Myosteatosis is associated with poor outcomes in various liver diseases. However, standardized methods for assessing, defining, and diagnosing myosteatosis in the context of liver diseases remain unclear. Furthermore, the underlying mechanisms by which myosteatosis leads to pathophysiological progression and adverse health outcomes remain elusive. Therefore, in this review, we elaborate on the currently available measures, definitions, and diagnostic criteria of myosteatosis in the existing literature. We thoroughly clarify the recent evidence and data regarding the possible involvement of myosteatosis in the progression and deterioration of various liver diseases and resulting complications, including liver cirrhosis, chronic viral hepatitis, non-alcoholic/metabolic-associated fatty liver disease, primary sclerosing cholangitis, liver transplantation, and hepatocellular carcinoma. Additionally, it synthesizes insights from basic research on the pathogenesis of myosteatosis, which involves multifactorial mechanisms, including insulin resistance, mitochondrial dysfunction, and chronic inflammation. Finally, from an operational and pragmatic perspective, several regimens, including physical, nutritional, and pharmacological therapies, have been discussed as potential treatments for myosteatosis.

Researchers from Universidad Carlos III de Madrid (UC3M), the National Center for Cardiovascular Research (CNIC), and Yale University (USA) have published a comprehensive review article in the journal Cell that proposes a new framework for understanding neutrophils, the most abundant cells of the immune system. Drawing on extensive evidence from recent research, the authors describe neutrophils as a dynamic and adaptable collective, capable of functional diversification and forms of immunological memory, far beyond their traditionally assigned roles.

A prospective phase I/II clinical trial led by QST Hospital reports that carbon-ion radiotherapy achieved five-year local control and disease-free survival rates of 92%, with no grade ≥2 toxicities, in selected patients with stage I breast cancer who did not undergo surgery. Excellent cosmetic outcomes were maintained. These findings position carbon-ion therapy as a promising alternative for medically inoperable patients or those who decline surgery and support the need for larger, controlled studies.

Hepatocellular carcinoma (HCC), characterized by high aggressiveness and recurrence, poses a significant global health challenge. The interplay between the tumour microenvironment and exogenous exposures disrupts homeostasis, and tumour biological behaviours, then accelerating tumour progression. Sorafenib, a first-line targeted therapy, often faces resistance due to tumour heterogeneity and microenvironmental changes. Understanding the link between adverse exposures and drug resistance, identifying key molecules, and developing precise interventions are crucial for improving the management of advanced/drug-resistant HCC.

Chemotherapy exerts systemic effects that extend beyond direct tumor cell killing, according to a new study led by Tatiana Petrova, professor at the Faculty of Biology and Medicine at the University of Lausanne, and published in Nature Communications.

A new preclinical study from researchers at The University of Texas MD Anderson Cancer Center, published today in Nature Communications, identifies a powerful strategy to overcome drug resistance in breast cancer by simultaneously targeting two key cell-cycle regulators, CDK2 and CDK4/6.

Why do some tumours spread while others remain localised? The mechanisms governing the metastatic potential of tumour cells remain largely unknown — yet understanding this is crucial for optimising patient care. Using cells from colon cancers, scientists at the University of Geneva (UNIGE) have pinpointed the criteria that influence the risk of metastasis, and identified gene expression signatures that can be used to assess its probability. The team then created an artificial intelligence tool (MangroveGS) capable of transforming these data into predictions for many cancers with unparalleled reliability. These results, published in Cell Reports, pave the way for more precise care and the discovery of new therapeutic targets.

Researchers at Nano Life Science Institute (WPI-NanoLSI) and the Cancer Research Institute at Kanazawa University led have uncovered how targeted lung cancer drugs alter the shape and behavior of a key cancer-driving protein—revealing a hidden mechanism that helps explain why some treatments stop working over time.