This study aimed to evaluate the diagnostic accuracy of the apparent diffusion coefficient (ADC) derived from diffusion weighted imaging (DWI) for detecting lymph node metastasis in breast cancer.

Hypopharyngeal carcinoma (HC) is one of the rarest and worst head and neck cancers (HNC) with insidious location, atypical early symptoms, and frequently diagnosed in advanced stages. The risk factors of HC mainly include smoking and drinking. Preventive interventions directed towards environmental risk factors are highly likely to yield far-reaching beneficial effects in reducing the incidence of this disease. The majority of advanced HC patients undergo multimodal treatments that encompass radiotherapy, chemotherapy and surgery, with poor oncological and functional outcomes. The early diagnosis and management of HC are vital for improving the prognosis of patients. Currently, there are few reviews specifically focusing on early HC, thus this review aims to summarize the current advancements in the diagnosis and management of early HC. Magnifying endoscopy with narrow-band imaging (ME-NBI) can improve the detection rate of early lesions and assess the invasion depth by enhancing the visualization of microvascular patterns. In recent years, artificial intelligence (AI) presents a promising prospect in the detection of early HC through deep learning algorithms. Larynx-preserving surgery or radiotherapy alone is predominantly recommended for individuals diagnosed at an early stage, aiming to achieve optimal oncological control while preserving crucial functions. With the increasing detection rates of early HC and the development of surgical equipment, transoral minimally invasive surgery is becoming more widely applied in HC. Its minimally invasive nature offers reduced morbidity and faster recovery, making it an attractive option for eligible patients with early HC.

Colorectal cancer (CRC) continues to be a leading cause of cancer-related mortality globally, and accurately predicting lymph node metastasis (LNM) in T1 and T2 lesions is vital for informing treatment strategies. This study aimed to assess the diagnostic accuracy of artificial intelligence (AI)-based models, particularly deep learning (DL) and machine learning (ML) approaches, in predicting LNM risk in CRC.

Gallbladder (GB) malignancy is the most common biliary malignancy; however, squamous cell carcinoma of the gallbladder (GBSCC) is extremely rare. Synchronous primary GB and colon cancers are very rare, but they are still adenocarcinomas.

Although several studies have suggested that sarcopenia is associated with adverse outcomes in kidney cancer patients undergoing nephrectomy, the results have been inconsistent. Therefore, this meta-analysis was conducted to investigate the relationship between sarcopenia and post-nephrectomy survival in kidney cancer patients.

Cellular senescence, characterized by partially irreversible cell cycle arrest, has a dual role in cancer progression via the senescence-associated secretory phenotype (SASP). SASP encompasses a wide range of bioactive chemicals, including cytokines, chemokines, growth factors, and proteases, all of which can have a significant impact on the tumor microenvironment (TME). Initially, SASP can enhance tumor suppression by attracting immune cells and inhibiting cancer cell proliferation, but its long-term presence at TME can promote tumor growth, metastasis, and treatment resistance. Moreover, therapy-induced senescence, a common side effect of cancer treatments, can result in an increase of senescent cells and pro-tumorigenic SASP. Therefore, recent research has highlighted the potential of targeting SASP to improve cancer therapy. Among the therapeutic strategies, senolytic therapies selectively eliminate senescent cells, whereas senomorphic drugs decrease SASP without cytotoxicity, and there is also combined therapy targeting SASP for oncotherapy. Therefore, it is of crucial importance to develop more specific senotherapeutics and investigate the clinical applications of SASP modulation, such as using SASP components as biomarkers for therapy monitoring and personalized medicine. Taken together, understanding the molecular processes of SASP induction and their function in TME, including its heterogeneity across cell types and tissues, and designing personalized treatment are critical for optimizing cancer therapy and improving patient outcomes.

The cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) pathway is critical for innate immunity, as it detects cytoplasmic DNA and drives type I interferon signaling. Pharmacological stimulation of this pathway has been recognized as a valuable approach for cancer immunotherapy, especially when used together with immune checkpoint inhibitors (ICIs). Preclinical studies have demonstrated synergistic antitumor effects of cGAS-STING agonists and ICIs across various tumor models, while early-phase clinical trials are exploring their safety and efficacy in patients. Nonetheless, intrinsic tumor resistance, an immunosuppressive tumor microenvironment (TME), and therapy-associated immune toxicities continue to pose substantial obstacles to clinical application. In this review, we provide an overview of the present status of cGAS-STING agonists, emphasizing preclinical and clinical advances in combination therapy with ICIs, and discusses the challenges and future directions to optimize efficacy, improve safety, and expand the therapeutic potential of this strategy in oncology.

