While severe postoperative complications (SPCs) impact cancer prognosis, their effect on locally advanced esophageal squamous cell carcinoma (ESCC) patients with varying immunonutritional statuses after minimally invasive esophagectomy (MIE) is unclear.

This retrospective study analyzed 442 patients with locally advanced ESCC who underwent MIE, investigating the relationship between SPCs and survival based on preoperative immunonutritional status, determined by the prognostic nutritional index (PNI). Nomograms were developed for patients with preserved immunonutritional status using Cox regression, and their performance was assessed.

Of the patients, 102 (23.1%) experienced SPCs after MIE. Five-year overall survival (OS) and disease-free survival (DFS) were significantly different between SPCs and non-SPCs groups (p < 0.001). In the preserved immunonutritional group, SPCs significantly reduced 5-year OS (p = 0.008) and DFS (p = 0.011), but not in the poor immunonutritional group (OS p = 0.152, DFS p = 0.098). Multivariate Cox regression identified SPCs as an independent risk factor for OS (HR = 1.653, p = 0.013) and DFS (HR = 1.476, p = 0.039). A nomogram for predicting OS and DFS in preserved immunonutritional patients demonstrated excellent performance.

SPCs significantly affect prognosis in ESCC patients with preserved immunonutritional status after MIE. Nomograms based on SPCs can predict OS and DFS in these patients.

Polysaccharides from algae provide a range of biology and health benefits. Lately, there has been a significant interest in how algal polysaccharides affect the immune microenvironment around tumors.

To elucidate the subtle interactions between algal polysaccharides and the tumor immune microenvironment to further understand the medicinal potential of algal polysaccharides.

To give a summary of the sources, bioactivities and characteristics of the tumor immune microenvironment of algal polysaccharides, and to analyze alteration of the immunological milieu surrounding tumors by algal polysaccharides and their potential as immunomodulators of chemotherapeutic agents.

Search popular academic search engines using selected keywords for articles ending before September 2024 using selected keywords Google Scholar, PubMed, ScienceDirect, Scopus, Web of Science, Springer, and official websites.

Algal polysaccharides can fight tumors by changing how immune cells work and affecting inflammation in different ways. Moreover, algal polysaccharides have shown promise in mitigating the adverse effects associated with conventional cancer treatments, such as chemotherapy. Algal polysaccharides, through their immunomodulatory effects, can alleviate some of these side effects, leading to an enhanced overall treatment outcome.

As research continues to uncover the underlying mechanisms of their antitumor effects, algal polysaccharides are poised to become a vital component in the development of novel cancer treatments, providing new hope for patients and advancing the field of oncology.

To develop a deep learning-based method for robust and rapid estimation of the fatty acid composition (FAC) in mammary adipose tissue.

A physics-based unsupervised deep learning network for estimation of fatty acid composition-network (FAC-Net) is proposed to estimate the number of double bonds and number of methylene-interrupted double bonds from multi-echo bipolar gradient-echo data, which are subsequently converted to saturated, mono-unsaturated, and poly-unsaturated fatty acids. The loss function was based on a 10 fat peak signal model. The proposed network was tested with a phantom containing eight oils with different FAC and on post-menopausal women scanned using a whole-body 3T MRI system between February 2022 and January 2024. The post-menopausal women included a control group (n = 8) with average risk for breast cancer and a cancer group (n = 7) with biopsy-proven breast cancer.

The FAC values of eight oils in the phantom showed strong correlations between the measured and reference values (R2 > 0.9 except chain length). The FAC values measured from scan and rescan data of the control group showed no significant difference between the two scans. The FAC measurements of the cancer group conducted before contrast and after contrast showed a significant difference in saturated fatty acid and mono-unsaturated fatty acid. The cancer group has higher saturated fatty acid than the control group, although not statistically significant.

The results in this study suggest that the proposed FAC-Net can be used to measure the FAC of mammary adipose tissue from gradient-echo MRI data of the breast.

Prostate cancer (PCa) is globally the second most diagnosed malignancy in men, with >1.5 million new cases reported in 2020. Given the limitations of classical detection methods, the discovery of new predictive PCa biomarkers is critical. MicroRNAs (miRs), which are small, single-stranded, non-coding RNA molecules, have emerged as potential biomarkers for cancer diagnosis and prognosis. The present study aimed to evaluate the diagnostic value of miR-21 and miR-221 in PCa and their association with clinicopathological parameters. The expression of miR-21 and miR-221 was assessed using reverse transcription-quantitative PCR in 50 tumour and 50 control tissue samples. The results demonstrated that miR-21 and miR-221 were significantly upregulated in PCa tissues compared with that of the normal control tissues. Receiver operating characteristic curve analysis revealed that miR-21 had an area under the curve (AUC) of 0.90, with a sensitivity of 70% and a specificity of 96%. Similarly, miR-221 demonstrated an AUC of 0.89, with a sensitivity of 86% and a specificity of 78%. High expression of miR-21 and miR-221 was also demonstrated to be associated with higher Gleason scores and advanced tumour stages. The findings of the present study indicate the potential role of miR-21 and miR-221 as biomarkers in the diagnosis of PCa. However, further studies in non-invasive samples such as serum, blood and urine are needed to support the results of the present study.

The C-Reactive Protein (CRP)-Albumin-Lymphocyte (CALLY) index is an established immuno-nutritional scoring system. We screened relevant literature from the major databases up until May, 2024, and extracted the data for analysis. A total of 2829 gastric cancer (GC) patients from six studies were included in this meta-analysis, the results of which revealed that the CALLY index was an independent prognostic factor for OS and RFS in both univariate analyses and multivariate analyses, and that a high CALLY index was a favorable prognostic factor. Moreover, GC patients in the high CALLY index group seemed to have better 5-year OS and 5-year RFS than those in the low CALLY index group. There was a higher proportion of patients with T1 status in the high CALLY index group than in the low CALLY index group. However, the opposite results were found in the analyses of lymph node metastasis positivity, lymph-vascular invasion positivity, postoperative complications, differentiated histological type, anastomotic leakage, and adjuvant chemotherapy. The present meta-analysis concluded that the CALLY index was a simple and useful independent prognostic biomarker for GC patients after gastrectomy.

Adipose tissue is an immunologically active organ that controls host physiology, partly through the release of mediators termed adipokines. In obesity, adipocytes and infiltrating leukocytes produce adipokines, which include the hormones adiponectin and leptin and cytokines such as tumour necrosis factor and IL-1β. These adipokines orchestrate immune responses that are collectively referred to as metabolic inflammation. Consequently, metabolic inflammation characterizes metabolic disorders and promotes distinct disease aspects, such as insulin resistance, metabolic dysfunction-associated liver disease and cardiovascular complications. In this unifying concept, adipokines participate in the immunological cross-talk that occurs between metabolically active organs in metabolic diseases, highlighting the fundamental role of adipokines in obesity and their potential for therapeutic intervention. Here, we summarize how adipokines shape metabolic inflammation in mice and humans, focusing on their contribution to metabolic disorders in the setting of obesity and discussing their value as therapeutic targets.

