Chemokine ligand 2 (CCL2) is a key regulatory molecule in the tumor microenvironment (TME) participating in the occurrence, progression, and metastasis of tumors through complex mechanisms. This paper systematically reviews the production and regulation of CCL2 in tumors and its pleiotropic effects. CCL2 can be continuously produced by tumor cells, stromal cells, and host-tumor interactions through constitutive secretion, microenvironmental stimulation response, and interaction network. Its expression is regulated by transcription factors such as Nuclear factor-kappa B (NF-κB), signal transducer and activator of transcription 3 (STAT3), and activator protein 1 (AP-1); single nucleotide polymorphisms (SNPs); and epigenetic modifications such as DNA methylation and noncoding RNA. Inflammatory factors (such as tumor necrosis factor [TNF]-α, interleukin [IL]-1β, and IL-6) and hypoxia signal in the TME further amplify CCL2 secretion through the activation of NF-κB, MAPK, and other pathways, forming a positive feedback loop. CCL2 directly promotes the proliferation, migration, and epithelial-mesenchymal transition of cancer cells by activating CCR2 receptor and its downstream PI3K/AKT, MAPK, and other signaling pathways and remodels the immunosuppressive microenvironment by recruiting tumor-associated macrophages and myeloid-derived suppressor cells. Furthermore, CCL2 drives tumor invasion and distant metastasis by inducing angiogenesis, enhancing matrix metalloproteinase activity, and promoting premetastatic niche formation. Although clinical trials targeting the CCL2-CCR2 axis have been carried out, the efficacy is limited by the redundancy of CCL2 expression and its crosstalk with other factors. Given our incomplete understanding of its mechanism, the development of combined strategies or miRNA, epigenetic intervention, and other source regulation methods is necessary. This study provides a theoretical basis for understanding the tumor regulatory network of CCL2 and the development of precise targeted therapy.

Esophageal squamous cell carcinoma (ESCC) remains a global health challenge, with immune checkpoint inhibitors (ICIs) reshaping therapeutic strategies. However, heterogeneous responses underscore the urgent need for robust predictive biomarkers. While PD-L1 expression remains the most widely used marker, its limitations, including spatial heterogeneity and inducible expression, have prompted exploration of alternative and composite indicators. Recent advances highlight the predictive potential of tumor immune microenvironment (TME) features such as tumor-infiltrating lymphocytes (TILs), tertiary lymphoid structures (TLSs), stromal maturity, and T cell-inflamed gene expression profiles. Concurrently, tumor-intrinsic biomarkers, including microsatellite instability, tumor mutational burden, neoantigen load, and chromosomal alterations-have shown promise in stratifying immunotherapy responders. Multi-omics approaches, liquid biopsies, and integration of host factors such as gut microbiota are emerging to refine patient selection. This review comprehensively examines evolving biomarkers and therapeutic trials, emphasizing the need for integrative precision strategies to optimize immunotherapy efficacy in ESCC.

Colorectal cancer (CRC) is a prominent worldwide health concern because of its high prevalence and mortality rates. This study explored the role of Ursolic Acid (UA) in preventing the development of CRC and clarified potential mechanisms.

Differential genes between human normal tissues and colon adenocarcinoma tumor tissues, plus survival analysis were generated on GEPIA2 website. RNA-seq was utilized to screen therapeutic targets after UA added into HT29 cells. AutoDock Vina 1.2.3 was used to carry out molecular docking between GPX4 and UA. Dual-luciferase reporter method was applied to evaluate miR-214-3p/GPX4 and miR-214-3p/Stat3 sponging. Gene overexpression plasmids, miRNA mimics and inhibitors transfection assays were carried out. The morphological alterations in mitochondria were detected based on transmission electron microscopy (TEM). In vivo, the xenograft model of HT29 cells transfected with luciferase gene (HT29-luc) was constructed in nude mice.

We found that UA substantially inhibited the proliferation of CRC cells, induced cellular ferroptosis by decreasing the expression of system xc^- (SLC7A11 and SLC3A2) and GPX4. Overexpression of Stat3 increased GPX4 expression level. MiR-214-3p mimics can reduce GPX4, p-Stat3 and Stat3 expression levels. MiR-214-3p can bind both GPX4 and Stat3 mRNA 3'UTR. Overexpression of GPX4 and miR-214-3p inhibitors accelerated CRC cells proliferation. MiR-214-3p inhibitors can reverse UA-reduced GPX4 and Stat3 mRNA expression levels. TEM images showed that mitochondrial volume decreased, bilayer membrane density increased, mitochondrial cristae decreased after intervention with UA or miR-214-3p mimics. According to in vivo experiments, UA inhibited CRC tumor growth by regulation of above genes.

