Direct inhibition of PI3K in combination with dual HER2 inhibitors is required for optimal antitumor activity in HER2+ breast cancer cells.
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Epidermal growth factor-receptor activation modulates Src-dependent resistance to lapatinib in breast cancer models.Niche-localized tumor cells are protected from HER2-targeted therapy via upregulation of an anti-apoptotic program in vivo.Activation of EGFR-PI3K-AKT signaling is required for Mycoplasma hyorhinis-promoted gastric cancer cell migration.MYC-xing it up with PIK3CA mutation and resistance to PI3K inhibitors: summit of two giants in breast cancersIn situ single-cell analysis identifies heterogeneity for PIK3CA mutation and HER2 amplification in HER2-positive breast cancer.Dual inhibition of Type I and Type III PI3 kinases increases tumor cell apoptosis in HER2+ breast cancersThe pan-class I phosphatidyl-inositol-3 kinase inhibitor NVP-BKM120 demonstrates anti-leukemic activity in acute myeloid leukemia.Chemical probing of HER2-amplified cancer cells identifies TORC2 as a particularly effective secondary target for combination with lapatinibShort-term early exposure to lapatinib confers lifelong protection from mammary tumor development in MMTV-erbB-2 transgenic mice.Is There any Concordance between of IHC with FISH in HER2-Positive Breast Cancer Patients?Application of pharmacologically induced transcriptomic profiles to interrogate PI3K-Akt-mTOR pathway activity associated with cancer patient prognosis.Therapeutic targeting of ERBB2 in breast cancer: understanding resistance in the laboratory and combating it in the clinic.Inhibiting the PI3K signaling pathway: buparlisib as a new targeted option in breast carcinoma.BRAF, KRAS and PIK3CA Mutation and Sensitivity to Trastuzumab in Breast Cancer Cell Line ModelHER2 Reactivation through Acquisition of the HER2 L755S Mutation as a Mechanism of Acquired Resistance to HER2-targeted Therapy in HER2+ Breast Cancer.Combined inhibition of PI3K and PARP is effective in the treatment of ovarian cancer cells with wild-type PIK3CA genes.Extracellular Matrix/Integrin Signaling Promotes Resistance to Combined Inhibition of HER2 and PI3K in HER2+ Breast Cancer.Cancer-associated fibroblasts induce trastuzumab resistance in HER2 positive breast cancer cells.Phase I dose-escalation and -expansion study of buparlisib (BKM120), an oral pan-Class I PI3K inhibitor, in patients with advanced solid tumors.Transcriptome- and proteome-oriented identification of dysregulated eIF4G, STAT3, and Hippo pathways altered by PIK3CA H1047R in HER2/ER-positive breast cancer.Cooperative oncogenic effect and cell signaling crosstalk of co‑occurring HER2 and mutant PIK3CA in mammary epithelial cells.Common and cell-type specific responses to anti-cancer drugs revealed by high throughput transcript profiling.HER2-Overexpressing Breast Cancers Amplify FGFR Signaling upon Acquisition of Resistance to Dual Therapeutic Blockade of HER2.Combined inhibition of AKT and HSF1 suppresses breast cancer stem cells and tumor growth.The crossroads of breast cancer progression: insights into the modulation of major signaling pathways.Neoadjuvant buparlisib plus trastuzumab and paclitaxel for women with HER2+ primary breast cancer: A randomised, double-blind, placebo-controlled phase II trial (NeoPHOEBE).Efficacy of buparlisib in treating breast cancer.Revisiting the IGF-1R as a breast cancer target.Microenvironmental Signals and Biochemical Information Processing: Cooperative Determinants of Intratumoral Plasticity and Heterogeneity.Novel treatment strategies for patients with HER2-positive breast cancer who do not benefit from current targeted therapy drugs
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Direct inhibition of PI3K in combination with dual HER2 inhibitors is required for optimal antitumor activity in HER2+ breast cancer cells.
description
article científic
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article scientifique
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articolo scientifico
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artigo científico
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bilimsel makale
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scientific article published on 23 January 2014
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vedecký článok
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vetenskaplig artikel
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videnskabelig artikel
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vědecký článek
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name
Direct inhibition of PI3K in c ...... in HER2+ breast cancer cells.
@en
Direct inhibition of PI3K in c ...... in HER2+ breast cancer cells.
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type
label
Direct inhibition of PI3K in c ...... in HER2+ breast cancer cells.
@en
Direct inhibition of PI3K in c ...... in HER2+ breast cancer cells.
@nl
prefLabel
Direct inhibition of PI3K in c ...... in HER2+ breast cancer cells.
@en
Direct inhibition of PI3K in c ...... in HER2+ breast cancer cells.
@nl
P2093
P2860
P356
P1476
Direct inhibition of PI3K in c ...... in HER2+ breast cancer cells.
@en
P2093
Brent N Rexer
Carlos L Arteaga
Kimberly Dahlman
Siprachanh Chanthaphaychith
P2860
P2888
P356
10.1186/BCR3601
P577
2014-01-23T00:00:00Z
P5875
P6179
1020419960