Mesenchymal stem cells (MSCs), due to their tumor-targeting homing properties, are present in the tumor microenvironment (TME) and influence the biological behaviors of tumors. The purpose of this paper is to establish a signature based on the MSC secretome to predict the prognosis and treatment of bladder cancer (BLCA).

The presence of MSCs in BLCA was validated through flow cytometry and multiplex fluorescence immunohistochemistry (mFIHC), and the relationships between MSCs and clinical characteristics were explored. Unsupervised clustering analysis was performed on BLCA according to the differential proteins detected in MSC-conditioned medium (MSCCM) using a cytokine array. Using the TCGA-BLCA, GSE32548, and GSE32894 datasets as background data, a risk signature was constructed according to the differential proteins in MSCCM through machine learning. For the risk groups with high and low prognoses, we calculated Kaplan-Meier (K-M) curves. Additionally, we explored the relationships between the signature and the tumor immune landscape, response to immunotherapy, and chemotherapy drugs.

Both flow cytometry and mFIHC confirmed the presence of MSCs in bladder tumors, and clinical samples revealed correlations between MSCs and the pathological grade, T stage, and Ki67 in BLCA. Based on differential proteins and unsupervised clustering analysis, BLCA patients were divided into two groups, and significant differences were found between these groups in terms of TME, immune response, and clinical treatments. Using machine learning, a signature was constructed with the combination algorithm Stepcox (both) + plsRcox, revealing significant survival differences between the high- and low-risk MSC groups. Regression analyses, along with ROC curves, further demonstrated that risk score independently predict the prognosis of patients with high predictive performance. Moreover, there were notable differences between the high- and low-risk groups in terms of the TME scores, immune infiltration, and immune checkpoints. For BLCA immunotherapy, the low-risk group suggested better efficacy, while conventional chemotherapy drugs such as gemcitabine and cisplatin might be less effective in the low-risk group.

The signature based on MSC secreted protein profiles could effectively predict the prognosis of BLCA and provided valuable guidance for treatment and drug resistance.

The ketogenic diet (KD) has attracted attention in recent years for its potential anticancer effects. KD is a dietary structure of high fat, moderate protein, and extremely low carbohydrate content. Originally introduced as a treatment for epilepsy, KD has been widely applied in weight loss programs and the management of metabolic diseases. Previous studies have shown that KD can potentially inhibit the growth and spread of cancer by limiting energy supply to tumor cells, thereby inhibiting tumor angiogenesis, reducing oxidative stress in normal cells, and affecting cancer cell signaling and other processes. Moreover, KD has been shown to influence T-cell-mediated immune responses and inflammation by modulating the gut microbiota, enhance the efficacy of standard cancer treatments, and mitigate the complications of chemotherapy. However, controversies and uncertainties remain regarding the specific mechanisms and clinical effects of KD as an adjunctive therapy for cancer. Therefore, this review summarizes the existing research and explores the intricate relationships between KD and cancer treatment.

Tumor-associated macrophages (TAMs) play crucial roles in development and progression of malignant diseases. Notably, CD163+ TAMs likely perform specific pro-tumorigenic functions, suggesting that this subset may serve as both prognostic biomarkers and targets for future anti-cancer therapy. We conducted a scoping review to map the current knowledge on the prognostic role of CD163+ TAMs in the five most lethal cancers worldwide: Lung, colorectal, gastric, liver, and breast cancer. For all cancer types, most studies showed that high tumoral presence of CD163+ cells was associated with poor patient outcome, and this association was more frequently observed when CD163+ cells were measured at the tumor periphery compared to more central parts of the tumor. These results support that CD163+ TAMs represent a biomarker of poor patient outcome across a variety of solid tumors, and highlight the relevance of further investigations of CD163+ TAMs as targets of future immunotherapies.

Colorectal cancer (CRC) is the world's third most frequent cancer, and both its incidence and fatality rates are rising. Despite various therapeutic approaches, neither its mortality rate nor its recurrence frequency has decreased significantly. Additionally, conventional treatment approaches, such as chemotherapy and radiotherapy, have several side effects and risks for patients with CRC. Accordingly, the need for alternative and effective treatments for CRC patients is critical. Immunotherapy that utilizes dendritic cells (DCs) harnesses the patient's immune system to combat cancer cells effectively. DCs are the most potent antigen-presenting cells (APCs), which play a vital role in generating anti-cancer T cell responses. A significant barrier to the immune system's ability to eliminate CRC is the establishment of a potent immunosuppressive tumor milieu by malignant cells. Since DCs are frequently defective in this milieu, the tumor setting significantly reduces the effectiveness of DC-based therapy. Determining central mechanisms contributing to tumor growth by unraveling and comprehending the interaction between CRC tumor milieu and DCs may lead to new therapeutic approaches. This study aims to review DC biology and discuss its role in T-cell-mediated anti-tumor immunity, as well as to highlight the immunosuppressive effects of the CRC tumor milieu on the function of DCs. We will also highlight the tumor microenvironment (TME)-related factors that interfere with DC function as a possible therapeutic target to enhance DC-based cell therapy efficacy.

Increasing evidence has showed that tumorigenesis is closely linked to inflammation, regulated by multiple signaling pathways. Among these, the cyclooxygenase-2/prostaglandin E2 (COX-2/PGE2) axis plays a crucial role in the progression of both inflammation and cancer. Inhibiting the activity of COX-2 can reduce PGE2 secretion, thereby suppressing tumor growth. Therefore, COX-2 inhibitors are considered potential therapeutic agents for cancers. However, their clinical applications are greatly hindered by poor physicochemical properties and serious adverse effects. Fortunately, the advent of nanotechnology offers solutions to these limitations, enhancing drug delivery efficiency and mitigating adverse effects. Given the considerable progress in this area, it is timely to review emerging COX-2 inhibitors-based nanotherapeutics for cancer diagnosis and therapy. In this review, we first outline the various antineoplastic mechanisms of COX-2 inhibitors, then comprehensively summarize COX-2 inhibitors-based nanotherapeutics for cancer monotherapy, combination therapy, and diagnosis. Finally, we highlight and discuss future perspectives and challenges in the development of COX-2 inhibitors-based nanomedicine.

Classical myeloproliferative neoplasms (MPN) are clonal stem cell disorders characterized by driver mutations that affect the constitutive activation of JAK-signaling. Mutations additional to an MPN-driver occur in a large number of patients and have been shown be associated with disease presentation and progression. In this review, we outline the current hypotheses regarding how clonal evolution in MPN is thought to occur and the functional mechanisms as to how concomitant somatic mutations (i.e., mutations in genes other than the 'driver' genes) contribute to disease progression. We discuss the definitions of high molecular risk MPN, provide an overview of how concomitant mutations influence the clinical management of MPN and suggest how the rapidly developing genetic risk stratification can be utilized to improve clinical outcomes.

