The peripheral nervous system significantly determines the fate of solid tumors and their microenvironment. In neurotropic malignancies such as pancreatic and prostate cancer, denervation in animal models demonstrate significantly delays in tumor initiation and progression, underscoring the critical neural dependency of these cancers. While tumor innervation establishes a structural basis for the neuromodulatory effects, the degree of innervation exhibits marked heterogeneity across tumor types, and its regulatory mechanisms remain poorly characterized. In this study, we screened genes associated with innervation status in pancreatic cancer and identified the splicing factor SRSF12 as a critical gene related to tumor innervation. In clinical samples, SRSF12 was expressed at low levels in pancreatic cancer tissues, and its downregulation was linked to poor prognosis in patients. Then we crossed Kras mutation and Srsf12 knockout mice (KrasG12DSrsf12 fl/fl) together with Srsf12 fl/flPdx1cre mice and found that depletion of Srsf12 accelerated Kras-driven pancreatic tumorigenesis and enhanced tumor innervation. Furthermore, we demonstrated that SRSF12 inhibits neurite outgrowth primarily by generating a LAMA3 splice isoform that lacks the fourth and fifth LG (G45) domains. Mechanistically, G45 promotes tumor innervation by activating ITGB1 and FAK in neurons. Together, our findings delineate SRSF12 as a novel suppressor of tumor innervation and pancreatic tumorigenesis, while also identifying a tumor-specific target for SRSF12-deficient pancreatic cancer.

Prostate cancer (PC) contributes to male mortality worldwide. The objective of this study is to comprehensively depict the scientific accomplishments and research trends in nanotechnology for PC applications.

Utilizing the Web of Science Core Collection database, publications were gathered on the basis of inclusion and selection criteria. The publications were analyzed and visualized using VOSviewer, R-studio and CiteSpace software tools.

A total of 1949 studies were incorporated. Farokhzad was the most productive author. The United States and China released 58.13% of the total publications. The Chinese Academy of Sciences was the most influential institution, and the International Journal of Nanomedicine stood out as a prominent journal in this field. The most frequently referenced publication and research subject category were identified. The most extensively investigated area was nanoparticle-based drug delivery, while recent research has focused on anticancer with novel nanocarriers.

A bibliometric analysis in the PC and nanotechnology was conducted between 2004 and 2023. The overview and characteristics of the publications were identified. We discussed the application and restrictions faced by nanotechnology in PC management. The study of nanotechnology in PC treatment needs to be further studied.

Krukenberg tumour is defined by the development of metastasis in both ovaries, characterised by the presence of mucine secreting cells, hence the name carcinoma mucocellular; However, the term "Krukenberg" has often been broadly applied to any metastases to the ovaries, irrespective of the site of origin. It is uncommon representing about 1%-2% of all ovarian tumours. It is in general secondary to a gastric adenocarcinoma but other sites have been found to be responsible of krukenberg's tumour, notably large bowels adenocarcinoma, pancreas, breast cancer, lung adenocarcinoma and biliary tract cholangiocarcinoma. In this article we will report the case of a 29 years old patient presenting with metachronous krukenberg tumour and peritoneal carcinosis with a history of surgery for a gallbladder adenocarcinoma 9 month prior. This case study sheds light on this pathology, familiarizing us with its clinical and radiological picture, as well as its prognosis.

Several diseases affect the female reproductive system, and both disease factors and treatments impact its integrity and function. Consequently, understanding the mechanisms of disease occurrence and exploring treatment methods are key research focuses in obstetrics and gynecology. However, constructing accurate disease models requires a microenvironment closely resembling the human body, and current animal models and 2D in vitro cell models fall short in this regard. Thus, innovative in vitro female reproductive system models are urgently needed. Additionally, female reproductive system diseases often cause tissue loss, yet effective tissue repair and regeneration have long been a bottleneck in the medical field. 3D bioprinting offers a solution by enabling the construction of implants with tissue repair and regeneration capabilities, promoting cell adhesion, extension, and proliferation. This helps maintain the long-term efficacy of bioactive implants and achieves both structural and functional repair of the reproductive system. By combining live cells with biomaterials, 3D bioprinting can create in vitro 3D biomimetic cellular models, facilitating in-depth studies of cell-cell and cell-extracellular microenvironment interactions, which enhances our understanding of reproductive system diseases and supports disease-specific drug screening. This article reviews 3D bioprinting methods and materials applicable to the female reproductive system, discussing their advantages and limitations to aid in selecting optimal 3D bioprinting strategies. We also summarize and critically evaluate recent advancements in 3D bioprinting applications for tissue regeneration and in vitro disease models and address the prospects and challenges for translating 3D bioprinting technology into clinical applications within the female reproductive system.

In pancreatic ductal adenocarcinoma, neural invasion is being increasingly recognized as an unfavorable predictor of patient outcomes. Neural invasion severity seems to have a stronger clinical impact on patient prognosis than neural invasion status alone. Therefore, this study aims to assess the impact of severity of neural invasion on overall survival and disease-free survival in pancreatic ductal adenocarcinoma.

To assess the impact of intrapancreatic neural invasion severity, tumor specimens resected from patients with pancreatic ductal adenocarcinoma between 2007 and 2014 were systematically re-evaluated, and neural invasion severity was determined using the standardized neural invasion severity score.

In our cohort (n = 216), an increased neural invasion severity score was associated with markedly shorter overall survival in pancreatic head ductal adenocarcinoma (neural invasion severity score low: 22.8 months vs neural invasion severity score high: 17.6 months: P = .001). An external European validation cohort confirmed these results and showed significantly better survival of patients with lower neural invasion (20.5 vs 15.4 months, P = .026). The disease-free survival time was also substantially decreased in patients with pancreatic head pancreatic ductal adenocarcinoma and increased neural invasion severity (neural invasion severity score low: 19.1 months vs neural invasion severity score high: 10.4 months; P = .004). Moreover, the neural invasion severity score was an important independent factor influencing overall survival (hazards ratio 1.024, P = .04) and disease-free survival (hazards ratio 1.03, P = .01) using an adjusted Cox proportional hazards model. Importantly, higher neural invasion severity score leads to significantly more and earlier local recurrence than to distant tumor recurrence.

Neural invasion severity is a powerful independent factor influencing overall survival and local recurrence in patients with pancreatic ductal adenocarcinoma. Therefore, individuals with high neural invasion severity score values should be regarded as a specific subgroup of pancreatic ductal adenocarcinoma patients and may benefit from more tailored postoperative oncologic therapy.

