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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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Recurrent molecular deletion of the 12p13 region, centromeric to ETV6/TEL, in T-cell prolymphocytic leukemia.

TL;DR: Deletion of the 12p13 region is a highly recurrent genetic event in T-cell prolymphocytic leukemia and is defined as a minimal region of deletion of less than one Mb flanked by the markers b312C2T7 and D12S320.
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Backbone dynamics and solution structure refinement of the 15N-labeled human oncogenic protein p13MTCP1: comparison with X-ray data.

TL;DR: The refined structure of p13MTCP1 benefits from 520 additional NOEs, extracted from either 15N-edited 3D experiments or homonuclear 2D NOESY recorded at 800 MHz, and from a nearly complete set of φ angular restraints.
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Ultraviolet radiation drives mutations in a subset of mucosal melanomas.

TL;DR: In this paper, the role of ultraviolet radiation (UVR)-induced DNA damage in mucosal melanoma is poorly defined, and the authors show that UVR-associated single base substitution signature 7 (SBS7) is dominant in the majority of the cases.
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Molecular characterization of different ataxia telangiectasia T-cell clones. I. A common breakpoint at the 14q11.2 band splits the T-cell receptor alpha-chain gene.

TL;DR: It is demonstrated that the T-cell receptor α-gene is split in at least two of these translocations, the first direct evidence of the involvement of a gene from the immunoglobulin superfamily in chromosomal rearrangements in ataxia telangiectasia.
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No germline ATM mutation in a series of 16 T-cell prolymphocytic leukemias

TL;DR: In their review, Vanasse et al state that up to half of the individuals without ataxia telangiectasia who contract T-cell prolymphocytic leukemia (T-PLL) were heterozygote carriers of mutations with the ATM gene.