Hepatitis B virus (HBV) remains an important risk factor for hepatocellular carcinoma (HCC), and inflammation plays an essential role in tumor development. This study aimed to investigate the impact of inflammatory markers in the postoperative outcomes of patients with HBV-related HCC, providing valuable prognostic indicators after hepatectomy.

We retrospectively analyzed 222 patients with HBV-related HCC after surgical resection. The ROC curve was used to calculate biomarker cutoff values. The Kaplan-Meier method was used to estimate overall survival (OS) and recurrence-free survival (RFS), and univariate and multivariate analyses were used to identify the prognostic factors.

The Kaplan-Meier analysis revealed that patients with high albumin-bilirubin (ALBI) score, aspartate aminotransferase to platelet ratio index (APRI), and monocyte to lymphocyte ratio (MLR) had worse OS, while those with high ALBI score and MLR had shorter RFS. Multivariate Cox regression analysis identified alpha-fetoprotein >400 ng/mL (hazard ratio [HR]: 2.447, 95% confidence interval [CI]: 1.273-4.706, p = 0.007), alanine aminotransferase (HR: 0.377, 95% CI: 0.171-0.834, p = 0.016), platelet to lymphocyte ratio (HR: 0.385, 95% CI: 0.196-0.755, p = 0.006), systemic inflammatory response index (HR: 1.844, 95% CI: 1.049-3.239, p = 0.033), ALBI score (HR: 1.808, 95% CI: 1.020-3.203, p = 0.043), APRI score (HR: 3.193, 95% CI: 1.662-6.137, p < 0.001), tumor diameter (HR: 1.083, 95% CI: 1.012-1.160, p = 0.022), and portal vein tumor thrombosis (PVTT) (HR: 6.083, 95% CI: 2.774-13.338, p < 0.0001) as independent predictors for OS. MLR (HR: 2.285, 95% CI: 1.290-4.048, p = 0.005) and PVTT (HR: 2.672, 95% CI: 1.280-5.579, p = 0.009) were confirmed as significant prognostic markers of RFS in patients with HBV-related HCC.

ALBI score, APRI, and MLR are effective prognostic predictors in patients with HBV-related HCC after curative resection. Close monitoring and adjuvant therapies should be considered for high-risk patients.

Cancer cachexia, a multifactorial syndrome characterized by body weight loss, muscle, and adipose tissue wasting, affects patients with cancer. Over time, the definition of cachexia has been modified, including inflammation as one of the main causal factors. Evidence has suggested that a range of proinflammatory mediators may be involved in the regulation of intracellular signaling, resulting in enhanced resting energy expenditure, metabolic changes, and muscle atrophy, all of which are typical features of cachexia. Physiologically speaking, however, inflammation is a response aimed at facing potentially damaging events. Along this line, its induction in the cancer hosts could be an attempt to restore the physiological homeostasis. Interesting observations have shown that cytokines such as interleukins 4 and 6 could improve muscle wasting, supporting the view that the same mediator may exert pro- or anti-inflammatory activity depending on the immune cells involved as well as on the tissue metabolic demand. In conclusion, whether inflammation is crucial to the occurrence of cachexia or just one contributor among others, is still unclear. Indeed, while inflammation is a trigger of cachexia, the alterations of energy and protein metabolism and of the hormonal homeostasis occurring in cachexia likely act as inflammatory stimuli on their own. Whether the causative role prevails over the compensatory one likely depends on the tumor type and stage, patient lifestyle, the presence of comorbidities, and the response to anticancer treatments paving the way to a holistic, personalized approach to cancer cachexia.

Prostate cancer (PCa), a significant health concern among middle-aged and elderly men globally, has increasingly been associated with metabolic and inflammatory processes. The advanced lung cancer inflammation index (ALI), a novel marker reflecting nutritional and inflammatory status, has not yet been thoroughly investigated in the context of PCa. This study investigated the potential link between ALI and PCa.

We first conducted a cross-sectional study utilizing data from the National Health and Nutrition Examination Survey (NHANES). The relationship between ALI and PCa was examined by NHANES-provided survey weights. Smoothed curve fitting and threshold effect analyses were conducted to evaluate possible nonlinear associations. Then we analyzed the correlation between the prognosis of PCa patients and ALI.

Out of 15,042 adult participants, 683 (4.54%) were diagnosed with PCa. The risk of PCa decreased across increasing quartiles of ALI. Multivariate logistic regression analysis revealed that compared to participants in the lowest ALI quartile (Q1: 2.89-41.94), those in higher quartiles (Q2: 41.94-59.08, Q3: 59.08-80.88, and Q4: ≥80.88) had progressively lower odds of developing PCa in both unadjusted and adjusted models. Smoothed curve fitting indicated a U-shaped relationship between ALI and PCa. Longitudinal follow-up data indicated that lower ALI values were positively correlated with a poor survival in cancer patients.

Our study revealed a non-linear relationship between ALI and the risk of PCa development. Specifically, there was a negative correlation between ALI and PCa risk when the ALI value was < 100. Furthermore, we found that lower ALI levels are strongly associated with a poor survival in cancer patients. Additional large-scale prospective studies are needed to confirm these findings and investigate the underlying mechanisms.

This study aimed to investigate the role of immunotrophic inflammatory markers in assessing the prognosis and treatment-related toxicity in patients with esophageal squamous cell carcinoma (ESCC) undergoing first-line radiotherapy and chemotherapy combined with immunotherapy. We retrospectively enrolled 67 patients with ESCC and determined the optimal cutoff values for prognostic nutrition index (PNI), neutrophil to lymphocyte ratio (NLR), and platelet to lymphocyte ratio (PLR) using receiver operating characteristic (ROC) curve analysis. Statistical analysis was performed using SPSS 25.0. The one-, two-, and three-year overall survival (OS) rates were 88.1%, 62.3%, and 57.6%, respectively. The overall effective rate was 82.1% (55/67). ROC curve analysis revealed optimal cutoff values for PNI, NLR, and PLR as 48.35, 3.84, and 150.49, respectively. Patients in the high PNI group, low NLR group and PLR group exhibited significantly higher mOS and mPFS time compared to the control group. Notably, the incidence of grade 2 toxicity and side effects in the PNI ≥ 48.35 group was significantly lower than that in the PNI < 48.35 group. Our findings suggest that pretreatment values of PNI, NLR, and PLR can serve as valuable biomarkers for evaluating the prognosis of ESCC patients undergoing first-line radiotherapy and chemotherapy combined with immunotherapy. Further studies with larger cohorts are warranted to validate these results.

Although the systemic inflammation response index (SIRI) is often associated with prognostic significance in esophageal cancer (EC) patients, the results continue to be conflicting. We focused on identifying SIRI's precise role in forecasting EC prognosis through performing this meta-analysis.