Prostate cancer is the second leading cause of cancer-related among men globally, with a rising incidence rate, particularly in developing countries. This highlights the urgent need to identify novel therapeutic agents. Roemerine, a naturally abundant alkaloid, has demonstrated antibacterial and antitumor properties, suggesting its potential utility in prostate cancer treatment. This study evaluates the effects of roemerine on RM-1 prostate cancer cells using in vitro assays and an in vivo nude mouse subcutaneous xenograft tumor model. Through Cell Counting Kit-8(CCK8), MTT, Wound-Healing, and Transwell assays, we assessed roemerine's impact on RM-1 cell proliferation, migration, and invasion. Additionally, the antitumor efficacy of roemerine was evaluated in nude mice bearing subcutaneous RM-1 tumors. Our findings reveal that roemerine significantly inhibits RM-1 cell activity, migration, invasion, and tumor growth. These results highlight the potential of roemerine as a novel antitumor agent for prostate cancer, providing a foundation for further mechanistic and pharmacological investigations.

Thioredoxin reductase (TrxR) is a pivotal regulator of redox homeostasis. It is frequently overexpressed in various cancer cells, including prostate cancer, making it a promising target for the development of anti-cancer drugs. In this study, we screened a series of newly designed complexes of gold(I) phosphine. Specifically, Compound 5 exhibited the highest cytotoxicity against prostate cancer cells and demonstrated stronger antitumor effects than commonly used drugs, such as cisplatin and auranofin. Importantly, our mechanistic study revealed that Compound 5 effectively inhibits the TrxR system in vitro. Additionally, Compound 5 promoted intracellular accumulation of reactive oxygen species (ROS), leading to mitochondrial dysfunction and irreversible apoptosis in prostate cancer cells. Our in vivo xenograft study further demonstrated that Compound 5 has excellent antitumor activity against prostate cancer cells, but does not cause severe side effects. These findings provide a promising lead Compound for the development of novel antitumor agents targeting prostate cancer and offer a valuable tool for investigating biological pathways involving TrxR and ROS modulation.

Cigarette smoke (CS) creates a "cancer field" in the lung that promotes malignant transformation. The molecular changes within this field are not fully characterized. We examined the significance of microRNA-1 (miR-1) downregulation as one of these changes. We found that tumor miR-1 levels in three non-small cell lung cancer cohorts show inverse correlations with the smoking burden. Lung MiR-1 levels follow a spatial gradient, have prognostic significance, and correlate inversely with the molecular markers of injury. In CS-exposed lungs, miR-1 is specifically downregulated in the endothelium. Exposure to CS induces angiogenesis by selectively degrading mature miR-1 via a vascular endothelial growth factor-driven pathway. Applying a multi-step molecular screen, we identified angiogenic genes regulated by miR-1 in the lungs of smokers. Knockdown of one of these genes, Notch homolog protein 3, simulates the anti-angiogenic effects of miR-1. These findings suggest that miR-1 can be used as an indicator of malignant transformation.

It is generally accepted that ZEB1 and ZEB2 act as master regulators of the epithelial-mesenchymal transition, which arguably is the key mechanism of metastasis. Accordingly, they are deemed as negative predictors of the survival of cancer patients by promoting the emergence of secondary foci of the disease. Paradoxically, in some types of cancer types the opposite effect is observed, i.e. ZEB1 and ZEB2 are associated with better prognosis for cancer patients. In this review, we discuss the hypothesis that the tumorigenic effects of ZEB1/ZEB2 can be different in various tissues depending on the initial status of these proteins in the corresponding healthy tissues. Emerging evidence suggests that ZEB1 and ZEB2 are constitutively expressed in several healthy tissues, performing vital functions. Consequently, reducing the expression of ZEB1 and ZEB2 could negatively affect these tissues causing various diseases, including cancer. Finally, the dualistic role of ZEB1 and ZEB2 as immune modulators and their effect on tumor microenvironment is also discussed.

Several patient-derived tumor models have emerged recently. However, soft tissue sarcomas (STSs) present a challenge in developing preclinical drug-testing models due to their non-epithelial and complex nature. Here, we report a model termed patient-derived tumor-like cell clusters (PTCs) derived from STS patients. PTCs result from the self-assembly and proliferation of mesenchymal stem cells (MSCs), epithelial cells, and immune cells, faithfully recapitulating the morphology and function of the original tumors. Through standardized culture and drug-response assessment protocols, PTCs facilitate personalized drug testing, evaluating hundreds of therapies within two weeks. Notably, PTCs exhibit 100% accuracy in distinguishing between complete or partial response and disease progression. We demonstrate the utility of PTCs in guiding chemotherapy selection for a patient with relapse and metastases following conventional therapy, who exhibited a positive response after non-conventional therapy identified through PTC. These findings underscore the potential of PTCs for prospective use in clinical decision-making regarding therapy selection.

Advances in medical care have made cancer rehabilitation an essential component of comprehensive cancer treatment. However, bibliometric analyses in this field remain limited. This study maps the global research landscape of cancer rehabilitation over the past decade.

Relevant publications on cancer rehabilitation from 2013 to 2023 were retrieved from the Web of Science Core Collection (WoSCC) database. Bibliometric analysis was conducted using VOSviewer, CiteSpace, and the R package "Bibliometrics."

A total of 6743 publications from 98 countries demonstrated sustained growth, peaking in 2022. The USA (1581 publications) and China (974) led in research output, while the Netherlands recorded the highest citation impact (32.75 citations per paper). Key institutions included the University of Texas MD Anderson Cancer Center (148 publications) and Memorial Sloan Kettering Cancer Center (40.58 citations per paper). Supportive Care in Cancer ranked as the most influential journal. Research efforts primarily focused on exercise interventions (n = 404), quality of life (n = 688), and breast cancer rehabilitation (n = 440). Recent trends highlighted telemedicine, digital health, and breast cancer-related lymphedema.

This analysis highlights the dominance of high-income countries in cancer rehabilitation research and identifies exercise, quality of life, and breast cancer as enduring focal points. Emerging priorities include technology-driven interventions and lymphedema management. However, critical gaps remain, such as the underrepresentation of low-resource regions, limited focus on pediatric populations, and insufficient integration of advanced technologies (e.g., AI, wearables). Future efforts should emphasize equitable resource distribution, evidence-based pediatric rehabilitation models, and scalable technology-driven solutions to address global disparities and improve survivorship care.

