The tumor microenvironment (TME) plays a pivotal role in cancer progression, with cancer-associated fibroblasts (CAFs) significantly influencing tumor behavior. Especially, elevated COX2 expressing fibroblasts within the TME, notably in collagen-dense tumors like breast cancer, has been recently emphasized in the literature. However, the specific effect of COX2-expressing CAFs (COX2+ CAFs) on neighboring cells and their consequent role in cancer progression is not fully elucidated.

Alternative splicing (AS) is consistently linked to tumor progression. SRSF1, the first identified proto-oncogene in the serine/arginine-rich splicing factor (SRSF) protein family, plays a crucial role. However, the specific functions and potential mechanisms of SRSF1 in advancing bladder cancer (BCa) progression and influencing chemosensitivity remain largely unexplored.

As machine learning (ML) continuously develops in cancer diagnosis and treatment, some researchers have attempted to predict the expression of programmed death ligand-1 (PD-L1) in non-small cell lung cancer (NSCLC) by ML. However, there is a lack of systematic evidence on the effectiveness of ML.

The potential of glioblastoma (GBM) photodynamic therapy (PDT) is limited by inadequate GBM drug delivery, and the development of resistance to PDT as a result of cellular damage response that critically involves the hypoxia-inducible factor-1α (HIF-1α) and yes-associated protein (YAP). Herein, addressing these challenges, we demonstrated a strategy of photo-controlled, targeted co-delivery of verteporfin (Vp), a photosensitizer and YAP inhibitor as well, and acriflavine (Af), a HIF-1α inhibitor via platelets for enhanced GBM PDT. Mouse platelets were separately loaded with Vp (Vp@Plt) and Af (Af@Plt) and the mixture thereof is termed Vp@Plt + Af@Plt. Alternatively, platelets were simultaneously loaded with Vp and Af to yield (Vp + Af)@Plt. First, both Vp@Plt + Af@Plt and (Vp + Af)@Plt were shown to achieve rapid and efficient laser-triggered, GBM-targeted delivery of Vp and Af, which led to markedly higher phototoxicity in the GBM cells (GBCs) and ultimately more potent GBM PDT than Vp@Plt in mice. Next, a mechanistic study revealed the induction of a mutually promotional interaction of HIF-1α and YAP in the GBCs in response to PDT-inflicted DNA damage. This interaction protected HIF-1α from degradation and meanwhile assisted in the nuclear translocation of YAP leading to increased nuclear presence of both HIF-1α and YAP and escalated DNA damage repair activity under their regulation. Both Af and Vp were found to block the PDT-induced HIF-1α-YAP interaction and thereby severely impaired DNA damage repair, eventually resulting in exacerbated cell death. In conclusion, Af and Vp can be adequately co-delivered in GBM via platelets in a photo-controlled manner to achieve efficacious GBM PDT through double blocking of the HIF-1α-YAP interaction in the GBCs.

To investigate the current situation of nosocomial infections in oral cancer patients after surgery, explore possible risk factors for nosocomial infections, screen high-risk populations for nosocomial infections after oral cancer surgery in the early stage, and provide scientific basis for the prevention and control of nosocomial infections in oral cancer patients after surgery.

Ferroptosis is a novel iron-dependent type of programmed cell death that is characterized by the oxidation of lipids by divalent iron ions to produce lipid peroxides, which leads to cell death. Fucosyltransferase 11 (FUT11) is highly expressed in most tumors and is involved in tumorigenesis. However, there have been few studies regarding the relationship between FUT11 and ferroptosis. In this study, we found that FUT11 expression was abnormally high in gastric cancer (GC) cells and that the prognosis of patients with GC and high expression of FUT11 was poor. FUT11 expression was significantly correlated with the TNM stage of GC.Specific knockdown of FUT11 significantly inhibited the proliferation of GC cells, reduced the abundance of the key anti-ferroptotic protein glutathione peroxidase 4(GPX4), induced lipid peroxidation and ferroptosis in GC cells, and inhibited the proliferation of these cells. The overexpression of GPX4 reduced the inhibitory effect of FUT11 on GC cells. In addition, the knockdown of FUT11 significantly inhibited GC tumor growth in mice, and this inhibitory effect was reduced by the overexpression of GPX4. In conclusion, we have shown that FUT11 promotes GC progression by targeting GPX4, thereby inhibiting ferroptosis in GC cells. These findings suggest that FUT11 is a potential therapeutic target for GC.