This study demonstrated that UA could effectively inhibit CRC proliferation by inducing ferroptosis via regulation of system xc^- subunits and miR-214-3p/Stat3/GPX4 axis, suggesting UA could serve as a promising anti-colorectal cancer candidate requiring further validation and optimization.

In the last decade, chimeric antigen receptor (CAR)-modified T cells have revolutionized the treatment of hematologic malignancies. However, antitumor responses in solid tumors remain poor, and the difficulty in finding truly tumor-specific target antigens leads to a high risk of on-target/off-tumor toxicity. Transient modification with mRNA is gaining momentum as an alternative approach to viral transduction in order to achieve a better safety profile. On the other hand, generation of T cells secreting bispecific T cell engagers (TCEs) has been reported to outperform the antitumor efficacy of T lymphocytes expressing membrane-anchored CARs, due to the ability of the soluble TCEs to recruit unmodified bystander T cells.

We have electroporated human primary T cells with in vitro transcribed mRNA encoding an anti-EGFR x anti-CD3 bispecific T cell engager. Such mRNA-modified T cells (STAR^EGFR-T cells) have been analyzed for anti-EGFR bispecific TCE secretion and for their ability to drive anti-tumor responses against EGFR-expressing cells, both in vitro and in vivo.

STAR^EGFR-T cells transiently secrete bispecific TCEs capable of redirecting T lymphocytes to exert tumor cell-specific killing in in vitro assays. Moreover, STAR^EGFR-T cells efficiently control tumor growth in in vivo xenograft models of solid malignancy.

Our results strongly support mRNA-engineered TCE-secreting T cells as a promising therapeutic strategy for solid tumors.

Focal xanthogranulomatous pyelonephritis (XGP) is a rare chronic renal inflammatory disorder in children that often mimics renal neoplasms, complicating diagnosis and management.

We describe two pediatric cases of focal XGP managed at our institution and provide a descriptive review of the literature (1975-2024), analyzing clinical presentation, imaging features, management strategies, and outcomes of this disease.

Case 1: A 2-year-old boy presented with a febrile right flank mass and systemic inflammation. CT Scan revealed an 80 mm multilocular renal mass. Surgical drainage and biopsy confirmed focal XGP, and targeted antibiotics led to complete resolution with preserved renal function at two-year follow-up. Case 2: A 10-year-old girl presented with a 40 mm left renal mass and systemic inflammatory signs. CT-guided aspiration and histopathology confirmed focal XGP. She was managed conservatively with intravenous and oral antibiotics, achieving complete resolution and normal renal function at seven-year follow-up. Literature review of 34 pediatric XGP cases (median age 11.1 years) showed that 53% were focal lesions. Conservative management with antibiotics, with or without drainage, succeeded in 64% of cases, and overall outcomes were favorable, with stable renal function and no reported mortality.

This combined case series and descriptive literature review highlights that conservative, kidney-sparing management is a feasible and effective approach in selected pediatric focal XGP cases. Multicenter collaborations are needed to define standardized diagnostic and therapeutic protocols.

Cancer, ranging from early stages to metastatic spread, is one of the leading causes of death globally. Current treatment options, including chemotherapy, radiotherapy, and targeted drugs, have limitations, such as significant side effects, drug resistance, and high cost. To overcome these challenges, extensive studies have explored the anticancer potential of various drugs such as clotrimazole (CLZ), which has shown promising anticancer effects. CLZ was first developed as an antifungal agent. Recently significant anticancer effects have been observed making it a suitable candidate for drug repurposing. Compared with other azole-based antifungals, CLZ has shown distinct therapeutic effects on cancer cells via several pathways. Its ability to disrupt glycolysis by inhibiting phosphofructokinase (PFK) and hexokinase (HK) distinguishes it from other azoles. Furthermore, CLZ obstructs calcium homeostasis and critical survival pathways, such as extracellular signal-regulated kinase (ERK)-p65, phosphatidylinositol 3-kinase (PI3K), and mitochondrial apoptotic pathways, inhibiting tumor growth, inducing apoptosis, and attenuating metastasis. This review explores the potential of repurposing CLZ in cancer and its well-established safety profile and cost-effectiveness to highlight current treatment gaps. It briefly examines in vitro and in vivo assessments to understand the mechanisms and effects of CLZ on various cancer types. Furthermore, novel strategies such as nanoformulations and combination therapies with existing chemotherapeutic drugs have been highlighted to improve therapeutic outcomes. Preclinical studies have provided promising evidence for the efficacy of CLZ in different cancers, showing tumor regression and improved responses to conventional chemotherapy or targeted therapies. Given its evident preclinical results and diverse mechanisms of action, CLZ may be considered an antineoplastic agent. Further clinical research is required to fully elucidate its anticancer potential, potentially positing it as a valuable addition to currently available cancer treatments.