The objective of this study was to evaluate the effectiveness of folate-conjugated nano-lipid constructs (F-NLCs) for targeting lung squamous carcinoma through both ex-vivo and in-vivo studies. Ligand-conjugated (F-NLCs) and non-conjugated (P-NLCs) formulations were prepared using the solvent evaporation method, with paclitaxel as the reference drug. The formulations were characterized for particle size, zeta potential, encapsulation efficiency, and drug loading capacity. The average particle size of P-NLCs and F-NLCs was found to be 190.1 ± 1.9 nm and 231.3 ± 2.3 nm, respectively. The percent entrapment efficiency of P-NLCs and F-NLCs was 85.14 ± 1.4 % and 82.42 ± 1.2 %, respectively. The drug loading for P-NLCs and F-NLCs was 25.3 ± 1.1 % and 24.2 ± 1.3 %, respectively. The haemolytic study revealed lower toxicity for F-NLCs (4.36 ± 0.6 %) compared to P-NLCs (12.36 ± 0.8 %) and paclitaxel (25.41 ± 0.4 %). Ex-vivo studies, employing the SRB method, demonstrated GI50 (µM) values of 9.72 for P-NLCs and 5.84 for F-NLCs, compared to 18.51 for the paclitaxel solution. Cellular uptake studies using Rhodamine-B dye-loaded NLCs (F-D-NLCs), observed through fluorescence microscopy, indicated higher accumulation in the lung sac compared to D-NLCs. In vivo research, focusing on biodistribution and pharmacokinetics, was conducted on Wistar rats to confirm the efficacy of F-NLCs. Biodistribution results showed concentrations of 25.86 ± 0.39 % for F-NLCs and 3.14 ± 0.46 % for the paclitaxel solution in lung squamous carcinoma cells, indicating a significant improvement in drug concentration within carcinogenic squamous cells with F-NLCs. The findings conclude that F-NLCs are a safe, stable, and promising drug delivery system for the targeted treatment of lung squamous carcinoma.

We sought to study the expression of FGFR2 and c-Met and evaluate the correlation between the two proteins in a series of endometrial cancer patients as well as the prognostic significance of the two markers in endometrium carcinoma.

Patients who were diagnosed with endometrial cancer and had undergone surgical treatment in Beijing Chao-Yang Hospital, Capital Medical University from November 2004 to June 2011 were included in this study. Tissue microarray construction, immunohistochemical staining and scoring were employed to study the expression of FGFR2 and c-Met. SPSS version 22.0 was used to evaluate the correlation between FGFR2 and c-Met expression and the prognosis prediction value of the two markers.

In total, 109 patients were included in this study. The median age was 56 years (ranges, 30-79). The most common histologic tumor subtype was adenocarcinoma (86.2%). The five-year survival rate was 87.2%. Significantly different FGFR2 expression was observed among patients with different disease stages (p < 0.001), depths of myometrial invasion (p = 0.001) and lymph node status (p < 0.001). C-Met expression was also increased in tissues from patients with advanced stage disease, deep myometrial invasion and lymph node metastasis (p < 0.001, p = 0.031 and p < 0.001, respectively). The expression of FGFR2 and c-Met was increased in the group with poorer prognosis (overall survival < 5 years) (p = 0.002 and p = 0.023, respectively). Moreover, a strong positive correlation was observed between FGFR2 and c-Met expression (p < 0.01, r = 0.656). FGFR2 was a significant factor that influence the FIGO stage.

Higher expression of FGFR2 and c-Met is associated with more advanced stage, deeper myometrial invasion and lymph node metastasis in endometrial cancer and poorer prognosis. In addition, high expression of FGFR2 is correlated with high c-Met expression.

More research has been done on the correlation between exercise and cancer, which has revealed several ways that physical activity decreases the risk of developing the disease. The developing function of lncRNAs as an important molecular link between exercise and cancer suppression is the main topic of this review. According to recent research, regular physical exercise also alters the expression levels of several lncRNAs, which are generally elevated in cancer. A complex network of interactions that may provide protective effects against carcinogenesis is suggested by the contribution of these lncRNAs in various cellular processes, such as epigenetic alterations, proliferation, and apoptosis regulation. We offer a comprehensive summary of the existing information regarding specific lncRNAs that are influenced by physical activity and could potentially impact cancer-related processes. We also go over the difficulties in interpreting these alterations, taking into account the fact that several lncRNAs have a dual function in promoting and preventing cancer in various physiological settings. To understand the complex impacts of exercise-induced lncRNA regulation in cancer biology, more study is required. The critique strongly highlights the possibility of lncRNAs serving as both indicators and treatment prospects for cancer-preventive strategies.

Pancreatic ductal adenocarcinoma (PDAC) is the most common and aggressive type of pancreatic cancer, with a five-year survival rate below 8%. Its high mortality is largely due to late diagnosis, metastatic potential, and resistance to therapy. Epithelial-mesenchymal transition (EMT) plays a key role in metastasis, enabling cancer cells to become mobile. Partial EMT, where cells maintain both epithelial and mesenchymal traits, is more frequent in tumors than complete EMT and contributes to cancer progression. The long non-coding RNA MIR31 host gene (MIR31HG) has recently emerged as a critical factor in PDAC oncogenesis. This study aimed to investigate MIR31HG's role in partial EMT and its association with the basal-like PDAC subtype.

We analyzed the relationship between MIR31HG expression, partial EMT, and the basal-like subtype of PDAC by integrating data from public databases. We reanalyzed public data from PDAC patient-derived organoids to assess MIR31HG expression and gene signatures under hypoxic and normoxic conditions. RNA sequencing and bioinformatics analyses, including gene set enrichment analysis (GSEA), were used to investigate differentially expressed genes and pathway enrichments. EMT, partial EMT, and hypoxia scores were calculated based on the expression levels of specific gene sets.

We observed that MIR31HG overexpression strongly correlates with higher partial EMT scores and the stabilization of the epithelial phenotype in PDAC. MIR31HG is highly expressed in the basal-like subtype of PDAC, which exhibits partial EMT traits. Hypoxia, a hallmark of basal-like PDAC, was shown to significantly induce MIR31HG expression, thereby promoting the basal-like phenotype and partial EMT. In patient-derived organoids, hypoxic conditions increased MIR31HG expression and enhanced basal-like and partial EMT gene signatures, while normoxia reduced these expressions. These findings suggest that hypoxia-induced MIR31HG expression plays a crucial role in driving the aggressive basal-like subtype of PDAC.

Our results indicate that MIR31HG is crucial in regulating PDAC progression, particularly in the aggressive basal-like subtype associated with hypoxia and partial EMT. Targeting the MIR31HG-mediated network may offer a novel therapeutic approach to combat hypoxia-driven PDAC.

This study aimed to validate the clinical feasibility, safety, and effectiveness of using the fluorescence endoscopy with second window indocyanine green (FESWICG) technique for resection of malignant brain tumors.

