ObjectiveThis retrospective case-control study aimed to explore the correlations of blood lipid levels, triglyceride-glucose index, systemic immune-inflammation index, and platelet-to-lymphocyte ratio with colorectal cancer and evaluate their potential value in early risk prediction.MethodsA total of 120 patients admitted to Anqing First People's Hospital between July 2022 and March 2025 were categorized into a control group (n = 60, normal colonoscopy) and an observation group (n = 60, colorectal cancer). Clinical and laboratory data, including sex, age, body mass index, lipid profile, blood glucose, and blood counts, were collected. Triglyceride-glucose index, systemic immune-inflammation index, and platelet-to-lymphocyte ratio were calculated accordingly.ResultsThe observation group had significantly higher rates of drinking history, body mass index, triglyceride, total cholesterol, low-density lipoprotein cholesterol, triglyceride-glucose index, systemic immune-inflammation index, and platelet-to-lymphocyte ratio (P < 0.05). Triglyceride was strongly positively correlated with triglyceride-glucose index (r = 0.921) and negatively correlated with platelet-to-lymphocyte ratio (r = -0.189). Logistic regression identified drinking history (odds ratio = 5.015) and triglyceride-glucose index (odds ratio = 5.937) as independent risk factors. The receiver operating curve of triglyceride-glucose index showed an area under the curve of 0.713, with 78.3% specificity and 65% sensitivity.ConclusionTriglyceride-glucose index, along with blood lipid levels, systemic immune-inflammation index, and platelet-to-lymphocyte ratio, is closely associated with colorectal cancer. Triglyceride-glucose index may be a promising biomarker for early screening.

As a major contributor to cancer-associated deaths, advanced colorectal cancer (CRC) has a constrained range of effective treatment options. The short isoform of bromodomain-containing protein 4 (BRD4-S) has recently been implicated as a potential oncogenic driver; however, its regulatory mechanisms and functional role in CRC remain incompletely understood.

Osteosarcoma (OS) is a highly aggressive primary bone malignancy with a prominent propensity for metastasis. The identification of the key molecular drivers for OS progression is paramount to developing effective therapies. Although kinesin family member 18A (KIF18A) has previously been suggested to play a role as a potential oncogene in the development and metastatic progression of several types of cancer, little is known about its exact functional role in OS.

Since its introduction in 2008, sorafenib has remained the standard first-line systemic treatment for advanced hepatocellular carcinoma (HCC). Nevertheless, its clinical benefits are often compromised by the rapid emergence of drug resistance. This study explores the molecular mechanisms underlying sorafenib resistance, with particular emphasis on the involvement of connective tissue growth factor (CCN2/CTGF) in the regulation of c-Met signaling pathways.

Macrophage infiltration is prevalent in lung cancer tissues, significantly influencing disease progression and clinical outcomes. Lung squamous cell carcinoma (LUSC) is often diagnosed at advanced stages, resulting in poor prognosis. Identifying effective diagnostic biomarkers, particularly those associated with macrophage infiltration, is crucial for early detection and improved treatment outcomes. This study aims to identify diagnostic markers specifically linked to M1 macrophages in LUSC.

Ankyrin G (ANK3), belonging to the ankyrin family, contributes to cellular structural integrity by linking the cytoskeleton to the plasma membrane. Abnormal ANK3 expression has been reported across several human malignancies, yet the regulatory mechanisms involved are still poorly understood. The process of dividing introns into several steps is referred to as recursive splicing (RS). RS can control the quality of transcripts produced by regulating the retention of the RS-exon. Hundreds of annotated RS-exons in human mRNAs are attributed to the inhibition of RS by the exon junction complex (EJC).

Resistance to anoikis is a critical mechanism that enables metastatic dissemination. Abrogation of this cellular safeguard is therefore a hallmark of aggressive cancer progression. Despite the importance of anoikis, there are still few biomarkers among anoikis-related genes (ARGs) that could aid in the prognostication of bladder cancer (BC) patients and potentially serve as drug targets.

Research on the molecular progression of esophageal squamous dysplasia to cancer remains limited. The majority of prior studies have focused on morphological precancerous lesions sampled adjacent to tumors, and have relied primarily on the analysis of data from whole-exome sequencing.