Uveal melanoma (UM) is the most prevalent primary intraocular malignancy in adults, originating from the melanocytes within the uvea. Currently, the treatment of ocular tumors predominantly relies on conventional approaches such as brachytherapy and enucleation. Despite the limited pharmaceutical treatment options for uveal melanoma (UM), the effectiveness of ocular drug delivery is hindered by the ocular barrier to local drug administration and the complex tumor microenvironment (TME). In response, biomimetic low-density lipoprotein nanoparticles (LD-DPVP NPs) with active targeting capabilities were designed. This nanodrug system combined photosensitizer (verteporfin, VP) with the tumor vascular normalization drug (dexamethasone, DEX) to achieve low-toxicity, high-efficacy treatment of intraocular tumors. After intravenous injection, the nanoparticles selectively targeted the tumor site and induced VP to produce reactive oxygen species (ROS) that killed tumor cells under near-infrared laser stimulation. The produced ROS could also trigger the cleavage of the DEX prodrug (DPD) and rapid release of DEX via breakage of the thioether bond (TK). Additionally, DEX could modulate the TME, improving the delivery of nanoparticles to the tumor and further enhancing the efficacy of LD-DPVP NPs. We believe the biomimetic nanoparticles designed in this study have a potential clinical application value in inhibiting UM growth and provided a promising strategy for addressing other ocular malignancies.

Helicobacter pylori (H. pylori) infection and the resulting gastric inflammation are major contributors to gastric cancer development. Probiotics, particularly Lactobacillus, are promising for their anti-inflammatory potential, yet their exact mechanisms in inhibiting H. pylori-induced inflammation are unclear. In our previous study, Lactiplantibacillus plantarum ZJ316 (L. plantarum ZJ316) demonstrated strong anti-inflammatory effects against H. pylori infection in vivo, but its precise mechanisms were not fully understood. Here, we aimed to investigate how L. plantarum ZJ316 inhibits the inflammatory response to H. pylori infection. Our results demonstrated that L. plantarum ZJ316 effectively reduced the expression of pro-inflammatory cytokines in H. pylori-infected AGS cells. Mechanistically, L. plantarum ZJ316 inhibited the NF-κB signaling pathway by preventing the degradation of IκBα, suppressing p65 phosphorylation, and blocking the nuclear translocation of phosphorylated p65. Treatment with the NF-κB inhibitor BAY 11-7082 further decreased tumor necrosis factor-α (TNF-α), interleukin-8 (IL-8), and interleukin-1β (IL-1β) levels, confirming the inhibitory effect of L. plantarum ZJ316 on the NF-κB pathway. In H. pylori-infected mice, oral administration of L. plantarum ZJ316 significantly alleviated inflammatory cell infiltration, reduced TNF-α and pepsinogen II (PGII) levels, and increased interleukin-10 (IL-10) levels in serum. A comparative metagenomic analysis of the gastric microbiota revealed a decrease in Prevotella and Desulfovibrio, alongside an increase in Ligilactobacillus and Akkermansia, supporting the protective effects of L. plantarum ZJ316 and correlating with their decreased inflammatory response. In summary, administration of L. plantarum ZJ316 demonstrated robust anti-inflammatory effects against H. pylori infection by suppressing NF-κB signaling and promoting favorable changes in the gastric microbiota composition. Therefore, L. plantarum ZJ316 holds promise as a novel functional food for protecting the body against H. pylori infection.

Cancer patients often experience significant weight loss due to metabolic changes, increased resting energy expenditure (REE), and poor nutrient intake, particularly exacerbated by treatments like chemotherapy and radiation. This study aimed to determine whether combining Oral Nutrition Supplements (ONS) with dietary education is more effective than dietary education alone in improving nutritional outcomes for cancer patients. An open-label randomized clinical trial at Persahabatan Hospital in Jakarta, Indonesia, involved 108 patients with lung or gynecological cancer, with 87 completing the study. Participants were assigned to receive either dietary education plus ONS (intervention group) or dietary education alone (control group). Results indicated that while both groups improved their nutrition knowledge, the intervention group experienced significant increases in body weight (1.68 ± 3.96 kg) and body mass index (BMI) (0.86 ± 1.96 kg/m2), whereas the control group lost weight. Additionally, the intervention group had a lower rate of anemia (60% vs. 80.9%), though no significant differences were found in albumin levels or inflammation status. These findings suggest that ONS combined with dietary education may help improve weight and BMI in cancer patients, warranting further research to confirm these benefits and assess long-term effects.

Osteosarcoma, a primary malignant bone tumor commonly found in adolescents, is highly aggressive, with a high rate of disability and mortality. It has a profound negative impact on both the physical and psychological well-being of patients. The standard treatment approach, comprising surgery and chemotherapy, has seen little improvement in patient outcomes over the past several decades. Once relapse or metastasis occurs, prognosis worsens significantly. Therefore, there is an urgent need to explore new therapeutic approaches. In recent years, the successful application of immunotherapy in certain cancers has demonstrated its potential in the field of cancer treatment. Macrophages are the predominant components of the immune microenvironment in osteosarcoma and represent critical targets for immunotherapy. Macrophages exhibit dual characteristics; while they play a key role in maintaining tumor-promoting properties within the microenvironment, such as inflammation, angiogenesis, and immune suppression, they also possess antitumor potential as part of the innate immune system. A deeper understanding of macrophages and their relationship with osteosarcoma is essential for the development of novel therapeutic strategies.

Systemic inflammation and nutritional status are key factors affecting the prognosis of patients with cancer cachexia. This study aims to evaluate the prognostic value of a new nutritional and inflammatory index, Prognostic Nutritional CRP Ratio (NCR), in patients with cancer cachexia.

This prospective multicenter study analyzed 3,447 patients diagnosed with cancer cachexia across over 40 clinical centers in China, from June 2012 to December 2023. The NCR was calculated as BMI × albumin / CRP. The Cox proportional hazards regression model was utilized to analyze hazard ratios (HRs) for all-cause mortality. The relationship between NCR and all-cause mortality was assessed using restricted cubic spline modeling. The optimal cutoff value for NCR was determined through maximally selected rank statistics.

Among the 3,447 individuals diagnosed with cancer cachexia in our study, 2,296 (66.6%) were men, and 1,151 (33.4%) were women. With a median follow-up duration of 45.33 months, the mean age of the participants was 63.8 ± 11.4 years. We observed that lower NCR levels were prevalent among cachexia patients across a spectrum of cancer types, including lung, colorectal, liver, esophageal, breast, ovarian, and cervical cancers. We observed that lower NCR levels were prevalent among cachexia patients across a spectrum of cancer types, including lung, colorectal, liver, esophageal, breast, ovarian, and cervical cancers. This correlation held true across diverse patient subgroups, delineated by gender, age, smoking status, BMI, TNM stage, and tumor types, underscoring the broad applicability of NCR as a prognostic marker. Moreover, our findings highlighted that cancer cachexia patients with higher NCR levels experienced a significantly improved quality of life.