Twenty-two patients undergoing surgery for malignant brain tumor resection were examined. Intravenous ICG (250 mg) was administered within 24 hours prior to surgery. All procedures were performed under endoscopic guidance. The fluorescence intensity of the tumors was monitored using fluorescence mode endoscopy. Specimens including resection margins were harvested and submitted for histopathological analysis. The sensitivity and specificity of FESWICG were validated using contrast-enhanced cranial magnetic resonance imaging performed within 24 hours of surgery and histopathology. The Karnofsky performance scale was used to assess overall functional status before and after surgery.

The tumor diagnoses were as follows: glioma (n = 14), ependymoma (n = 1), metastasis (n = 5), lymphoma (n = 1), and choroid plexus papilloma (n = 1). Intraoperative tumor fluorescence was strong in 20 patients and weak in 2. Postoperative contrast-enhanced imaging revealed complete tumor resection in 18 patients (81.82%). Sixty-four tumor specimens were collected, including 42 obtained from tumor margins. Using histopathology as the reference, the sensitivity, specificity, positive predictive value, and negative predictive value of FESWICG for detection of malignant brain tumors were 91.42%, 41.38%, 65.31%, and 80%, respectively. The median Karnofsky performance scale score was 85 before surgery and 93 at the 3-month follow-up.

SWICG notably enhanced intraoperative visualization of malignant brain tumors, particularly the delineation between tumor and normal brain. Its utility for margin detection is promising. When utilized in conjunction with a full endoscopic system, the visual acuity and overall effectiveness of surgical procedures can be substantially enhanced. However, ICG remains a low-specificity technique.

Clear cell renal cell carcinoma is the most predominant type of renal malignancies, characterized by high aggressiveness and probability of distant metastasis. Renin angiotensin system (RAS) plays a crucial role in maintaining fluid balance within the human body, and its involvement in tumorigenesis is increasingly being uncovered, while its role in ccRCC remains unclear.

WGCNA was used to identify RAS related genes. Machine learning was applied to screen hub genes for constructing risk model, E-MTAB-1980 dataset was used for external validation. Transwell and CCK8 assays were used to investigate the impact of SLC6A19 to ccRCC cells.

SLC6A19, SLC16A12 and SMIM24 were eventually screened to construct risk model and the predictive efficiency for prognosis was validated by internal and external cohorts. Moreover, the differences were found in pathway enrichment, immune cell infiltration, mutational landscapes and drug prediction between high and low risk groups. Experimental results indicated that SLC6A19 could inhibit invasion and proliferation of ccRCC cells and GSEA pinpointed that SLC6A19 was intimately correlated with fatty acid metabolism and CPT1A.

The risk model based on the three RAS-related genes have a robust ability to predict the prognosis and drug sensitivity of ccRCC patients, further providing a valid instruction for clinical care.

Renal cell carcinoma (RCC) is a heterogeneous group of cancers originating from renal tubular and epithelial cells, constituting 2-4% of global cancer cases. Incidence patterns vary internationally, with the Czech Republic and European Baltic countries experiencing higher rates. Despite the majority of cases being sporadic, approximately 4% have a hereditary basis.

This study, conducted in Erbil, Iraq, investigates RCC survival rates and influential factors at Nanakaly Hospital and Rizgary Oncology Center. A retrospective analysis spanning January 2017 to December 2020, covering 93 patients, explores demographic, clinical, and treatment variables.

Out of a total of 93 cases, there were 68 deaths, and 25 cases were censored. This means that 73.12% of the cases resulted in death, and 26.88% of the cases were censored. The Kaplan-Meier survival analysis indicates a mean survival time of approximately 5.517 years. Clinical characteristics such as tumor side and histology show no significant associations with survival status, except for the TNM stage (p-value < 0.001). While smoking, alcohol history, history of malignancy, and comorbidities demonstrate no significant impact on survival, the study identifies a potential trend associating comorbidities with poorer outcomes (p-value = 0.051). Significant associations emerge with treatment types; radical nephrectomy (p-value = 0.004) and systemic treatments (p-value < 0.001) influence survival. Strikingly, recurrence was significantly associated with mortality (p-value < 0.001).

The study reveals a higher RCC had a shorter survival in Erbil compared to international survival. This is attributed to delayed referrals and advanced disease stages. Additionally, the absence of crucial antineoplastic agents negatively affects outcomes. Comorbidities are also found to significantly reduce survival rates. These findings underscore the necessity for an enhanced referral system, improved access to oncological services, and the approval of essential therapies in Erbil.

Head and neck cancer (HNC) patients face substantial morbidity and mortality. Despite the potential benefits of palliative care (PC) in improving quality of life, many HNC patients do not receive these services. This study aimed to quantify the proportion of HNC patients receiving PC, the timing of PC referrals, and the mental health and clinical outcomes of this population.

A retrospective cohort study was conducted using the TriNetX database with de-identified electronic medical records. HNC patients were categorized based on whether they had at least one PC encounter. We examined time to first PC encounter, mortality rates, mental health diagnoses, and access to ACP and supportive care.

Of 304,404 HNC patients, only 22,470 (7.4 %) had at least one PC encounter. The median time from cancer diagnosis to initial PC referral was 318 days. After propensity score matching, the cohorts consisted of 24,916 patients each. Those who received PC had a significantly higher risk of mortality (RR 3.05, 95 % CI 2.97-3.14), depression (RR 1.38, 95 % CI 1.33-1.45), anxiety (RR 1.47, 95 % CI 1.42-1.53), failure to thrive (RR 3.26, 95 % CI 3.03-3.51), and were more likely to engage in advance care planning (RR 4.97, 95 % CI 4.39-5.62) and access supportive care services compared to patients who did not receive PC.

PC utilization among HNC patients is low, with patients often waiting nearly a year before their first PC encounter. This delay highlights a significant unmet need for early integrated PC in this population.

We aimed to evaluate the prognostic value of stage IIIB non-small-cell (NSCLC) lung cancer patients and to construct a nomogram to effectively predict their overall survival (OS).

In total, 4323 patients with stage IIIB NSCLC diagnosed between 1975 and 2018 were selected from the Surveillance, Epidemiology, and End Results (SEER) database. Multiple prognostic factors were combined to construct a nomogram for predicting OS of patients with stage IIIB NSCLC. The discrimination and calibration of the nomogram were evaluated by C-indexes and calibration curves. The nomogram was evaluated for predictive ability using receiver operating characteristic (ROC) curves, decision curve analysis curve (DCA), and clinical impact curve (CIC).