Previous meta-analyses have shown TAS-102's potential in metastatic colorectal cancer (mCRC). Thus, we conducted a meta-analysis to investigate the efficacy and safety of TAS-102 combined with bevacizumab versus TAS-102 monotherapy in the treatment of mCRC.

Gastric cancer with peritoneal involvement is becoming increasingly common, particularly among younger patients with diffuse-type disease. This aggressive subtype carries a high symptom burden and severely impacts quality of life (QoL). Novel therapeutic strategies targeting peritoneal metastases, including normothermic intraperitoneal and systemic chemotherapy (NIPS), pressurised intraperitoneal aerosol chemotherapy (PIPAC), and cytoreductive surgery with HIPEC, are reshaping the treatment landscape. Among these, only NIPS has demonstrated a clear overall survival benefit, as shown in the phase III DRAGON-01 trial. PIPAC and CRS with HIPEC hold promise and are currently being investigated in randomised studies. However, patient-reported outcomes (PROs) remain inconsistently captured. For example, neither DRAGON-01 nor PHOENIX-GC reported QoL data despite their clinical impact. By contrast, PERISCOPE II and PIPAC VER-ONE have incorporated PRO measures, including EORTC QLQ-C30 and QLQSTO22, which are expected to provide more patient-centred insights. These instruments, while valuable, may not fully capture peritoneal-specific symptoms, highlighting the need for tailored tools. Routine integration and standardised reporting of PROs are critical to ensure that survival gains are accompanied by meaningful improvements in patient experience. As therapeutic strategies evolve, embedding PROs in trial design is essential for delivering value-based, patient-centred care in gastric cancer with peritoneal metastases. [KD1]LE: Structured abstract is required in this type of journal. Please consider providing the aforesaid.

Claudin 18.2 (CLDN18.2) is a novel treatment target for patients with unresectable or stage IV gastric cancer. However, it remains unclear whether the expression of CLDN18.2 affects survival outcomes. In total, 586 patients with GC were enrolled in this study. CLDN18.2 expression in cancer cells was analyzed by immunohistochemistry. Correlations between CLDN18.2 expression and several clinicopathological factors and survival outcomes were investigated. We also performed a systematic review and a meta-analysis. CLDN18.2 expression was mainly observed in the cell membrane. The CLDN18.2 expression was not significantly correlated with any clinicopathological factor. In all patients, CLDN18.2 did not significantly affect OS. In patients with the diffuse type, the overall survival of patients with CLDN18.2-high expression was worse than that of patients with CLDN18.2-low expression, although the difference was not significant (p = 0.092). Meta-analyses revealed that CLDN18.2 was not significant prognostic factor in resected cases, although CLDN18.2 negative cases showed a trend for worse survival. In, conclusion, CLDN18.2 was not a significant prognostic factor in general, although CLDN18.2 negative cases showed a trend for worse survival. We revealed that patients with CLDN18.2 high expression showed worse survival outcomes especially in the diffuse type.

Colorectal cancer (CRC) remains a leading cause of cancer-related mortality worldwide, highlighting the critical need for the development of innovative and effective therapeutic strategies. Baicalein, a bioactive flavonoid derived from Scutellaria baicalensis, has emerged as a promising anticancer agent with multifaceted effects against colorectal cancer. This work summarizes into the molecular and immunomodulatory mechanisms underlying baicalein's anticancer activity. Baicalein inhibits proliferation, suppresses metastasis, induces apoptosis, and modulates key pathways like PI3K/Akt, MAPK, and TLR4/NF-κB. It enhances the tumor microenvironment by promoting immune cell infiltration, regulating cytokines, and activating CD4 + and CD8 + T cells, amplifying antitumor immunity. By targeting critical oncogenic and immune pathways, baicalein disrupts tumor progression while simultaneously enhancing immune recognition and suppressing tumor-promoting mechanisms in CRC. Additionally, baicalein influences redox homeostasis by modulating reactive oxygen species (ROS) generation and restoring oxidative balance, thereby impacting cancer cell survival and proliferation. Its anti-oxidative properties further mitigate tumor-promoting oxidative stress while sensitizing CRC cells to apoptosis. Baicalein have poor solubility and rapid metabolism limits its effectiveness against colorectal cancer, where nanotechnology-based drug delivery can overcome these challenges. By using nanoparticles (NP) and other nano-carriers to improve stability, targeting, and controlled release, baicalein's anticancer potency and safety can be significantly enhanced for future CRC therapies. Thus, baicalein-NP conjugates can strengthen the immune defense and blocks cancer-promoting signals in colorectal cancer.