The NCR, indicative of nutritional status and inflammation, is associated with reduced all-cause mortality and could be a valuable prognostic marker for patients with cancer cachexia.

Predicting chemoradiotherapy (CRT) response in esophageal cancer is essential as outcomes vary among patients. This study aimed to evaluate the impact of osteosarcopenia on the effectiveness of neoadjuvant CRT (NACRT).

Ninety-five patients with advanced esophageal cancer who underwent surgical resection post-NACRT were included. Sarcopenia and osteopenia were determined using pre-NACRT skeletal muscle index and bone density at L3 and Th11 levels. Patients were categorized based on osteosarcopenia status.

Thirty-seven patients (39%) had osteosarcopenia. Among tumors, 49 (51.6%) were grade 1 (non-responders), 12 (12.6%) were grade 2, and 34 (35.8%) were grade 3 (responders). NACRT was significantly more effective in patients with above-median body mass index, shallow tumor depth, low squamous cell carcinoma antigen levels, and without osteosarcopenia. Osteosarcopenia was independently correlated with the histopathologic response to NACRT. No significant differences in overall or relapse-free survival were observed based on osteosarcopenia status.

Osteosarcopenia may predict NACRT response in esophageal cancer.

Cancer remains a formidable adversary in global health, necessitating the development of innovative strategies to curb the proliferation, invasion, and metastasis of cancer cells for effective treatment outcomes. Traditional cancer therapies often fall short in addressing the diverse therapeutic requirements of patients. Consequently, the exploration of novel therapeutic targets has become increasingly vital. Olfactory receptors (ORs) belonging to the G protein-coupled receptor (GPCR) subfamily, are present in non-nasal tissues and contribute to a wide range of physiological functions. ORs are specifically expressed in malignant tumors and have emerged as potential biomarkers for cancer detection. They can regulate diverse tumor biological behaviors and are involved in the development of malignant tumors, indicating that they might serve as potential targets for cancer treatment. This paper provides a comprehensive review of the ectopic expression of ORs, their functions in malignancies and odor-based therapeutics targeting ectopic olfactory receptors (EORs) in cancer, and aims to clarify their connection with cancer, providing new clues for probing the tumor biology and developing therapeutic strategies against cancer.

Triple negative breast cancer (TNBC) is an immunogenic tumor; however, its tumor immune microenvironment (TIME) is densely packed with immune suppressive cytokines and immune checkpoints. The immune-suppressive features of TNBC TIME represent a considerable obstacle to any immunotherapeutic approach. The objective of this study was to develop a multimodal in-vitro strategy to manipulate the TNBC TIME and enhance patients' outcomes by employing carefully tailored hybrid chitosan-lipid Nanoparticles (CLNPs), metformin and chlorin e6 (Ce-6)-mediated PDT, alone or combined. Special focus is directed towards evaluation of the role of the selected treatment agents on the non-coding RNAs (ncRNAs) involved in tuning the immuno-oncogenic profile of TNBC, for instance, the miR-30a-5p/MALAT1 network.

This study enrolled 30 BC patients. CLNPs and ce-6-loaded CLNPs with different physicochemical features were synthesized and optimized using ionotropic gelation. The intracellular concentration and effects on MDA-MB-231 cellular viability were investigated. UHPLC was used to quantify ce-6. MDA-MB-231 cells were transfected with miR-30a-5p oligonucleotides and MALAT1 siRNAs using lipofection to investigate the interaction between MIF, PD-L1, TNF-α, IL-10, and the miR-30a-5p/MALAT1 ceRNA network. qRT-PCR was used to evaluate IL-10, TNF-α, and MIF expression levels, whereas flow cytometry was used for PD-L1.

Immunophenotyping of BC biopsies revealed significantly elevated levels of immunosuppressive markers, including IL-10, TNF-α, PD-L1, and MIF in BC biopsies compared to its normal counterparts. Upon patient stratification, it was shown that MIF and IL-10 are upregulated in TNBC patients compared to non-TNBC patients. Nonetheless, immune suppressive biomarkers expression investigated in the current study was generally correlated with signs of poor prognosis. CLNPs with mean particle size ranging from 50-150 nm were obtained. CLNPs exhibited different patterns of intracellular uptake, cytotoxicity and modulation of the immunosuppressive markers based on their physicochemical properties and composition. In particular, CLNP4 in-vitro effectively reduced IL-10, TNF-α, MIF, and PD-L1. Loading of Ce-6 into CLNP4 (Ce6-CLNPs) improved the in-vitro cytotoxic effects via PDT. In addition, PDT with Ce6-CLNP4 enhanced the expression of tumor-suppressive miR-30a-5p and decreased oncogenic lncRNA MALAT1 expression in MDA-MB-231 cells, suggesting a potential for modulating the TNBC immuno-oncogenic profile.

This study demonstrated that CLNPs and Ce-6-mediated PDT can modulate several key immunosuppressive factors and the miR-30a-5p/MALAT1 axis in TNBC cells. These findings provide a rationale for further in-vivo investigation of this multimodal therapeutic strategy.

The prototypical type I natural killer T (NKT) cell agonist, α-galactosylceramide (α-GalCer), has shown only minimal effects against solid tumors in the clinic. The most promising clinical application of α-GalCer currently entails ex vivo priming of patient-derived dendritic cells; however, this technology suffers from cost, logistical concerns, and safety issues. As a parenteral dendritic cell-targeted alternative, we demonstrate that poly(L-lysine succinylated) (PLS)-α-GalCer, a novel scavenger receptor-A1 targeted α-GalCer prodrug has enhanced antitumor activity compared with α-GalCer.

To compare the antitumor activity of PLS-α-GalCer and α-GalCer, we used mouse syngeneic subcutaneous pancreatic and cervical tumor models using Panc02 and TC-1 cells, respectively. Intratumoral immune cell infiltration was evaluated using flow cytometry and immunohistochemistry whole-slide scan analysis. Serum cytokine levels were examined by ELISA and LEGENDplex analysis. Type I NKT cell intracellular interferon-gamma (IFN-γ) levels were determined by flow cytometry. Immunofluorescence was used to test the uptake and processing of PLS-α-GalCer and α-GalCer in antigen-presenting cells (APCs).

The scavenger receptor A1 (SR-A1)-mediated targeting of α-GalCer to APCs by PLS-α-GalCer significantly improves the antitumor function against solid tumors compared with α-GalCer. The Panc02 and TC-1 tumor models demonstrated that PLS-α-GalCer increases intratumoral antigen-specific T, NKT and T cells, and increases the M1/M2 macrophage ratio. In the TC-1 tumor model, we demonstrated that PLS-α-GalCer synergizes with an E7 tumor vaccine to significantly suppress tumor growth and increase the survival of mice. Furthermore, the antitumor function of PLS-α-GalCer is dependent on type I NKT cells and requires SR-A1 targeting. In addition, using SR-A1 knockout RAW cells, a murine macrophage cell line, we showed that PLS-α-GalCer uptake and processing in APCs are more efficient compared with α-GalCer. PLS-α-GalCer also induces significantly less serum Th2 and Th17 cytokines while stimulating significantly more IFN-γ for a longer period and increases Th1:Th2 cytokine ratios compared with α-GalCer.