The nomogram was built on data of 4323 patients with stage IIIB NSCLC and consisted of the following prognostic factors: age, race, sex, primary labeled, pathology, T stage, whether to receive surgery, whether to receive radiotherapy, and whether to receive chemotherapy. The C-index in the training and validation sets for the nomogram was 0.672 (95% CI: 0.661-0.683) and 0.675 (95% CI: 0.656-0.694), respectively. According to scores of the nomogram, patients in the complete set, validation set, and training set were classified into two risk groups, low risk and high risk.

We developed the first validated nomogram to estimate the OS of patients with stage IIIB NSCLC. The nomogram was based on nine prognostic factors and provided an individualized risk estimate of 3-year and 5-year OS survival in patients with stage IIIB NSCLC.

Six separated compounds were identified from Artemisia capillaris Thunb., and they were 7-methoxycoumarin (1), 6,7-dimethoxycoumarin (2), 7-hydroxy-6-methoxycoumarin (3), quercetin (4), chlorogenic acid (5) and caffeic acid (6). Among them, 6,7-dimethoxycoumarin, as known as scoparone, was the most effective on scavenging ABTS free radicals (IC50 = 0.97 μΜ) and was then tested by cytotoxic activity and pro-apoptotic activity against HepG2 cells. Scoparone dose-dependently and time-dependently inhibited the cell proliferation. Furthermore, scoparone induced the expression of Bax, concurrently suppressing the expression of Bcl-2, resulting in a noteworthy elevation in the Bax/Bcl-2 ratio to up-regulate Caspase-3 activity, thus inducing cell apoptosis via the intracellular pathway. Meanwhile, scoparone promoted the expression of Fas, FasL, FADD, Caspase-8 and Caspase-3, indicating that scoparone also triggered apoptosis via the extracellular pathway. In a word, scoparone demonstrated remarkable antitumor capability to induce apoptosis of HepG2 cells through both intracellular and extracellular pathways.

Innovative therapeutic strategies are urgently needed to address the ongoing global health concern of hepatobiliary pancreatic malignancies. This review summarizes the latest and most comprehensive research of chimeric antigen receptor (CAR-T) cell engineering immunotherapy for treating hepatobiliary pancreatic cancers. Commencing with an exploration of the distinct anatomical location and the immunosuppressive, hypoxic tumor microenvironment (TME), this review critically assesses the limitations of current CAR-T therapy in hepatobiliary pancreatic cancers and proposes corresponding solutions. Various studies aim at enhancing CAR-T cell efficacy in these cancers through improving T cell persistence, enhancing antigen specificity and reducing tumor heterogeneity, also modulating the immunosuppressive and hypoxic TME. Additionally, the review examines the application of emerging nanoparticles and biotechnologies utilized in CAR-T therapy for these cancers. The results suggest that constructing optimized CAR-T cells to overcome physical barrier, manipulating the TME to relieve immunosuppression and hypoxia, designing CAR-T combination therapies, and selecting the most suitable delivery strategies, all together could collectively enhance the safety of CAR-T engineering and advance the effectiveness of adaptive cell therapy for hepatobiliary pancreatic cancers.

In patients with metastatic non-small cell lung cancer (NSCLC) with high programmed death-ligand 1 (PD-L1) expression, there is still a lack of biomarkers to identify patients with maximum benefit from first-line treatment with checkpoint inhibitor therapy (CIT) alone. This work examines the impact of different ABO blood groups (BG) on the response to CIT monotherapy.

Retrospective analysis of patients with stage IV NSCLC and high PD-L1 expression (tumor proportional score/TPS ≥ 50%), receiving first-line therapy with pembrolizumab alone or in combination with chemotherapy at the West German Cancer Center from 2017 to 2022. Study endpoints were overall survival (OS) and progression-free survival (PFS).

Eighty-two patients were included in the analysis. Twenty-two patients (27%) received first-line therapy with pembrolizumab alone (monoimmunotherapy cohort/MIC), of which seven patients (32%) had BGO. Sixty patients (73%) were treated with pembrolizumab combined with platinum-based chemotherapy (chemoimmunotherapy cohort/CIC), of which 38 (63%) had BGO. In MIC, younger age and BGO were independent predictors of favorable OS (BGO vs. other ABO-BG: HR 0.22, 95% CI: 0.1-0.9; p = 0.037; median OS 62 versus 19 months) and PFS (BGO vs. other ABO-BG: HR 0.21, 95% CI: 0.1-0.8; p = 0.024; median PFS 39 vs. 4 months). There was no significant impact of ABO-BG in patients treated with CIC. In support, a historical control group treated with chemotherapy alone also showed no prognostic impact of the ABO-BG.

BGO associates with favorable survival in patients with NSCLC receiving pembrolizumab monotherapy, but not in patients with chemo-immunotherapy or chemotherapy. Further validation of this promising strategy for personalized decision-making is warranted.

Lung cancer is a highly prevalent neoplastic disease in various regions of the world, but the mechanism of its occurrence, development, and metastasis is not clear. Different hormone levels have different potential roles in the occurrence, development, and metastasis of lung cancer, but the association between hormone levels and lung cancer is not clear.

This study aims to explore the causal relationship between hormone levels and lung cancer using Mendelian randomization. Sensitivity and heterogeneity tests were conducted to ensure the reliability of the results, offering insights into the prevention, diagnosis, and treatment of lung cancer.

We employed a two-sample Mendelian randomization (MR) analysis using large-scale publicly available genome-wide association studies (GWAS) data to assess the causal relationship between hormone levels and lung cancer. We explored the causal relationship between 15 hormones and three subtypes of lung cancer. The inverse variance weighted (IVW) method was used as the primary analysis, while MR-Egger, weighted median, weighted mode, and simple median were applied as supplementary methods. Sensitivity and heterogeneity tests were conducted to ensure the robustness of the findings.

We identified six hormone levels to be significantly associated with lung squamous cell carcinoma (LUSC): total testosterone, oestradiol, thyrotropin-releasing hormone, insulin, parathyroid hormone, and glucocorticoid. Among them, total testosterone, estradiol, and thyrotropin-releasing hormone were negatively correlated with morbidity. Insulin, prolactin levels, and parathyroid hormone were positively correlated with morbidity. Five hormone levels were significantly associated with lung adenocarcinoma (LUAD): luteinizing hormone, thyroid hormones, insulin, prolactin levels, and parathyroid hormone. Luteinizing hormone and thyroid hormones were negatively correlated with morbidity, while insulin, prolactin levels, and parathyroid hormone were positively correlated with morbidity. Similarly, five hormone levels were linked to small cell lung cancer (SCLC): total testosterone, luteinizing hormone, estradiol, PTHrP, and insulin. Total testosterone and luteinizing hormone were negatively correlated with morbidity, while estradiol, Parathyroid Hormone-Related Peptide (PTHrP), and insulin were positively correlated with morbidity. Several hormones were associated with different subtypes of lung cancer. Insulin was significantly associated with all three types of lung cancer. Testosterone showed positive effects in LUSC and SCLC, and estradiol had varying effects, with a negative correlation in SCLC and a positive correlation in LUSC. Testosterone and estradiol were not significantly associated with LUAD. Luteinizing hormone showed positive effects in LUAD and SCLC, and parathyroid hormone showed negative effects in LUSC and LUAD.