Faust Akl et al. revealed in Nature a paradigm-shifting mechanism distinct from myeloid-driven immunosuppression, whereby glioblastoma induces T-cell apoptosis via tumor-derived IL-11, prompting astrocytes to reprogram into immunosuppressive tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)+ effectors, thereby establishing astrocytes as active immunomodulators. Therapeutically, herpes simplex virus type 1 (HSV-1) (anti-TRAIL) achieves a dual therapeutic effect, offering novel strategies to overcome glioblastoma (GBM)'s evasion tactics.

The tumor microenvironment, especially the extracellular matrix (ECM), plays a critical role in cancer initiation and progression, although its underlying mechanisms remain incompletely understood. Conventional therapies (such as chemotherapy, surgery, and radiotherapy) often produce unsatisfactory outcomes. Immunotherapy, while showing limited clinical success to date, holds considerable promise. Growing evidence indicates that the biophysical properties of the ECM interact with immune cells, contributing to mechanisms of immunotherapy resistance in cancer. Alterations in these ECM properties can impair immune cell infiltration and function, thereby diminishing the effectiveness of immunotherapeutic approaches. This review explores how the biophysical features of the ECM and their crosstalk with tumor immune evasion pathways highlight the potential of ECM-targeted immunotherapy as an innovative strategy for cancer treatment.

Liver cancer, particularly hepatocellular carcinoma (HCC), represents a global health challenge. The tumor microenvironment (TME) plays a pivotal role in the progression and therapeutic resistance of HCC. Interventional therapies have emerged as pivotal modalities in the treatment of liver cancer, especially in cases that are unsuitable for surgical resection. The evolution of these techniques has been markedly enhanced by the integration of artificial intelligence (AI), which has the potential to increase precision, improve outcomes, and personalize patient care. This review covers modern interventional therapies for liver cancer, highlighting recent advances in minimally invasive procedures. It describes the intricate liver TME and emphasizes the importance of characterizing its diversity and identifying therapeutic targets. Additionally, we discuss how AI can decipher TME complexities, predict responses, categorize patients, and personalize treatments. By elucidating connections between the TME, therapeutic interventions, and AI, this review aims to improve the management and care of patients with liver cancer.

Clonal hematopoiesis (CH) is characterized by the expansion of hematopoietic stem and progenitor cells harboring somatic mutations, which confers an increased risk of hematologic malignancies and cardiovascular disease. Among CH-associated mutations, mutations affecting splicing factors (SFs), including splicing factor 3b subunit 1 (SF3B1), serine/arginine-rich splicing factor 2 (SRSF2), U2 small nuclear RNA auxiliary factor 1 (U2AF1), and zinc finger CCCH-type, RNA binding motif and serine/arginine rich 2 (ZRSR2), play a unique role in promoting clonal expansion and leukemogenesis. In this review, we summarize recent findings on the role of SF mutations in CH progression, their interplay with other mutations (e.g., DNA methyltransferase 3 alpha (DNMT3A), ten-eleven translocation methylcytosine dioxygenase 2 (TET2) and isocitrate dehydrogenase 2 (IDH2)), and their impact on hematopoietic homeostasis. Epidemiological studies have demonstrated that SF-mutant CH exhibits an accelerated clonal expansion compared to other CH clones. Furthermore, murine models suggest that SF mutations alone do not inherently confer a growth advantage for clonal expansion but rather enhance disease phenotypes when co-existing with epigenetic mutations, such as IDH2 and TET2. These findings suggest that SF mutations contribute to CH expansion and malignant transformation through a synergistic interplay with other mutations and external factors such as inflammation. Given the clinical significance of SF mutations, ongoing research is focused on developing targeted therapies that modulate aberrant RNA splicing and prevent CH-driven leukemogenesis. Understanding the mechanisms underlying mutant spliceosome-mediated CH expansion may provide novel insights into early detection, risk stratification, and therapeutic interventions in hematologic malignancies.