PLS-α-GalCer is a promising immunotherapy for the treatment of solid tumors that has superior antitumor activity compared with α-GalCer and could be combined with tumor vaccines and potentially other immunotherapies such as immune checkpoint inhibitors.

Inflammation appears to play a crucial role in the development and progression of penile cancer (PeCa). Two molecular pathways of PeCa are currently described: HPV-dependent and HPV-independent. The tumor immune microenvironment (TIME) of PeCa is characterized by the presence of tumor-associated macrophages, cancer-associated fibroblasts, and tumor-infiltrating lymphocytes. The components of the TIME produce pro-inflammatory cytokines and chemokines, which have been found to be overexpressed in PeCa tissues and are associated with tumor progression and unfavorable prognoses. Additionally, the nuclear factor kappa B (NF-κB) pathway and secreted phosphoprotein 1 (SPP1) have been implicated in PeCa pathogenesis. Elevated C-reactive protein (CRP) levels and the neutrophil-to-lymphocyte ratio (NLR) have been identified as potential prognostic biomarkers in PeCa. This overview presents the complex contribution of the inflammatory process and collates projects aimed at modulating TIME in PeCa.

Introduction: Diethyl nitrosamine (DEN), a known carcinogen, has been used for validating the RasH2 and P53 transgenic models in chemical testing and has been shown to enhance primary liver tumor growth in the ATT-Myc transgenic mouse model of liver cancer. Material and Methods: to better understand the mechanism of hepatocellular carcinoma acceleration following DEN, BHT and vehicles treatments in ATT-Myc, transgenic and non-transgenic, mice. We employed an exon array, RT-PCR, Western blotting, and IHC to investigate the complex interplay between the c-Myc transgene and other growth factors in treated mice versus control transgenic and non-transgenic mice. Results: Notably, DEN treatment induced a 12-fold increase in c-Myc expression compared to non-transgenic mice. Furthermore, tumor growth in the DEN group was strongly associated with increased proliferation of transformed or carcinogenic hepatocytes, as evidenced by proliferative cell nuclear antigen and bromodeoxyuridine expression. Internally, the loss of c-Met signaling, enriched transcription factors, and the diminished expression of antioxidants, such as superoxide dismutase (SOD1) and NRF2, further enhanced c-Myc-induced liver tumor growth as early as four months post-DEN treatment. Discussion: Extensive tumor growth was observed at 8.5 months, coinciding with the downregulation of tumor suppressors such as p53. In contrast, at these time points, ATT-Myc transgenic mice exhibited only dysplastic hepatocytes without tumor formation. Additionally, the antioxidant butylated hydroxytoluene maintained c-Met expression and did not promote liver tumor formation. Conclusions: the persistent upregulation of c-Myc in the ATT-Myc liver cancer model, at both the gene and protein levels following DEN treatment inhibited the ETS1 transcription factor, further exacerbating the decline of c-Met signaling, SOD1, and NRF2. These changes led to increased reactive oxygen species production and promoted rapid liver tumor growth.

The effect of the controlling nutritional status (CONUT) score on forecasting multiple myeloma (MM) prognosis is previously analyzed, whereas the results remained inconsistent. The present meta-analysis focused on identifying the exact function of CONUT in forecasting MM prognosis.

Web of Science, PubMed, Embase, CNKI, and Cochrane Library were comprehensively searched between inception and 1 February 2025. The effect of CONUT on forecasting MM overall survival (OS) and progression-free survival (PFS) was determined by computing pooled hazard ratios (HRs) together with 95% confidence intervals (CIs).

There were nine studies with 1,176 patients being recruited into the present work. As indicated by our pooled data, elevated CONUT was related to the dismal OS (HR = 1.87, 95% CI = 1.37-2.54, p < 0.001) of patients with MM. Nonetheless, CONUT was not significantly related to PFS (HR = 1.33, 95% CI = 0.81-2.19, p = 0.254) of MM. Furthermore, higher CONUT score showed a significant relationship to bone marrow plasma cells >30% (OR = 2.30, 95% CI = 1.32-3.99, p = 0.003). On the other hand, CONUT was not markedly correlated with gender (OR = 2.68, 95% CI = 0.81-8.82, p = 0.105), ISS stage (OR = 1.28, 95% CI = 0.94-1.75, p = 0.119), or ECOG PS (OR = 1.30, 95% CI = 0.84-2.01, p = 0.234) of MM.

Collectively, according to our results in this meta-analysis, higher CONUT score is markedly related to dismal OS, but not PFS in patients with MM. CONUT score can be used as a candidate marker used to predict MM prognosis in the clinic in the future.

Though not specifically designed for cancer therapy, several FDA-approved drugs such as metformin, aspirin, and simvastatin have an effect in lowering the incidence of cancer. However, there is a great discrepancy between in vitro concentrations needed to eliminate cancer cells and the plasma concentration normally tolerated within the body. At present, there is no universal explanation for this discrepancy and several mechanisms have been proposed including targeting cancer stem cells (CSCs) or cellular senescence. CSCs are cells with the ability of self-renewal and differentiation known to be resistant to chemotherapy. Senescence is a response to damage and stress, characterized by permanent cell-cycle arrest and apoptotic resistance. Although, for both situations, there are few examples where low concentrations of the FDA-approved drugs were the most effective, there is no satisfactory data to support that either CSCs or cellular senescence are the target of these drugs. In this review, we concisely summarize the most used FDA-approved drugs for non-cancer conditions as well as their potential mechanisms of action in lowering cancer incidence. In addition, we propose that prolonged low-dose administration (PLDA) of specific FDA-approved drugs can be useful for effectively preventing metastasis formation in selected patients.

Background/Objectives: Chronic inflammation has been implicated in cancer development, but the association between allergic rhinitis (AR) and head and neck cancer (HNC) remains unclear. This study aims to investigate this potential relationship using a population-based dataset. Methods: Utilizing the Taiwan Longitudinal Health Insurance Database 2010, we conducted a case-control study encompassing 14,913 HNC patients and 59,652 propensity-score matched controls. Multivariate logistic regression analyses were performed to quantitatively evaluate the association between HNC and prior AR, adjusting for demographic factors and medical comorbidities such as hyperlipidemia, diabetes, hypertension, tobacco use disorder, HPV infection, and alcohol-related disorders. Results: This study identified that 20.19% of the entire cohort had a prior diagnosis of AR, with a significantly higher prevalence in HNC patients relative to controls (26.2% vs. 18.70%). The adjusted odds ratio (OR) for previous AR in HNC patients was 1.559 (95% CI = 1.494-1.627). Furthermore, site-specific analysis revealed increased odds ratios for AR among patients with cancers of the larynx (OR = 1.537, 95% CI = 1.307-1.807), hypopharynx (OR = 1.220, 95% CI = 1.035-1.437), nasopharynx (OR = 2.933, 95% CI = 2.722-3.160), sinonasal (OR = 3.100, 95% CI = 2.424-3.964), salivary glands (OR = 1.470, 95% CI = 1.158-1.865), and thyroid (OR = 1.566, 95% CI = 1.447-1.693). Conclusions: The findings robustly support a significant link between AR and an elevated risk of developing HNC, notably affecting the nasopharynx, sinonasal cavities, larynx, salivary glands, and thyroid.