This work searched PubMed, Web of Science, Embase, Cochrane Library, and CNKI till November 16, 2024, and determined pooled hazard ratios (HRs) and 95% confidence intervals (CIs) for evaluating EC prognosis forecasting efficiency of SIRI. The inclusion criteria: (1) pathologic confirmation of EC; (2) those reporting associations of SIRI with EC survival outcomes; (3) those reporting HRs and 95% CIs; (4) those with an available cut-off value of SIRI; and (5) no restriction in language. The exclusion criteria: (1) case reports, reviews, meeting abstracts, comments and letters; (2) those enrolling duplicate cases; and (3) animal studies.

We enrolled six studies comprising 2176 cases into the present work. Based on our combined findings, elevated SIRI showed significant relation to dismal overall survival (OS) (HR = 1.43, 95%CI = 1.20-1.71, p < 0.001; I2 = 48.8%, p = 0.098) and shortened progression-free survival (PFS) (HR = 2.00, 95%CI = 1.35-2.98, p = 0.001; I2 = 0, p = 0.409) in EC. Moreover, high SIRI exhibited obvious relation to male gender (OR = 1.86, 95%CI = 1.07-3.22, p = 0.027; I2 = 69.4%, p = 0.020), TNM stage of III-IV (OR = 1.52, 95%CI = 1.18-1.94, p = 0.001; I2 = 24.3%, p = 0.265), T3-T4 stage (OR = 1.73, 95%CI = 1.12-2.69, p = 0.014; I2 = 61.0%, p = 0.053), and lymph node metastasis (OR = 1.29, 95%CI = 1.02-1.64, p = 0.036; I2 = 42.7%, p = 0.155). However, SIRI was not markedly related to age, tumor location, tumor differentiation, or smoking history.

In summary, high SIRI is significantly related to dismal OS and shortened PFS of EC cases, together with advanced tumor stage, T3-T4 stage, and lymph node metastasis of EC. Due to some limitations, large prospective studies that utilize standardized threshold SIRI should be conducted to validate our results in the future.

Lung cancer, a malignant neoplasm that is globally prevalent and characterized by high incidence and mortality rates, has seen the rise of immune checkpoint inhibitors (ICIs) as a crucial systemic treatment. However, a subset of patients exhibits suboptimal responses to ICIs. Recently, studies revealed the role of vitamin D in inflammation modulation, cell differentiation, and cancer prevention. Vitamin D precisely modulates immune responses and inflammatory states within the tumor microenvironment (TME) by targeting both innate and adaptive immunity. These effects may reduce immune tolerance to ICIs and synergistically enhance their therapeutic efficacy. Here, we review vitamin D metabolism in lung cancer patients, as well as its anti-tumor mechanisms, immune regulation, and the significant promise of vitamin D in lung cancer immunotherapy and adjuvant therapeutic strategies. Further research is imperative to surmount these challenges and fully realize vitamin D's potential in improving lung cancer immunotherapy outcomes.

Lung cancer has become a significant global health concern due to the increasing number of cases and deaths. Recent research has suggested a potential link between parasites and lung cancer. This review aims to comprehensively analyse existing literature to highlight relevant studies evaluating this relationship. A thorough search in different databases revealed four key associations: parasites as a potential risk factor for lung cancer, suppressors of lung cancer, mimics of lung cancer leading to misdiagnosis, and coincidental infections with lung cancer. The review indicates a significant relationship between parasites and the suppression of lung cancer, emphasising the importance of further research to explore this novel avenue in the hope of identifying and developing novel biological cancer therapeutic and preventive strategies. It also stresses the importance of recognising pulmonary parasitic infections in the differential diagnosis of lung cancer to prevent misdiagnosis and subsequent unnecessary surgical intervention. Additionally, in patients with concurrent pulmonary parasitic infections and lung cancer, which may be easily overlooked, persistent symptoms despite applying appropriate anti-parasitic treatment should raise concern about the need for repetitive evaluation by appropriate diagnostic protocols and imaging follow-up for potential underlying lung cancer.

This study investigated the correlation between tongue coating thickness (TCT), micro-inflammatory state (MIS), and oral microbiome in maintenance hemodialysis (MHD) patients.

Forty MHD patients (20 thin-tongue coating [BTZ], 20 thick-tongue coating [HTZ]) and 15 healthy controls (DZZ) were enrolled. Blood microinflammatory markers were analyzed in all patients. Saliva samples from 15 HTZ, 15 BTZ, and 15 DZZ underwent 16S rRNA sequencing.

HTZ patients exhibited higher microinflammatory marker levels than BTZ. Oral microbiome species richness in DZZ surpassed that of the MHD groups, with distinct structural differences, particularly between HTZ and DZZ. HTZ showed higher abundances of Actinobacillus, Peptostreptococcus, and Lachnospiraceae NK4A136 group than BTZ. Correlation analysis revealed a positive correlation between the levels of IL-6 and TNF-α and the abundance of Fusobacterium, but a negative correlation with Streptococcus. Additionally, the TNF-α level positively correlated with Campylobacter.

Thick tongue coating in MHD patients is associated with elevated microinflammation and altered oral microbiome, suggesting a link between inflammation and microbial dysbiosis.

Adenosine kinase (ADK, EC: 2.7.1.20) is an evolutionarily ancient ribokinase, which acts as a metabolic regulator by transferring a phosphoryl group to adenosine to form AMP. The enzyme is of interest as a therapeutic target because its inhibition is one of the most effective means to raise the levels of adenosine and hence adenosine receptor activation. For these reasons, ADK has received significant attention in drug discovery efforts in the early 2000s for indications such as epilepsy, chronic pain, and inflammation; however, the report of adverse events regarding cardiovascular and hepatic function as well as instances of microhemorrhage in the brain of preclinical models prevented further development efforts. Recent findings emphasize the importance of compartmentalization of the adenosine system reflected by two distinct isoforms of the enzyme, ADK-S and ADK-L, expressed in the cytoplasm and the cell nucleus, respectively. Newly identified adenosine receptor independent functions of adenosine as a regulator of biochemical transmethylation reactions, which include DNA and histone methylation, identify ADK-L as a distinct therapeutic target for the regulation of the nuclear methylome. This newly recognized role of ADK-L as an epigenetic regulator points toward the potential disease-modifying properties of the next generation of ADK inhibitors. Continued efforts to develop therapeutic strategies to separate nuclear from extracellular functions of adenosine would enable the development of targeted therapeutics with reduced adverse event potential. This review will summarize recent advances in the discovery of novel ADK inhibitors and discuss their potential therapeutic use in conditions ranging from epilepsy to cancer.

While growing evidence highlights the role of gut microbiota and inflammatory proteins in cancer, with cancer-related inflammation now considered the seventh hallmark of cancer, the direct causal relationships between specific microbiota, cancer, and the potential mediating effects of inflammatory proteins have not been fully established.

We employed Mendelian randomization (MR) to assess the causal relationships between gut microbiota, inflammatory proteins, and eighteen distinct cancers using data from extensive genome-wide association studies (GWAS). The primary statistical method utilized was inverse variance weighting (IVW). We also investigated whether inflammatory proteins could mediate the effects of gut microbiota on cancer development.

