Cancers are complex diseases characterized by dynamic perturbations of regulatory networks across multiple hierarchical levels, which cannot be fully captured by alterations in a small number of genes. To this end, based on the concept of Hallmarks of Cancer, a whole genomic data-driven approach is proposed to capture the dynamic variation from normal to cancerous cells. This framework focuses on the characteristic functional modules of cancer via hallmarks of cancer by constructing a coarse-grained gene regulatory network of hallmarks. Through this framework, with stochastic differential equations, macroscopic dynamic changes in tumorigenesis are simulated and further explored. The analysis results reveal that network topology undergoes significant reconfiguration before shifts in hallmark levels, serving as an early indicator of malignancy. A pan-cancer examination across 15 cancer types uncovers universal patterns, for example, the "Tissue Invasion and Metastasis" hallmark exhibits the most significant difference between normal and cancer states, while "Reprogramming Energy Metabolism" shows the least pronounced differences. These findings reinforce the systemic nature of cancer evolution, highlighting the potential of network-based systems biology methods for understanding critical transitions in tumorigenesis.

Radiation pneumonitis (RP) is a major dose-limiting toxicity in concurrent chemoradiotherapy (CRT) for stage III non-small cell lung cancer (NSCLC). Existing models often analyze a single lung region and rely on a single algorithm, limiting accuracy and external validity.

The COMS (Collaborative Ocular Melanoma Study) eye plaques are based on the application of low-energy photon sources such as iodine-125 (125I) and palladium-103 (103Pd). Compared to 125I, 103Pd is characterized by different radiobiological and physical parameters, which include the half-life, relative biological effectiveness (RBE), and average photon energy. Variation of these parameters may increase or decrease the integrated cell-killing effect of eye plaques; therefore, quantitative evaluation of biological effects may be used to optimize the dose prescription and improve the therapeutic ratio.

Metastatic head and neck squamous cell carcinoma (mHNSCC) poses a significant threat to patient survival. Previous studies have identified cathepsin L (CTSL) as a key driver of tumourigenesis, metastasis and chemoresistance. However, the regulatory mechanisms underlying CTSL expression remain poorly understood.

Immunotherapy resistance in microsatellite-stable colorectal cancer (CRC) remains a major therapeutic challenge. Recent strategies to overcome the immunosuppressive tumor microenvironment have focused on reactivating innate immune pathways, particularly the cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) axis, which links cytosolic DNA sensing to proinflammatory cytokine production and T cell activation. Although STING agonists show promise, their clinical application is limited by poor drug stability and cytokine storms triggered by excessive STING activation. This study establishes valosin-containing protein (VCP/p97) as a druggable target to potentiate cGAS-STING-driven antitumor immunity, offering a promising therapeutic strategy to overcome immunotherapy resistance in CRC.

Neoadjuvant chemoimmunotherapy (NACI) shows promise for locally advanced cervical cancer (LACC), but drug-tolerant persister (DTP) cells and immunosuppressive microenvironmental adaptations limit clinical efficacy. The underlying determinants governing heterogeneous responses to NACI regimens remain poorly understood, particularly regarding how dynamic tumor-immune interactions shape therapeutic outcomes.

Despite remarkable advances in cancer immunotherapy, including immune checkpoint inhibitors and adoptive cell therapies, many patients fail to achieve durable responses due to factors such as immunosuppressive tumor microenvironments, poor tumor antigenicity, and systemic toxicity. These limitations underscore the need for alternative platforms that can elicit robust and localized antitumor immune responses. Bacteria have emerged as promising candidates owing to their natural ability to selectively colonize tumors, stimulate innate and adaptive immunity, and be engineered for therapeutic delivery. However, the therapeutic potential of naturally occurring marine bacterial strains remains largely unexplored in colorectal cancer.

The goal of this review is to describe data for nonendoscopic screening techniques for the detection of Barrett's esophagus (BE). Endoscopic screening is currently the primary modality for BE detection. A more effective strategy could use risk-based models that integrate clinical factors and are embedded in electronic health records to guide screening. High-risk patients may need endoscopy, while low-risk patients could benefit from less invasive tools like cell collection devices with biomarkers. Integrating BE screening into primary care will be critical in improving early detection of esophageal adenocarcinoma.

Endoscopic Barrett's esophagus (BE) screening detects premalignant changes, enabling the detection of BE and endoscopic surveillance to detect dysplasia/esophageal adenocarcinoma (EAC). Endoscopic therapy for BE dysplasia reduces EAC risk and can treat early stage EAC effectively. Screening is advised for those with multiple risk factors: chronic reflux, age over 50 years, male sex, Caucasian race, smoking, central obesity, hiatal hernia, or family history. Risk prediction tools are evolving. High-definition endoscopy with biopsies enables detection; precise landmark identification is key.

Barrett's Esophagus (BE) is a key precursor to esophageal adenocarcinoma that requires quality management to improve patient outcomes. This article explores current evidence-based practices in the diagnosis, surveillance, and endoscopic treatment of BE, with a focus on quality indicators including biopsy protocols, dysplasia detection techniques, and adherence to surveillance intervals. We examine emerging technologies, such as image-enhanced endoscopy and artificial intelligence, with emphasize on the importance of training, audit, and standardization in clinical practice. By aligning care with established quality benchmarks, clinicians can enhance the early detection and prevention of neoplastic progression in patients with BE.