Inflammation, a hallmark of cancer, has been associated with tumor progression, transition into malignant phenotype and efficacy of anticancer treatments in cancer. It affects all stages of cancer, from the initiation of carcinogenesis to metastasis. Chronic inflammation induces immunosup-pression, providing an environment conducive to carcinogenesis, whereas acute inflammation induces an antitumor immune response, leading to tumor suppression. Solid tumors have an inflammatory tumor microenvironment (TME) containing cancer cells, immune cells, stromal cells, and soluble molecules, which plays a key role in tumor progression and therapy response. Both cancer cells and stromal cells in the TME are highly plastic and constantly change their phenotypic and functional properties. Cancer-associated inflammation, the majority of which consists of innate immune cells, plays an important role in cancer cell plasticity, cancer progression and the development of anticancer drug resistance. Today, with the combined used of advanced technologies, such as single-cell RNA sequencing and spatial molecular imaging analysis, the pathways linking chronic inflammation to cancer have been largely elucidated. In this review article, we highlighted the molecular and cellular mechanisms involved in cancer-associated inflammation and its effects on cancer progression and treatment response. We also comprehensively review the mechanisms linking chronic inflammation to cancer in the setting of GI cancers.

The biological mechanisms by which postdiagnosis physical activity improves disease-free survival in colorectal cancer survivors remain incompletely understood. This trial tested the hypothesis that 12 wk of moderate-intensity aerobic exercise, when compared with a control group, would change inflammation, CTCs, and ctDNA in a manner consistent with an improved cancer prognosis.

This trial randomized Stages I-III colorectal cancer survivors to 12 wk of home-based moderate-intensity aerobic exercise or a waitlist control group. The co-primary endpoints were high-sensitivity C-reactive protein (hs-CRP) and interleukin-6 (IL-6), secondary endpoints were soluble tumor necrosis factor-α receptor 2 (sTNFαR2) and circulating tumor cells (CTCs), and the exploratory endpoint was tumor fraction quantified from circulating tumor DNA.

Sixty subjects were randomized (age = 60.6 ± 10.8 years, mean ± SD; 39 (65%) females; 46 (77%) colonic primary tumor), and 59 (98%) subjects completed the study. Over 12 wk, exercise adherence was 92% (95% confidence interval (95%CI): 86‒99). Exercise improved submaximal fitness capacity (0.36 metabolic equivalents; 95%CI: 0.05‒0.67; p = 0.025) and objectively measured moderate-to-vigorous-intensity physical activity (34.8%, 95%CI: 11.3‒63.1; p = 0.002) compared to control. Exercise did not change hs-CRP (20.9%, 95%CI: -17.1 to 76.2; p = 0.32), IL-6 (11.4%, 95%CI: -7.5 to 34.0; p = 0.25), or sTNFαR2 (-3.6%, 95%CI: -13.7 to 7.7; p = 0.52) compared to control. In the subgroup of subjects with elevated baseline hs-CRP (n = 35, 58.3%), aerobic exercise reduced hs-CRP (-35.5%, 95%CI: -55.3 to -3.8; p = 0.031). Exercise did not change CTCs (0.59 cells/mL, 95%CI: -0.33 to 1.51; p = 0.21) or tumor fraction (0.0005, 95%CI: -0.0024 to 0.0034; p = 0.73). In exploratory analyses, higher aerobic exercise adherence correlated with a reduction in CTCs (ρ = -0.37, 95%CI: -0.66 to -0.08; p = 0.013).

Colorectal cancer survivors achieved high adherence to a home-based moderate-intensity aerobic exercise prescription that improved fitness capacity and physical activity but did not reduce inflammation or change tumor endpoints from a liquid biopsy.

Background: Colorectal cancer affects a large number of patients worldwide, with numerous factors being involved in its etiopathogenesis and chronic inflammation playing an essential role in tumor development. In this study, we analyzed and compared several markers of inflammation that are relatively easy to obtain for a rapid and accurate diagnosis and prognosis. Methods: This study included 219 patients diagnosed with colorectal cancer, analyzing the inflammation scores derived from their blood cells and inflammatory circulating proteins. These inflammatory markers are neutrophil-to-lymphocyte ratio-NLR; platelet-to-lymphocyte ratio-PLR; lymphocyte-to-monocyte ratio-LMR; systemic immune inflammation index-SII; systemic inflammatory response index-SIRI; aggregate index of systemic inflammation-AISI; derived neutrophil-to-lymphocyte ratio-dNLR; C-reactive protein-to-albumin ratio-CAR; and fibrinogen-to-albumin ratio-FAR. In the analysis of patients with colorectal cancer, we have also introduced two new recently developed inflammatory markers: the cumulative inflammatory index (IIC) and the ratio between the mean corpuscular volume and lymphocytes (MCVL). This study aimed to correlate the inflammatory markers' levels with the colorectal cancer diagnostic stage, the tumor and clinical characteristics of the colorectal cancer patients, and 36 months' survival time and to evaluate the diagnostic and prognostic capacity and accuracy of these inflammatory markers in this type of cancer. Results: We showed that the levels of the analyzed inflammation markers correlate with the TNM stage, the tumor pathological differentiation grade, the age and gender of the patients, and overall survival, with their increased levels being associated with a lower survival rate. Conclusions: The analyzed markers, which are easy to perform right from the patient's admission, can be helpful both in diagnosis and, mostly, in prognosis, sustaining the role of inflammation in cancer. By comparing them, we showed which one can be useful for increased sensitivity and specificity in the diagnosis and prognosis of colorectal cancer patients.

The immune system provides defense against foreign agents that are considered harmful for the organism. Inorganic nanomaterials can be recognized by the immune system as antigens, inducing an immune reaction dependent on the patient's immunological anamnesis and from several factors including size, shape, and the chemical nature of the nanoparticles. Furthermore, nanomaterials-driven immunomodulation might be exploited for therapeutic purposes, opening new horizons in oncology and beyond. In this scenario, we present a critical review of the state of the art regarding the preclinical evaluation of the effects of the most promising metals for biomedical applications (gold, silver, and copper) on the immune system. Because exploiting the interactions between the immune system and inorganic nanomaterials may result in a game changer for the management of (non)communicable diseases, within this review we encounter the need to summarize and organize the plethora of sometimes inconsistent information, analyzing the challenges and providing the expected perspectives. The field is still in its infancy, and our work emphasizes that a deep understanding on the influence of the features of metal nanomaterials on the immune system in both cultured cells and animal models is pivotal for the safe translation of nanotherapeutics to the clinical practice.

