Metabolic dysfunction-associated steatotic liver disease (MASLD) is now the most common chronic liver disease in the Western world, driven by obesity, insulin resistance, and systemic inflammation. Its progressive form, metabolic dysfunction-associated steatohepatitis (MASH), can culminate in cirrhosis and hepatocellular carcinoma (HCC). While lifestyle modification remains central to MASLD management, there is growing interest in pharmacological interventions, particularly nutrient-stimulated hormone-based therapies (NuSHs), such as GLP-1 receptor agonists. NuSHs exert metabolic and anti-inflammatory effects primarily via weight loss and improved insulin sensitivity. Emerging clinical data support their efficacy in resolving MASH without worsening fibrosis. However, benefits in cirrhotic patients are less evident, suggesting greater utility in early intervention. Observational studies and clinical trials suggest a reduction in liver-related morbidity with GLP-1 receptor agonist use, though fibrosis regression remains inconsistent. Preclinical models indicate that NuSHs may also reduce MASH-related HCC incidence and tumor burden, likely through systemic metabolic improvements rather than direct antineoplastic action. Observational human data following bariatric surgery reinforce this link, suggesting that weight loss itself plays a key preventive role. Herein, we propose that NuSHs are promising candidates for MASH-related HCC prevention. We provide mechanistic suggestions for how this may occur. Furthermore, incorporating NuSHs into the post-locoregional treatment pathway for HCC may delay the need for systemic anti-cancer therapies, improve immunotherapy synergy and transplant eligibility, and even slow disease progression through reversal of carcinogenic drivers. Future studies are needed to target oncological endpoints and clarify immunometabolic mechanisms to guide the integration of NuSHs into MASLD treatment algorithms.

Sterol regulatory element-binding protein 1 (SREBP1), a key regulator of lipogenesis, is highly expressed in tumors, but the mechanisms sustaining its elevated levels remain unclear. The role of UFMylation, a posttranslational modification, in modulating SREBP1 stability and tumor progression has not been explored. This study aimed to investigate the role of UFMylation in the progression of liver cancer.

Liquid chromatography-tandem mass spectrometry was employed to investigate the interacting proteins of ubiquitin-fold modifier 1-specific ligase 1 (UFL1). Knockdown of UFL1 and DDRGK domain-containing protein 1 (DDRGK1) was performed to assess SREBP1 stability. In vitro and in vivo models of hepatocellular carcinoma (HCC) were used to evaluate tumor progression. Clinical correlations between UFL1/DDRGK1 and SREBP1 levels were analyzed in HCC patient samples.

SREBP1 undergoes UFMylation, which synergizes with ubiquitination to reduce its stability. Depletion of UFL1 or DDRGK1 increased SREBP1 stability, driving HCC progression. Clinically, UFL1 and DDRGK1 levels were reduced in HCC tissues and inversely correlated with SREBP1 expression. Fatostatin (an SREBP1 inhibitor) enhanced the therapeutic effect of Lenvatinib in HCC models with low UFL1 expression.

UFMylation is a critical posttranslational modification that destabilizes SREBP1, and its dysregulation contributes to HCC progression. Targeting the UFMylation-SREBP1 axis, particularly through Fatostatin and Lenvatinib combination therapy, represents a novel therapeutic strategy for HCC.

Medulloblastoma (MB) is a malignant neoplasm that is relatively common in children but rare in young adults, accounting for less than 1% of all intracranial tumors. This study reports a rare case of MB metastasis to the right temporoparietal region in a 42-year-old woman, presenting with focal neurological symptoms such as weakness in the left arm and leg, speech disturbances, and impaired coordination. The patient had a history of cerebellar MB and underwent surgical resection, radiation therapy, and chemotherapy. Despite treatment, metastasis occurred, highlighting the diagnostic and therapeutic challenges in adult MB cases. The article also reviews the literature on MB in young adults, emphasizing the importance of dynamic neuroclinical monitoring and timely instrumental diagnosis for early detection and management of MB metastases.

Chimeric antigen receptor (CAR)-T cell therapy faces significant challenges in treating solid tumors, including immune evasion, suppressive tumor microenvironments, and on-target/off-tumor toxicity, which limit its clinical efficacy. Although it has revolutionized treatment for hematological malignancies, these obstacles hinder its broader application in solid tumors. Nanotechnology offers innovative strategies to address these limitations through enhanced delivery, localization, and control. This review summarizes recent advances in nanotechnology-assisted CAR-T cell therapies for gynecologic cancers, with a particular focus on messenger RNA (mRNA)-based delivery systems, lipid nanoparticles, hydrogels, and external activation techniques such as photothermal and acoustogenetic modulation. The integration of nanotechnology, especially mRNA-based delivery systems, holds transformative potential for overcoming these barriers. mRNA enables transient, non-integrating expression of CARs, meaning the genetic modifications are temporary. This improves safety and allows flexible control over treatment intensity, while rational sequence optimization (e.g., codon usage, guanine-cytosine content, secondary structure) enhances mRNA stability and protein translation efficiency. Lipid nanoparticles, the leading delivery platform, can be engineered for cell-type specificity and tissue targeting through modulation of their components and surface functionalization. Recent innovations, including siloxane-modified lipid nanoparticles, injectable hydrogels, and photothermal or acoustogenetic activation strategies, enable precise spatiotemporal control of CAR-T cell function in vivo. In ovarian cancer, preclinical studies targeting nfP2X7 and employing multifunctional nanoparticles have demonstrated synergistic efficacy and tumor-specific delivery. This review highlights how nanotechnology platforms can be integrated with CAR-T cell therapies to enhance safety, precision, and therapeutic outcomes in ovarian cancer.