Our findings revealed 42 positive and 49 inverse causal impacts of gut microbiota on cancer risk (P < 0.05). Additionally, we identified 32 positive and 28 inverse causal relationships between inflammatory proteins and cancer risk. Moreover, genus Collinsella decreased the risk of lung cancer by decreasing levels of T-cell surface glycoprotein CD5 (mediating effect = 16.667%), while genus Ruminococcaceae UCG005 increased the risk of mesothelioma by increasing levels of CCL4 (mediating effect = 5.134%).

Our study provides evidence for a causal association between gut microbiota, inflammatory proteins, and eighteen different cancer types. Notably, the T-cell surface glycoprotein CD5 and CCL4 were identified as mediators linking the genus Collinsella with lung cancer and the genus Ruminococcaceae UCG005 with mesothelioma, respectively.

Inflammation is a hallmark of cancer. It contributes to a heterogeneous, hyperpermeable, and poorly perfused tumor vasculature, as well as to a dense and disorganized extracellular matrix, which together negatively affect drug delivery. Reasoning that glucocorticoids have pleiotropic effects, we use clinical-stage dexamethasone liposomes (LipoDex) to prime the tumor microenvironment for improved drug delivery and enhanced treatment efficacy. We show that LipoDex priming improves tumor vascular function and reduces extracellular matrix deposition. Single-cell sequencing corroborates LipoDex-mediated inhibition of pro-inflammatory, pro-angiogenic, and pro-fibrogenic gene expression in mononuclear cells, tumor-associated macrophages, and cancer-associated fibroblasts. Multimodal optical imaging illustrates that LipoDex pre-treatment increases the tumor accumulation and intratumoral distribution of subsequently administered polymeric and liposomal drug delivery systems. Using Doxil as a prototypic nanodrug, we finally show that LipoDex priming promotes antitumor treatment efficacy. Altogether, our findings demonstrate that desmoplastic tumors can be primed for improved drug targeting and therapy using clinical-stage glucocorticoid liposomes.

Inflammation within tumor microenvironments has been correlated to numerous malignancies. This study aims to explore its significance in thyroid cancer (TC).

Retrospective analysis of 157 thyroid carcinomas and 40 benign cases involved initial univariate analysis. The value of neutrophils/value of lymphocytes (NLR), value of platelets/value of lymphocytes (PLR), value of lymphocytes/value of monocytes (LMR), and value of platelets × value of neutrophils/value of lymphocytes (SII) indexes were related to TC characteristics and number and location of involved lymph nodes using χ2 or Fischer's exact tests for categorical variables and Student's t-tests for continuous ones. A 1:1 propensity score matching balanced malignant and benign TC groups based on age, sex, and tumor size was used. Post-matching, a multivariate logistic model integrated sex, age, Central lymph node metastases (CLNM), and SII index. Statistically significant immune index values underwent ROC curve analysis for determining cut-offs. Among the 157 malignant TC, median test and density plots were performed.

The SII index emerged as a predictor of malignancy in both univariate and multivariate analyses (p-value = 0.0202). The ROC curve indicated a cut-off SII value of 465.71, (specificity = 58% [95% CI: 0.43-0.73]; sensitivity = 80% [95% CI: 0.68-0.93]). Median SII index values for tumor sizes of 1 and >1 were 522.8 and 654.8, respectively (p-value = 0.016). When central lymph nodes metastases(CLNMs) was considered (CLNM = 0 vs. CLNM > 0), median SII values were 530.7 and 1121.7, respectively (p-value = 0.011).

The SII index appears to be a valuable tool in the presence of TC, showing correlations with malignancy, tumor size, and CLNMs.

A cell is governed by the interaction of myriads of macromolecules. Inferring such a network of interactions has remained an elusive milestone in cellular biology. Building on recent advances in large foundation models and their ability to learn without supervision, we present scPRINT, a large cell model for the inference of gene networks pre-trained on more than 50 million cells from the cellxgene database. Using innovative pretraining tasks and model architecture, scPRINT pushes large transformer models towards more interpretability and usability when uncovering the complex biology of the cell. Based on our atlas-level benchmarks, scPRINT demonstrates superior performance in gene network inference to the state of the art, as well as competitive zero-shot abilities in denoising, batch effect correction, and cell label prediction. On an atlas of benign prostatic hyperplasia, scPRINT highlights the profound connections between ion exchange, senescence, and chronic inflammation.

Tumor growth and spread are sustained by the tumor microenvironment. Inflammatory cells and pathways have a fundamental role in the tumor microenvironment, driving or conditioning the functional activation of other leukocyte subsets and favoring evasion of anti-tumor immunity. One of the inflammatory pathways contributing to cancer-related inflammation is the complement system. Complement has long been considered an immune mechanism associated with immunosurveillance. More recently it emerged as a tumor promoting pathway, due to direct effects on cancer cells or indirect effects via immunosuppression driven by myeloid cells. The role of complement in cancer is complex and ambiguous, and depends on the tumor type and stage, as well as other factors including oncogenic drivers, leukocyte infiltration, interactions with other tumor microenvironment components or tumor cells. Other factors of complexity include the source of complement molecules, its canonical or non-canonical extracellular functions, its potential intracellular activation, and the interaction with other systems, such as the coagulation or the microbiome. Preclinical studies generally demonstrate the involvement of complement activation in smouldering inflammation in cancer and promotion of an immunosuppressive environment. These studies paved the way for clinical trials aimed at enhancing the potential of immunotherapy, in particular by targeting complement-dependent myeloid-sustained immunosuppression. However, the complex role of complement in cancer and the multiplicity of complement players may represent stumbling blocks and account for failures of clinical trials, and suggest that further studies are required to identify patient subsets who may benefit from specific complement molecule targeting in combination with conventional therapies or immunotherapy. Here, we will discuss the anti- or pro-tumor role of complement activation in cancer, focusing on the interactions of complement with immune cells within the tumor microenvironment, in particular the myeloid compartment. Furthermore, we will examine the potential of complement targeting in cancer treatment, particularly in the context of macrophage reprogramming.

With low early detection rates and high incidence and mortality, Gastrointestinal cancer (GIC) imposes a significant global health burden. Emerging evidence indicates that periodontitis may be a potential risk factor for GIC development; however, epidemiological data remains inconclusive.

This study aimed to examine the impact of periodontitis on the incidence, recurrence, and metastasis of GIC in Southwest China, thereby offering epidemiological evidence to support GIC prevention and management.

Between September 2022 and August 2024, a case-control study was conducted at the Affiliated Hospital of North Sichuan Medical College. Five hundred GIC patients were included as the case group based on the predefined inclusion and exclusion criteria, while 1005 healthy individuals were recruited for the control group. Multivariate analyses were performed to examine the associations between periodontitis and GIC incidence, recurrence, and metastasis while controlling for potential confounding factors.

