Small-cell lung cancer (SCLC) is a highly aggressive neuroendocrine malignancy characterized by rapid growth, early metastatic dissemination, and a dismal prognosis. For decades, treatment paradigms remained largely stagnant, particularly for extensive-stage disease (ES-SCLC). However, the last five years have witnessed a significant evolution in the therapeutic landscape.

Background/Objectives: The aim of our study was to evaluate clinical outcomes in patients with small pleomorphic adenoma (PA) after extracapsular dissection (ED) versus superficial parotidectomy (SP). Methods: Following the PRISMA guidelines, a systematic review covering the years from 1950 to 2025 was conducted using the Pubmed/MEDLINE, Cochrane Library, Scopus, Ovid MEDLINE and Embase databases. A single-arm meta-analysis was performed to evaluate intraoperative capsular rupture, recurrence, transient and permanent facial nerve palsy, Frey's syndrome, salivary fistula, seroma and hematoma of patients who underwent ED vs. those who underwent SP, and funnel plots were constructed to evaluate the robustness of the findings. Results: Of the 1793 identified papers, 21 articles met the inclusion criteria. The meta-analysis (2507 patients) reported the following: (1) the risk of recurrence is similar in patients treated with ED and SP; (2) the transient facial nerve palsy rate is lower after ED (p < 0.05), while the permanent facial nerve palsy rate is similar with ED and SP; (3) post-operative complications, especially Frey's syndrome (p < 0.05), are more common after SP. Conclusions: Given the similar recurrence rate and the lower morbidity compared to SP, ED could be considered the treatment of choice for pleomorphic adenomas of the parotid gland that are up to 3 cm in size, mobile and located in the superficial lobe of the parotid gland.

Endothelial transdifferentiation represents a multifaceted process wherein glioma stem cells (GSCs) gradually adopt endothelial characteristics, marked by the expression of endothelial markers (CD31, CD34) and functional traits, while concurrently relinquishing their stem-like properties. This phenomenon is heterogenous in glioblastoma (GBM) samples, but holds importance in terms of prognosis. Typically occurring within hypoxic environments, particularly in perinecrotic regions, endothelial transdifferentiation is influenced by the secretome of neighboring cells, which orchestrates the activation of various signaling pathways including Notch during endothelial lineage commitment, PI3K/AKT, Wnt/β-catenin and epithelial-mesenchymal transition (EMT) during both commitment and maturation. Initially, GSCs organize into vascular-like channels resembling vasculogenic mimicry and express CD144; however, this signature diminishes as endothelial maturation progresses. GSC-derived endothelial cells (ECs) eventually integrate with normal ECs from the tumor periphery, yielding a mosaic pattern. Endothelial transdifferentiation plays a role in response to standard treatments such as temozolomide chemotherapy and radiotherapy.

5-Methylcytosine (m5C), an important RNA modification, has been extensively studied in colorectal cancer (CRC). In recent years, with advances in high-throughput sequencing technology and RNA modification detection tools, the role of m5C modification in tumorigenesis and development has been gradually elucidated and regulated by "writers," "erasers," and "readers," m5C modification affects many biological processes and cancer progression, including cell proliferation, autophagy, invasion, and apoptosis. In CRC, m5C modification affects cancer cell proliferation, migration, invasion, drug resistance, and immunotherapy resistance by regulating RNA stability, metabolic reprogramming, signalling pathway activation, and immune escape. Moreover, m5C modification provides potential biomarkers and targets for early diagnosis and efficacy prediction. In addition, studies on drugs that target m5C modification related proteins have shown that intervention in m5C modification may provide new directions for immunotherapy and molecular therapy for patients with CRC. In summary, m5C modification, an important epigenetic regulators in CRC, provides a new perspective on the mechanism underlying cancer therapy and precision medicine research. Future research should focus on revealing the specific role of m5C modification in the tumor microenvironment and drug resistance mechanisms and promote its clinical translation in diagnosis and treatment.

Systems biology approaches have been applied to prostate cancer to model how individual cellular and molecular components interact to influence cancer development, progression, and treatment responses. The integration of multi-omic experimental data with computational models has provided insights into the molecular characteristics of prostate cancer and emerging treatment strategies that have the potential to improve patient outcomes. Here, we highlight recent advancements that have emerged from systems modeling in prostate cancer. These include descriptions of the molecular landscape of prostate cancer and how genomic alterations inform computational models of disease progression, how evolutionary processes give rise to mechanisms of therapeutic resistance, and the development of innovative treatment strategies such as adaptive therapy. We also highlight current challenges in prostate cancer that can be addressed through systems biology approaches. These include tumor heterogeneity, poor immunotherapy response, a paucity of experimental model systems, and the ongoing translation of computational models for clinical decision making. Leveraging systems biology approaches has the potential to lead to a better understanding of the disease and better patient outcomes in the treatment of prostate cancer.