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.

Nicotinic acetylcholine receptors (nAChRs) are widely expressed in a variety of cell types and are involved in multiple physiological regulatory mechanisms in cells, tissues and systems. Increasing evidence suggests that the α5 nicotinic acetylcholine receptor (α5-nAChR), encoded by the CHRNA5 gene, is one of a key mediator involved in lung cancer development and immune responses. Several studies have shown that it is a regulator that stimulates processes via various signaling pathways, including STAT3 in lung cancer. In addition, α5-nAChR has a profound effect on lung immune response through multiple immune-related factor pathways. In this review, we focus on the perspectives on α5-nAChR in lung cancer progression, which indicates that targeting α5-nAChR could provide novel anticancer and immune therapy strategies for lung cancer.

NF-κB, a multifunctional transcription factor, is linked to cancer initiation and progression. As a key immune mediator, it may play a crucial role in HPV-induced cervical carcinogenesis. However, consensus is lacking on the activation timing of NF-κB during the transition from cervical intraepithelial neoplasia (CIN) to cervical squamous cell carcinoma (CSCC). In this study, immunohistochemical analysis was performed to examine RELA, one of the important members of the NF-κB family, and phospho-RELA expression in different cervical lesions. Then, we analyzed NF-κB regulation of differentially expressed genes (DEGs) in cervical lesions vs. normal tissues. Gene enrichment identified oncogenic DEGs, followed by expression and survival analyses. The impact of NF-κB activation on cervical cell proliferation, migration, and oncogenic regulation, as well as the effects of inhibiting NF-κB, were examined. Our study showed that NF-κB activation starts in cervical simple hyperplasia and intensifies as CIN evolves to CSCC. NF-κB-regulated DEGs show stage-specific functions: immune regulation in CIN and cancer promotion in CSCC. Short-term NF-κB activation boosts cervical cell proliferation and migration, which is reversible by an NF-κB inhibitor. Long-term NF-κB activation promotes the expression of cancer-promoting genes in normal cells and also maintains them in cancer tissues, which is linked to poorer prognosis. Inhibiting NF-κB downregulates these genes in cancer cells and suppresses the oncogenic abilities of cervical cancer cells. Collectively, NF-κB activation initiates during the simple hyperplasia stage of cervical cells, stimulating proliferation, migration, and oncogene expression. Throughout the transition from CIN to CSCC, NF-κB activation progressively intensifies, and its long-term activation promotes carcinogenesis. Thus, NF-κB is crucial in mediating cervical oncogenic transformation.

Lactylation plays an important role in tumor progression. This study aimed to clarify the impact of lactylation on cancer-associated fibroblasts(CAFs).

Single-cell and bulk RNA sequence data, along with survival information, were obtained from TCGA and GEO datasets. Significant lactylation-associated genes were acquired by differential analysis and used to construct a prognostic model via Cox and LASSO regression analyses. Next, single-cell analysis, enrichment and pathway analysis, pseudotemporal trajectory and survival analysis were used to identify significant lactylation-associated fibroblast subclusters in colon cancer. IMvigor210 and PRJEB23709 cohorts were applied to assess the response to immunotherapy. In vitro experiments were conducted to explore how lactylation affect fibroblasts.

We established a lactylation-associated prognostic model with 17 risk genes in TCGA and further validated it in GEO datasets. Single-cell analysis revealed the lactylation level of fibroblasts in colon cancer was greater than that in normal tissues. Moreover, five lactylation-associated fibroblast subclusters were identified via the NMF algorithm. Patients with lower scores of FB_2_CALD1, FB_3_TPM4 and FB_4_AHNAK subclusters had better clinical prognosis in colon cancer and were more likely to benefit from immunotherapy. Further experiments demonstrated that lactylation could enhance the proliferation, migration and invasion ability of fibroblasts and up-regulate the expression of COL1A1, which was similar to the effect of colon cancer cells.

This study identified key fibroblast subclusters with prognostic value and implied that lactylation might help transform fibroblasts into CAFs in colon cancer for the first time, which provides new paths for understanding the evolution of CAFs and cancer therapeutic strategies.

Due to drug resistance, a majority of patients with non-small cell lung cancer (NSCLC) experience disease progression following immunotherapy. Therefore, there is an urgent need to develop novel biomarkers to predict the prognosis of NSCLC patients. Clinical data from 544 patients with advanced NSCLC who underwent immune checkpoint blockers (ICBs) at our clinical center were collected in this study. The results indicated that low Albumin-Globulin Ratio (AGR) and Lymphocyte-Monocyte Ratio (LMR) and high Systemic Immune-Inflammation Index (SIRI) were significantly correlated with both poor overall survival (OS) and progression-free survival (PFS) in NSCLC patients (P < 0.01). These three indicators collectively formed the most effective combined model for predicting the prognosis of NSCLC. Importantly, risk stratification based on AGR, LMR and SIRI was better than that based on the TNM stage, and served as an independent predictor of OS and PFS. Notably, the nomogram model developed by risk stratification, sex, age, smoking history, and pathological type demonstrated a good ability to predict the 1 to 5-year OS rates for NSCLC patients. In summary, AGR, LMR, and SIRI represented the optimal combined models for forecasting the prognosis of patients with advanced NSCLC who underwent ICBs, offering promising potential as biomarkers to direct personalized clinical interventions.

This study aimed to evaluate the therapeutic effect of Terminalia chebula (TC) on Tibetan yak-origin Salmonella-induced diarrhea and dysentery in mice. The levels of pro-inflammatory cytokines (IL-1β, IL-6, IL-8, and TNF-α), anti-inflammatory cytokines (IL-4 and IL-10), and the oxidative stress markers malondialdehyde (MDA), superoxide dismutase (T-SOD), total antioxidant capacity (T-AOC), reduced glutathione (GSH-PX), and catalase (CAT) in the serum of mice were measured using ELISA kits. Using microbial diversity sequencing and non-targeted metabolomics detection techniques, the relevant mechanisms of TC treatment in a mouse Salmonella infection model were evaluated. The results showed the following: TC can effectively reduce the diarrhea rate; alleviate weight loss caused by Salmonella invasion; reduce the pro-inflammatory cytokines IL-1β, IL-6, IL-8, and TNF-α in serum; and increase the concentrations of the anti-inflammatory cytokines IL-4 and IL-10. TC can improve the body's antioxidant levels to heal the damage caused by oxidative stress and lipid peroxidation. The histological section results show that TC can significantly improve gastric and intestinal tissue lesions and has no toxic effects on the liver and kidneys. 16S rRNA and ITS sequencing analysis suggests that Lactobacillus, Enterorhabdus, Alistipes (bacterial community), Lodderomyces, Saccharomyces, and Penicillium (fungal community) may be key functional microbial communities in TC. Non-targeted metabolomics also suggests that the antibacterial treatment of dysentery with chebulic acid may be related to regulation of the Ras signaling pathway, long-term potentiation, the MAPK signaling pathway, metabolic pathways, and gut microbiome composition. Conclusion: TC has clear clinical efficacy in treating bacterial diarrhea, presenting anti-inflammatory and antioxidant effects. Its roles in regulating the gut microbiome and metabolic pathways and products were determined as the main reason for its therapeutic effect in a mouse gastroenteritis model caused by Salmonella infection.