The results of this study demonstrated that periodontitis was significantly associated with the incidence of esophageal, gastric, and colorectal cancer. Even after adjusting for potential confounders, it remained a significant risk factor for esophageal cancer (OR = 2.810, 95% CI 1.032-7.649, P = 0.043), colon cancer (OR = 2.330, 95% CI 1.072-5.067, P = 0.033), and rectal cancer (OR = 2.730, 95% CI 1.247-5.379, P = 0.012). Compared to non-periodontitis subjects, periodontitis showed a significant association with distant metastasis of rectal cancer (aHR = 5.332, 95% CI 1.406-20.220, P = 0.014). Moreover, severe periodontitis was identified as an risk factor for distant metastasis in rectal cancer (aHR = 10.138, 95% CI 1.824-56.354, P = 0.008).

This study highlights significant associations between periodontitis and an increased risk of esophageal and colorectal cancers. Additionally, patients with rectal cancer and periodontitis exhibited an increased risk of distant metastasis compared to those without periodontitis.

Emerging concerns link periodontitis to an array of cancers, notably thyroid cancer, though investigations into these associations are still in the nascent stages. This population-based study aimed to investigate the association of thyroid cancer with chronic periodontitis using Taiwan's Longitudinal Health Insurance Database 2010 (LHID2010).

This case-control study utilized LHID2010, selecting 2,775 patients diagnosed with thyroid cancer, matched with 8,325 controls based on age, sex, income, and the presence of diabetes, hypertension, hyperlipidemia, human papillomavirus infection, and tobacco use disorder using propensity-score matching. Multivariate logistic regression models were used to evaluate the association of thyroid cancer with chronic periodontitis.

A chi-squared analysis demonstrated a significant disparity in the prevalence of chronic periodontitis between those diagnosed with thyroid cancer and the controls, with prevalence rates of 38.5% and 24.1% respectively, and a p-value less than 0.001. The odds ratio (OR) for having prior chronic periodontitis among patients with thyroid cancer compared to controls was 1.991, with a 95% confidence interval (CI) of 1.816-2.184 and a p-value less than 0.001. The association was similar between sexes, yielding adjusted ORs of 1.991 (95% CI = 1.816∼2.184) for men and 1.962 (95% CI = 1.765-2.182) for women, indicating a statistically significant higher prevalence of chronic periodontitis in both male and female patients diagnosed with thyroid cancer compared to their control counterparts.

The findings highlight chronic periodontitis as a potential risk factor for thyroid cancer, underscoring the importance of integrated health surveillance and preventive strategies that encompass oral health.

This study aimed to explore the link between thyroid cancer and chronic periodontitis. Using Taiwan's Longitudinal Health Insurance Database 2010 (LHID2010), we selected 2,775 patients with thyroid cancer and matched them with 8,325 individuals without the disease based on age, sex, income, and other health conditions such as diabetes, hypertension, high cholesterol, HPV infection, and smoking habits. The study used statistical models to examine the relationship between thyroid cancer and chronic periodontitis. The findings showed that 38.5% of thyroid cancer patients had chronic periodontitis, compared to 24.1% of the control group. The odds of having chronic periodontitis were nearly twice as high in thyroid cancer patients. This pattern was consistent for both men and women. The study underscores the strong connection between chronic periodontitis and thyroid cancer, emphasizing the importance of raising public awareness about the potential risks of periodontitis.

Thyroid cancer is rapidly increasing worldwide, with some patients facing poor prognosis and recurrence despite current treatments. Chitosan-based nanoparticles have exhibited exciting antitumor efficacy both in vitro and in vivo, which indicates that there is vast scope of clinical application. This study develops a anhydride-modified chitosan and anhydride-modified chitosan‑silver nanoparticles, encapsulated in γ-cyclodextrin to help drug delivery by safe way and enhance thyroid cancer therapy.

5H pyrolo(3,4-b)pyrazin-5,7-(6H)-dione-6-(N-chitosanimide nanoparticle(composite constructed with nano silver (B1) was prepared and the optimized formula was further investigated regarding FT-IR, X-RD, SEM and TEM. Furthermore, it was encapsulated in γ-CD, and an in vivo study was conducted to investigate its anticancer activity. The binding affinities of 2,3-Pyrazinedicarboxylic anhydride to inhibitor of kappa B kinase beta (IKK-β) was demonstrated by molecular docking.

SEM and TEM revealed that Ag NPs were mostly uniformly incorporated into the 5H pyrolo(3,4-b)pyrazin-5,7-(6H)-dione 6-(N-chitosanimide nanoparticle, while FT-IR and X-RD findings verified the formation of 5H pyrolo(3,4-b)pyrazin-5,7-(6H)-dione-6-(N-chitosanimide nanoparticle)/composite constructed with nano silver and encapsulated in γ-CD (B2). γ-CD encapsulation induced a significant enhancement in pyrazine thyroid antitumor activity in xenografic model.

B2 could be considered a promising formula for suppression of thyroid cancer by modulating NF-κB signaling pathway, and hence, future studies could be planned to transfer our formula to the clinical field.

Lipid nanoparticles are obtaining significant attention in cancer treatment because of their efficacy at delivering drugs and reducing side effects. These things are like a flexible platform for getting anticancer drugs to the tumor site, especially upon HA modification, a polymer that is known to target tumors overexpressing CD44. HA is promising in cancer therapy because it taregtes tumor cells by binding onto CD44 receptors, which are often upregulated in cancer cells. Lipid nanoparticles are not only beneficial in improving solubility and stability of drugs; they also use the EPR effect, meaning they accumulate more in tumor tissue than in healthy tissue. Adding HA to these nanoparticles expands their biocompatibility and makes them more accurate and specific towards tumor cells. Studies show that HA-modified nanoparticles carrying drugs such as paclitaxel or doxorubicin improve how well cells absorb the drugs, reduce drug resistance, and make tumor shrinking. These nanoparticles can respond to tumor microenvironment stimuli in targeted delivery. This targeted delivery diminishes side effects and improves anti-cancer activity of drugs. Thus, lipid-based nanoparticles conjugated with HA are a promising way to treat cancer by delivering drugs effectively, minimizing side effects, and giving us better therapeutic results.