This review aims to provide a comprehensive description of the clinical presentation, treatment, and histopathological features of extrauterine sites of leiomyomatosis (ESL), such as disseminated peritoneal leiomyomatosis (DPL), parasitic myoma (PM), benign metastatic leiomyoma (BML), and intravascular leiomyoma (IVL). The impact of previous surgery (hysterectomy or myomectomy) on development of intra-abdominal extrauterine leiomyomas (IAELs) and extra-abdominal extrauterine leiomyomas (EAELs) has been evaluated.

RNA is a fundamental biological macromolecule that undergoes several post-transcriptional modifications, including adenosine to inosine (A-to-I) editing by adenosine deaminases acting on RNA (ADARs). These essential enzymes catalyze the conversion of A-to-I in double-stranded RNA (dsRNA) molecules, influencing RNA stability, splicing, and translation, all of which impact various cellular functions. More recently, RNA editing has emerged as a pivotal mechanism in cancer biology, where ADARs, primarily ADAR1 and ADAR2, exert context-dependent roles as either oncogenic drivers or tumor suppressors. Beyond their catalytic editing function, ADARs also regulate cancer-relevant pathways through editing-independent mechanisms, including RNA binding and protein-protein interactions. Dysregulated ADAR activity facilitates carcinogenesis by altering oncogene expression, impairing tumor suppressor pathways, and reprogramming the transcriptome to promote tumor progression. Furthermore, RNA editing may contribute to tumor cell immune evasion by affecting interferon signaling and altering neoantigen presentation, as well as modulating immune surveillance. Additionally, ADAR-mediated RNA modifications contribute to therapy resistance by modifying drug targets and pathways involved in cell survival and repair. This review comprehensively analyzes the multifaceted roles of RNA-editing ADAR enzymes in cancer pathogenesis, emphasizing editing-dependent and -independent mechanisms contributing to tumor progression, immune evasion, and resistance to therapy. Moreover, we highlight the potential of ADARs as prognostic biomarkers and promising therapeutic targets in oncology. This review aims to spark novel precision oncology and cancer immunotherapy strategies by bridging molecular insights with translational applications.

Chemokines are tiny chemotactic cytokines which play a crucial role in pathophysiology by maintaining homeostasis and inflammation. Their role in the tumour microenvironment is very much puzzling because of both pro- and anti-tumourigenic effects. Chemokines have gained much attention today, since it has been recognized that they are game changers in the TME via controlling immune cell recruitment, angiogenesis, metastasis, tumour growth and drug resistance. In this review, we are exploring the role of several chemokines and their receptors in the TME with special focus on immune cell recruitment, immune surveillance, regulation of immune checkpoints and epithelial mesenchymal transition. We are also reviewing the possibility of targeting chemokines along with immunotherapy for better outcome and disease-free survival. A better understanding on the dual role of chemokine in the TME might help to implement novel therapeutic interventions and adopt precision in targeted therapy.

Adenomatoid tumors (ATs) of the Fallopian tube are rare benign neoplasms, accounting for approximately 0.5-1% of all ATs of the female genital tract. They are often asymptomatic and discovered incidentally. Due to their mesothelial origin, histopathological (HP) diagnosis may be uncertain, requiring immunohistochemical (IHC) tests for definitive confirmation.

Background∕Objectives: Appendiceal neuroendocrine tumors (aNETs), though rare and often incidentally discovered, have shown a rising incidence, particularly among younger individuals, due to improved diagnostic practices, and are generally associated with favorable prognosis, with current evidence supporting conservative, individualized management and tailored surveillance strategies based on tumor size, grade, histopathological features, and imaging findings. Study selection for review: A PubMed search was performed to explore the current understanding of aNETs, with emphasis on their etiopathogenesis, diagnostic criteria, and therapeutic strategies. Case presentation: A 42-year-old man underwent an uneventful laparoscopic appendectomy for acute appendicitis, during which a 5 cm appendix with a pale, nodular tip suggestive of a lesion was resected, leading to the incidental discovery of an aNET. Conclusions: aNETs, though rare, are increasingly detected incidentally and have a favorable prognosis, with individualized management and follow-up guided by tumor features and supported by multidisciplinary care.

Breast cancer brain metastases (BCBM) are a significant clinical challenge, especially in aggressive subtypes like HER2-positive and triple-negative breast cancer. This review discusses hormone receptor discordance, it's existence and contributing factors, the role of the bloodbrain barrier (BBB) in metastatic progression, and therapeutic modalities. While local treatments such as surgery and radiotherapy remain foundational, advances in systemic and immunotherapeutic approaches show promising potential. A deeper understanding of molecular mechanisms driving BCBM is essential to guide effective treatments and improve patient outcomes.

