Capucine Héraud
A5062247058- Advanced Breast Cancer Therapies
- Cancer-related Molecular Pathways
- Breast Cancer Treatment Studies
- Cancer Treatment and Pharmacology
- HER2/EGFR in Cancer Research
- Mitochondrial Function and Pathology
- Cellular Mechanics and Interactions
- PI3K/AKT/mTOR signaling in cancer
- Cancer Research and Treatments
- Glycosylation and Glycoproteins Research
- Ubiquitin and proteasome pathways
- Protein Tyrosine Phosphatases
- Protein Kinase Regulation and GTPase Signaling
- Cancer, Hypoxia, and Metabolism
- Endoplasmic Reticulum Stress and Disease
- Cytokine Signaling Pathways and Interactions
Harvard University
2023-2024
Dana-Farber Cancer Institute
2023-2024
Inserm
2017-2022
Université de Bordeaux
2017-2022
Bordeaux Population Health
2022
Fondation pour la Recherche Médicale
2019
Translational Research in Oncology
2019
Resistance to endocrine therapy (ET) and CDK4/6 inhibitors (CDK4/6i) is a clinical challenge in estrogen receptor (ER)-positive (ER+) breast cancer. Cyclin-dependent kinase 7 (CDK7) candidate target endocrine-resistant ER+ cancer models selective CDK7 (CDK7i) are development for the treatment of Nonetheless, precise mechanisms responsible activity CDK7i remain elusive. Herein, we sought unravel these mechanisms.
Objective The AAA+ ATPase Reptin is overexpressed in hepatocellular carcinoma and preclinical studies indicate that it could be a relevant therapeutic target. However, its physiological pathophysiological roles vivo remain unknown. This study aimed to determine the role of mammalian adult liver. Design results We generated an inducible liver-specific knockout ( Repin LKO ) mouse model. Following invalidation, mice displayed decreased body fat mass, hypoglycaemia hypolipidaemia. was...
<p>Focal CNVs in PDX1526-Mut and PDX1415-WT enriched transcription pathways between the two PDX models.</p>
<p>MYC transcription is impaired by CDK7 inhibition.</p>
<p>On-target effect of SY-1365 and modulation WT/DOX-Y537S mutant MCF7 cells gene expression after treatment over time.</p>
<p>Effect of samuraciclib on PalboS and PalboR T47D cells.</p>
<p>Effect of samuraciclib on PalboS and PalboR T47D cells.</p>
<p>MYC transcription is impaired by CDK7 inhibition.</p>
<p>The combination of SY-1365 and fulvestrant inhibits proliferation CDK7 targets in PDX1415-WT.</p>
<p>The combination of SY-1365 and fulvestrant inhibits proliferation CDK7 targets in PDX1415-WT.</p>
<p>Effect of SY-1365 on WT and KI-Y537S mutant MCF7 cells after treatment over time</p>
<p>On-target effect of SY-1365 and modulation WT/DOX-Y537S mutant MCF7 cells gene expression after treatment over time.</p>
<p>Focal CNVs in PDX1526-Mut and PDX1415-WT enriched transcription pathways between the two PDX models.</p>
<p>PalboS and PalboR T47D MCF7 transcriptomic proteomic profile.</p>
<p>PalboS and PalboR T47D MCF7 trancrisptomic proteomic profile after treatment with SY-1365.</p>
<p>Effect of SY-1365 on WT and KI-Y537S mutant MCF7 cells after treatment over time</p>
<p>PalboS and PalboR T47D MCF7 trancrisptomic proteomic profile after treatment with SY-1365.</p>
<div>AbstractPurpose:<p>Resistance to endocrine therapy (ET) and CDK4/6 inhibitors (CDK4/6i) is a clinical challenge in estrogen receptor (ER)-positive (ER<sup>+</sup>) breast cancer. Cyclin-dependent kinase 7 (CDK7) candidate target endocrine-resistant ER<sup>+</sup> cancer models selective CDK7 (CDK7i) are development for the treatment of Nonetheless, precise mechanisms responsible activity CDK7i remain elusive. Herein, we sought unravel these...
<p>PalboS and PalboR T47D MCF7 transcriptomic proteomic profile.</p>
<div>AbstractPurpose:<p>Resistance to endocrine therapy (ET) and CDK4/6 inhibitors (CDK4/6i) is a clinical challenge in estrogen receptor (ER)-positive (ER<sup>+</sup>) breast cancer. Cyclin-dependent kinase 7 (CDK7) candidate target endocrine-resistant ER<sup>+</sup> cancer models selective CDK7 (CDK7i) are development for the treatment of Nonetheless, precise mechanisms responsible activity CDK7i remain elusive. Herein, we sought unravel these...
The GTPase-activating protein (GAP) p190RhoGAP (p190A) is encoded by ARHGAP35 which found mutated in cancers. p190A a negative regulator of the GTPase RhoA cells and must be targeted to RhoA-dependent actin-based structures fulfill its roles. We previously identified functional region called PLS (protrusion localization sequence) required for lamellipodia but also regulating GAP activity p190A. Additional effects on need further characterization. Here, we demonstrated that target...
Resistance to endocrine treatment and CDK4/6 inhibitors (CDK4/6i) is a major clinical challenge in estrogen receptor (ER) positive (ER+) breast cancer (BC). Previously, we identified cyclin-dependent kinase 7 (CDK7) as an essential gene ER mutant BC models showed that CDK7 silencing suppressed mutant-dependent cell growth. Selective (CDK7i) are currently development for the of ER+ BC. However, since has diverse roles biology, it critical decipher which functions govern anti-tumor activity...