Oxidative stress and inflammation may initiate carcinogenesis and facilitate metastasis via activation of pro-inflammatory signaling network. The side product of arachidonic acid processing by cyclooxygenase-2 (COX-2), the prostaglandin E2 (PGE2), plays a key role in various metabolic disorders and during inflammation-mediated tumorigenesis. It has been demonstrated that PGE2 increases the proliferation, migration, invasion, metastasis, and resistance of cancer cells to apoptosis and other forms of programmed cell death. The expression level of PGE2 metabolizing enzyme 15-hydroxyprostaglandin dehydrogenase (15-PGDH) is often decreased in various malignancies. However, the role of 15-PGDH and PGE2 in the regulation of carcinogenesis remains controversial. Numerous cancer cell lines and mouse models have demonstrated the role of 15-PGDH as a tumor suppressor. Downregulation of 15-PGDH increased cancer cell proliferation, migration, anchorage independent growth, colony formation while overexpression reversed these effects, by inducing apoptosis and cell cycle arrest in vitro and in vivo. The expression of 15-PGDH is regulated by various mechanisms, including (a) epigenetic alterations (methylation of promoter region, histone deacetylases, microRNAs (miR-21, miR-26a/b, miR-106b-5p, miR-146b-3p, miR-155, miR-218-5p, and miR-620)); and (b) dysregulated oxidative stress and associated mediators (elevated levels of growth factors and proinflammatory cytokines (such as IL1β and TNFα)). Several transcription factors, such as HNF3β, β-catenin, Snail, Slug, can bind to 15-PGDH promoter region and downregulate the enzyme expression. In contrast, the expression of 15-PGDH can be upregulated by several anti-inflammatory cytokines and anti-cancer agents, such as IL10 and vitamin D. The functional activity of 15-PGDH protein can be modulated by signaling effectors and oxidative stress, including increased production of reactive oxygen species (ROS). However, the role of oxidative stress regulator protein, i.e., nuclear factor erythroid 2-related factor 2 (Nrf2), in the control of 15-PGDH expression remains unclear. This article provides insights and comprehensive overview of the tumor suppressor role of 15-PGDH in various cancers. Epigenetic and post-translational mechanisms regulating 15-PGDH expression and the role of novel ROS-Nrf2-15-PGDH axis were discussed and accented as potential drug targets.

Hashimoto's thyroiditis (HT) and papillary thyroid carcinoma (PTC) co-occurrence raises significant questions regarding the immune microenvironment and molecular mechanisms in thyroid tumor development. This review synthesizes recent literature to explore the immune microenvironment and molecular characteristics of PTC patients with HT, and to analyze how these characteristics influence disease onset, progression, and treatment. We focused on the immunological and molecular biological mechanisms underlying the interaction between HT and PTC, particularly the recruitment and activation of immune cells and alterations in key signaling pathways. Studies indicate that PTC with HT exhibits distinctive immune microenvironmental features, such as the role of regulatory T cells (Tregs), activation of the IFN-γ-mediated CXCR3A-CXCL10 signaling axis, and NF-κB pathway activation. Additionally, thyroid-stimulating hormone (TSH) stimulation, RET/PTC gene rearrangements, and changes in STAT6 and DMBT1 gene expression levels also play significant roles in PTC development. Notably, while HT may increase the risk of PTC, patients with concurrent HT tend to have better prognoses. Future research should further elucidate the complex interplay between these two diseases to prevent the transformation of HT into PTC and offer more personalized treatment plans for PTC patients, including considerations for preoperative thyroidectomy and lymph node dissection strategies, as well as postoperative TSH suppression therapy risk assessment. This review underscores the importance of a deeper understanding of HT and PTC interactions and offers new perspectives for future research directions and therapeutic strategies.

Anxiety and depression are common in many cancers but, to our knowledge, have not been systematically studied in patients with histiocytic neoplasms (HNs). We sought to estimate rates of anxiety and depression and identify clinical features and patient-reported outcomes (PROs) associated with anxiety and depression in patients with HNs. A registry-based cohort of patients with HNs completing PROs including the hospital anxiety and depression scale (HADS) from 2018 to 2023 was identified. Moderate or severe anxiety or depression were respectively defined as a score of ≥11 on the HADS anxiety or depression subscales. Associations of variables, including other validated PROs, with moderate or severe anxiety or depression were modeled with logistic regression to estimate odds ratios and 95% confidence intervals. In 215 patients, ∼1 in 3 met the criteria for anxiety or depression, and 1 in 7 met the criteria for moderate or severe anxiety or depression. These estimates remained stable over a 12-month trajectory. Rates of depression, but not anxiety, significantly differed across HN types, with patients with Erdheim-Chester disease experiencing the highest rate. In addition, neurologic involvement, unemployment, and longer undiagnosed illness interval were significantly associated with increased risk of depression. Financial burden, financial worry, and severe disease-related symptoms were correlated with increased risk of both anxiety and depression. Conversely, increased general and cognitive health-related quality of life (HRQoL) were correlated with decreased risk of both anxiety and depression. In patients with HN, anxiety and depression are prevalent, stable over time, and correlated with financial burden, symptom severity, and HRQoL. This trial was registered at www.clinicaltrials.gov as #NCT03329274.

Vascular cell adhesion molecule (VCAM)-1 has garnered significant research attention due to its potential as a disease biomarker and drug target across several inflammatory pathologies-including atherosclerosis, asthma, rheumatoid arthritis, and inflammatory bowel disease (IBD). The VCAM-1 protein has also been noted for its functional involvement in cancer metastasis and drug resistance to conventional chemotherapeutics. Although the anti-inflammatory and anti-cancer facets of VCAM-1 antagonisation have been examined separately, there is yet to be a review that explicitly addresses the functional interrelationship between these mechanisms. Furthermore, the pleiotropic mechanisms of anti-VCAM-1 therapies may present a useful paradigm for designing drug candidates with synergistic anti-inflammatory and anti-tumorigenic effects. The pathological overlap between inflammatory bowel disease (IBD) and colitis-associated colorectal cancer (CRC) serves as the quintessential disease model to observe this therapeutic duality. This review thereby details the adhesive mechanisms of VCAM-1 in colorectal disease-specifically, driving immune cell infiltration during IBD and tumour cell metastasis in CRC-and posits the potential of this receptor as a common drug target for both diseases. To explore this hypothesis, the current progress of novel VCAM-1-directed drug candidates in experimental models of IBD and CRC is also discussed.

Epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) are standard therapies for EGFR-mutated non-small-cell lung cancer (NSCLC); however, their efficacy is inconsistent. Secondary mutations in the EGFR or other genes that lead to resistance have been identified, but resistance mechanisms have not been fully identified. Chromosomal instability (CIN) is a hallmark of cancer and results in genetic diversity. In this study, we demonstrated by transcriptomic analysis that CIN activates the cGAS-STING signaling pathway, which leads to EGFR-TKI refractoriness in a subset of EGFR-mutated NSCLC patients. Furthermore, EGFR-mutated H1975dnMCAK cells, which frequently underwent chromosomal mis-segregation, demonstrated refractoriness to the EGFR-TKI osimertinib compared to control cells. Second, H1975dnMCAK cells exhibited activation of cGAS-STING signaling and its downstream signaling, including tumor-promoting cytokine IL-6. Finally, chromosomally unstable EGFR-mutated NSCLC exhibited enhanced epithelial-mesenchymal transition (EMT). Blockade of cGAS-STING-TBK1 signaling reversed EMT, resulting in restored susceptibility to EGFR-TKIs in vitro and in vivo. These results suggest that CIN may lead to the activation of cGAS-STING signaling in some EGFR-mutated NSCLC, resulting in EMT-associated EGFR-TKI resistance.