Metastatic prolactinomas are an extremely rare type of neuroendocrine tumors, comprising <0.2% of all pituitary tumors. These tumors are typically associated with poor prognosis, with an average survival of 10 months. Temozolomide, an alkylating chemotherapy agent, has previously been shown to be effective in treating these rare cases once first-line medical and surgical therapies have failed. We present a patient with metastatic prolactinoma to the cerebellopontine angle, thoracic spine, and lumbar spine who has achieved 12 years of survival with clinical improvement and stabilization after 4 years of temozolomide therapy.

This study aims to assess the knowledge, attitudes, and practices (KAP) of liver cancer patients and their family members regarding hepatitis B and liver cancer in hospitals in central and western China.

A multicenter cross-sectional survey was conducted on liver cancer patients and their families between February 2023 and August 2024. Data were collected using a validated, self-developed questionnaire.

A total of 810 valid questionnaires were analyzed, with 432 (53.33%) respondents being family members. The mean scores for knowledge, attitude, and practice were 7.19 ± 3.68, 43.71 ± 4.30, and 39.93 ± 6.06, respectively. Multivariate logistic regression identified education (OR = 3.009 for high school/technical school; OR = 6.771 for associate degree or above), hepatitis B diagnosis (OR = 1.530), and duration of liver cancer diagnosis (OR=1.690) as significant predictors of knowledge scores. Positive attitudes were linked to higher knowledge scores (OR=1.212), high school/technical school education (OR=1.831), and a monthly per capita income of 10,000-20,000 Yuan (OR=2.964). For practices, predictors included higher knowledge scores (OR=1.067), higher attitude scores (OR=1.241), non-disclosure of income (OR=3.311), current alcohol consumption (OR=0.303), and diabetes (OR=2.175).

Liver cancer patients and their family members demonstrated inadequate knowledge but relatively positive attitudes and proactive practices regarding hepatitis B and liver cancer in hospitals in central and western China. This knowledge-practice gap may reflect cultural norms, family support, or public health campaigns, yet improving knowledge remains essential to sustain positive behaviors. Targeted educational interventions should therefore be integrated into clinical and community care. In particular, future interventions should be tailored to address urban-rural disparities and to actively involve family members in supporting patients. These findings provide practical implications for enhancing health literacy, guiding policymaking, and improving counseling strategies to strengthen disease management and prevention.

Osteosarcoma (OSA) is the most common primary bone neoplasm affecting dogs and the appendicular bones are frequently affected, accounting for up to 80% of reported cases. After tumor diagnosis and staging, surgery followed by adjuvant chemotherapy is the standard treatment of care. The purpose of this narrative literature review is to describe the anatomical landmarks and amputation techniques performed in the treatment of canine appendicular OSA, also using cadaveric models to demonstrate it. Surgical treatment options may include amputation of the affected limb, considered the standard of care. For thoracic limbs anterior quarter amputation, amputation with shoulder disarticulation, and midhumeral amputation. For pelvic limbs, amputation with hemipelvectomy, amputation with hip disarticulation, and midfemoral amputation. Anatomical knowledge is fundamental for performing a meticulous and correct technique, which allows a lower risk of recurrence and intra-operative and post-surgical complications.

One of the most common malignant tumors in women worldwide is breast cancer, which affects even more than one-third of all female tumor patients. Patient outcomes and effective therapeutic strategies are frequently determined by molecular subtypes in breast cancer. However, the underlying epigenetic characteristics that could further divide breast cancer patients into groups and affect their outcomes could be the reason for the differences in therapeutic response. It is true that there have been recent findings about the role of epigenetic abnormalities in cancer, and that therapeutics targeting particular epigenetic pathways have been developed. Phytochemicals function as gene regulators in a variety of cancers and are crucial to the pathophysiology of many human cancers, including breast cancer. Preclinical studies have revealed that phytochemicals exhibit promising therapeutic efficacy against breast carcinoma by modulating several epigenetic alterations including DNA methylation, histone modifications, non-coding RNA and estrogen associated epigenetic changes. Nevertheless, despite promising in vitro and in vivo results, the clinical application of phytochemicals targeting epigenetic markers in breast cancer is limited. Further research is required to confirm their effectiveness and safety in clinical settings. Thus, this study provides a thorough summary of how epigenetic changes contribute to the development of breast cancer. This article also explores the potential benefits of phytochemicals, such as flavonoids, terpenoids, alkaloids, isothiocyanates, and quinones, in modulating these epigenetic markers in preclinical models of breast cancer.