patients' prognosis. After surgery, Patients' Jitter (%), Shimmer (%) showed significant improvement from pre-surgery, in contrast to Harmonic noise ratio and maximum phonation time, which underwent a significant decrease. The study assessed success and recurrence rates over 3- and 5-year follow-up periods, revealing a disease control rate of 86.79%, with 3- and 5-year recurrence rates of 14.62% and 20.28%, respectively. Patients were categorized into favorable and unfavorable prognosis groups based on the 3-year recurrence. Univariate analysis identified significant risk factors for recurrence, including age, tumor-node-metastasis (TNM) stage, clinical stage, and cumulative anterior commissure involvement (P < 0.05). Further multivariate logistic regression confirmed the above indexes as independent risk factors impacting patient prognosis. In conclusion, TEPR effectively treats early GLC, though recurrence risk persists, with age, TNM stage, clinical stage, and anterior commissure involvement identified as prognostic risk factors, suggesting the need for targeted preventive measures in clinical practice.

Glioblastoma (GBM) is the most common and deadly tumor in the central nervous system. Although much has been done to optimize treatment options for GBM, the clinical prognosis is still very poor. The recent development of organoid models are emerging as cutting-edge tools in GBM research. However, the established and applications of organoid in cancer neuroscience are still elusive. In this study, we successfully established patient-derived GBM organoids (GBOs) with conserved pathological properties of parental GBM. Moreover, GBO-neuron co-culture system was also investigated and interactions between GFP labeled neurons and mCherry labeled GBOs have been observed. We further used an in-situ stereotaxic instrument to implant GBO into the brains of nude mice and established intracranial orthotopic GBM models based on these GBOs. Thus, we proposed a system to generate and bank patient-derived GBOs and verified its application in cancer neuroscience, which might be an important way to illustrate the mechanism of GBM.

RNA-binding proteins (RBPs) are essential regulators of RNA expression during both transcriptional and post-transcriptional processes. Recent evidence indicates that dysregulation of RBPs is associated with cancer initiation and progression. Among these, RBFOX2 has been identified as exhibiting variable expression patterns across different cancers and is implicated in various malignant processes, including tumor growth, metastasis, ferroptosis, stemness, and chemoresistance. Despite these findings, the precise mechanisms by which RBFOX2 contributes to carcinogenesis remain largely unexplored. In this comprehensive review, we systematically examine the multifaceted functions of RBFOX2 in tumorigenesis, with a particular focus on its roles in alternative splicing, mRNA stability, and microRNA processing. Upon elucidating the specific roles of RBFOX2 in various cancers, targeted drugs can be devised to inhibit cancer development. Furthermore, we evaluate the specific roles of RBFOX2 in various cancer types, including pancreatic ductal adenocarcinoma, myeloid leukemia, and nasopharyngeal carcinoma. By providing an in-depth analysis, we aim to establish RBFOX2 as a potential diagnostic and therapeutic target in cancer biology and treatment, thereby offering new insights for future research.

Thyroid cancer (TC) is one of the most prevalent endocrine malignancy with a steadily increasing incidence globally. Although standard treatments like thyroidectomy and radioiodine therapy effectively manage most cases of differentiated thyroid cancers (DTC), certain recurrent cases or those involving poorly differentiated thyroid cancers (PDTC) demand more specialized interventions. Follicular thyroid cancer (FTC) is the second most common type of DTC, and frequently metastasizes through the bloodstream to distant sites such as bones and lungs which is a leading cause of metastatic and recurrent DTC and significantly affects survival. However, existing drugs primarily address symptom management without offering a curative solution. Therefore, it is urgent to develop a new therapeutic agent for these challenging cases. Evodiamine (EVO), extracted from Evodia rutaecarpa, has shown potential as an anti-cancer agent in multiple types of human cancers including anaplastic thyroid cancer (ATC) and papillary thyroid cancer (PTC) cells. However, the anti-cancer effects of EVO on FTC have remained unclear. Therefore, the present study aims to investigate the anti-cancer effects of EVO in FTC cells. Our data showed that EVO effectively inhibits FTC cell growth, induces cell cycle arrest, and triggers apoptosis. Additionally, our study explored the underlying mechanisms through which EVO affects signaling pathways. To verify the anti-cancer effects of combination chemotherapy, EVO and doxorubicin were used together in FTC cells. In conclusion, this study demonstrates that EVO shows significant anti-human FTC activity, making it a promising therapeutic candidate for the treatment of follicular thyroid cancers.

