PI3K inhib 
Welcome,         Profile    Billing    Logout  
 67 Companies  59 Products   59 Products   344 Diseases   342 Trials   12240 News 


«12...103104105106107108109110111112113...229230»
  • ||||||||||  Venclexta (venetoclax) / Roche, AbbVie, Calquence (acalabrutinib) / AstraZeneca
    Review, Journal:  Current Treatment Options in CLL. (Pubmed Central) -  Jun 3, 2021   
    Venetoclax, an inhibitor of the anti-apoptotic BCL2 protein and, to a lesser extent, phosphoinositide-3 kinase (PI3K) delta inhibitors, add to the armamentarium of targeted agents for the treatment of CLL...An even bigger challenge poses the determination of the optimal combination and sequence of those drugs. Here, we give an overview of current treatment options in CLL, weighing the advantages and disadvantages of each approach in the light of different clinical settings.
  • ||||||||||  Journal:  Evaluation of SARS-CoV-2 Spike S1 Protein Response on PI3K-Mediated IL-8 Release. (Pubmed Central) -  Jun 3, 2021   
    To that end, the current studies were sought to determine the response of the SARS-CoV-2 Spike S1 protein on PI3K-mediated IL-8 release using relevant and widely used cellular models. Overall, these studies indicate that PI3K signaling does not directly mediate Spike S1 protein-induced IL-8 release in these cellular models.
  • ||||||||||  Erbitux (cetuximab) / Eli Lilly, EMD Serono
    Journal:  Inactivation of NF1 promotes resistance to EGFR inhibition in KRAS/NRAS/BRAFV600-wildtype colorectal cancer. (Pubmed Central) -  Jun 2, 2021   
    Loss of NF1 may be a useful biomarker to identify patients that are less likely to benefit from single agent anti-EGFR therapy in CRC and may direct potential combination strategies. Implications: This study suggests that further clinical validation of NF1 status as predictor of response to anti-EGFR targeting antibodies in CRC patients with KRAS/NRAS/BRAFV600-wildtype tumours is warranted.
  • ||||||||||  cisplatin / Generic mfg.
    Preclinical, Journal:  PIK3CA and p53 mutations promote 4NQO-initated head and neck tumor progression and metastasis in mice. (Pubmed Central) -  Jun 2, 2021   
    Given the prevalence of mutations in p53 and the PI3K pathways in HNSCC in conjunction with loss of p16 genetically or epigenetically, this universal increased sensitivity to cisplatin and BYL719 combination therapy in cancer cells with PIK3CA mutation represents an opportunity to a subset of HNSCC patients. Implications: Our results suggest that combination therapy of cisplatin and PI3K inhibitor may be worthy of consideration in HNSCC patients with PIK3CA mutation.
  • ||||||||||  Journal:  Rapid membrane effect of estrogens on stimulation of corticotropin-releasing hormone. (Pubmed Central) -  Jun 2, 2021   
    Furthermore, BS-KS seems to inhibit macrophage M1 polarization and promote M2 polarization via the PPAR gamma /NF-κB signaling pathway, thus playing an inhibitory role in atherosclerosis. MIES can efficiently upregulate CRH expression via various intracellular kinase pathways and may thus be a crucial component in the stress response.
  • ||||||||||  Journal:  Class IA PI3K regulatory subunits: p110-independent roles and structures. (Pubmed Central) -  Jun 2, 2021   
    Factors that influence the monomer-dimer equilibrium of p110-independent p85 offer additional control over this system, disruption to which likely results in disease. Here we review the current knowledge of the structure and functions of p110-independent class IA PI3K regulatory subunits.
  • ||||||||||  quercetin (LY294002) / Eli Lilly
    Journal:  Knockdown of ZFAS1 Inhibits Hippocampal Neurons Apoptosis and Autophagy by Activating the PI3K/AKT Pathway via Up-regulating miR-421 in Epilepsy. (Pubmed Central) -  Jun 2, 2021   
    The phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) pathway was blocked by LY294002 and related protein levels were detected via western blot...Inhibition of the PI3K/AKT pathway reversed the effect of ZFAS1 knockdown on SE hippocampal neurons apoptosis and autophagy. Interference of ZFAS1 attenuated hippocampal neurons apoptosis and autophagy in SE by increasing miR-421 and activating the PI3K/AKT pathway, indicating a new mechanism for understanding the pathogenesis of SE.