This study demonstrates significant causal relationships between specific hormone levels and various types of lung cancer, providing valuable insights for prevention, diagnosis, and treatment strategies of lung cancer.

This study aimed to identify periodontal pathogens involved in the onset and progression of OSCC.

Saliva samples were collected from 112 patients without oral mucosal diseases (OMDs) as controls; 36 patients with oral potentially malignant disorders (OPMDs); and 104 patients with OSCC. Periodontal examinations were performed on all patients. Endpoint PCR was performed for seven species of oral pathogens. The 16S rRNA analysis was performed using 20 DNA samples from each group.

Periodontitis tended to worsen in the OMDs group compared to the control group. The number of oral bacteria was significantly higher in the OSCC group than in the other groups. The detection rates of P. gingivalis and Aggregatibacter actinomycetemcomitans (A. actinomycetemcomitans) were significantly higher in the OSCC group than those in the control group. From 16S rRNA analysis, the relative abundance of Prevotella buccae and intermedia was significantly higher in OSCC than in the control. Moreover, LPS derived from P. gingivalis contributes to the early development of oral epithelial precancerous lesions and carcinomas in mice.

Specific periodontal pathogens are present in the oral cavities of patients with OPMDs and OSCC, and changes in the bacterial flora due to their presence may contribute to the onset and progression of OMDs.

Forkhead box (FOX) genes are a family of transcription factors that participate in many biological activities, from early embryogenesis to the formation of organs, and from regulation of glucose metabolism to regulation of longevity. Given the extensive influence in the multicellular process, FOX family proteins are responsible for the progression of many types of cancers, especially lung cancer, breast cancer, prostate cancer, and other cancers. Breast cancer is the most common cancer among women, and 2.3 million women were diagnosed in 2020. So, various drugs targeting the FOX signaling pathway have been developed to inhibit breast cancer progression. While the role of the FOX family gene in cancer development has not received enough attention, discovering more potential drugs targeting the FOX signaling pathway is urgently demanded. Here, we review the main members in the FOX gene family and summarize their signaling pathway, including the regulation of the FOX genes and their effects on breast cancer progression. We hope this review will emphasize the understanding of the role of the FOX gene in breast cancer and inspire the discovery of effective anti-breast cancer medicines targeting the FOX gene in the future.

The epithelial mesenchymal transition (EMT) is a biological process in which epithelial cells lose their polarity and adhesion characteristics, and adopt a mesenchymal phenotype. While the EMT naturally occurs during tissue fibrosis, wound healing, and embryonic development, it can be exploited by cancer cells and is strongly associated with cancer stem cell formation, tissue invasiveness, apoptosis, and therapy resistance. Transcription factors (TFs) such as SNAIL, ZEB, and TWIST play a pivotal role in driving the EMT. This systematic review aims to assess the impact of EMT-TFs on hematological malignancy and solid tumors.

English-language literature published between 2010 and 2024 was systematically reviewed, utilizing databases such as PubMed and Google Scholar.

A total of 3250 studies were extracted. Of these, 92 publications meeting the inclusion criteria were analyzed to elucidate the role of EMT-TFs in cancer. The results demonstrated that the EMT-TFs play a critical role in both hematological and solid tumor development and progression. They promote invasive, migratory, and metastatic properties in these tumors, and contribute to therapeutic challenges by enhancing chemoresistance. A strong correlation between EMT-TFs and poor overall survival has been identified.

Our research concluded that EMT-TFs may serve as important predictive and prognostic factors, as well as potential therapeutic targets to mitigate cancer progression.

Age alone should not be an absolute contraindication for any contraceptive methods. However, medical eligibility criteria for combined hormonal contraception (CHC) use must be taken into consideration when choosing an appropriate contraceptive method. Women should be counseled on the benefits and risks of CHC while in their 40s. If there are no contraindications, women may use CHC for contraception up until the age of 50 years. Loss of libido is a common symptom during the late 40s. While women associate this with hormone levels, libido is multifactorial and is influenced by family and work stress, tiredness, self-image, medications and the physical changes in their partner. During this stage, women might experience urogenital issues such as vaginal dryness, dyspareunia and bladder problems, which can further affect the woman's sexual function. Before attributing the cause of sexual dysfunction to CHC use, a complete gynecologic examination and a full biopsychosocial assessment of the woman and her partner should be conducted to define other potential causes. When CHC-related female sexual dysfunction is suspected, using an oral CHC with a higher estrogen dose, a vaginal contraceptive ring or a transdermal contraceptive patch, or switching to a progesterone-only pill or non-hormonal method, might be suggested.

Hodgkin lymphoma (HL) constitutes 10% of all lymphoma diagnoses and accounts for 5% of lymphoma-related deaths. Accurate prognostication in HL remains crucial, particularly given that 10%-20% of patients may receive either insufficient or excessive treatment. This study investigates the effect of hemoglobin, albumin, lymphocyte, and platelet (HALP) score, which is a marker of inflammation status and nutrition, at the time of diagnosis for the patients with HL on prognosis.

A total of 147 patients diagnosed with cHL were included in the study, and their data were analyzed retrospectively. The significance of the HALP score and hematological indices [neutrophil-lymphocyte ratio (NLR), lymphocyte-monocyte ratio (LMR), and platelet-lymphocyte ratio (PLR)] as predictors of overall survival (OS) and disease-free survival (DFS) was evaluated.

Patients were grouped according to median values for the HALP score and hematological indices. High HALP score (p = 0.034), low NLR (p = 0.033), high LMR (p = 0.003), and low PLR (p = 0.014) were statistically significant in the early-stage favorable group. DFS and OS were not statistically significant according to the HALP score NLR, LMR, and PLR groups.

The need for readily applicable, reliable prognostic markers in cHL, where immunotherapy treatments have led to significantly improved survival outcomes, remains persistent.

