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  • ||||||||||  Review, Journal:  Defining Bronchial Asthma with Phosphoinositide 3-Kinase Delta Activation: Towards Endotype-Driven Management. (Pubmed Central) -  Jan 8, 2020   
    Defining subpopulations of asthma patients with PI3K-δ activation, namely PI3K-δ-driven asthma endotype, may therefore provide us with a novel framework for the treatment of the disease, particularly for corticosteroid-resistant severe form, an important unresolved aspect of the current asthma management. In this review, we specifically summarize the recent advancement of our knowledge on the critical roles of PI3K-δ in the pathogenesis of bronchial asthma.
  • ||||||||||  Journal:  Effect of silencing FABP3 gene on LPS-induced apoptosis and endoplasmic reticulum stress in alveolar epithelial cells (Pubmed Central) -  Jan 8, 2020   
    Apoptosis rate [(10.5±1.1)%], IL-6[(301.3±30.0) ng/L], IL-8[(189.4±19.0) ng/L], TNF-α [(400.1±40.1) ng/L], cleaved-caspase-3 (0.45±0.05), GRP78 (0.48±0.05), ATF4 (0.60±0.06), CHOP (0.55±0.05), cleaved-caspase-12 (0.60±0.06), p-Akt (0.50±0.05) and PI3Kp110α(0.45±0.05) in LPS+si-FABP3 group were significantly lower than those in LPS+si-con group [(28.1±2.8)%, (536.3±53.6) ng/L, (400.2±40.2) ng/L, (623.1±62.3) ng/L, (0.96±0.10), (1.02±0.10), (1.15±0.12), (1.10±0.11), (1.15±0.12), (0.90±0.09), (0.72±0.07)] (all P<0.05). Silencing FABP3 gene can inhibit LPS-induced alveolar epithelial cell apoptosis and endoplasmic reticulum stress, which may act by inhibiting the PI3K/Akt signaling pathway.
  • ||||||||||  [VIRTUAL] Therapeutic Vulnerabilities and Resistance Mechanisms in Estrogen Receptor-Positive Breast Cancer (Room 30 A-E - Upper Lvl - SDCC) -  Jan 8, 2020 - Abstract #AACR2020AACR_614;    
    In this session, 4 KOLs in the field will discuss their new findings on genetic vulnerabilities, tumor evolution, drug resistance mechanisms, and novel therapeutic opportunities in this subset of breast cancer. Moreover, a 2020 Next Gen Star recipient will present his new, exciting findings on dual PIK3CA mutations as a hallmark of oncogene addiction and determinant of sensitivity to PI3K inhibitors.
  • ||||||||||  doxycycline / Generic mfg.
    Journal:  A Ras-LSD1 axis activates PI3K signaling through PIK3IP1 suppression. (Pubmed Central) -  Jan 6, 2020   
    Using doxycycline-inducible PIK3IP1, here we confirm that reversing the effect of Ras by inducing expression of PIK3IP1 suppresses Ras-induced anchorage-independent growth, supporting the central role of PIK3IP1 in transformation...We find that Ras activity represses PIK3IP1 expression via the recruitment of lysine-specific demethylase 1 (LSD1) to the PIK3IP1 gene promoter and enhancer, resulting in erasure of active histone marks. These studies demonstrate cross-activation of Ras/Raf/MEK/ERK and PI3K/AKT/mTOR pathways, where Ras decommissions PIK3IP1 gene expression by enhancing LSD1 and its corepressor activities to suppress PIK3IP1 transcription.
  • ||||||||||  Review, Journal:  Roles of long-non-coding RNAs in cancer therapy through the PI3K/Akt signalling pathway. (Pubmed Central) -  Jan 5, 2020   
    In summary, lncRNAs have tremendous potential in cancer diagnosis, assessing cancer patient prognosis and in developing new therapeutic options for patients with resistance to current cancer therapies. Thus, understanding how lncRNAs influence the Akt pathway is essential for the development of novel and effective cancer therapies.
  • ||||||||||  Review, Journal:  Hormonal treatment combined with targeted therapies in endocrine-responsive and HER2-positive metastatic breast cancer. (Pubmed Central) -  Jan 5, 2020   
    The analyses included efficacy and toxicity data from earlier studies with a single anti-HER2 drug combined with hormonal therapy up to more recent studies testing new molecules targeting these signaling pathways. The aims of this review are to summarize current knowledge and to discuss research development including the possibility to spare chemotherapy in this subgroup of HER2-positive breast cancer patients.
  • ||||||||||  cisplatin / Generic mfg.
    Journal:  AFAP1-AS1 induces cisplatin resistance in non-small cell lung cancer through PI3K/AKT pathway. (Pubmed Central) -  Jan 5, 2020   
    Silencing of EZH2 inhibited the activation of PI3K/AKT pathway. In conclusion, AFAP1-AS1 accelerates the proliferative and metastatic abilities of A549/DDP cells, whereas inhibits the apoptosis of A549/DDP cells, by interacting with EZH2 to activate the PI3K/AKT pathway; thus, inducing DDP resistance in NSCLC.
  • ||||||||||  Journal:  Cryptotanshinone Inhibites Bladder Cancer Cell Proliferation and Promotes Apoptosis via the PTEN/PI3K/AKT Pathway. (Pubmed Central) -  Jan 5, 2020   
    In addition, CTT modulated the expression of proteins via the PI3K/AKT pathway, and the inhibition of PI3K/AKT signalling was due to induction of PTEN expression. Taken together, the results of the present study demonstrated the anticancer effect of CTT on bladder cancer cells, which might be associated with the downregulation of PI3K/AKT/mTOR and NF-κB signalling pathway proteins, and this inhibition was mediated by the induction of PTEN.