Over the past 30 years, advancements in radiotherapy have transformed the treatment of pediatric ependymoma, improving tumor control and reducing treatment-related complications. Early protocols, such as RT1 and ACNS0121, demonstrated the efficacy of immediate post-operative radiotherapy, particularly for children as young as 12 months, setting benchmarks for modern treatment strategies. The introduction of conformal photon therapy revolutionized tumor targeting by minimizing radiation exposure to surrounding normal tissues, while proton therapy has emerged as the preferred modality in developed countries due to its superior normal tissue-sparing properties. Despite these advances, long-term comparative data between photon and proton therapy remains limited. Critical factors in radiotherapy planning include tumor location, patient age, molecular features, and the potential for neuraxis dissemination. Advances in imaging, such as high-resolution MRI and emerging molecular staging techniques, have enhanced precision in treatment planning and risk stratification. However, challenges persist for patients with residual or recurrent disease. Reirradiation has emerged as a promising option for relapse, demonstrating high rates of tumor control and low risks of complications when combined with timely surgical intervention and multidisciplinary care. This chapter highlights the importance of leveraging data from three separate clinical trials to refine treatment strategies and address cognitive outcomes, which have been identified as a major area of clinical importance and research. Future trials are expected to explore molecular risk stratification and the integration of systemic therapies alongside radiotherapy to optimize outcomes, ensuring continued progress in the care of children with ependymoma.

Recent advancements in the molecular understanding of pediatric brain tumor biology have significantly contributed to the development of innovative therapeutic strategies aimed at improving clinical outcomes for affected children. These scientific breakthroughs have facilitated the identification of specific molecular targets and signaling pathways integral to the oncogenesis of pediatric brain tumors, thereby enabling the design of targeted therapies that disrupt these pathogenic processes. Furthermore, the incorporation of immunotherapy and precision medicine approaches has unveiled novel therapeutic avenues, offering the potential for more efficacious and less toxic treatment modalities. As research in this domain continues to progress, these cutting-edge therapeutic interventions are anticipated to enhance survival rates and improve the quality of life for pediatric patients. This review delineates emerging interventional treatments in pediatric brain tumor management and examines the persistent challenges within the field.

Non-germinomatous germ cell tumors (NGGCTs) are rare, histologically diverse malignancies that primarily affect children and adolescents. Unlike germinomas, NGGCTs are less responsive to chemotherapy and radiation, resulting in a less favorable prognosis and necessitating intensified multimodal therapy. This chapter provides a comprehensive overview of NGGCTs, including histological subtypes, clinical presentation, diagnostic strategies, and established as well as emerging treatment paradigms. We discuss current classification systems, the roles of tumor markers and neuroimaging, and challenges in histopathologic diagnosis. Treatment approaches vary globally but typically include intensive chemotherapy combined with craniospinal or whole-ventricular irradiation. Long-term outcomes remain suboptimal for high-risk subtypes, especially those with yolk sac tumor, choriocarcinoma or embryonal carcinoma components. Recent genomic and epigenomic studies have revealed recurrent alterations in the RTK/MAPK and PI3K/mTOR pathways, along with distinctive methylation signatures and copy number aberrations, offering insights into tumorigenesis and potential therapeutic targets. Ongoing trials continue to focus on refining risk stratification and minimizing treatment-related toxicities. These efforts, along with advances in molecular characterization, may ultimately improve survival and long-term quality of life in patients with CNS NGGCTs.

Central Nervous System (CNS) germinomas are rare, malignant germ cell tumors that predominantly affect children, adolescents and young adults (AYA). These tumors are highly sensitive to irradiation and chemotherapy, making them one of the most curable intracranial malignancies. This review provides a comprehensive overview of germinoma, covering epidemiology, pathogenesis, clinical presentation, diagnostic approaches, treatment strategies, and long-term outcomes. We also discuss recent advances in molecular biology and their implications on future therapeutic developments.