Autophagy was considered to induce resistance in chemotherapy, which was significantly associated with proliferation of cancer; however, few bibliometric studies on the relation between autophagy and chemotherapy in lung cancer are available. The aim of the present study was to provide a comprehensive overview of the knowledge structure and research hotspots of autophagy and chemotherapy in lung cancer by bibliometric analysis. Publications related to autophagy and chemotherapy in lung cancer from 2003 to 2023 were searched on the Web of Science Core Collection (WoSCC) database. The bibliometric analysis was conducted by using VOSviewers, CiteSpace, and the R package "bibliometrix." A total of 675 articles from 70 countries, led by China and the United States, were included in the analysis. The number of publications related to autophagy and chemotherapy in lung cancer is increasing year by year. Nanjing Medical University, Zhejiang University, China Medical University, and Sichuan University are among the main research institutions contributing to this field. The journal Cancers is the most popular publication in this area, with Autophagy being the most co-cited journal. These publications involve 4481 authors, with Chiu Chien-chih and Gewirtz David having published the most papers, and Noboru Mizushima being the most frequently co-cited author. Studying the relation between autophagy and chemotherapy in the occurrence and development of lung cancer, and exploring therapeutic strategies involving autophagy and chemotherapy in lung cancer, are the primary topics in this research field. "Tumor stem cells," "microRNA," and "EGFR" emerge as the primary keywords in the emerging research hotspots. Indeed, this bibliometric study provides valuable insights into the research trends and developments concerning autophagy and chemotherapy in lung cancer. By identifying recent research frontiers and highlighting hot directions, this study serves as a valuable reference for scholars interested in understanding the relationship between autophagy and chemotherapy in lung cancer. The comprehensive summary of findings offers a foundation for further exploration and advancement in this critical area of cancer research.

To evaluate clinicopathological features in women with mucinous breast cancer (MBC), distinguishing between pure (PMC) and mixed (MMC) subtype.

A retrospective analysis of all 358 women with MBC treated at Vietnam National Cancer hospital from June 2015 to December 2020. PMC was defined by ≥ 90% mucinous components.

We identified 358 women with MBC (245 PMC and 113 MMC) representing 2.7% of all 13,254 BC patients. The proportions of stage I, II, III and IV were 34.9%, 50.8%, 10.4% and 3.9% respectively. The rate of HER2 overexpression was 12%, and only 1.4% of patients was treated with anti-HER2. 193 patients (53.9%) had chemotherapy, including 55 patients (15.4%) treated in the neoadjuvant setting. Only 3 patients (5.5%) achieved pCR. PMC patients were older (54.4 ± 13.3 vs 51.1 ± 13.1 years), had lower Ki67 expression, lower incidence of nodal metastasis (N +) (p values < 0.05). At a median follow-up of 58 months, the 5-year overall survival rate of non-metastatic patients was 86.6%. Multivariate analysis showed N + to be the most significant prognostic factor (HR = 3.3; 95%CI 1.5-7.1), followed by T-stage (HR = 2.9; 95%CI 1.4-6.3), HER2 + (HR = 2.5; 95%CI 1.2-5.3) and MMC subtype (HR = 1.9; 95%CI 1.0-3.9).

Poor prognostic factors of MBC include high T-stage, N-positivity, HER2 overexpression and MMC subtype. Given the low response rate to neoadjuvant CT, upfront surgery is appropriate for MBC patients.

Gallbladder cancer (GBC) is a rare but aggressive malignancy, accounting for most biliary tract cancers. It typically presents at an advanced stage, leading to a poor prognosis, with a mean survival of six months and a five-year survival rate of 17.6 %. Early detection is critical due to its insidious onset and rapid progression.

We report a case of a 46-year-old African male who presented with a two-week history of colicky abdominal pain. Diagnostic imaging revealed a gallbladder mass, and the patient underwent surgical resection followed by adjuvant therapy. Postoperative recovery was initially satisfactory; however, 18 months later, the patient developed peritoneal carcinomatosis and succumbed to the disease.

This case highlights the challenges of managing GBC in resource-limited settings, where late-stage presentation is common. Early surgical intervention remains the mainstay of potentially curative treatment. Adjuvant therapies may improve outcomes but are often less effective in advanced disease stages.

Early detection and surgical management are pivotal for improving survival outcomes in gallbladder cancer. This case emphasizes the need for heightened clinical awareness and improved diagnostic capabilities in resource-constrained environments.

Renal cell carcinoma (RCC) constitutes the most frequent kidney cancer of the adult population and one of the most lethal malignant tumors worldwide. RCC often presents without early symptoms, leading to late diagnosis. Prognosis varies widely based on the stage of cancer at diagnosis. In the early-stage, localized RCC has a relatively good prognosis, while advanced or metastatic RCC has a poor outcome. Obesity, smoking, genetic mutations and family history are all considered risk factors for RCC, while inherited disorders, such as Tuberous Sclerosis and von Hippel-Lindau syndrome, are causally associated with RCC development. Genetic screening, deep sequencing analysis, quantitative proteomics and immunostaining analysis on RCC tissues, biological fluids and blood samples have been employed to identify novel biomarkers, predisposing factors and therapeutic targets for RCC with important clinical implications for patient treatment. Combined approaches of gene-targeting strategies coupled to a deep functional analysis of cancer cell biology, both in vitro and in appropriate animal models of RCC, significantly contributed to identify and characterize relevant pathogenic mechanisms underlying development and progression of RCC. These studies provided also important cues for the generation of novel target-specific therapeutics that selectively restore deranged cancer cell signalling and dysfunctional immune checkpoints, positively impacting on the survival rate of treated RCC patients. In this review, we will describe the recent discoveries concerning the most relevant pathogenic mechanisms of RCC and will highlight novel therapeutic strategies that interrupt oncogenic pathways and restore immune defences in RCC patients.

Ovarian cancer is one of the most prevalent malignancies among women. CircRNAs play key roles in the progression of ovarian cancer. This study aimed to investigate the mechanism of action of hsa_circ_0000129 and its effects on ovarian cancer. Expression of hsa_circ_0000129, tropomyosin 3 (TPM3), and miR-383-5p in ovarian cancer cell lines and tissue specimens was detected using qRT-PCR or western blotting. Cell counting kit-8 (CCK-8), colony formation, and transwell assays were performed to assess viability, proliferation, and migration of ovarian cancer cells. A xenograft model was used to study tumorigenicity of ovarian cancer cells in vivo. Luciferase and RNA immunoprecipitation assays were performed to determine binding between miR-383-5p and hsa_circ_0000129 or TPM3. Upregulation of hsa_circ_0000129 and TPM3 and downregulation of miR-383-5p were observed in ovarian cancer. Low hsa_circ_0000129 and TPM3 expression repressed viability, migration, and proliferation of ovarian cancer cells. Inhibition of miR-383-5p had a contrary effect. Furthermore, knockdown of hsa_circ_0000129 restricted the tumorigenicity of ovarian cancer cells. Mechanistically, hsa_circ_0000129 has a sponging effect on miR-383-5p, which targets TPM3. Hsa_circ_0000129 stimulated development of the malignant ovarian cancer phenotype by sponging miR-383-5p and releasing TPM3.