  • ||||||||||  Journal:  VEGF Induce Vasculogenic Mimicry of Choroidal Melanoma through the PI3k Signal Pathway. (Pubmed Central) -  Jan 4, 2020   
    These results indicate that VEGF induce VM formation in CM by activating PI3K/AKT signaling pathway. VEGF promoted VM formation by the PI3K signal transduction pathway, indicating a molecular mechanism which may be used to develop new therapeutic targets for the clinical treatment of CM.
  • ||||||||||  Journal:  Resolving PI3K-δ inhibitor resistance in CLL. (Pubmed Central) -  Jan 2, 2020   
    The above results suggested that compound 7m could be considered as a promising PI3Kα inhibitor. No abstract available
  • ||||||||||  Preclinical, Journal, PARP Biomarker, IO Biomarker:  Anti-liver cancer effect and the mechanism of arsenic sulfide in vitro and in vivo. (Pubmed Central) -  Jan 2, 2020   
    PI3K inhibitors such as PI-103, PI-828 and PX-866 may be developed as potential therapeutic agents for effective treatment of oral squamous cell carcinoma (OSCC) patients, associated with activated PI3K/Akt pathway. These findings suggested that AsS could induce apoptosis of liver cancer cells in vitro and in vivo, which was related to PI3K/AKT-mediated mitochondrial pathway and may provide a novel promising therapeutic agent for liver cancer treatment.
  • ||||||||||  Journal:  A novel monoallelic gain of function mutation in p110δ causing atypical activated phosphoinositide 3-kinase δ syndrome (APDS-1). (Pubmed Central) -  Jan 2, 2020   
    These findings suggested that AsS could induce apoptosis of liver cancer cells in vitro and in vivo, which was related to PI3K/AKT-mediated mitochondrial pathway and may provide a novel promising therapeutic agent for liver cancer treatment. This study reports on a novel activating p110δ mutation causing adult-onset hypogammaglobulinemia with lymphopenia without the classical presentation of atypical Activated phosphoinositide 3-kinase δ syndrome (ADPS-1), underlining thus the heterogeneous clinical and immunological presentation of p110δ mutated individuals and offers additional data on the role of p110δ in early and late B cell development in humans.
  • ||||||||||  Piqray (alpelisib) / Novartis
    Journal, IO Biomarker:  Casticin inhibits nasopharyngeal carcinoma growth by targeting phosphoinositide 3-kinase. (Pubmed Central) -  Jan 2, 2020   
    Casticin is a newly emerging selective PI3K inhibitor with potential for use as a targeted therapeutic treatment for nasopharyngeal carcinoma. Accordingly, casticin might represent a novel and effective agent against NPC and likely has high potential for combined use with pharmacological agents targeting PI3K/AKT.
  • ||||||||||  paclitaxel / Generic mfg.
    Biomarker, Journal:  Resveratrol enhances chemosensitivity of renal cell carcinoma to paclitaxel. (Pubmed Central) -  Jan 1, 2020   
    Furthermore, decrease of survivin by inhibition of PI3K/AKT pathway significantly inhibits the effect of PTX in Caki-1 cells. These data show that RES increases the sensitivity of PTX resistant renal cells to drug treatment.
  • ||||||||||  Journal:  UBE2T promotes proliferation and regulates PI3K/Akt signaling in renal cell carcinoma. (Pubmed Central) -  Jan 1, 2020   
    Similarly, the UBE2T overexpression‑induced promotion of 786‑O cell proliferation was also attenuated by wortmannin. In conclusion, UBE2T promoted the proliferation of RCC cells by regulating PI3K/Akt signaling, suggesting it may be a novel target for the treatment of patients with RCC.
  • ||||||||||  Journal:  TEEG Induced A549 Cell Autophagy by Regulating the PI3K/AKT/mTOR Signaling Pathway. (Pubmed Central) -  Jan 1, 2020   
    In addition, increased TEEG concentration enhanced the expression of Class III p-PI3K and reduced the expression of Class I p-PI3K, p-AKT, p-mTOR, and p-P70S6K. These results indicate that TEEG induces autophagy of A549 cells through regulation of the PI3K/AKT/mTOR signaling pathway.
  • ||||||||||  quercetin (LY294002) / Eli Lilly
    Journal:  Arctigenin promotes bone formation involving PI3K/Akt/PPARγ signaling pathway. (Pubmed Central) -  Dec 30, 2019   
    Furthermore, arctigenin prevented OVX-induced osteoporosis in rats by increasing BMD and ALP activity and inhibiting the loss of Ca and P. In contrast, treatment with LY294002, a selective inhibitor of the phosphatidylinositol 3-kinase (PI3K), produced the opposite phenotype. These data suggest that the protective effects of arctigenin on BMSCs and OVX rat models result from the induction of osteogenesis involving the PI3K/Akt/PPAR γ axis.
  • ||||||||||  Journal, IO Biomarker:  Aclidinium Bromide holds promising inhibitory effects in A549 lung cancer cells potentials by regulating PI3K / AKT signaling pathway. (Pubmed Central) -  Dec 29, 2019   
    Taken together, these results indicate that Apigenin could inhibit the growth of cisplatin-resistant colon cancer cells in vitro and in vivo and may be used for the improvement of therapy of colon cancer. Our results reveals that Aclidinium Bromide behaves as a novel M3R antagonist, and may inhibit lung cancer cell growth by regulating the PI3K/AKT signaling pathway, which sheds some light on that it might be a potential therapeutic agent for lung cancer.