The stability of messenger RNA (mRNA) is controlled by proteins that bind to adenosine-uridine-rich sequences (AREs) in their 3' untranslated regions (3'UTR), known as AU-binding proteins. One of these proteins is tristetraprolin (TTP; encoded by Zfp36), which promotes degradation of mRNAs with AREs in their 3'UTR. TTP accelerates the decay of its target transcripts, many of which encode proinflammatory mediators that promote tumorigenesis. TTP underexpression has been reported in multiple cancer types. Oral squamous cell carcinoma is an aggressive disease characterized by high morbidity and few therapeutic options. The role of TTP has not been studied in oral epithelium homeostasis nor in its carcinogenesis. Herein, using tissue-specific TTP knockout mice (TTP-KO), we show that TTP expression is relevant for oral epithelium homeostasis. TTP-KO mice developed dysplastic lesions in the tongue along with inflammatory infiltrates in the connective tissue. Analysis of the inflammatory infiltrate revealed the presence of mast cells (MCs), CD45+ cells, and CD11b+ cells, with the MCs being the most abundant cell type and associated with cyclooxygenase-2 expression. Recruitment of MCs was dependent on tumor necrosis factor-α (TNFα) upon TTP ablation in the tongue. Although the infiltration of MCs was dependent on TNFα activity, this did not affect the development of tongue dysplasia. We analyzed the status of the NF-κB pathway, finding its activation. In addition, we demonstrate that K-ras activation combined with Zfp36 deletion leads to the rapid onset of the oral tongue phenotype and significantly reduces mouse survival. Our results support the notion that TTP expression protects against oral carcinogenesis, regulates the inflammatory infiltrate, and maintains the epithelial microenvironment, potentially serving as a barrier to tumorigenesis.

The intricate relationship between cancer, circadian rhythms, and aging is increasingly recognized as a critical factor in understanding the mechanisms underlying tumorigenesis and cancer progression. Aging is a well-established primary risk factor for cancer, while disruptions in circadian rhythms are intricately associated with the tumorigenesis and progression of various tumors. Moreover, aging itself disrupts circadian rhythms, leading to physiological changes that may accelerate cancer development. Despite these connections, the specific interplay between these processes and their collective impact on cancer remains inadequately explored in the literature. In this review, we systematically explore the physiological mechanisms of circadian rhythms and their influence on cancer development. We discuss how core circadian genes impact tumor risk and prognosis, highlighting the shared hallmarks of cancer and aging such as genomic instability, cellular senescence, and chronic inflammation. Furthermore, we examine the interplay between circadian rhythms and aging, focusing on how this crosstalk contributes to tumorigenesis, tumor proliferation, and apoptosis, as well as the impact on cellular metabolism and genomic stability. By elucidating the common pathways linking aging, circadian rhythms, and cancer, this review provides new insights into the pathophysiology of cancer and identifies potential therapeutic strategies. We propose that targeting the circadian regulation of cancer hallmarks could pave the way for novel treatments, including chronotherapy and antiaging interventions, which may offer important benefits in the clinical management of cancer.

Extraction and fractionation of Barleria trispinosa growing in Saudi Arabia yielded four iridoid compounds identified by spectroscopic techniques as acetylbarlerin (1), barlerin (2), shanzhiside methyl ester (3) and 6-⍺-L-rhamnopyranosyl-8-O-acetylshanzihiside methyl ester (4). Preliminary experiments confirmed that compound 1 acts as an inducer of chemopreventive NAD(P)H:Quinone oxidoreductase 1 (NQO1) enzymatic activity in a murine hepatoma (Hepa1c1c7) chemoprevention model. It also demonstrated the ability to inhibit the lipopolysaccharides (LPS)-induced nitric oxide (NO) production in the RAW264.7 macrophage model. Western blotting revealed the ability of compound 1 to up-regulate the protein expression of the NQO1 marker. Furthermore, compound 1 elicited NO suppression in RAW264.7 macrophages by inhibiting iNOS protein expression. Molecular docking and molecular simulation studies of 1 supported its experimental results as an inhibitor of the nuclear factor erythroid 2-Kelch-like ECH-associated protein 1 (Nrf2-KEAP1) complex, resulting in Nrf2-mediated induction of chemopreventive NQO1.Communicated by Ramaswamy H. Sarma.

Uveal melanoma (UM) is a rare disease, with the highest incidence in people with fair skin and light eyes. Eye color is largely genetically determined and is defined by a set of single nucleotide polymorphisms (SNPs). We set out to determine whether we could identify a SNP related to prognosis.

We sequenced DNA from peripheral blood mononuclear cells of 392 patients with UM and obtained the genotype of 6 common eye color-related SNPs. Clinical and histopathologic tumor characteristics, tumor chromosome status, and patient survival were compared among patients with different genotypes.

Three hundred ninety-two patients who underwent enucleation for UM at the Leiden University Medical Center, Leiden, The Netherlands.

We isolated DNA from peripheral blood leukocytes of 392 patients with UM and performed sequencing, using 6 eye color SNPs from the HIrisPlex-S assay (Erasmus MC, Walsh lab). The genotypes extracted from the sequencing data were uploaded onto the HIrisPlex webtool (https://hirisplex.erasmusmc.nl/) for eye color prediction. We tested the association of eye color SNPs with tumor characteristics and chromosome aberrations using Pearson's chi-square test and the Mann-Whitney U test and evaluated survival with Kaplan-Meier curves with the log-rank test and Cox regression.

Uveal melanoma-related survival.

Of 392 patients with analyzable genotype data, 307 patients (78%) were assigned blue eyes, 74 patients (19%) were assigned brown eyes, and 11 patients (3%) could not be assigned to either blue or brown. Patients with a genetically blue eye color showed worse survival (P = 0.04). This was related to 1 genotype: patients with the G/G genotype of rs12913832 (HERC2), which codes for blue eye color showed a worse prognosis (P = 0.017) and more often had high-risk tumors (monosomy of chromosome 3; P = 0.04) than in patients with an A/G or A/A genotype.

The G/G genotype of rs12913832 (HERC2), which is related to blue eye color, not only is a genetic factor related to the risk of UM develop, but also is linked to a worse prognosis because of an association with a higher risk of a high-risk UM developing (carrying monosomy of chromosome 3).

The author(s) have no proprietary or commercial interest in any materials discussed in this article.

