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<p>Cancer-associated thrombosis (CAT) and cancer-associated cachexia (CAC) are the most common comorbidities in patients with malignant diseases. Their development is modulated by several factors related to the patient, tumour and antineoplastic treatments. Intriguingly, they share a pro-inflammatory setting induced by cytokines released by cancer and host cells in the tumour microenvironment, which leads to metabolic and endocrine derangements across organ systems. The insulin-like growth factor 1 (IGF-1) axis, implicated in metabolism, tissue homeostasis, and tumourigenesis, may play a key role in this interface. Specifically, the dysregulation of the IGF1R-PI3K-Akt-mTOR pathway, which governs protein synthesis (anabolism) and degradation (catabolism), has been involved in muscle wasting associated with CAC. Concerning CAT, while less explored, the roles of the IGF-1 axis in angiogenesis and endothelial stability suggest a potential connection. To address knowledge gaps, this comprehensive narrative review examined the current literature on the IGF-1 pathway’s involvement in CAT and CAC, including the implications of genetic markers. As the IGF-1 axis may serve as a signalling bond between these paraneoplastic syndromes, further investigation may lead to the identification of disease predictors, supporting risk stratification and early intervention. </p> Graphical Abstract <p></p>

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IGF-1 axis: The signalling bond in cancer-associated thrombosis and cachexia?

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年6月30日

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  • Mariana Moreira Pires,
  • Valéria Tavares,
  • Tiago Ferreira,
  • Ana Carolina Leão Silva,
  • Inês Guerra de Melo,
  • Rui Medeiros

摘要

Cancer-associated thrombosis (CAT) and cancer-associated cachexia (CAC) are the most common comorbidities in patients with malignant diseases. Their development is modulated by several factors related to the patient, tumour and antineoplastic treatments. Intriguingly, they share a pro-inflammatory setting induced by cytokines released by cancer and host cells in the tumour microenvironment, which leads to metabolic and endocrine derangements across organ systems. The insulin-like growth factor 1 (IGF-1) axis, implicated in metabolism, tissue homeostasis, and tumourigenesis, may play a key role in this interface. Specifically, the dysregulation of the IGF1R-PI3K-Akt-mTOR pathway, which governs protein synthesis (anabolism) and degradation (catabolism), has been involved in muscle wasting associated with CAC. Concerning CAT, while less explored, the roles of the IGF-1 axis in angiogenesis and endothelial stability suggest a potential connection. To address knowledge gaps, this comprehensive narrative review examined the current literature on the IGF-1 pathway’s involvement in CAT and CAC, including the implications of genetic markers. As the IGF-1 axis may serve as a signalling bond between these paraneoplastic syndromes, further investigation may lead to the identification of disease predictors, supporting risk stratification and early intervention.

Graphical Abstract