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  • ||||||||||  Journal:  PI3K-AKT-mTOR signaling pathway: the intersection of allergic asthma and cataract. (Pubmed Central) -  Sep 21, 2020   
    Considering that they are all induced by immune imbalance, inflammation, etc., there may be some correlation in the mechanism, and many clues showed that both diseases are associated with activation of the PI3K-AKT-mTOR signaling pathway. Therefore, we hypothesized that the PI3K-AKT-mTOR signaling pathway produces inflammatory or immune imbalance based on allergy leading to cataract.
  • ||||||||||  Journal:  GANT61 and Curcumin loaded PLGA Nanoparticles for GLI-1 and PI3K/Akt Mediated Inhibition in Breast Adenocarcinoma. (Pubmed Central) -  Sep 21, 2020   
    The nanoparticles induced cytotoxic effects to breast cancer cells at a mid-minimal dosage followed by cell death via autophagy and apoptosis, reduction in their target protein expression along with compromising the self-renewal property of CSCs as revealed by their in vitro cell studies. The dual drug NPs thus provides a novel perspective on the aid of existing anti-cancer nano-medicine therapies to target a heterogeneous tumor mass effectively.
  • ||||||||||  Journal, IO Biomarker:  DAla2GIP antagonizes HO-induced chondrocyte apoptosis and inflammatory factor secretion. (Pubmed Central) -  Sep 19, 2020   
    Further, molecular biology experiments confirmed that DAla2GIP inhibited the HO mediated inflammation vis up-regulating the expressions of Sox9 and Col2a1 and inhibiting PI3K/Akt/NF-κB pathway. The results demonstrate that DAla2GIP has protective properties in HO-induced chondrocyte injury, this finding shows that novel GIP analogues have the potential as a novel therapeutic for osteoarthritis patients.
  • ||||||||||  Journal:  Cbl-PI3K interaction regulates Cathepsin K secretion in osteoclasts. (Pubmed Central) -  Sep 19, 2020   
    Further, we found that in contrast to WT, conditioned media derived from YF osteoclasts promoted increased numbers of alkaline phosphatase (ALP)-positive colonies, and increased expression of osteogenic markers in WT calvarial cultures. Cumulatively, our results suggest that the Cbl-PI3K interaction regulates Cathepsin K secretion required for proper bone resorption, and secretion of factors which promote osteogenesis.
  • ||||||||||  doxorubicin hydrochloride / Generic mfg.
    Journal:  Co-targeting CK2α and YBX1 suppresses tumor progression by coordinated inhibition of the PI3K/AKT signaling pathway. (Pubmed Central) -  Sep 19, 2020   
    Further results demonstrated that CK2α could interact with YBX1 and PI3K/AKT antagonist decreased cell resistance to doxorubicin induced by co-activation of CK2α and YBX1. These results indicated that combined inhibition of CK2α and YBX1 showed synergistic effects in inactivating the PI3K/AKT signaling pathway and may be one of the mechanisms involved in tumor growth and migration.
  • ||||||||||  sirolimus / Generic mfg.
    Journal:  Inhibition of Growth of TSC2-Null Cells by a PI3K/mTOR Inhibitor but Not by a Selective MNK1/2 Inhibitor. (Pubmed Central) -  Sep 19, 2020   
    In contrast, a PI3K/mTOR inhibitor omipalisib blocked the phosphorylation of Akt and both S6K/S6 and 4E-BP/eIF4E branches, and additively decreased the growth of TSC2-null cells with rapamycin. Omipalisib, or another inhibitor of both major mTORC1 growth pathways and pAkt, might provide therapeutic options for TSC2-deficient cancers including, but not limited to, LAM.
  • ||||||||||  Piqray (alpelisib) / Novartis
    Journal:  Alpelisib to treat breast cancer. (Pubmed Central) -  Sep 18, 2020   
    Although clinical activity has been observed independently of PIK3CA mutation status, clinical improvement has been mostly seen in a higher proportion of patients with PIK3CA-mutated tumors. In this review I share current data on alpelisib in breast cancer treatment.
  • ||||||||||  everolimus / Generic mfg., paclitaxel / Generic mfg.
    Journal:  Synergistic Anti-Tumor Activity by Targeting Multiple Signaling Pathways in Ovarian Cancer. (Pubmed Central) -  Sep 18, 2020   
    Furthermore, the triple combination also synergistically increased the anti-tumor activity of paclitaxel, both in vitro and in vivo. Taken together, our results demonstrate that simultaneous inhibition of several signaling pathways results in better anti-tumor activity compared to inhibiting any of these signaling pathways alone.
  • ||||||||||  Clinical, Review, Journal:  Targeting PI3K/Akt/mTOR in AML: Rationale and Clinical Evidence. (Pubmed Central) -  Sep 18, 2020   
    In this article, we review the laboratory-based evidence of the critical role of PI3K/Akt/mTOR pathway in AML, and outcomes from current clinical studies using PI3K/Akt/mTOR inhibitors. Based on these results, we discuss the putative mechanisms of resistance to PI3K/Akt/mTOR inhibition, offering rationale for potential candidate combination therapies incorporating PI3K/Akt/mTOR inhibitors for precision medicine in AML.
  • ||||||||||  Zolinza (vorinostat) / Merck (MSD)
    Journal, IO Biomarker:  Hydroxamic Acid Derivatives of β-Carboline/Hydroxycinnamic Acid Hybrids Inducing Apoptosis and Autophagy through the PI3K/Akt/mTOR Pathways. (Pubmed Central) -  Sep 17, 2020   
    Compound 12b enhanced the acetylation levels of histone H3 and α-tubulin and induced greater cancer cell apoptosis than the FDA-approved HDAC inhibitor SAHA by regulating expression of apoptotic proteins Bax, Bcl-2, and caspase 3...Finally, 12b significantly inhibited PI3K/Akt/mTOR signaling, an important cell-growth-promoting pathway aberrantly activated in many cancers. Together, the results suggest that these hydroxamic-acid-containing β-carboline derivatives may be new leads for the discovery of agents for the treatment of human carcinoma cancers.
  • ||||||||||  Preclinical, Journal:  The effect of miR-579 on the PI3K/AKT pathway in human glioblastoma PTEN mutant cell lines. (Pubmed Central) -  Sep 17, 2020   
    Furthermore, the Western blot analysis showed that miR-579 could downregulate the AKT1 and Rheb protein expression. Overall, our findings propose that miR-579 functions as a novel tumor suppressor gene in GBM by regulating the PI3K/AKT signaling pathway and may serve as a therapeutic target for clinical therapy of glioblastoma multiform.