Herein, nine square planar trans-arylbis(triphenylphosphine)palladium halides (PdX(PPh3)2Ar) were synthesized and fully characterized. The molecular structure of two complexes (1 and 2) have been determined by both X-ray diffraction and described thanks to Hirshfeld surface analysis. Investigation of the antioxidant activities showed that most of the complexes exhibit a strong dose-dependent radical scavenging activity towards DPPH radical as well as in the ABTS radical scavenging test. Complexes 1 [PdI(PPh3)2(4-MeOC6H4)] and 3 [PdCl(PPh3)2(4-MeOC6H4)] showed the highest activity in the DPPH assay with EC50 values of 1.14 ± 0.90 and 1.9 ± 0.87 µM, respectively. In contrast, for the ABTS assay, quercetin (5.56 ± 0.97 µM) was slightly more efficient than the three complexes 1 (5.78 ± 0.98 µM), 2 (7.01 ± 0.98 µM), and 3 (11.12 ± 0.94 µM). The use of kinetic studies as a powerful parameter shows that complexes 1, 2, and 3 displayed the best antioxidant efficiency. The antioxidant effect of the nine palladium complexes has been also evaluated on the enzyme-catalyzed oxidation of the L012 probe (using HRP/H2O2) by using a chemiluminescence technique. As with the last model, complexes 1, 2, and 3 showed the best activity, with EC50 values of 3.56 ± 1.87, 148 0.71, and 5.8 ± 2.60 µM, respectively. Interestingly, those complexes (1, 2, and 3) even exhibited a higher dose-dependent activity than the quercetin (7.06 ± 2.56 µM) used as a standard. Taken together, the combined results reveal that the antiradical and enzyme (HRP) inhibitory activity of complexes decrease following the ligand order of p-OMePh > p-OAcPh >> Ph.

Physical exercise is an essential component of human health. In recent years, scientific research has focused on identifying natural compounds and formulating new supplements aimed at enhancing athletic performance, accelerating muscle recovery, and minimizing the damage caused by physical exertion. The use of antioxidants to counteract the formation of reactive oxygen species (ROS) following physical activity (PA) is already a widely adopted practice. Resveratrol (RES), a polyphenol belonging to the stilbene class, is well known for its potent antioxidant activity and anti-inflammatory effects primarily attributed to the activation of sirtuins. RES possesses multiple nutraceutical properties used for the prevention and treatment of inflammatory, cardiovascular, neoplastic, and infectious diseases, thus attracting attention to study its use in combination with physical exercise to promote well-being. Animal trials combining RES and PA have mainly reported improvements in muscle, energy, and cardiovascular functions. The data presented and discussed in this narrative review are from Pubmed, Scopus, and the Human Gene Database (search limited to 2011 to 2025 with the keywords RES, sirtuins, and physical activity altogether or in combination with each other). This review gathers several studies on RES focusing on its nutraceutical properties, epigenetic activities via sirtuins, and the potential benefits of combining RES with PA in maintaining health and well-being based on trials performed first in animals and later in humans. Human studies have been conducted on various populations, including active adults, sedentary individuals, patients with diseases, and elderly individuals. Some studies have confirmed the benefits of RES observed in animal experiments. However, in some cases, no substantial differences were found between RES supplementation and the control group. In conclusion, the benefits of RES on PA reported in the literature are still not fully evident, given the contrasting studies and the still limited number of trials, but both RES and PA are successful tools for the maintenance of health and wellbeing.

As one part of the innate immune response to external stimuli, chronic inflammation increases the risk of various cancers, and tumor-promoting inflammation is considered one of the enabling characteristics of cancer development. Recently, there has been growing evidence on the role of anti-inflammation therapy in cancer prevention and treatment. And researchers have already achieved several noteworthy outcomes. In the review, we explored the underlying mechanisms by which inflammation affects the occurrence and development of cancer. The pro- or anti-tumor effects of these inflammatory factors such as interleukin, interferon, chemokine, inflammasome, and extracellular matrix are discussed. Since FDA-approved anti-inflammation drugs like aspirin show obvious anti-tumor effects, these drugs have unique advantages due to their relatively fewer side effects with long-term use compared to chemotherapy drugs. The characteristics make them promising candidates for cancer chemoprevention. Overall, this review discusses the role of these inflammatory molecules in carcinogenesis of cancer and new inflammation molecules-directed therapeutic opportunities, ranging from cytokine inhibitors/agonists, inflammasome inhibitors, some inhibitors that have already been or are expected to be applied in clinical practice, as well as recent discoveries of the anti-tumor effect of non-steroidal anti-inflammatory drugs and steroidal anti-inflammatory drugs. The advantages and disadvantages of their application in cancer chemoprevention are also discussed.

Cervical cancer, ranking as the fourth most common cancer in women globally, is closely linked to chronic inflammation resulting from persistent human papillomavirus (HPV) infection. Chronic inflammation mediated by cyclooxygenase (COX) has been identified as a factor in cancer onset and progression, with HPV oncoproteins E6 and E7 inducing COX activation. Nonsteroidal anti-inflammatory drugs (NSAIDs) have demonstrated the capability to significantly inhibit COX activity, playing a crucial preventive and therapeutic role in various tumors. This paper explores the therapeutic value and potential clinical applications of NSAIDs in cervical cancer by examining the mechanistic interactions between HPV and COX and the carcinogenic effects of COX in cervical cancer.

Burn-induced sepsis is a critical clinical challenge marked by systemic inflammation, immune dysregulation, and high mortality. Macrophage-driven inflammatory pathways are central to sepsis pathogenesis, while immune cell metabolic reprogramming plays a key role in both sepsis and cancer progression.

Bioinformatics analyses using GEO, TCGA, and GTEx datasets identified MLIP-modulated genes linked to immune responses and prognosis. In vitro, LPS-stimulated HUVEC cells were used to study MLIP's effects on inflammation and macrophage function through cell viability, ROS levels, cytokine expression, qRT-PCR, and immunofluorescence assays.

MLIP-modulated genes were associated with immune-related metabolic pathways in both sepsis and cancer. Epigenetic analysis showed MLIP expression is regulated by promoter methylation and chromatin accessibility. Prognostic analyses revealed MLIP's impact on survival outcomes across cancer types. In vitro, MLIP reduced inflammation, oxidative stress, and macrophage hyperactivation.

MLIP regulates immune-metabolic dynamics in burn-induced sepsis, influencing macrophage activity and oxidative stress. Its role in metabolic reprogramming suggests MLIP as a potential therapeutic target linking immune modulation and cancer progression. Further research on MLIP's role in immune evasion and tumor metabolism may inform novel therapeutic strategies.

This study aims to explore the relationship between body adipose tissue characteristics and clinical outcomes in cancer patients receiving immune checkpoint inhibitor (ICI) therapy.

We conducted an extensive literature search across three major online databases-Embase, PubMed, and the Cochrane Library-to identify studies examining the link between body adipose tissue and treatment outcomes in cancer patients undergoing ICI therapy, from the inception of each database until February 20, 2024. The quality of the included studies was evaluated using the Newcastle-Ottawa Scale. The primary outcomes analyzed were hazard ratios (HRs) for overall survival (OS) and progression-free survival (PFS), as well as odds ratios (ORs) for disease control rate (DCR). Pooled estimates and 95% confidence intervals (CIs) were calculated.

