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Cancer-associated cachexia (CAC) is a prevalent condition that accelerates cancer progression and heightens treatment-related adverse effects in patients by affecting multiple organ systems. Despite the profound impact of CAC on clinical management and treatment outcomes of patients with cancer, the current understanding of mechanisms associated with the condition, as well as the tools necessary for early diagnosis, are limited. Currently, the clinical diagnosis of CAC relies on weight change-based assessments, which have limited sensitivity and cannot identify patients at risk for CAC. In this context, noninvasive imaging-based biomarkers, such as the composition and properties of adipose and muscle tissues, may allow for diagnosis of CAC before substantial weight loss occurs. Such early detection can potentially enable more timely and effective interventions. Furthermore, imaging allows for quantitative assessment of CAC, enabling monitoring of prognosis and treatment response. This article reviews current applications and future developments of imaging techniques, particularly those employed in current clinical radiology, that can reveal diagnostic information and facilitate early detection of CAC and quantitative evaluation of associated metabolic alterations. Molecular Imaging, Cancer, MRI, PET/CT, Ultrasound, Muscular, Oncology © RSNA, 2025.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC12304533 | PMC |
http://dx.doi.org/10.1148/rycan.240291 | DOI Listing |
Mol Cancer
September 2025
School of Chinese Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China.
Chin Clin Oncol
August 2025
School of Medicine, Valladolid University, Valladolid, Spain; Internal Medicine Unit, Río Hortega University Hospital, Valladolid, Spain.
Malnutrition and cachexia in cancer patients, particularly those with lung cancer, represent a pervasive clinical challenge that compromises treatment outcomes, quality of life, and overall survival. This article analyzes the multifactorial etiology of oncological malnutrition, highlighting the chronic inflammatory state, tumor-induced anorexia, and metabolic abnormalities that accelerate muscle and weight loss. It underscores that rates of malnutrition can range from 30% to 80% across different tumor types, with lung cancer patients especially vulnerable due to their high inflammatory burden.
View Article and Find Full Text PDFInt J Mol Sci
August 2025
Department of Physiology, Faculty of Medicine, Jagiellonian University Medical College, 31-531 Cracow, Poland.
Cancer-associated cachexia is a multifaceted wasting syndrome characterized by progressive loss of skeletal muscle mass, systemic inflammation, and metabolic dysfunction and is particularly prevalent in gastrointestinal cancers. Physical activity has emerged as a promising non-pharmacological intervention capable of attenuating key drivers of cachexia. Exercise modulates inflammatory signaling (e.
View Article and Find Full Text PDFClin Nutr
September 2025
Department of Medical Oncology, Cochin University Hospital, Université Paris Cité, Institut du Cancer Paris CARPEM, Paris, France; Centre de Recherche des Cordeliers, UMR1138, Université Paris Cité, Sorbonne Université, INSERM, CNRS, France; Université Paris Cité, 75006, Paris France. Electro
Background And Aims: Clinical complexity of patients with cancer represents a challenge when aiming to implement individualized clinical management strategies. Despite their impact on patient outcomes, the burden of cancer-associated cachexia and inflammation remains underestimated by cancer physicians. We aimed to evaluate the performances of an early multi-dimensional patient assessment, integrating a comprehensive nutritional and inflammatory evaluation, for patient categorization and prognostication, independently of tumor features.
View Article and Find Full Text PDFJ Cachexia Sarcopenia Muscle
August 2025
Department of Anatomy, Korea University College of Medicine, Seoul, Republic of Korea.
Background: Cancer-associated cachexia (CAC) is a multifactorial syndrome characterised by progressive loss of muscle mass with limited Food and Drug Administration treatments. Although emerging evidence suggests that l-leucine and β-hydroxy-β-methyl butyrate (HMB) have potential for treating CAC, the role of α-ketoisocaproate (KIC), a metabolite of l-leucine, remains unclear. Therefore, this study explored the use of KIC as a therapeutic agent for CAC-induced muscle atrophy by targeting myostatin.
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