  • ||||||||||  Journal:  FOXO1 promotes tumor progression by increased M2 macrophage infiltration in esophageal squamous cell carcinoma. (Pubmed Central) -  Jun 2, 2021   
    FOXO1 facilitated M0-to-M2 polarization and the recruitment of M2 macrophages in the TME via the transcriptional modulation of CCL20 and CSF-1. Our data deciphered the FOXO1-dependent mechanism in M2 macrophage infiltration in the TME of ESCC, which has implications for the development of novel prognostic and therapeutic targets to optimize the current treatment against ESCC.
  • ||||||||||  [VIRTUAL] Fibroblast-induced paradoxical PI3K pathway activation in colorectal cancer: Role of PTEN and potential implications for PI3K/mTOR inhibition () -  Jun 1, 2021 - Abstract #ESMOGI2021ESMO_GI_408;    
    Methods Sensitivity of cell lines to single (alpelisib, everolimus, MK-2206) and double PI3K/mTOR (gedatolisib and dactolisib) pathway inhibitors was investigated using Crystal Violet assay under differing culture conditions (wo FBS, in the presence of fibroblast-conditioned medium -CM- or in direct co-culture)...Results Based on results obtained in PTEN isogenic cell lines (HCT116 Parental and HCT116 PTEN-/-) under different culture conditions, we show that sensitivity to MEK inhibition (trametinib) is dictated mainly by the genetic background of the cancer cells; conversely, the effect of PI3K/mTOR double inhibition is profoundly influenced by exposure to fibroblast CM...Paradoxical PI3K activation involves the assembly and cellular relocalization of macromolecular complexes orchestrated by the PDZ domain of PTEN, resulting in activation of the mTORC1/p70S6K pathway. Therefore, TME-mediated pathway modulation could be potentially exploited to improve the treatment of PTEN-competent CRC patients and overcome therapeutic resistance to PI3K/mTOR inhibitor.
  • ||||||||||  Journal:  Modulation of phagosome phosphoinositide dynamics by a Legionella phosphoinositide 3-kinase. (Pubmed Central) -  Jun 1, 2021   
    We also show that MavQ is associated with the LCV and the ∆mavQ mutant displays phenotypes in the anchoring of a PtdIns4P-binding effector similar to those of ∆lepB or ∆sidF mutants. Our results establish a mechanism of de novo PtdIns4P biosynthesis by L. pneumophila via a catalysis axis comprised of MavQ, LepB, and SidF on the surface of its phagosome.
  • ||||||||||  dizocilpine (MK801) / Merck (MSD)
    Journal:  Reversible Changes in BDNF Expression in MK-801-Induced Hippocampal Astrocytes Through NMDAR/PI3K/ERK Signaling. (Pubmed Central) -  Jun 1, 2021   
    Similarly, MK-801-induced BDNF upregulation was blocked by pretreatment with inhibitors of PI3K and ERK1/2, but not by inhibitors of p38 and JNK. These findings suggested that astrocytes may contribute to the acute neurological and behavioral response to MK-801 treatment via a transient increase in BDNF expression involving NMDA-R-PI3K-ERK signaling.
  • ||||||||||  quercetin (LY294002) / Eli Lilly
    Journal, IO biomarker:  MiR-122 Participates in Oxidative Stress and Apoptosis in STZ-Induced Pancreatic β Cells by Regulating PI3K/AKT Signaling Pathway. (Pubmed Central) -  Jun 1, 2021   
    Then, LY294002 (LY, PI3K inhibitor) was used to treat INS-1 cells, and oxidative stress and apoptosis were measured...Finally, the addition of LY increased insulin levels; reduced the activities of SOD, CAT, and GSH-px; and promoted apoptosis in STZ-induced INS-1 cells. In conclusion, interference with miR-122 can inhibit oxidative stress and apoptosis in STZ-induced INS-1 cells, involving a mechanism of action related to the PI3K/AKT pathway.
