Phosphorylated S6 kinase-1: a breast cancer marker predicting resistance to neoadjuvant chemotherapy

Anticancer Res. 2013 Sep;33(9):4073-9.

Abstract

Background: Pre-clinical data support a link between the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling pathway and chemoresponsiveness. We evaluated whether the expression of phosphorylated AKT (p-AKT) or phosphorylated S6 kinase-1 (p-S6K1), a key effector of the mTOR pathway, could be a predictive marker for chemoresponsiveness in breast cancer.

Patients and methods: A total of 209 patients with locally advanced breast cancer who received neoadjuvant chemotherapy between April 2005 and July 2012 were analyzed. Patients without a minimum of 10% tumor reduction, after neoadjuvent chemotherapy, were classified as non-responders.

Results: Overall, 184 (88%) patients were classified as responders and 25 (12%) as non-responders. The positive expression rate for p-AKT and p-S6K1 was 31.6% and 45%, respectively. There was no difference in the pre-chemotherapy clinical stage according to p-S6K1 or p-AKT expression status. p-AKT expression was slightly higher in non-responders compared to responders (48% vs. 30.9%; p=0.088). However, p-S6K1 expression was significantly higher in non-responders than responders (68% vs. 41.8%; p=0014). Following multivariate analysis, p-S6K1 positivity remained an independent predictor of non-responder status (hazard ratio=3.81; 95% confidence interval=1.28-11.31; p=0.016).

Conclusion: The expression of p-S6K1 may be a predictive marker of resistance to neoadjuvant chemotherapy in patients with breast cancer.

Keywords: AKT; Breast cancer; S6 kinase 1 (S6K1); chemoresponsiveness; neoadjuvant chemotherapy.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Antineoplastic Agents / therapeutic use*
  • Biomarkers, Tumor / metabolism*
  • Breast Neoplasms / drug therapy
  • Breast Neoplasms / enzymology*
  • Breast Neoplasms / pathology
  • Chemotherapy, Adjuvant
  • Drug Resistance, Neoplasm*
  • Female
  • Humans
  • Middle Aged
  • Phosphorylation
  • Proto-Oncogene Proteins c-akt / metabolism
  • Ribosomal Protein S6 Kinases / metabolism*
  • TOR Serine-Threonine Kinases / metabolism

Substances

  • Antineoplastic Agents
  • Biomarkers, Tumor
  • MTOR protein, human
  • Proto-Oncogene Proteins c-akt
  • Ribosomal Protein S6 Kinases
  • TOR Serine-Threonine Kinases