Tislelizumab, a PD-1-targeting monoclonal antibody, can potentially treat advanced esophageal squamous cell carcinoma (ESCC). Using pooled clinical data, this study evaluates Tislelizumab's efficacy and safety in advanced ESCC.

Oncolytic viruses (OV) are an emerging form of immunotherapy that utilize naturally occurring or engineered viruses to specifically infect and lyse tumor cells. They achieve tumor treatment through direct tumor cell killing or by inducing immunogenic cell death to enhance immune responses. However, the efficacy of OV has been suboptimal in clinical trials. This review comprehensively examines mechanisms of resistance to OV through three interconnected dimensions: The characteristics of tumors and tumor cells, factors related to stromal cells and the extracellular matrix (ECM) and the host immune status. Potential solutions targeting these mechanisms are also proposed. For instance, OV typically achieve tumor selectivity through tumor‑specific receptors or specific promoters. However, due to inter‑ and intratumoral heterogeneity, the lack of such specific receptors or promoters in tumor cells can lead to off‑target effects of OV, resulting in treatment resistance. The ECM in the tumor microenvironment, such as hyaluronic acid, may also impede viral transport. Additionally, the clearance of OV by immune cells can contribute to suboptimal therapeutic outcomes of OV treatment. Consequently, investigating predictive biomarkers of OV efficacy, utilizing ECM‑degrading enzymes and combining with immune checkpoint inhibitors represents a promising strategy to augment the therapeutic effects of OV. Synthesizing current evidence, it is anticipated that future investigations will optimize the therapeutic effects of OV treatment and bring better immunotherapeutic outcomes for cancer patients.

Radiotherapy improves survival rates in patients with cancer; however, the development of radioresistance hinders its effectiveness, resulting in unfavorable outcomes. A key factor in cancer progression is the dysregulation of autophagy, a lysosomal degradation process governed by various evolutionarily conserved autophagy‑related genes (ATGs). Long non‑coding RNAs (lncRNAs) serve a crucial role in the regulation of autophagy. lncRNAs modulate ATGs and their signaling pathways, contributing to the emergence of radioresistance. The present review offers a comprehensive examination of the critical roles of autophagy and lncRNAs in mediating radioresistance. By enhancing the understanding of these mechanisms, novel therapeutic strategies aimed at increasing tumor radiosensitivity through the modulation of autophagy may be revealed.

Lung cancer (LC) is the second most frequently diagnosed malignancy worldwide and has the highest mortality rate among all types of cancer. Despite advancements in treatment strategies, the overall survival rate for affected individuals remains low. Ferroptosis, a form of regulated cell death characterized by iron‑dependent lipid peroxidation and accumulation of reactive oxygen species, serves a role in LC. The present review aimed to explore the dual role of ferroptosis in LC, examining both its pathological and therapeutic implications. Ferroptosis contributes to tumor progression, modulates the immune microenvironment and influences treatment resistance. Conversely, it also enhances the efficacy of immunotherapy, increases radiosensitivity and decreases chemotherapy resistance. The present study aimed to summarize the potential of ferroptosis‑based strategies, including the use of nanomaterials and combination therapy, to inform future research and therapeutic approaches.

Nasopharyngeal carcinoma (NPC) is an epithelial malignancy closely associated with Epstein‑Barr virus (EBV) infection. Although patients with early‑stage NPC can achieve a high cure rate through radiotherapy, recurrence and distant metastasis remain the primary causes of treatment failure in patients with advanced‑stage NPC. Circular RNA (circRNA) is a class of covalently closed non‑coding RNAs involved in multiple aspects of tumor biology. Recent evidence has shown that certain circRNAs can encode functional peptides, which participate in the regulation of tumor‑related signaling pathways. In NPC, circRNAs have been implicated in the modulation of signaling pathways, including NF‑κB and JAK/STAT, both of which are activated in the EBV‑infected microenvironment. Furthermore, frequently mutated genes in NPC, such as TNF receptor‑associated factor 3 and cylindromatosis lysine 63 deubiquitinase, are known regulators of the NF‑κB pathway, suggesting a potential link between genetic alterations and circRNA‑related mechanisms. This article systematically reviews the biological mechanisms of circRNA‑encoded peptides, summarizes the expression and function of circRNA in NPC and focuses on discussing the potential roles of circRNA‑encoded peptides in tumor microenvironment regulation, immune escape and clinical application prospects. By integrating existing research results, this article aims to provide a new perspective and theoretical basis for the in‑depth exploration of circRNA‑encoded peptides in the field of NPC.