To develop a multiclass radiomics model for differentiating chondroid bone tumors using preoperative MRI.

The synchronous occurrence of adenocarcinoma and squamous cell carcinoma in distinct cervical regions is exceptionally rare. This report highlights a case of HPV-associated adenocarcinoma and squamous cell carcinoma at distinct sites in a patient with primary stage IA1 cervical cancer.

Next-generation sequencing (NGS) allows for the simultaneous sequencing of multiple cancer predisposition genes. We assessed the frequency and spectrum of germline variations in individuals with ovarian cancer (OC), using whole exome sequencing (WES).

Hormone receptor (HR) positive (HR +) and human epidermal growth factor receptor 2 (HER2) negative (aka HER2 -) breast cancer (BC) is the most frequently diagnosed subtype. Recent development of next-generation endocrine therapies (e.g. selective estrogen receptor degraders (SERDs); third-generation aromatase inhibitors (AI) and targeted therapies (e.g., CDK4/6, PI3K, and mTOR inhibitors)) as well as antibody drugs conjugates (ADC, eg. T-DXd and SG) showed promising results with meaningful improvements in survival for patients with metastatic HR + HER2 - BC. Therapy selection is mainly based on clinical, tumor pathological and molecular characteristics as well as on efficacy based on trial data, nevertheless, side effect profiles are key differentiators of treatments in the metastatic setting. Therefore, understanding how patients evaluate various treatment attributes and how these change in different clinical situations is fundamental toward the choice of optimal therapeutic strategies for treating metastatic HR + HER2 - Stage IV patients. Here, we investigated treatment preferences of a total of 102 stage IV HR + HER2 - breast cancer patients in Italy by developing and applying a survey instrument based on discrete choice experiment (DCE). Treatment efficacy was the top valued attribute across all patient segments and the second most important attribute was the risk of grade ≥ 3 adverse events (AE). Overall, therapies with better outcomes of PFS or AE grade 3 or higher would have a higher impact on the preference to choose a treatment from a patient perspective.

Bladder cancer represents a heterogeneous disease with distinct clinical challenges. Non-muscle invasive bladder cancer (NMIBC) typically presents as indolent and slow-growing, yet a critical clinical challenge remains: identifying which patients will progress to muscle-invasive disease requiring radical interventions. Early detection of progression propensity is essential, as once muscle invasion occurs, the risk of distant metastasis increases substantially, and treatment shifts from conservative TURBT (Transurethral Resection of Bladder Tumor) to aggressive surgical interventions with significant morbidity. Current risk stratification methods fail to adequately predict this transition in approximately 30% of cases, highlighting the urgent need for more accurate prognostic tools.

Colorectal cancer (CRC) is a prevalent and highly malignant neoplasm on a global scale, ranking as the second most widespread cause of cancer-associated death. Long noncoding RNAs (lncRNAs) control tumorigenic processes in CRC by modulating inflammatory signals. However, the precise mechanisms remain unknown.

Women with metastatic breast cancer (MBC) face unique challenges throughout their disease journey. Unfortunately, there is limited research on the specific needs of patients with MBC in low- and middle-income countries such as Mexico. Understanding the priorities of this population is crucial for improving their care.

Bladder cancer is uncommon in individuals under the age of 45, and its clinical and molecular characteristics in this population differ significantly from those observed in older patients. This systematic review aims to evaluate recurrence, progression, survival outcomes, and molecular profiles of bladder cancer in young adults.