Gastrointestinal (GI) malignancies represent a significant global health burden, characterized by high mortality rates and profound resistance to conventional therapies. This necessitates the exploration of novel therapeutic vulnerabilities, and two recently discovered forms of regulated cell death, ferroptosis and cuproptosis, offer promising metabolism-centered strategies. Ferroptosis is a non-apoptotic pathway driven by iron-dependent lipid peroxidation, canonically suppressed by the glutathione peroxidase 4 (GPX4) axis. In contrast, cuproptosis is a distinct process wherein excess copper induces lethal proteotoxic stress through direct binding to lipoylated components of the tricarboxylic acid (TCA) cycle. Critically, these pathways are not mutually exclusive; instead, they are intricately connected through shared molecular nodes and metabolic dependencies, including redox homeostasis, key signaling proteins, and mitochondrial integrity. This review systematically examines the molecular crosstalk between ferroptosis and cuproptosis, highlighting the synergistic potential of their co-activation as a powerful anti-cancer strategy in GI tumors. We systematically evaluate both preclinical evidence and clinical studies for therapeutic interventions, ranging from small-molecule inducers to advanced nanoplatforms and immunotherapy combinations. Furthermore, we discuss the pressing challenges of identifying predictive biomarkers for patient stratification and overcoming adaptive resistance. Ultimately, deciphering the ferroptosis-cuproptosis nexus holds immense potential to unlock a new paradigm of synergistic therapies, paving the way for more effective clinical management of GI malignancies.

Oral squamous cell carcinoma (OSCC) is the most common oral malignancy, often associated with poor outcomes due to metastasis and late detection. The epithelial-to-mesenchymal transition (EMT) is central to OSCC progression, but the prognostic role of EMT markers remains unclear. This systematic review and meta-analysis evaluated five key EMT markers-E-cadherin, EpCAM, Vimentin, TWIST, and SNAIL-in OSCC.

Decreased tobacco use has resulted in substantial declines in the prevalence of upper aerodigestive tract malignancies. However, the prevalence of oral cavity squamous cell carcinomas has been steadily increasing despite decreases in tobacco-related malignancies both within the United States and worldwide. The cause driving the increasing prevalence is unknown and may reflect a combination of viral, environmental, and genetic mechanisms. Radiologists must be familiar with the imaging appearance of oral cavity carcinomas to achieve proper staging and to guide surgical and/or radiation therapy management. This article will review the emerging trends in oral cavity carcinoma, the basics of oral cavity anatomy relevant to subsites of cancer involvement, the imaging appearance of this entity, and the information critical for appropriate staging to direct surgical management, medical treatment, and/or radiation therapy. Keywords: Ear/Nose/Throat, Head/Neck, Tongue, Neoplasms-Primary, Oncology, CT, MR Imaging, Diagnosis, PET/CT, PET/MRI © RSNA, 2025.

Glioblastoma multiforme (GBM), the most invasive primary malignant tumor of the central nervous system, is characterized by an extremely poor prognosis and a high recurrence rate. Its significant molecular heterogeneity challenges precise diagnosis and treatment. Recently, with the rapid development of molecular pathology, the combination of histological and molecular typing has become the mainstream method for GBM diagnosis. Here, we review the impact of classic molecular markers on patient prognosis in GBM, as well as the different values of traditional and novel molecular markers in prognosis assessment. We initially discuss the correlation between molecular markers and recurrence, as well as the research progress of molecular markers in emerging technological fields. Moreover, we propose the challenges currently faced by molecular markers in glioblastoma and discuss future research directions in this field.