A total of 23 studies were included, encompassing 2741 cancer patients. The analysis revealed that patients with higher levels of visceral adipose tissue (VAT) exhibited significantly improved OS (HR: 0.72, 95% CI: 0.59-0.89, p < 0.001) and PFS (HR: 0.80, 95% CI: 0.67-0.96, p = 0.015), along with a higher DCR (OR: 1.81, 95% CI: 1.26-2.60, p = 0.001), compared to those with lower VAT levels. Additionally, increased subcutaneous adipose tissue (SAT) levels were associated with significantly better OS (HR: 0.69, 95% CI: 0.58-0.82, p < 0.001) and PFS (HR: 0.82, 95% CI: 0.68-1.00, p = 0.049), and a higher DCR (OR: 1.99, 95% CI: 1.15-3.44, p = 0.014). Elevated total adipose tissue (TAT) levels were also linked to longer OS (HR: 0.73, 95% CI: 0.55-0.97, p = 0.028). However, a higher visceral-to-subcutaneous adipose tissue ratio (VSR) was associated with a shorter OS (HR: 1.43, 95% CI: 1.09-1.87, p = 0.010). No significant relationship was found between TAT (HR: 0.81, 95% CI: 0.54-1.23, p = 0.332) and VSR (HR: 1.20, 95% CI: 0.95-1.51, p = 0.131) with PFS in ICI-treated patients.

This study highlights the prognostic relevance of VAT and SAT in predicting treatment response and survival outcomes in cancer patients receiving ICIs. These findings suggest that assessments of VAT and SAT should be incorporated into prognostic evaluations for this patient population.

Immune status critically affects cancer progression and therapy responses. This study aimed to identify plasma proteome changes in immunosuppressive cancer and potential biomarkers predicting systemic immunosuppression. Mouse models of syngeneic breast tumors (benign 67NR and malignant 4T1) were used to collect plasma samples. Plasma samples from naive mice and both early- and late-stage tumor-bearing mice were subjected to liquid chromatography-mass spectrometry (LC-MS) analysis. 4T1-bearing mice showed systemic immunosuppression characterized by significant generation of myeloid-derived suppressor cells (MDSCs) as early as 7 days after tumor implantation, unlike 67NR tumors. LC-MS identified 1086 proteins across the five experimental groups, with 27 proteins showing group-specific expression in 4T1 blood compared with 67NR blood. Immune-related proteins osteopontin, lactotransferrin, calreticulin, and peroxiredoxin 2 were selected as potential biomarkers of MDSC-producing breast cancer. These markers were expressed in cancer cells or MDSC in the 4T1 model, and osteopontin and peroxiredoxin 2 were associated with low survival probability and high recurrence in patients with triple-negative breast cancer. Our findings suggest that MDSC-producing immunosuppressive cancers have unique plasma proteomes, offering additional insights into cancer immune status.

To investigate the relationship between obesity and Microsatellite Instability (MSI) in endometrial cancer (EC), determine which mismatch repair (MMR) protein loss is influenced by obesity, and assess the correlation between BMI and MSI probability.

This retrospective cohort study included 89 endometrial cancer patients treated at the Gynaecologic oncology unit of the University of Campania "Luigi Vanvitelli" from August 2023 to October 2024, and stratified by BMI: normal weight (n = 26), overweight (n = 31), obese (n = 26), and severely obese (n = 6). Microsatellite instability (MSI) was determined through immunohistochemical assessment of mismatch repair (MMR) protein expression: MLH1, PMS2, MSH2, and MSH6. Tumors were considered MSI if at least one of the four MMR proteins showed loss of expression. Univariate and multivariate logistic regression models were constructed to evaluate the correlation between BMI and MSI RESULTS: 89 patients were enrolled. Obese and severely obese groups showed significantly higher MSI rates (50 % each) compared to normoweight (12 %) and overweight (29 %) groups (P = .013). MLH1 and PMS2 loss of expression were significantly higher in obese and severely obese women (MLH1: P = .003; PMS2: P = .014). Univariate logistic regression showed a significant positive correlation between BMI and MSI (OR 1.02, 95 % CI 1.01-1.04, P = .007). In multivariate analysis, adjusting for grading, stage, histotype, and age, BMI maintained a significant positive correlation with MSI (OR 1.02, 95 % CI 1.01-1.04, P = .048).

This study demonstrates a significant association between obesity and MSI in EC, particularly affecting MLH1 and PMS2 expression. The findings suggest that obesity may contribute to EC development also through MMR deficiency.

The gut microbiome, a complex community of trillions of microorganisms in the intestines, is crucial in maintaining human health. Recent advancements in microbiome research have unveiled a compelling link between the gut microbiome and cancer development and progression. Alterations in the composition and function of the gut microbiome, known as dysbiosis, have been implicated in various types of cancer, including, esophageal, liver, colon, pancreatic, and gastrointestinal. However, the specific gut microbial strains associated with the development or progression of cancers in various tissues remain largely unclear. Here, we summarize current research findings on the gut microbiome of multiple cancers. This review aims to identify key gut microbial targets that closely influence cancer development based on current research findings. To accurately evaluate the effectiveness of the gut microbiome as a clinical tool for cancer, further research is needed to explore its potential as a biomarker and therapeutic strategy.

Djon Djon is a particularly special black mushroom indigenous to Haiti that has a long history in both their cuisine and in traditional medicine. Centuries of folkloric utilization of theses "medicinal" botanicals tend to indicate the presence of a potentially efficacious western medicine entity.

With the advantages afforded by both traditional medicines and fermentation, we endeavored to investigate if fermentation of Djon Djon mushrooms can provide skin care benefits.

In this study, active Djon Djon fermentation broth (DDF) was obtained using Saccharomyces, and anti-inflammatory efficacy was assessed in cultured systems using human keratinocytes and fibroblasts, exposed to either UVB or H2O2 respectively. In addition, RNA-Seq technology was employed to further characterize the mechanisms of DDF following ultraviolet irradiation.

Characterization of the DDF displayed a high number of polysaccharides and peptides present following fermentation, that function to scavenge intracellular ROS, decrease MDA content, while increasing the levels of CAT, COL-I, and HA in HSF induced by H2O2. In addition, levels of pro-inflammatory factors (IL-6, IL-1β, and TNF-α) were decreased in UVB irradiated HaCaT cells that had been treated with DDF. Analysis of cellular RNA indicated that DDF altered the DEGs involved in the AGE-RAGE signaling pathway suggesting that this signaling cascade is inhibited by DDF. Additionally, DDF also influenced the metabolism of arachidonic acid, histidine, and phenylalanine, which are involved in inflammatory processes.

DDF can alleviate oxidative stress damage caused by hydrogen peroxide and photodamage caused by UVB, and the mechanism by which DDF protects skin cells is revealed, displaying the potential benefits of fermented DjonDjon in skincare.