Radiotherapy (RT) is a relevant treatment for head and neck squamous cell carcinoma (HNSCC) patients but radioresistance, which depends on DNA damage response (DDR), restrains outcome. Therefore, manipulating DDR by small molecule inhibitors (SMI) is a promising treatment option. The main DNA double strand break (DSB) repair mechanisms in healthy mammalian cells are homologous recombination (HR) and non-homologous end joining (NHEJ). It is known that HR is already often impaired in tumors because of cancerous transitions. Therefore, additionally inhibiting NHEJ is a possibility to specifically target tumor cells and spare healthy tissue, which has the alternative DSB repair mechanism available. We treated HNSCC and healthy fibroblast cell lines with 30 µM of the ligase IV inhibitor SCR130 and a single dose of 2 Gy (Gy) ionizing radiation (IR) to investigate the inhibitor's radiosensitizing effect. In short, the effect of SCR130 in combination with IR on cell death, clonogenicity, and DNA damage is limited and highly cell line specific. Nevertheless, SCR130 increases the number of cells in G0/G1 phase concomitant with gained p21 expression consistently. We suggest that SCR130 in combination with IR has anti-proliferative effects, but an escape of the cells by upregulation of ligase IV resulting from the treatment is possible.

Metastatic bladder cancer is characterized by its aggressive behavior and complex molecular mechanisms that remain largely undefined. This study explores the therapeutic potential of targeting peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) using liposomal nanoparticles to deliver PGC-1α siRNA to bladder cancer cells. We employed comprehensive transcriptomic, proteomic, and metabolomic analyses to investigate the impact of PGC-1α silencing. Our in vitro results demonstrate that targeting PGC-1α significantly impairs mitochondrial function and disrupts energy metabolism, affecting critical pathways such as glycolysis and the citric acid cycle, as well as altering mRNA nuclear export. In vivo experiments in animal models show that nanoparticles loaded with si-PGC-1α effectively reduce lung metastasis, indicating a significant impact on metastatic progression. These findings highlight PGC-1α as a key regulator of metabolic reprogramming in metastatic bladder cancer and suggest that its inhibition could serve as a promising therapeutic strategy. By elucidating the role of PGC-1α in cancer metabolism, this study provides new insights into the molecular underpinnings of bladder cancer metastasis and offers potential avenues for developing targeted therapies aimed at the metabolic vulnerabilities of this malignancy.

This study aimed to address the prognostic value of positive lymph node ratio for oral cavity squamous cell carcinoma (OCSCC) patients after neoadjuvant treatment, and build a prediction nomogram model. Patients with OCSCC with neoadjuvant treatment were retrieved from the Surveillance, Epidemiology, and End Results database from 2004 to 2021. The primary outcome was overall survival (OS), and the second outcome was disease-specific survival (DSS). Kaplan-Meier and log-rank tests were used to analyze the survival outcomes. Univariable and multivariable analyses were conducted, and then a nomogram was constructed. A total of 419 were included in this study. The optimal cutoff value of the positive lymph node ratio (LNR) was 7.0%. The 5-year OS of patients with low LNR was significantly improved over those with high LNR (p < 0.0001). LNR > 7.0% (HR 50.7, 95% CI 19.7-130.5), and unmarried status (HR 1.33, 95% CI 1.03-1.70) were the independent risk factors for OS (all p < 0.05). LNR > 7.0% (HR 35.8, 95% CI 9.63-132.7), gum primary site (HR 0.330, 95% CI 0.132-0.827), and preoperative chemotherapy and radiotherapy (HR 2.91, 95% CI 1.78-4.73) were the independent risk factors for DSS (all p < 0.05). According to the nomogram, patients were stratified into the high-risk group and the low-risk group for OS and DSS. Patients in the low-risk group were predicted with superior survival (both p < 0.05). The LNR was an independent prognostic factor of the OS and DSS for OCSCC patients after neoadjuvant treatment. The tools may be valuable to guide multidisciplinary teams in making treatment decisions.

