Analyzing the evolution of research on autophagy of pancreatic cancer (PC) across years, countries, institutions, journals, citations, and keywords was the core objective of this study, followed by the projection of future research focuses.
The Web of Science Core Collection served as the source for a search of publications. An analysis of the contributions from various countries/regions, institutions, authors, identified research hotspots, and promising future trends was conducted using VOSviewer16.16. The CiteSpace66.R2 programs are essential. In addition, we synthesized clinical trial data for PC, specifically those connected to autophagy.
Among the papers reviewed for this study were 1293 papers focused on autophagy in PC, all published between 2013 and 2023. In the average article, 3376 citations were found. China led in the number of publications, with the United States a strong contender. Co-citation analysis revealed 50 highly influential articles. Metabolic reprogramming, ER stress, mTOR-mediated apoptosis, and extracellular traps emerged as significant clusters from the clustering analysis. M6620 nmr The co-occurrence cluster analysis in recent research reveals pancreatic stellate cells, autophagy-dependent ferroptosis, autophagy-related pathways, metabolic rewiring, and on-coding RNAs as highly investigated research subjects.
Over the past few years, there has been a general increase in the amount of published research and areas of scholarly interest. China and the United States have both made notable contributions to research on PC autophagy. Research hotspots currently center on the modulation, metabolic reprogramming, and ferroptosis of tumor cells, along with the tumor microenvironment, including autophagy within pancreatic stellate cells and novel treatments aimed at autophagy.
The past few years have witnessed a general uptick in the number of research publications and areas of research interest. In the investigation of cellular autodigestion, the contributions of China and the United States regarding PC cells are noteworthy. Current research hotspots are not limited to the modulation, metabolic reprogramming, and ferroptosis processes in tumor cells, but also extend to the study of the tumor microenvironment, including autophagy within pancreatic stellate cells, and treatments specifically targeting autophagy.
This study aimed to determine the predictive value of a radiomics signature (R-signature) regarding clinical outcomes for patients suffering from gastric neuroendocrine neoplasms (GNEN).
Eighteen-two GNEN patients undergoing dual-phase enhanced CT scans were the focus of this retrospective study. Using LASSO-Cox regression analysis, features were screened to establish the R-signature patterns for the arterial, venous, and arteriovenous phases, in that order. Stem cell toxicology A study examined how effectively the optimal R-signature predicted overall survival (OS) in the training group, and subsequently confirmed this link in the validation group. Clinicopathological factors influencing overall survival (OS) were investigated using univariate and multivariate Cox regression analyses. In addition, the efficacy of a combined radiomics-clinical nomogram, incorporating the R-signature alongside independent clinicopathological risk factors, was assessed.
The arteriovenous phase combined R-signature achieved the highest accuracy in predicting overall survival, resulting in a better C-index compared to the independent arterial and venous phase R-signatures (0.803 vs 0.784, and 0.803 vs 0.756, respectively, P<0.0001). The training and validation cohorts displayed a significant association between the optimal R-signature and OS. GNEN patients were classified into high and low prognostic risk groups using the median value of their radiomics scores. capacitive biopotential measurement The predictive capacity of a radiomics-clinical nomogram, which incorporates a novel R-signature and independent risk factors (sex, age, treatment protocols, tumor stage, lymph node status, distant metastasis, tumor borders, Ki67 expression, and CD56 expression), was markedly superior to that of existing clinical nomograms, the R-signature alone, and the TNM system, as demonstrated by the concordance index (C-index) values (0.882 versus 0.861, 0.882 versus 0.803, and 0.882 versus 0.870, respectively; P<0.0001). Across all calibration curves, a noteworthy correspondence was evident between projected and observed survival rates, with decision curve analysis further affirming the clinical utility of the combined radiomics-clinical nomogram.
The R-signature allows for the stratification of GNEN patients, dividing them into high-risk and low-risk categories. The combined radiomics-clinical nomogram displayed better predictive accuracy than alternative models, thereby enhancing the capacity for therapeutic decision-making and patient counseling by clinicians.
The R-signature's use in stratifying patients with GNEN into high- and low-risk groups remains a possibility. In addition, the radiomics-clinical nomogram's predictive capability outperformed alternative models, potentially assisting clinicians in therapeutic decision-making and providing valuable patient guidance.