Some of these include basal cell carcinoma (BCCs), squamous cell carcinoma (SCCs), and melanoma; skin cancer is a leading global health problem due to its high prevalence and possibly due to its serious health implications. Conventional and known therapies like surgeries, radiation therapies and chemotherapy although helpful are sometime deleterious and do not specifically attack the cancers. New advancement is half-breed technique has recently been recognized that photodynamic therapy (PDT) can be considered as a potentially effective modality by using photosensitizers which work through the generation of localized ROS on exposure to light. This review analyzes the recent progress in PDT and evaluation of its effectiveness in the cure of skin malignancies: with the emphasis on its applicability to BCCs and SCCs, as well as the limitations concerning the cure of melanomas. This review gives an insight to how PDT works and how it can be combined with other forms of therapy, and the prospects of photosensitizer carriers with special reference to nanotechnology. Also, the optimization of the parameters associated with the use of PDT is explored in an attempt to improve on its safety and efficacy in treatment. As such, the purpose of this systematic review of the literature is to advance the knowledge of PDT usage in contemporary dermatologic oncology and to contribute to the eventual expansion of this therapy into other skin diseases and potential use as a first-line treatment for skin neoplasia.

Lung cancer is the leading cause of cancer-related death globally and is often diagnosed at an advanced stage. Nivolumab represents a significant advancement for treating advanced non-small cell lung cancer (NSCLC). However, the absence of reliable biomarkers predicting treatment response hinders personalized therapy. Eosinophils play a notable role in cancer biology, particularly when treated with immune checkpoint inhibitors. Eosinophils can infiltrate tumor tissues, directly interacting with tumor cells or modifying the tumor microenvironment. This study aims to assess the potential of PD-L1 expression and peripheral blood eosinophil count in predicting treatment response and patient survival. This retrospective cohort study was conducted in three major cancer centers in Turkey, including 174 advanced NSCLC patients who had progressed after chemotherapy between July 2019 and November 2023. Demographic and clinical data, PD-L1 levels, and eosinophil counts were analyzed using SPSS 27.0. Survival analyses were performed with Kaplan-Meier and Cox regression models. Increased peripheral blood eosinophil count was positively associated with response to Nivolumab treatment and overall survival. Among treatment responders, 54.1% had eosinophil levels between 100-499 cells/mm³ before treatment, increasing to 70.8% post-treatment. In patients with high PD-L1 positivity (>50%), eosinophil levels averaged 266.0 cells/mm³, with improved survival outcomes (mean survival: 24.06 months, median: 20.0 months). Non-responders had a mean survival of 19.05 months and a median survival of 15.2 months. Peripheral eosinophil count appears to be a potential biomarker for predicting response to Nivolumab treatment and survival in NSCLC patients. Combined evaluation of eosinophil count and PD-L1 expression may enhance personalized treatment strategies. Further validation in prospective, randomized studies is necessary.

Pancreatic cancer (PC) has poor prognosis. PRKAA1 (AMPK-α1) is the catalytic subunit of 5'-adenylate-activated protein kinase (AMPK), which plays a critical role in multiple stages of tumorigenesis and development. However, the biological mechanisms of PRKAA1 in the tumor microenvironment have not been well studied. In this study, we performed a combined analysis of data from TCGA and GTEx databases to determine whether PRKAA1 is differentially expressed in a variety of tumors. Kaplan-Meier curve and Cox regression analyses indicated that the differential expression of PRKAA1 affected overall survival in a variety of tumors and was an independent prognostic factor for Brain Lower Grade Glioma (LGG), Brain Lower Grade Glioma (LAML), Liver hepatocellular carcinoma (LIHC), Pancreatic adenocarcinoma (PAAD), and Pancreatic adenocarcinoma (KICH). PRKAA1 was closely associated with various immune profiles, suggesting that PRKAA1 can be used for direct immunotherapy. We investigated the role of PRKAA1 in PC cells. We found that the downregulation of PRKAA1 expression reduced the proliferation, migration, and invasion of PC cells. In addition, we found that PRKAA1 regulated PC progression, possibly through the PI3K/AKT signaling pathway. Treatment of cells with the AKT inhibitors MK2206 and GSK2110183 revealed that the PRKAA1 overexpression group was less sensitive to AKT inhibitors than the negative control group. Taken together, PRKAA1 can be used as a potential prognostic marker and new target for tumor immunotherapy.

