Crosstalk of the Insulin-Like Growth Factor Receptor with the Wnt Signaling Pathway in Breast Cancer

Abstract

The insulin-like growth factor system has long been considered a pathway that promotes cell proliferation, survival, and transformation, and is thus a promoter of tumorigenesis. However, recent failure of clinical trials for IGF-1R inhibitors reveals the need for a better understanding of how this pathway functions in specific tumor subtypes. Ongoing studies are designed to uncover biomarkers and downstream targets to enhance therapeutic strategies. Other approaches in specific tumor models reveal complex interactions between IGF signaling and other tumor initiating pathways. Here, we review relevant background and recent studies suggesting that inhibiting the IGF-1R can amplify Wnt and Notch signaling pathways in a model of triple negative breast cancer.

<p>Higher Dietary Inflammatory Index Scores are Associated with Increased Odds of Benign Breast Diseases in a Case–Control Study</p>

“…20,52 DII scores can play an important role through these cytokines in breast cancer, such as induced methylation of the estrogen receptor via IL-1β 53 and TNF-α with proliferation effects on breast cancer tumors. 54 There are some limitations in this study that should be noted. Our study is a case-control research that does not allow cause and effect conclusion.…”

Hyperostosis frontalis interna in female historic skeletal populations: Age, sex hormones and the impact of industrialization

“…Nonetheless, our research indicates that, unlike the observations of the influence of suppressed androgens in HFI in males reported by May, Peled, Dar, Abbas, et al (2010), elevated FT and IGF‐1 are the key risk factors in HFI for females. High IGF‐1 serum levels have also been identified as a risk factor for breast cancer (Rota & Wood, ). Similarly, Schernhammer et al () found that despite the significant correlation between estradiol and all other hormones, only elevated levels of circulating FT was a significant risk factor in breast cancer development.…”

TROP-2 exhibits tumor suppressive functions in cervical cancer by dual inhibition of IGF-1R and ALK signaling

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