Advanced cancer patients commonly experience cachexia, a condition that leads to significant muscle loss and affects their treatment response, quality of life, and survival chances.
There are currently no effective treatments for cachexia, highlighting the urgent need for early detection and monitoring of muscle mass loss to implement timely interventions.
The study introduces simpler experimental cancer models using mice and human cancer cells, allowing for easier observation of muscle deterioration and evaluation of potential therapies for cachexia.
Metallothioneins are proteins that manage zinc storage and transport but are linked to increased levels during muscle atrophy.
Blocking metallothioneins 1 and 2 activates the Akt pathway, leading to larger muscle fibers and improved muscle strength.
The positive impact of metallothionein blockade on muscle mass and function also holds true even with glucocorticoid-induced atrophy, suggesting a potential treatment strategy for muscle wasting conditions.
Cachexia is a common condition in advanced cancer patients that negatively impacts treatment effectiveness, quality of life, and survival, with the role of ActRII inhibition in this context still unclear.
The study used a mouse model to test the effects of a neutralizing antibody (CDD866) against ActRII, in combination with two anti-cancer drugs, cisplatin and everolimus.
Results showed that cisplatin worsened weight loss and skeletal muscle degradation, while CDD866 helped protect against muscle loss; everolimus also protected muscle, and combining it with CDD866 suggested potential additional benefits.