about
ErbB-2 nuclear function in breast cancer growth, metastasis and resistance to therapyp42/p44 MAPK-mediated Stat3Ser727 phosphorylation is required for progestin-induced full activation of Stat3 and breast cancer growthHeregulin Co-opts PR Transcriptional Action Via Stat3 Role As a Coregulator to Drive Cancer Growth.Small interfering RNA targeted to IGF-IR delays tumor growth and induces proinflammatory cytokines in a mouse breast cancer modelClinical relevance of ErbB-2/HER2 nuclear expression in breast cancer.Inflammasome activation is critical to the protective immune response during chemically induced squamous cell carcinoma.Progesterone receptor activation downregulates GATA3 by transcriptional repression and increased protein turnover promoting breast tumor growthProgesterone receptor assembly of a transcriptional complex along with activator protein 1, signal transducer and activator of transcription 3 and ErbB-2 governs breast cancer growth and predicts response to endocrine therapy.Progesterone-induced stimulation of mammary tumorigenesis is due to the progesterone metabolite, 5α-dihydroprogesterone (5αP) and can be suppressed by the 5α-reductase inhibitor, finasteride.Targeting Stat3 induces senescence in tumor cells and elicits prophylactic and therapeutic immune responses against breast cancer growth mediated by NK cells and CD4+ T cells.Juvenile exposure to a high fat diet promotes behavioral and limbic alterations in the absence of obesity.Inhibition of MHC-I by Brucella abortus is an early event during infection and involves EGFR pathway.Progestin drives breast cancer growth by inducing p21(CIP1) expression through the assembly of a transcriptional complex among Stat3, progesterone receptor and ErbB-2.TNFα-Induced Mucin 4 Expression Elicits Trastuzumab Resistance in HER2-Positive Breast Cancer.Invasive micropapillary carcinoma of the breast overexpresses MUC4 and is associated with poor outcome to adjuvant trastuzumab in HER2-positive breast cancer.MiR-16 mediates trastuzumab and lapatinib response in ErbB-2-positive breast and gastric cancer via its novel targets CCNJ and FUBP1.Targeting ErbB-2 nuclear localization and function inhibits breast cancer growth and overcomes trastuzumab resistance.A Brucella spp. Protease Inhibitor Limits Antigen Lysosomal Proteolysis, Increases Cross-Presentation, and Enhances CD8+ T Cell ResponsesBlockade of Stat3 oncogene addiction induces cellular senescence and reveals a cell-nonautonomous activity suitable for cancer immunotherapy
P50
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P50
description
investigador
@es
researcher
@en
name
Roxana Schillaci
@en
type
label
Roxana Schillaci
@en
prefLabel
Roxana Schillaci
@en
P31
P496
0000-0002-7776-3378