  • ||||||||||  pictilisib (GDC-0941) / Roche
    [VIRTUAL] PI3K/AKT pathway is involved in fenhexamid-induced migration and angiogenesis in breast cancer cells via an ER-dependent manner () -  May 30, 2021 - Abstract #EACR2021EACR_2551;    
    Material and Methods ER positive MCF-7 and ER negative MDA-MB-231 breast cancer cells were exposed to 17β-estradiol (E2, 10-9 M), Fen (10-5 M and 10-7 M), ICI 182,780 (ICI; an ER antagonist, 10-8 M) or/and Pictilisib (Pic; a PI3K inhibitor, 10-7 M), and subsequently subjected to migration assay, live cell motility monitoring, trans-chamber assay, immunofluorescence, angiogenesis assay, tumor spheroid formation, and Western blot analysis...Conclusion Taken together, these results indicate that Fen as well as E2 promote the growth of breast cancer cells via the ER or/and PI3K pathways. Although a relatively safe pesticide, Fen may therefore play a role as an endocrine disrupting chemical in ER-positive breast cancer cells via the ER and PI3K signaling pathways.
  • ||||||||||  pictilisib (GDC-0941) / Roche
    [VIRTUAL] PI3K/AKT pathway is involved in fenhexamid-induced migration and angiogenesis in breast cancer cells via an ER-dependent manner () -  May 30, 2021 - Abstract #EACR2021EACR_2550;    
    Material and Methods ER positive MCF-7 and ER negative MDA-MB-231 breast cancer cells were exposed to 17β-estradiol (E2, 10-9 M), Fen (10-5 M and 10-7 M), ICI 182,780 (ICI; an ER antagonist, 10-8 M) or/and Pictilisib (Pic; a PI3K inhibitor, 10-7 M), and subsequently subjected to migration assay, live cell motility monitoring, trans-chamber assay, immunofluorescence, angiogenesis assay, tumor spheroid formation, and Western blot analysis...Conclusion Taken together, these results indicate that Fen as well as E2 promote the growth of breast cancer cells via the ER or/and PI3K pathways. Although a relatively safe pesticide, Fen may therefore play a role as an endocrine disrupting chemical in ER-positive breast cancer cells via the ER and PI3K signaling pathways.
  • ||||||||||  pictilisib (GDC-0941) / Roche
    [VIRTUAL] PI3K/AKT pathway is involved in fenhexamid-induced migration and angiogenesis in breast cancer cells via an ER-dependent manner () -  May 30, 2021 - Abstract #EACR2021EACR_2549;    
    Material and Methods ER positive MCF-7 and ER negative MDA-MB-231 breast cancer cells were exposed to 17β-estradiol (E2, 10-9 M), Fen (10-5 M and 10-7 M), ICI 182,780 (ICI; an ER antagonist, 10-8 M) or/and Pictilisib (Pic; a PI3K inhibitor, 10-7 M), and subsequently subjected to migration assay, live cell motility monitoring, trans-chamber assay, immunofluorescence, angiogenesis assay, tumor spheroid formation, and Western blot analysis...Conclusion Taken together, these results indicate that Fen as well as E2 promote the growth of breast cancer cells via the ER or/and PI3K pathways. Although a relatively safe pesticide, Fen may therefore play a role as an endocrine disrupting chemical in ER-positive breast cancer cells via the ER and PI3K signaling pathways.
  • ||||||||||  pictilisib (GDC-0941) / Roche
    [VIRTUAL] PI3K/AKT pathway is involved in fenhexamid-induced migration and angiogenesis in breast cancer cells via an ER-dependent manner () -  May 30, 2021 - Abstract #EACR2021EACR_2548;    
    Material and Methods ER positive MCF-7 and ER negative MDA-MB-231 breast cancer cells were exposed to 17β-estradiol (E2, 10-9 M), Fen (10-5 M and 10-7 M), ICI 182,780 (ICI; an ER antagonist, 10-8 M) or/and Pictilisib (Pic; a PI3K inhibitor, 10-7 M), and subsequently subjected to migration assay, live cell motility monitoring, trans-chamber assay, immunofluorescence, angiogenesis assay, tumor spheroid formation, and Western blot analysis...Conclusion Taken together, these results indicate that Fen as well as E2 promote the growth of breast cancer cells via the ER or/and PI3K pathways. Although a relatively safe pesticide, Fen may therefore play a role as an endocrine disrupting chemical in ER-positive breast cancer cells via the ER and PI3K signaling pathways.