Advances in endoscopic eradication therapy (EET) have improved the ability to achieve complete eradication of intestinal metaplasia. A multimodal approach of endoscopic resection followed by ablative therapy remains the cornerstone of EET for BE and BE-related dysplasia. However, challenges exist in patients with refractory and recurrent BE. Modifiable risk factors such as uncontrolled reflux should be addressed medically or surgically. Salvage therapy can be utilized in refractory BE, but endoscopists should be cautious of adverse effects such as stricture formation. Principles of management of recurrent BE are similar to patients undergoing initial EET.

Early detection of neoplastic lesions in Barrett's esophagus is essential for curative treatment. Endoscopic resection (ER) is effective for the treatment of these lesions and enables accurate histologic diagnosis. Most used ER techniques include band-assisted endoscopic mucosal resection (multiband mucosectomy [MBM]) and endoscopic submucosal dissection (ESD). MBM allows for quick removal of lesions less than 20 mm. ESD is a more challenging technique and enables en-bloc resection of larger, deeper invading lesions. Both have similar safety and efficacy outcomes. While we await data of prospective studies, the choice should be individualized based on lesion characteristics, patient factors, and endoscopist expertise.

Barrett's Esophagus (BE) is the precursor lesion of esophageal adenocarcinoma, which has a poor survival rate while having the fastest growing incidence of any cancer in the United States. Identifying patients with BE in the general population and optimizing surveillance programs to treat patients before the onset of adenocarcinoma are significant challenges. Clinical translation of advances in understanding BE pathogenesis and drivers of progression, along with improving pathologic diagnostic accuracy of precancerous lesions, holds promise to improve outcomes. This review highlights current concepts in BE-related surgical and molecular pathology and how these advances are being incorporated into daily clinical practice.

In this article, we aim to provide an in-depth review of the 2 primary ablative therapies, radiofrequency ablation and cryotherapy, for the treatment of dysplastic Barrett's esophagus (BE). Specifically for cryotherapy, the article will focus on liquid nitrogen spray cryotherapy and cryoballoon ablation. For each ablative modality, we will discuss the mechanisms of action, technical aspects, indications, patient selection, treatment protocols, efficacy, safety, and outcomes of both therapies. Additionally, we will provide an overview of the role of endoscopic eradication therapy within the broader management strategy of BE, including pretreatment assessment, patient counseling, and long-term surveillance.

Comparative analyses of normal esophageal tissue, Barrett's Esophagus (BE), and esophageal adenocarcinoma have identified distinctive molecular alterations in genomic DNA, epigenetics, non-coding RNA, and proteins that have shown promise as disease-specific biomarkers. Some of the best characterized and promising biomarkers for managing BE are multi-target esophageal cytology DNA assays based on methylated-DNA and immunohistochemical staining of Trefoil factor 3. Additional biomarkers including microRNA, measures of genomic instability, mixed-method panels, and other novel biomarkers (e.g. volatile organic compounds and saliva microbiome) remain in early development and will need further validation in large, prospective studies prior to clinical use.

Barrett's esophagus (BE), a premalignant condition linked to chronic gastroesohageal reflux disease, increases the risk of esophageal adenocarcinoma. Surveillance faces challenges including sampling error and subtle neoplastic changes. Enhanced imaging technologies like narrow band imaging and artificial intelligence improve dysplasia detection and risk stratification. This review explores their evolving roles in BE diagnosis and management.

Post-endoscopy esophageal neoplasia (PEEN) and post-endoscopy esophageal adenocarcinoma (PEEC) comprise a significant component of all Barrett's esophagus-related neoplasia diagnoses and rates of PEEN/PEEC may be rising. PEEN/PEEC occur primarily due to missed lesions or rapidly progressive disease. Root-cause analysis should be performed for cases and best practices should be implemented to decrease PEEN/PEEC rates - the most important intervention is a high-quality endoscopic exam. Future efforts should determine the role of biomarkers in identifying individuals at high risk of neoplastic progression, develop additional tissue-sampling techniques to reduce missed lesions, and improve education regarding the principles of a high-quality endoscopic examination.

Surveillance of Barrett's esophagus is essential for preventing and detecting esophageal cancer, particularly esophageal adenocarcinoma. This article examines the importance of ongoing surveillance before and after Barrett's endoscopic treatment to reduce the risk of progression to high-grade dysplasia or esophageal adenocarcinoma. It highlights the emerging role of adjunctive testing, including biomarkers, advanced imaging, and artificial intelligence to improve diagnostic accuracy. Additionally, the article reviews the latest clinical guidelines for surveillance intervals and timing. Overall, this article aims to provide insights into the evolving landscape of Barrett's Esophagus surveillance.

This article seeks to provide updated information on the pathogenesis of Barrett's esophagus (BE) including the possible cellular origins of esophageal columnar cells and the impact of chronic esophageal inflammation. Other considerations include clinical exposures and the importance of risk factor modifications such as weight loss and tobacco cessation. The article summarizes genetic risk factors in the pathogenesis of BE and discusses how familial risk and exposures are considered in current guidelines to identify those who may benefit from BE screening. Finally, insights gleaned from postablative therapy are integrated into this article for both clinical providers and researchers.

Therapeutic advances with the advent of molecularly targeted therapies and immunotherapy have been revolutionary in the management of advanced NSCLC and recently translated into major progress in earlier stages of NSCLC, reshaping the paradigm of neoadjuvant and adjuvant treatment. Novel therapies with bispecific antibodies and antibody-drug conjugates are now being introduced into the field with the aim to overcome acquired resistance mechanisms and improve patient outcomes. This article reviews new therapeutic models emerging in advanced NSCLC and highlights the role of biomarker testing in optimization of upfront treatment selection to inform potential future opportunities for patients with resectable NSCLC.