Studies of the mechanistic (mammalian) target of rapamycin inhibitors (mTOR) represent a step towards the targeted treatment of gynecological cancers. It has been shown that women with increased levels of mTOR signaling pathway targets have worse prognosis compared to women with normal mTOR levels. Yet, targeting mTOR alone has led to unsatisfactory outcomes in gynecological cancer. The aim of our review was therefore to provide an overview of the most recent clinical results and basic findings on the interplay of mTOR signaling and cold shock proteins in gynecological malignancies. Due to their oncogenic activity, there are promising data showing that mTOR and Y-box-protein 1 (YB-1) dual targeting improves the inhibition of carcinogenic activity. Although several components differentially expressed in patients with ovarian, endometrial, and cervical cancer of the mTOR were identified, there are only a few investigated downstream actors in gynecological cancer connecting them with YB-1. Our analysis shows that YB-1 is an important player impacting AKT as well as the downstream actors interacting with mTOR such as epidermal growth factor receptor (EGFR), Snail or E-cadherin.

Monitoring of low grade and early treatment of recurrent high grade squamous intraepithelial lesions (HSILs) are the cornerstones of cervical cancer prevention. Although current knowledge provides us with the ability to identify patients at risk for redeveloping HSIL, specifically patients with persistent human papilloma virus (HPV) 16 and 18 infection after conization, the danger of surgical overtreatment of these women with persistent infections remains. Complementary diagnostics encompassing the pathobiology of disease progression need to be evaluated. This perspective presents novel evidence that HPV methylation, c-MYC gene methylation, and co-expression of targeting protein for Xenopus kinesin-like protein and programmed death ligand 1 had a positive predictive value in determining which cervical lesions progress to high grade or spontaneously regress.