  • ||||||||||  pictilisib (GDC-0941) / Roche, buparlisib (BKM120) / Novartis, Adlai Nortye
    [VIRTUAL] Impact of PI3K inhibition in AIs-treated sensitive and resistant breast cancer cells: anti-proliferative effects and induction of apoptosis () -  May 30, 2021 - Abstract #EACR2021EACR_1691;    
    The third-generation of aromatase inhibitors (AIs), anastrozole (Ana), letrozole (Let) and exemestane (Exe) are a first-line treatment option for estrogen receptor-positive (ER+ ) breast tumors, in postmenopausal women...Therefore, in this work the combinations of two PI3K class I inhibitors, buparlisib (BKM120) and pictilisib (GDC-0941), with AIs were explored in AIs-sensitive (MCF-7aro) and AIs-resistant (LTEDaro) breast cancer cell models...All the combinations in the resistant cells induced apoptosis, through mitochondrial pathway, with a more pronounced effect for the combinations with Exe. Conclusion Despite the high toxicity associated with the use of PI3K class I inhibitors, these results support further studies combining new, less toxic and specific PI3K class I inhibitors with AIs, especially with Exe, in refractory ER+ tumors The authors thank Fundação para a Ciência e Tecnologia (FCT) for T. Augusto PhD grant (BD/128333/2017) funded in part by FCT PhD Programme in Medicines and Pharmaceutical Innovation (i3DU), for C. Amaral contract (DL 57/2016 – Norma Transitória) and by Post-doc grant (SFRH/BPD/98304/2013) and for financial support (UIDP/04378/2020, UIDB/04378/2020).
  • ||||||||||  pictilisib (GDC-0941) / Roche, buparlisib (BKM120) / Novartis, Adlai Nortye
    [VIRTUAL] Impact of PI3K inhibition in AIs-treated sensitive and resistant breast cancer cells: anti-proliferative effects and induction of apoptosis () -  May 30, 2021 - Abstract #EACR2021EACR_1690;    
    The third-generation of aromatase inhibitors (AIs), anastrozole (Ana), letrozole (Let) and exemestane (Exe) are a first-line treatment option for estrogen receptor-positive (ER+ ) breast tumors, in postmenopausal women...Therefore, in this work the combinations of two PI3K class I inhibitors, buparlisib (BKM120) and pictilisib (GDC-0941), with AIs were explored in AIs-sensitive (MCF-7aro) and AIs-resistant (LTEDaro) breast cancer cell models...All the combinations in the resistant cells induced apoptosis, through mitochondrial pathway, with a more pronounced effect for the combinations with Exe. Conclusion Despite the high toxicity associated with the use of PI3K class I inhibitors, these results support further studies combining new, less toxic and specific PI3K class I inhibitors with AIs, especially with Exe, in refractory ER+ tumors The authors thank Fundação para a Ciência e Tecnologia (FCT) for T. Augusto PhD grant (BD/128333/2017) funded in part by FCT PhD Programme in Medicines and Pharmaceutical Innovation (i3DU), for C. Amaral contract (DL 57/2016 – Norma Transitória) and by Post-doc grant (SFRH/BPD/98304/2013) and for financial support (UIDP/04378/2020, UIDB/04378/2020).
  • ||||||||||  pictilisib (GDC-0941) / Roche, buparlisib (BKM120) / Novartis, Adlai Nortye
    [VIRTUAL] Impact of PI3K inhibition in AIs-treated sensitive and resistant breast cancer cells: anti-proliferative effects and induction of apoptosis () -  May 30, 2021 - Abstract #EACR2021EACR_1689;    
    The third-generation of aromatase inhibitors (AIs), anastrozole (Ana), letrozole (Let) and exemestane (Exe) are a first-line treatment option for estrogen receptor-positive (ER+ ) breast tumors, in postmenopausal women...Therefore, in this work the combinations of two PI3K class I inhibitors, buparlisib (BKM120) and pictilisib (GDC-0941), with AIs were explored in AIs-sensitive (MCF-7aro) and AIs-resistant (LTEDaro) breast cancer cell models...All the combinations in the resistant cells induced apoptosis, through mitochondrial pathway, with a more pronounced effect for the combinations with Exe. Conclusion Despite the high toxicity associated with the use of PI3K class I inhibitors, these results support further studies combining new, less toxic and specific PI3K class I inhibitors with AIs, especially with Exe, in refractory ER+ tumors The authors thank Fundação para a Ciência e Tecnologia (FCT) for T. Augusto PhD grant (BD/128333/2017) funded in part by FCT PhD Programme in Medicines and Pharmaceutical Innovation (i3DU), for C. Amaral contract (DL 57/2016 – Norma Transitória) and by Post-doc grant (SFRH/BPD/98304/2013) and for financial support (UIDP/04378/2020, UIDB/04378/2020).