Introduction Adamantinomatous craniopharyngioma (ACP) is a significant source of morbidity in the pediatric brain tumor population. It predominantly arises from the parasellar space. The tumors proximity to key vital structures often makes gross total surgical resection challenging and sometimes clinically inadvisable. Compounding the problem, adjunct therapies are not yet capable of providing a definitive cure. Recent preclinical research has made significant progress towards elucidating the mutagenic drivers of ACP, however much work remains to translate this into safe and effective treatments. Content Overview and Key Takeaways In the following chapter, we discuss the most up-to-date understanding of ACP biology and management. ACP is a histologically low grade tumor characterized by a mutation involving the beta-catenin protein, resulting in pathologic stability of the protein that impairs cell death or apoptosis. A subpopulation of tumor cells then enter a transcriptomic state characterized by cellular oncogenic senescence. It is unclear how this state leads to feed forward loops resulting in tumorigenesis. Despite its benign nature, the consistent anatomic origin of ACP in the sellar/suprasellar space, often abutting or involving the hypothalamus, the infundibulum, and the optic chiasm, contributes to multiple long-term complications such as endocrinopathies, obesity, vision loss, and obstructive hydrocephalus. Surgically, the current trend is towards conservative approaches with the goal of maximal safe resection without perturbing the hypothalamus. Adjunct radiotherapy is standard in cases of residual or recurrent disease. Close coordination with endocrinology colleagues is vital to appropriately care for these patients as they often suffer from lifelong endocrinopathies that remain a significant source of burden in this population.

Atypical teratoid rhabdoid tumors (ATRT) are rare, often lethal embryonal tumors of the central nervous system (CNS) that primarily affect very young children. Intensive multimodal approaches have resulted in improvements in survival albeit with significant associated toxicity. Recent molecular studies have led to the discovery of SMARCB1 inactivation and resultant BAF47/INI1 loss as the near-universal key genetic event that leads to widespread epigenetic dysregulation. Rarely, SMARCA4 encoding BRG1 is impacted. SMARCB1 and SMARCA4 are core subunits of the SWI/SNF chromatin remodeling complex, which is a fundamental epigenetic regulator of gene transcription. Up to a third of patients diagnosed with ATRT have Rhabdoid Tumor Predisposition Syndrome (RTPS) characterized by germline SMARCB1 (or SMARCA4) alterations. Patients with RTPS are at increased risk of developing synchronous or metachronous rhabdoid tumors outside the CNS. At least three molecular subgroups of ATRT (ATRT-TYR, ATRT-SHH, ATRT-MYC) have been identified through large-scale DNA methylation and transcriptomic studies, with each subgroup having distinct transcriptional, epigenomic and clinicopathologic features. In this book chapter, we will summarize key epidemiological and clinical features of ATRT, review current conventional multimodal regimens, summarize key findings from conducted prospective trials and recently concluded (2020 to present) meta-analyses, as well as discuss emerging targeted treatment approaches that exploit potential therapeutic vulnerabilities of this epigenetically influenced tumor.

Medulloblastoma, once considered a uniform entity, is now accepted as a complex and heterogeneous group of tumors requiring a nuanced and multidisciplinary approach to diagnosis and treatment. The now four recognized primary subgroups have distinct genetic, epigenetic, and clinical characteristics that influence prognosis and treatment responses necessitating subgroup-specific strategies. Advances in diagnostics and risk stratification, largely driven by a deeper understanding in tumor biology, has led to an overall improvement in survival (>70 %), through risk-adapted treatment strategies. Contemporary clinical approaches incorporate a multimodality treatment strategy, integrating surgery, radiotherapy and intensive chemotherapy, each of which is associated with significant short- and long-term morbidity. Novel targeted therapeutics continue to be developed, investigated and explored in vitro, in vivo and through clinical trial design, particularly in the high risk and relapsed settings. As the therapeutic landscape continues to evolve, combining conventional therapies with these approaches holds promise to improve clinical outcomes. These innovations and developments expanding all disciplines aim to continue to provide precision-based care and enhance survival outcomes across all subgroups whilst mitigating the significant long-term burden of treatment-related sequelae disproportionately experienced by medulloblastoma survivors.

Pediatric-type diffuse low grade glioma are a novel subgrouping of pediatric glioma defined in the updated WHO 2021 classification of central nervous system tumors. The newly recognized pediatric-type diffuse low grade glioma family is comprised of four distinct entities, including diffuse astrocytoma MYB or MYBL1-altered, angiocentric glioma, polymorphous low-grade neuroepithelial tumor of the young, and diffuse low grade glioma MAPK-altered. Due to significant overlap in histopathology and molecular alterations between pediatric-type diffuse low grade glioma, accurate diagnosis of these tumor subtypes requires integration of both histology and molecular findings. Herein, we describe the epidemiologic, imaging, and molecular features of these pediatric diffuse glioma. In addition, we review current knowledge regarding management approach and treatment outcomes, including potential therapeutic implications of prevalent molecular alterations within this family of tumors.