This study aimed to develop a multimodal radiopathomics model utilising preoperative ultrasound (US) and fine-needle aspiration cytology (FNAC) to predict large-number cervical lymph node metastasis (CLNM) in patients with clinically lymph node-negative (cN0) papillary thyroid carcinoma (PTC).

This multicentre retrospective study included patients with PTC between October 2017 and June 2024 across seven institutions. Patients were categorised based on the presence or absence of large-number CLNM in training, validation, and external testing cohorts. A clinical model was developed based on the maximum diameter of thyroid nodules. Radiomics features were extracted from US images and pathomics features were extracted from FNAC images. Feature selection was performed using univariate analysis, correlation analysis, and least absolute shrinkage and selection operator regression. Six machine learning (ML) algorithms were employed to construct radiomics, pathomics, and radiopathomics models. Predictive performance was assessed using the area under the curve (AUC), and decision curve analysis (DCA).

A total of 426 patients with PTC (41.65 ± 12.47 years; 124 men) were included in this study, with 213 (50%) exhibiting large-number CLNM. The multimodal radiopathomics model demonstrated excellent predictive capabilities with AUCs 0.921, 0.873, 0.903; accuracies (ACCs) 0.852, 0.800, 0.833; sensitivities (SENs) 0.876, 0.867, 0.857; specificities (SPEs) 0.829, 0.733, 0.810, for the training, validation, and testing cohorts, respectively. It significantly outperformed the clinical model (AUCs 0.730, 0.698, 0.630; ACCs 0.690, 0.656, 0.627; SENs 0.686, 0.378, 0.556; SPEs 0.695, 0.933, 0.698), the radiomics model (AUCs 0.819, 0.762, 0.783; ACCs 0.752, 0.722, 0.738; SENs 0.657, 0.844, 0.937; SPEs 0.848, 0.600, 0.540), and the pathomics model (AUCs 0.882, 0.786, 0.800; ACCs 0.829, 0.756, 0.786; SENs 0.819, 0.889, 0.857; SPEs 0.838, 0.633, 0.714).

The multimodal radiopathomics model demonstrated significant advantages in the preoperative prediction of large-number CLNM in patients with cN0 PTC.

Question Accurate preoperative prediction of large-number CLNM in PTC patients can guide treatment plans, but single-modality diagnostic performance remains limited. Findings The radiopathomics model utilising preoperative US and FNAC images effectively predicted large-number CLNM in both validation and testing cohorts, outperforming single predictive models. Clinical relevance Our study proposes a multimodal radiopathomics model based on preoperative US and FNAC images, which can effectively predict large-number CLNM in PTC preoperatively and guide clinicians in treatment planning.

Cancer-associated fibroblasts (CAFs) are key components of the pancreatic adenocarcinoma (PAAD) tumor microenvironment (TME), where they promote tumor progression and metastasis through immunosuppressive functions. Although significant progress has been made in understanding the crosstalk between cancer cells and CAFs, many underlying mechanisms remain unclear. Recent studies have highlighted the importance of calcium signaling in enhancing interactions between tumor cells and the surrounding stroma, with the S100 family of proteins serving as important regulators. While the roles of some S100 proteins have been extensively studied, others, such as S100A13, remain less well understood.

Bioinformatic analysis was employed to predict the pathogenic potential of CAFs and S100A13. Stable S100A13 knockdown CAFs were generated using a short hairpin RNA system. Cellular viability and apoptosis rates were evaluated through CCK-8 and flow cytometry tests, respectively. Additionally, the wound healing and migration assays were conducted to assess the invasive and metastatic capabilities. Transcriptome analysis was conducted to identify differential gene expression and associated signaling pathways in PAAD cells derived from an indirect culture system. Furthermore, the protumoral role of S100A13 in PAAD was further verified using both 3D bioprinting and cell line-based xenograft tumor models.

In this study, we identified a strong association between S100A13, a calcium-binding protein, and CAFs in PAAD. Gene expression analysis revealed that S100A13 was highly expressed in CAFs and correlated with poor prognosis. Knockdown of S100A13 in CAFs reduced the metastatic potential of PAAD cells. In addition, S100A13 depletion impaired cell motility and calcium signaling pathways within the TME. Furthermore, silencing S100A13 in CAFs markedly slowed PAAD progression in both tumor spheroids and Balb/c nude mice.

Together, our findings underscore the critical role of CAFs-derived S100A13 in PAAD progression and suggest that targeting S100A13 may offer a promising therapeutic strategy for PAAD.

This study aims to develop a radiopathomics model based on preoperative ultrasound and fine-needle aspiration cytology (FNAC) images to enable accurate, non-invasive preoperative risk stratification for patients with papillary thyroid carcinoma (PTC). The model seeks to enhance clinical decision-making by optimizing preoperative treatment strategies.

A retrospective analysis was conducted on data from PTC patients who underwent thyroidectomy between October 2022 and May 2024 across six centers. Based on lymph node dissection outcomes, patients were categorized into high-risk and low-risk groups. Initially, a clinical predictive model was established based on the maximum diameter of the thyroid nodules. Radiomics features were extracted from preoperative two-dimensional ultrasound images, and pathomics features were extracted from 400x magnification H&E-stained tumor cell images from FNAC. The most predictive radiomics and pathomics features were identified through univariate analysis, Pearson correlation analysis and LASSO algorithm. The most valuable radiopathomics features were then selected by combining these predictive features. Finally, machine learning with the XGBoost algorithm was employed to construct radiomics, pathomics, and radiopathomics models. The performance of the models was evaluated using the area under the curve (AUC), decision curve analysis, accuracy, specificity, sensitivity, positive predictive value, and negative predictive value.

A total of 688 PTC patients were included, with 344 classified as intermediate/high-risk and 344 as low-risk. The multimodal radiopathomics model demonstrated excellent predictive performance, with AUCs of 0.886 (95% CI: 0.829-0.924) and 0.828 (95% CI: 0.751-0.879) in two external validation cohorts, significantly outperforming the clinical model (AUCs of 0.662 and 0.601), radiomics model (AUCs of 0.702 and 0.697), and pathomics model (AUCs of 0.741 and 0.712).

The radiopathomics model exhibits significant advantages in accurately predicting preoperative risk stratification in PTC patients. Its application is expected to reduce unnecessary lymph node dissection surgeries, optimize treatment strategies, and improve therapeutic outcomes.