Chronic inflammation of the intestine is a significant risk factor in the development of colorectal cancer. The emergence of colitis and colorectal cancer is a complex, multifactorial process involving chronic inflammation, immune regulation, and tumor microenvironment remodeling. Macrophages represent one of the most prevalent cells in the colorectal cancer microenvironment and play a pivotal role in maintaining intestinal health and the development of colitis-associated colon cancer (CAC). Macrophages are activated mainly in two ways and resulted in three phenotypes: classically activated macrophages (M1), alternatively activated macrophages (M2). The most characteristic of these cells are the pro-inflammatory M1 and anti-inflammatory M2 types, which play different roles at different stages of the disease. During chronic inflammation progresses to cancer, the proportion of M2 macrophages gradually increases. The M2 macrophages secrete cytokines such as IL-10 and TGF-β, which promote angiogenesis and matrix remodeling, and create the favorable conditions for cancer cell proliferation, infiltration, and migration. Therefore, macrophage polarization has a dual effect on the progression of colitis to CAC. The combination of immunotherapy with reprogrammed macrophages and anti-tumor drugs may provide an effective means for enhancing the therapeutic effect. It may represent a promising avenue for developing novel treatments for CAC. In this review, we focus on the process of intestinal macrophage polarization in CAC and the role of intestinal macrophage polarization in the progression of colitis to colon cancer, and review the immunotherapy targets and relevant drugs targeting macrophages in CAC.

The aim of this study is to analyze, through a literature review and the description of four clinical cases, whether prolonged tooth impaction may represent a trigger for the onset of oral carcinoma.

In this report, four cases of patients needing the extraction of third molars in complete mucosal or bone impaction are described, which, due to the presence of an unusual radiographic and/or clinical aspect, were found to represent cases of oral carcinomas on histologic analysis. Patients were then referred to the ENT department for further care. A review of the literature has been performed as well.

Literature analysis revealed the presence of only few case reports on the topic, suggesting therefore a lack of evidence on the correlation between tooth impaction and the onset of oral carcinomas.

Further studies are needed in order to give valid hypotheses. The concept of inflammation, that is at the base of oral carcinogenesis mechanism and tooth-related pathologies, such as pericoronitis, may be a common substrate to link these two phenomena.

A thorough analysis of the radiographic and clinical signs is strongly recommended prior and during surgical procedures, such as tooth extraction.

Sex-related differences in eating-related distress (ERD) experienced by cancer patients have not previously been clarified.

We conducted a multicenter survey among advanced cancer patients referred to palliative care. Data on patient characteristics were collected from the electronic medical records, and data on measurement outcomes were obtained from a questionnaire. Patients were categorized into male and female groups. We measured ERD using the Questionnaire for Eating-Related Distress among Patients with advanced cancer (QERD-P). The QERD-P comprises 3 items in each of the 7 factors, for a total of 21 items, and each item is rated on a 7-point Likert scale. High scores indicate worse distress. Comparisons were calculated using the Mann-Whitney U test. To assess associations between sexes and ERD, multivariate logistic regression analysis was performed.

A total of 192 patients were enrolled and divided into the male (n = 92) and female (n = 100) groups. The total score of the QERD-P was significantly higher in the male group (p = 0.018). The subtotal scores of "reasons why I cannot eat," "insufficient information," and "arguments with my family" were significantly higher in the male group (p = 0.035, 0.032, and 0.003, respectively). The male group had significantly higher risks for ERD associated with "arguments with my family" and "time with my family" (odds ratio [OR] 2.69, 95% confidence interval [CI] 1.38-5.24; OR 2.28, 95% CI 1.15-4.53).

Males had significantly worse ERD and were at higher risk of ERD in family relationships than females.

Bodyweight loss is a common occurrence in Nasopharyngeal Carcinoma (NPC) patients during Radiotherapy (RT). Previous studies found that the prognostic value of percentage weight loss (pWL) during RT is not credible. We aimed to develop a novel progression predictor surrogated to pWL by modelling all bodyweight records measured during the treatment interval. This retrospective study included two independent hospitals of 624 patients. The Predicted Progression Probability (PPP) was obtained from deep learning-guided differential equation solution, model by the patient's age, sex, body height, and the weekly measured bodyweight records. The performance of PPP in predicting disease progression was assessed, its association with prognosis and adjuvant chemotherapy response was evaluated. The PPP was learnt from the training cohort (N = 257) with 7 weeks of bodyweight records. The prediction performance was validated with 367 patients of the testing cohort sub-divided according to the number of bodyweight records found. The area under of curve for patients with 7 weeks (N = 155), 6 weeks (N = 176), and 5 weeks bodyweight records (N = 32) were 0.76, 0.73, and 0.95 respectively. PPP was significantly associated with progression-free and remained an independent prognostic factor adjusting for clinicopathologic variables in multivariate analysis in all study cohort (adjusted hazard ratio [HR] range: 2.50-7.04, all p < 0.001). Patients with high-PPP derived progression benefit from adjuvant chemotherapy (HR: 0.41-0.54, all p < 0.03), whereas those with low-PPP did not for both cohorts. The trajectory of bodyweight change during RT is more robust than the pWL to give a progression prediction after RT. The PPP is a reliable predictor for estimating the risk of residual diseases after RT course, which also helps to predict adjuvant chemotherapy response in locally advanced NPC patients.

Breast cancer (BC), which is the most common tumor in women, has greatly endangered women's lives and health. Currently, patients with BC receive comprehensive treatments, including surgery, chemotherapy, radiotherapy, endocrine therapy, and targeted therapy. According to the latest research, the development of BC is closely related to the inflammatory immune response, and the immunogenicity of BC has steadily been recognized. As such, immunotherapy is one of the promising and anticipated forms of treatment for BC. The potential values of miRNA in the diagnosis and prognosis of BC have been established, and aberrant expression of associated miRNA can either facilitate or inhibit progression of BC. In the tumor immune microenvironment (TME), miRNAs are considered to be an essential molecular mechanism by which tumor cells interact with immunocytes and immunologic factors. Aberrant expression of miRNAs results in reprogramming of tumor cells actively, which may suppress the generation and activation of immunocytes and immunologic factors, avoid tumor cells apoptosis, and ultimately result in uncontrolled proliferation and deterioration. Therefore, through activating and regulating the immunocytes related to tumors and associated immunologic factors, miRNA can contribute to the advancement of BC. In this review, we assessed the function of miRNA and associated immune system components in regulating the advancement of BC, as well as the potential and viability of using miRNA in immunotherapy for BC.