This study aimed to identify prognostic factors influencing the survival of angiosarcoma patients and to explore the relationship between peripheral blood indicators and patient prognosis. A retrospective analysis was conducted on the clinical data collected from 105 angiosarcoma patients treated at China-Japan Union Hospital of Jilin University from January 2004 to April 2019, with an additional 50 patients included as external validation cohort. The median survival time for the study cohort was 1395 days, with 66.7% of patients (n=70) dying during the follow-up period. Significant differences were observed between the survival and death groups in age (P=0.022), primary tumor site (P=0.013), tumor size (P=0.008), and metastasis (P=0.018). Analysis of peripheral blood indicators showed that white blood cell (WBC) (P=0.006), platelet (PLT) (P=0.019), platelet-to-lymphocyte ratio (PLR) (P<0.001), and systemic immune-inflammation index (SII) (P=0.036) were significantly lower in the survival group, while lymphocyte (LYM) (P<0.001), albumin (ALB) (P<0.001), and prognostic nutritional index (PIN) (P<0.001) were significantly higher in the survival group. Multivariate Cox regression analysis identified SII (P=0.049, HR=0.551, 95% CI: 0.304-0.998), primary tumor site (P=0.001, HR=0.405, 95% CI: 0.235-0.699), metastasis (P=0.029, HR=1.864, 95% CI: 1.066-3.26), and chemotherapy (P=0.004, HR=0.434, 95% CI: 0.245-0.768) as independent prognostic factors affecting patients' 5-year survival. A nomogram model constructed based on these factors demonstrated high accuracy and stability in predicting 1-year, 3-year, and 5-year survival rates, with area under the curve (AUC) values of 0.836, 0.837, and 0.803, respectively, as validated by calibration curves and receiver operating characteristic (ROC) analysis. External validation further confirmed the model's reliability. Additionally, significant interactions were found between SII and primary tumor site (P=0.005) as well as chemotherapy (P=0.045). In conclusion, SII, primary tumor site, metastasis, and chemotherapy are crucial prognostic factors for angiosarcoma, and the developed nomogram provides a reliable tool for predicting survival outcomes.

[This corrects the article on p. 13 in vol. 7, PMID: 28123844.].

Objective: To evaluate the potential of leukocyte-specific protein 1 (LCP1) and adenosine diphosphate-dependent glucokinase (ADPGK) as predictive biomarkers for immunotherapy-related adverse events in late-stage non-small cell lung cancer (NSCLC) patients with the KARS G12C mutation undergoing treatment with programmed cell death protein-1 (PD-1) monoclonal antibodies.

Methods: A total of 160 late-stage NSCLC patients with the KARS G12C mutation receiving PD-1 monoclonal antibody treatment were retrospectively analyzed. LCP1 and ADPGK expression levels were assessed at both mRNA and protein levels using validated methods. Statistical analyses, including correlation analysis, logistic regression, and receiver operating characteristic (ROC) curve analysis, were conducted to explore the association between LCP1 and ADPGK expression levels and the occurrence of immunotherapy-related adverse events.

Results: The mRNA levels of LCP1 (2.43 ± 0.72 vs. 2.14 ± 0.67, t=2.311, P=0.023) and ADPGK (2.31 ± 0.61 vs. 1.98 ± 0.59, t=3.145, P=0.002) were significantly elevated in patients with adverse reactions. Similarly, protein levels of LCP1 (1.22 ± 0.28 vs. 1.07 ± 0.25, t=3.179, P=0.002) and ADPGK (1.01 ± 0.18 vs. 0.93 ± 0.19, t=2.488, P=0.015) were higher in this group. Correlation and logistic regression analyses revealed positive correlations between LCP1 and ADPGK mRNA levels and adverse event occurrence (LCP1: rho=0.186, P=0.019, OR=1.842; ADPGK: rho=0.246, P=0.002, OR=2.549). Protein levels of LCP1 and ADPGK also correlated with immunotherapy-related adverse events (LCP1: rho=0.254, P=0.001, OR=9.554; ADPGK: rho=0.19, P=0.016, OR=10.058). The combined assessment of LCP1 and ADPGK expression showed strong predictive power for identifying patients at increased risk of adverse events during PD-1 treatment (AUC=0.808), with the validation group achieving an AUC of 0.751.

Conclusion: LCP1 and ADPGK are potential independent predictive biomarkers for immunotherapy-related adverse events in late-stage NSCLC patients with the KARS G12C mutation. Their combined assessment may offer a valuable tool for risk stratification during PD-1 monoclonal antibody treatment.