PI3K/AKT/mTOR inhibitors for hormone receptor-positive advanced breast cancer

Cancer Treat Rev. 2025 Jan:132:102861. doi: 10.1016/j.ctrv.2024.102861. Epub 2024 Nov 19.

Abstract

Dysregulation of the phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR) pathway plays a pivotal role in the development and progression of various cancers. In hormone receptor-positive (HR+)/human epidermal growth factor receptor 2-negative (HER2-) advanced breast cancer, aberrations in this pathway are increasingly recognized as key drivers of resistance to endocrine therapy and cyclin-dependent kinase 4/6 (CDK4/6) inhibitors, the first-line treatments for this disease subtype. Recognizing the urgent need for alternative therapeutic strategies, significant advancements have been made in developing PI3K/AKT/mTOR inhibitors for HR+ advanced/metastatic breast cancer. Among these inhibitors, capivasertib and alpelisib have received approval as targeted therapies for this indication. This review provides a comprehensive summary of the latest developments in PI3K/AKT/mTOR inhibitors for HR+ breast cancer. It also delves into different aspects, including sampling, testing method and timing, of PI3K/AKT/mTOR diagnostic testing. Additionally, the review discusses key considerations for integrating these inhibitors into clinical practice, such as timing and choice of PI3K/AKT/mTOR inhibitors, and management of treatment toxicities. By examining these different aspects, this review aims to provide valuable insights into optimizing the clinical utility of PI3K/AKT/mTOR inhibitors in HR+ advanced breast cancer.

Keywords: AKT inhibitor; Hormone receptor-positive breast cancer; PI3K inhibitor; PI3K/AKT/mTOR pathway; Precision therapy; Treatment.

Publication types

  • Review

MeSH terms

  • Antineoplastic Agents / pharmacology
  • Antineoplastic Agents / therapeutic use
  • Breast Neoplasms* / drug therapy
  • Breast Neoplasms* / metabolism
  • Breast Neoplasms* / pathology
  • Female
  • Humans
  • MTOR Inhibitors / pharmacology
  • MTOR Inhibitors / therapeutic use
  • Phosphoinositide-3 Kinase Inhibitors* / pharmacology
  • Phosphoinositide-3 Kinase Inhibitors* / therapeutic use
  • Protein Kinase Inhibitors / pharmacology
  • Protein Kinase Inhibitors / therapeutic use
  • Proto-Oncogene Proteins c-akt* / antagonists & inhibitors
  • Proto-Oncogene Proteins c-akt* / metabolism
  • Receptors, Estrogen / metabolism
  • Signal Transduction / drug effects
  • TOR Serine-Threonine Kinases* / antagonists & inhibitors
  • TOR Serine-Threonine Kinases* / metabolism

Substances

  • TOR Serine-Threonine Kinases
  • Proto-Oncogene Proteins c-akt
  • Phosphoinositide-3 Kinase Inhibitors
  • MTOR protein, human
  • MTOR Inhibitors
  • Protein Kinase Inhibitors
  • Receptors, Estrogen
  • Antineoplastic Agents