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Marc-Henri Stern

Researcher at Curie Institute

Publications -  196
Citations -  12240

Marc-Henri Stern is an academic researcher from Curie Institute. The author has contributed to research in topics: Gene & Breast cancer. The author has an hindex of 49, co-authored 168 publications receiving 9402 citations. Previous affiliations of Marc-Henri Stern include Necker-Enfants Malades Hospital & French Institute of Health and Medical Research.

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A Pan-Cancer Analysis Reveals High-Frequency Genetic Alterations in Mediators of Signaling by the TGF-β Superfamily

Anil Korkut, +760 more
- 24 Oct 2018 - 
TL;DR: An integromic analysis of gene alterations that modulate transforming growth factor β-Smad-mediated signaling in 9,125 tumor samples across 33 cancer types in The Cancer Genome Atlas provides a broad molecular perspective relevant for future functional and therapeutic studies of the diverse cancer pathways mediated by the TGF-β superfamily.
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VAMP: Visualization and analysis of array-CGH, transcriptome and other molecular profiles

TL;DR: A graphical user interface for visualization and first level analysis of molecular profiles is developed and currently in use at the Institut Curie for cancer research projects involving CGH arrays, transcriptome arrays, SNP (single nucleotide polymorphism) arrays, loss of heterozygosity results (LOH), and Chromatin ImmunoPrecipitation arrays (ChIP chips).
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The inactive X chromosome is epigenetically unstable and transcriptionally labile in breast cancer

TL;DR: This study provides the first integrated analysis of the inactive X chromosome in the context of breast cancer and establishes that epigenetic erosion of the active X can lead to the disappearance of the Barr body in breast cancer cells.
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Multiple tumor-suppressor gene 1 inactivation is the most frequent genetic alteration in T-cell acute lymphoblastic leukemia

TL;DR: MTS1 inactivation, observed in at least 80% of T-ALL, is the most consistent genetic defect found in this disease to date and strongly suggest that MTS1 is the functional target of rearrangements in T-all.