Pancreatic cancer remains one of the leading causes of mortality worldwide, largely due to the limitations of current clinical strategies for its treatment. As a result, identifying genetic alterations and potential therapeutic targets could offer new opportunities for improving the diagnosis and treatment of pancreatic cancer. The identification of differentially expressed genes (DEGs) and subsequent analyses, including signaling pathway enrichment, functional classification, and protein-protein interaction (PPI) network construction, were conducted using three public datasets: GSE32676, GSE71989, and GSE16515. Kaplan-Meier survival curves and receiver operating characteristic (ROC) curves were employed to investigate the correlation between hub genes and clinicopathological features in pancreatic cancer patients. Genetic alterations were analyzed using the CBioPortal web tool. Cell proliferation was assessed through CCK-8, colony formation, and EdU assays. Tumor migration, invasion, and angiogenesis were evaluated using transwell and tube formation assays, respectively. Protein and mRNA expression levels were measured via western blot analysis and qPCR assays. The subcutaneous xenografted nude mice models were generated to evaluate the potential effect of miR-485-3p/MELK cascade on tumor growth in vivo. Our analysis revealed that MELK expression is positively correlated with poor prognosis in patients with pancreatic cancer. The overexpression or knockdown of MELK significantly influences cell proliferation, tumor metastasis, and angiogenesis across various pancreatic cancer cell lines. Furthermore, we identified that miR-485-3p regulates MELK expression by directly targeting the MELK 3'UTR binding site in pancreatic cancer cells, which subsequently impacts tumor progression. Additionally, our findings demonstrate that the miR-485-3p/MELK cascade is closely associated with tumor progression in pancreatic cancer cells. Mechanistically, the miR-485-3p/MELK cascade promotes the phosphorylation of Akt to regulate pancreatic cancer cell progression, metastasis, and angiogenesis. Furthermore, overexpression of miR-485-3p inhibits the tumor growth induced by MELK overexpression in subcutaneous xenograft model. MiR-485-3p/MELK cascade may serve as a promising biomarker and therapeutic target for the diagnosis and treatment of pancreatic cancer.

Angiogenesis is one of the hallmarks of solid tumors. Exosomes are extracellular vesicles, which are involved in multiple stages of tumor progression. The role of macrophage-derived exosomes in angiogenesis in oral squamous cell carcinoma (OSCC), where macrophages are crucial components of the tumor microenvironment (TME), remains to be explored. The M2 macrophages and microvessels in OSCC were stained by immunohistochemistry. M2 macrophages were induced in vitro and exosomes were extracted by gradient centrifugation using ultracentrifugation. Fluorescence confocal microscopy was used to observe the uptake of M2 macrophage-derived exosomes by human umbilical vein endothelial cells (HUVECs). CCK-8 proliferation assay, TRANSWELL migration assay and tube formation assay were used to detect the effects of M2 macrophage-derived exosomes on the proliferation, migration and tube formation of HUVECs. Immunohistochemical study showed that M2 macrophage infiltration was positively correlated with microvessel density in OSCC. We induced M2 macrophages in vitro and successfully extracted its exosomes. The cellular internalization of fluorescence-labeled exosomes by HUVECs was dynamically monitored via laser scanning confocal microscopy. The M2 macrophage-derived exosomes promoted the proliferation, migration, and tube-forming ability of HUVECs. The results showed that M2 macrophage-derived exosomes could promote the proliferation, migration and tubulation of HUVECs.

We aimed to explore the effectiveness of CTH as a serum inflammation biomarker for HCC. Enzyme-linked immunosorbent assay was used to detect serum levels of CTH, interleukin-6 (IL-6), C-reactive protein (CRP), and IL-10. The Scheuer scoring system was used to assess the liver inflammation grading (significant liver inflammation: ≥ G2 grade). CTH levels in the HCC group were significantly elevated (P < 0.0001). Of 146 patients, 58.22% exhibited significant liver inflammation. CTH levels in patients with significant liver inflammation were significantly higher than those in patients with no or mild liver inflammation (< G 2) (p < 0.0001). The area under the Receiver Operating Characteristic (ROC) curve for CTH in predicting significant hepatitis was 0.77 (sensitivity, 81.2%; specificity,62.3%). There was a significant positive correlation (r = 0.50, p < 0.05) between serum CTH levels and histopathological parameter G. The area under the ROC curve for CTH in predicting hepatocellular carcinoma was 0.83 (sensitivity, 64.6%; specificity, 83.3%). CTH and AFP improved the diagnostic accuracy of HCC. CTH levels significantly decreased 6 months post-operation (p < 0.05). The recurrence of HCC caused significant increases in CTH levels. Thus, CTH can serve as a serum inflammation marker for HCC.