p-mTOR expression is associated with better prognosis in luminal breast carcinoma

Beça, Francisco; André, R; Martins, Daniel; Bilhim, Tiago; Martins, Diana; Schmitt, Fernando

doi:10.1136/jclinpath-2014-202320

Cited by 10 publications

(9 citation statements)

References 26 publications

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“…It has been shown that AKT hyperactivation could induce endocrine resistance in breast cancer and non-small-cell lung cancer 10–15. We also showed AKT hyperphosphorylation in PRCs with MPA treatment (Figures 2 and 3).…”

Section: Discussionsupporting

confidence: 62%

“…Aberrant hyperactivation of PI3K/AKT/mTOR pathway is one of the most common tumor-related signaling pathways that can be detected in a variety of tumor types, such as breast cancer, colorectal cancer, endometrial carcinoma, lung cancer, and glioblastoma, mainly including PIK3CA mutation, PTEN loss, and AKT1 mutation. In addition, KRAS mutation and BRAF mutation from the MAPK pathway can also result in PI3K/AKT/mTOR pathway activation 10–15. A previous study showed that progestin might activate PI3K/AKT signaling pathway independent of progesterone receptor (PR) in breast cancer 16…”

Section: Introductionmentioning

confidence: 99%

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PI3K/AKT/mTOR pathway promotes progestin resistance in endometrial cancer cells by inhibition of autophagy

Liu¹,

Zhang²,

xu-yan³

et al. 2017

OTT

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Endometrial cancer (EC) is now one of the most common malignant tumors in young women. In all, 90% of young patients with EC have a high expression of progesterone recep tor, can be treated with progestin, and have very good prognosis. However, some of the young EC patients are resistant to progestin, the mechanism of which is unclear. To illuminate the mechanism by which endometrial cells acquire progestin resistance, we treated Ishikawa cells by slowly increasing dosage of progestin and established a progestin-resistant cell subline. We show here that progesterone resistant cells acquire increased proliferation rate and interestingly decreased autophagy. To uncover the mechanism by which cells increase proliferation and bypass autophagy, we found higher activation of phosphatidylinositol 3-kinase/AKT/mTOR signaling pathway was necessary to this malignant acquirement by RNAi technique. Further, we elucidated that activation of mTOR was sufficient and necessary for progestin resistance. RAD001, an inhibitor of mTOR, decreased phosphorylation of mTOR and inhibited proliferation of progestin-resistant cancer cells by promoting autophagy. Thus, our results indicated that mTOR can be a target to treat the progestin-resistant EC.

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Section: Discussionsupporting

confidence: 62%

Section: Introductionmentioning

confidence: 99%

PI3K/AKT/mTOR pathway promotes progestin resistance in endometrial cancer cells by inhibition of autophagy

Liu¹,

Zhang²,

xu-yan³

et al. 2017

OTT

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“…Five [22–26, 29], three [24, 27, 28], and three [22, 28, 30]studies reported the HR and 95% CI for DFS, OS, and RFS, respectively. The results of the meta-analysis are shown in Figs 2–4.…”

Section: Resultsmentioning

confidence: 99%

P-mTOR Expression and Implication in Breast Carcinoma: A Systematic Review and Meta-Analysis

Ding

Zhou

et al. 2017

PLoS ONE

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ObjectivePhosphorylated mammalian target of rapamycin (p-mTOR) is a promising prognostic marker in many types of cancer. However, its survival benefit in patients with breast carcinoma remains unknown. The aim of the present study was to assess the relationship between p-mTOR expression and prognosis in breast carcinoma based on a systematic review and meta-analysis.Materials and MethodsElectronic databases (including Pubmed, Embase, ISI web of science, and Cochrane Library) were searched up to November 24, 2015. The outcome measures were hazard ratios (HRs) with 95% confidence interval (CI) for the association between the prognosis of breast carcinoma patients and p-mTOR expression. Primary end points were disease-free survival (DFS), overall survival (OS), and recurrence-free survival (RFS). Statistical analysis was performed with STATA 12.0.ResultsNine cohort studies including 3051 patients met full eligibility criteria. The pooled HRs (95% CI) for OS, DFS, and RFS were 0.84 (0.27–2.63), 0.71 (0.40–1.23), and 0.48 (0.20–1.18), respectively.ConclusionsOur findings suggested that p-mTOR overexpression was not significantly related to prognosis in breast carcinoma regarding OS and disease recurrence. Prospective studies are warranted to examine the association between p-mTOR expression and survival outcomes in breast carcinoma.

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“…In fact, the clinical relevance of hyperactive Akt/mTOR depends on the tumor type. Two recent meta‐analyses revealed that hyperactive mTOR is associated with worse prognosis in gynecologic and gastrointestinal cancers, whereas it is associated with good prognosis in some breast cancer types or in lung cancer . Although, García–Carracedo et al reported mTOR activation was correlated with improved clinical outcome in patients with laryngeal carcinomas.…”

Section: Discussionmentioning

confidence: 99%

Association between high expression of phosphorylated Akt and mammalian target of rapamycin and improved survival in salivary gland adenoid cystic carcinoma

Ouyang

Liang

et al. 2017

Head & Neck

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p-mTOR expression is associated with better prognosis in luminal breast carcinoma

Abstract: p-mTOR expression is associated with smaller, lower-grade and with luminal BC. In multivariable analysis, p-mTOR expression was associated with longer DFS and OS, independently of the size, grade and lymph node status, especially in luminal BCs.

Cited by 10 publications

References 26 publications

PI3K/AKT/mTOR pathway promotes progestin resistance in endometrial cancer cells by inhibition of autophagy

PI3K/AKT/mTOR pathway promotes progestin resistance in endometrial cancer cells by inhibition of autophagy

P-mTOR Expression and Implication in Breast Carcinoma: A Systematic Review and Meta-Analysis

Association between high expression of phosphorylated Akt and mammalian target of rapamycin and improved survival in salivary gland adenoid cystic carcinoma

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