Gastric cancer (GC) has a high incidence, resistance to chemotherapeutic drugs and a bleak prognosis. Helicobacter pylori (H. pylori) can promote GC development through Correa's cascade by impacting various forms of programmed cell death (PCD). As an iron‑dependent form of PCD, ferroptosis has emerged as a major focus in biomedical research. Notably, there have been developments in elucidating the mechanisms underlying ferroptosis dysregulation throughout Correa's cascade. On one hand, targeting ferroptosis may provide a promising direction for the development of drugs for chronic atrophic gastritis (CAG) and intestinal metaplasia (IM). On the other hand, targeting ferroptosis in GC may be a potential option to overcome the challenges in conventional therapies such as resistance to chemotherapy. Consequently, the present review aims to deliver a comprehensive understanding of the mechanisms underlying ferroptosis dysregulation in H. pylori‑associated GC and summarize the latest progress of ferroptosis‑related studies in CAG, IM and GC. The present study identifies key regulators of ferroptosis at distinct pathological stages, thereby providing insight of novel strategies for the management of precancerous lesion‑related diseases and GC.

The thioredoxin (Trx) system comprises four core components: Trx‑interacting protein (TXNIP), Trx, Trx reductase (TrxR) and NADPH. TrxR utilizes NADPH to reduce Trx, reducing target proteins through its conserved thiol groups, thereby maintaining cellular redox balance. TXNIP inhibits Trx activity by forming a disulfide exchange reaction with Trx. Beyond its role in redox regulation, the Trx system interacts with various cellular regulators and participates in intracellular signaling networks. The Trx system exhibits dual regulatory roles in autophagy, with Trx primarily exerting an inhibitory effect on ferroptosis and apoptosis, whereas TXNIP promotes these processes. Multiple molecular mechanisms are implicated in these regulatory functions. Furthermore, the Trx system mediates cross‑regulation between autophagy and ferroptosis, as well as autophagy and apoptosis, thereby influencing cellular responses to stress conditions. The present review examines the structural components of the Trx system and the cellular translocation of TXNIP. Additionally, it explores the involvement of the Trx system in various diseases, including neurodegenerative disorders, cardiovascular diseases and cancer, highlighting its potential as a therapeutic target. By analyzing the molecular mechanisms through which the Trx system modulates cell death pathways, including ferroptosis, autophagy and apoptosis, the present review may provide novel research perspectives and theoretical foundations for developing disease treatment strategies.

Amino acid (AA) sensing plays an important role in maintaining cellular metabolic homeostasis as well as tumorigenesis and progression. Studies on classic AA sensing pathways such as rapamycin complex 1 (mTORC1) and general control nonderepressible 2 (GCN2) have revealed their central position in cancer metabolic reprogramming. AA sensing pathways are often hijacked in tumors to adapt to the nutrient‑deprived microenvironment, promoting cell proliferation, anti‑apoptosis and treatment tolerance. In addition, the regulation of AA sensing and transport plays a crucial role in maintaining the metabolic flexibility of tumor cells. By targeting the AA sensing mechanism, it is expected to disrupt the metabolic homeostasis of cancer cells, providing new strategies for precision therapy. The present review summarized the latest advances in the research on the role of the mTORC1 and GCN2 AA sensing pathways in tumor metabolism, emphasizing their potential and the challenges faced in cancer diagnosis and treatment. Additionally, it provided novel insights into the therapeutic targeting of AA sensing pathways and proposes future research directions aimed at overcoming current limitations in cancer metabolism therapy.

Breast cancer (BC) ranks among the most prevalent malignant tumors in female patients. It represents a longstanding challenge to medical professionals in terms of diagnosis and treatment. Exploring BC pathogenesis offers insight into its complexity and facilitates the exploration of more effective treatment strategies. The present review aimed to describe the involvement of the immune system, inflammatory response and regulated cell death in BC development, offering avenues for novel therapeutic strategies against BC. Identifying novel treatment methods is key for enhancing the prognosis of patients with BC.

Ovarian cancer is one of the most malignant tumors in women. Long noncoding RNAs have been demonstrated to regulate multiple biological processes, including cell proliferation, migration, apoptosis, and drug resistance, in various cancers. Small nucleolar RNA (snoRNA) host genes (SNHGs) are a group of long noncoding RNAs. Studies have reported that SNHGs are aberrantly expressed in many kinds of cancers and are associated with poor patient prognosis. In ovarian cancer, SNHGs play critical roles in the development and progression of ovarian cancer via different pathways. However, there is a lack of systematic reports on the research progress of SNHGs in ovarian cancer. Therefore, we reviewed the studies on the roles of SNHGs in the early diagnosis, development, and treatment of ovarian cancer and explored the underlying mechanisms to provide new insights into the treatment of ovarian cancer.