The tumor microenvironment (TME) consists of tumor cells, stromal cells, infiltrating immune cells and non‑cellular components such as extracellular matrix, blood vessels and a wide variety of secreted proteins. Evidence shows that beyond supporting tumor growth, the TME also promotes tumor cell proliferation and invasion and contributes to treatment resistance, ultimately affecting patient prognosis. Cell‑to‑cell communication within the TME is driven by secreted proteins such as cytokines, chemokines, growth factors and interferons, which are produced not only by tumor cells but also by various stromal cells and immune cells. These proteins form a complex signaling network that promotes tumor cell proliferation and invasion and enables tumors to evade innate and adaptive immune responses. Antibody arrays are a technology that can simultaneously screen hundreds of secreted proteins in complex biological samples, aiding in the exploration of this complex signaling network. By combining high‑throughput multiplex immunoassays such as antibody arrays with cellular and molecular biology techniques, researchers have uncovered complex regulatory mechanisms of cytokine networks within the TME. The present review summarized recent findings on the communication between tumor cells and the TME, as well as key secreted proteins essential for tumor progression and the development of therapeutic resistance. In addition, it discusses how high‑throughput antibody arrays contribute to our understanding of regulatory networks of secreted proteins in the TME.

Endometrial cancer (EC) is a common gynecologic malignancy that often exhibits molecular features such as extensive somatic copy number alterations, microsatellite instability and frequent TP53 mutations, which considerably affect the physical and mental well‑being of women. The Fanconi anemia (FA) pathway is a DNA damage repair pathway involving multiple FA genes that play crucial roles in DNA damage repair as well as the maintenance of genome stability. Abnormalities in FA, such as deletions or mutations, may lead to defects in DNA damage repair, resulting in increased genomic instability and/or an abnormal cell cycle, ultimately leading to EC. This comprehensive review provides a systematic summary of EC‑related FA genes, elucidates the roles of various FA genes in EC and further speculates on their related mechanisms to facilitate the development of targeted therapies that specifically target key genes, leading to a more accurate and efficient treatment for EC. The present review searched PubMed and Google Scholar for articles published in English up to June 2025 using keywords such as Fanconi anemia pathway, 22 FA genes (FANCA, FANCB, FANCC, FANCD1/BRCA2, FANCD2, FANCE, FANCF, FANCG, FANCI, FANCJ/BRIP1, FANCL, FANCM, FANCN/PALB2, FANCO/RAD51C, FANCP/SLX4, FANCQ/XPF, FANCR/RAD51, FANCS/BRCA1, FANCT/UBE2T, FANCU/XRCC2, FANCV/REV7, FANCW/RFWD3), endometrial cancer (type I: Endometrioid adenocarcinoma; Type II Uterine serous carcinoma, clear‑cell carcinoma, carcinosarcoma), somatic copy number alterations, microsatellite instability, TP53 mutations, pathogenesis, genomic instability, target therapy.

Brain tumors, particularly gliomas, are among the most lethal malignancies, with high mortality driven by a delayed diagnosis and limited therapeutic efficacy. A central challenge lies in the presence of the blood‑brain barrier (BBB), which severely impedes the delivery of systemically administered therapeutics to tumor sites. Addressing this clinical urgency, nanoparticle (NP)‑based delivery systems have emerged as a transformative strategy to enhance brain‑specific drug accumulation, minimize off‑target toxicity and improve treatment outcomes. The present review systematically examined the recent advances in nanocarrier technologies for targeted brain tumor therapy, including liposomes, solid lipid NPs, dendrimers, polymeric nanoplatforms and inorganic nanomaterials. The design principles, mechanisms for BBB traversal, therapeutic payload compatibility and tumor‑targeting capabilities of NP technologies demonstrated in preclinical models have also been highlighted. In addition to drug delivery, emerging applications of nanocarriers in gene therapy were explored and the impact of protein corona formation on NP behavior in vivo was discussed. Finally, current translational bottlenecks were identified and future design considerations to achieve clinically viable, precision‑targeted nanomedicines for brain tumors were outlined.

Urothelial carcinoma (UC) presents considerable treatment challenges, primarily due to the high rates of therapeutic resistance observed in affected patients. Currently, therapeutic strategies often fail to yield satisfactory outcomes; therefore, there is a need for innovative treatment approaches. The tumor microenvironment (TME) serves a key role in driving treatment resistance in UC, revealing that components such as cancer‑associated fibroblasts, tumor‑associated macrophages and the extracellular matrix contribute to tumor survival and evasion of therapy. Understanding the mechanisms through which the TME influences treatment resistance is key for developing effective countermeasures. Targeting the TME may be an effective therapeutic strategy, as this approach may increase the efficacy of existing treatments and overcome barriers to response. The present review aims to summarize current knowledge regarding the role of the TME in UC treatment resistance, discuss potential strategies for targeting the TME and highlight future research directions. The translation of insights from studies on the TME into therapeutic strategies may improve clinical outcomes for patients suffering from this challenging malignancy.