Unfavorable prognoses are often associated with colorectal cancer (CRC) patients displaying BRAF mutations. The prompt identification of prognostic markers for BRAF-mutant colorectal cancers is essential. RNF43, an ENF ubiquitin ligase, is a component of the Wnt signaling machinery. Various human cancers exhibit a high incidence of RNF43 mutations. Nevertheless, a limited number of investigations have assessed the function of RNF43 in colorectal cancer. This research aimed to dissect the consequences of alterations in the RNF43 gene on the molecular makeup and prognosis of colorectal cancers that carry a BRAF mutation.
The retrospective analysis included 261 CRC patients with the BRAF mutation whose samples were reviewed. Targeted sequencing, using a gene panel of 1021 cancer-related genes, was performed on collected samples of tumor tissue and matching peripheral blood. Survival of patients was then assessed, considering the molecular characteristics that may have impacted it. Subsequently selected for further confirmation were 358 CRC patients from the cBioPortal database, all with a BRAF mutation.
This study's genesis was a CRC patient with both BRAF V600E and RNF43 co-mutations, who achieved a remarkable remission of 70% and a progression-free survival of 13 months. A genomic investigation revealed that the presence of an RNF43 mutation influenced the genomic traits of BRAF-mutated patients, including microsatellite instability (MSI), tumor mutation burden (TMB), and the prevalence of prevalent gene mutations. Predictive biomarker analysis of survival in BRAF-mutant colorectal cancer (CRC) identified RNF43 mutation as a factor correlated with enhanced progression-free survival (PFS) and overall survival (OS).
By aggregating our findings, we identified RNF43 mutations as correlated with beneficial genomic features, yielding better clinical outcomes in BRAF-mutant colorectal cancer cases.
A correlation between RNF43 mutations and favorable genomic features was established, which significantly influenced the clinical success of BRAF-mutant colorectal cancer patients.
Worldwide, hundreds of thousands succumb annually to colorectal cancer, a disease projected to increase in prevalence over the coming two decades. Within the realm of metastatic disease, there are few efficacious options for cytotoxic therapy, thus, only slight improvements in patient survival can be observed. Consequently, the investigation has transitioned to recognizing the mutation patterns within colorectal cancers and the design of therapeutic interventions specifically targeting them. This review analyzes the latest systemic treatment strategies for metastatic colorectal cancer, considering the actionable molecular alterations and genetic profiles of colorectal malignancies.
This research project investigated the connection of creatinine/cystatin C ratio to progression-free survival (PFS) and overall survival (OS) outcomes for colorectal cancer (CRC) patients undergoing surgical treatment.
The surgical resection of 975 colorectal cancer (CRC) patients from January 2012 through 2015 formed the basis of a retrospective analysis. The non-linear association between PFS/OS and creatinine-cystatin C ratio was graphed using a three-sample curve, subject to restrictions. A Cox regression model and Kaplan-Meier survival analysis were used to determine how the creatinine-cystatin C ratio affected the survival outcomes of colorectal cancer (CRC) patients. Using multivariate analysis, variables showing a p-value of 0.05 were selected as prognostic factors to construct prognostic nomograms. Using a receiver operator characteristic curve, the efficacy of prognostic nomograms was contrasted with the conventional pathological stage for evaluation.
There was an inverse linear relationship between the creatinine/cystatin C ratio and adverse progression-free survival (PFS) observed among CRC patients. A lower creatinine/cystatin C ratio was significantly associated with a poorer prognosis in terms of both progression-free survival (PFS) and overall survival (OS) for patients. The PFS rates were markedly different, 508% versus 639% (p = 0.0002), and OS rates were equally disparate (525% versus 689%, p < 0.0001). Multivariate analysis indicated a statistically significant association between low creatinine/cystatin C ratios and diminished progression-free survival (PFS) (hazard ratio [HR] = 1.286, 95% confidence interval [CI] = 1.007–1.642, p = 0.0044) and overall survival (OS) (hazard ratio [HR] = 1.410, 95% confidence interval [CI] = 1.087–1.829, p = 0.0010) in patients with colorectal cancer (CRC). With a concordance index exceeding 0.7, creatinine/cystatin C ratio-based prognostic nomograms provide strong predictive performance for 1-5 year prognosis.
The creatinine-to-cystatin C ratio could potentially be a significant prognostic factor for predicting progression-free and overall survival in colorectal cancer patients, supporting refined pathological staging, and, in concert with tumor markers, allowing for a more in-depth prognostic stratification of colorectal cancer patients.