R
Raphael Ceccaldi
Researcher at Harvard University
Publications - 18
Citations - 3990
Raphael Ceccaldi is an academic researcher from Harvard University. The author has contributed to research in topics: DNA repair & Homologous recombination. The author has an hindex of 14, co-authored 16 publications receiving 3110 citations. Previous affiliations of Raphael Ceccaldi include French Institute of Health and Medical Research & Paris Diderot University.
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Journal ArticleDOI
Repair Pathway Choices and Consequences at the Double-Strand Break
TL;DR: Alternative error-prone DSB repair pathways, namely alternative end joining (alt-EJ) and single-strand annealing (SSA) have been recently shown to operate in many different conditions and to contribute to genome rearrangements and oncogenic transformation.
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Homologous-recombination-deficient tumours are dependent on Polθ-mediated repair
Raphael Ceccaldi,Jessica Liu,Ravindra Amunugama,Ildiko Hajdu,Benjamin Primack,Mark I.R. Petalcorin,Kevin W O'Connor,Panagiotis A. Konstantinopoulos,Stephen J. Elledge,Simon J. Boulton,Timur Yusufzai,Alan D. D'Andrea +11 more
TL;DR: The results reveal a synthetic lethal relationship between the HR pathway and Polθ-mediated repair in EOCs, and identifyPolθ as a novel druggable target for cancer therapy.
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Homologous Recombination Deficiency: Exploiting the Fundamental Vulnerability of Ovarian Cancer
TL;DR: The genotypic and phenotypic characteristics of HR-deficient EOCs are described, current and emerging approaches for targeting these tumors are discussed, and present challenges associated with these approaches, focusing on development and overcoming resistance.
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The Fanconi anaemia pathway: new players and new functions
TL;DR: Current understanding of the functions of the Fanconi anaemia pathway in ICL repair is summarized, together with an overview of its connections with other repair pathways and its emerging roles in genome maintenance.
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Bone marrow failure in Fanconi anemia is triggered by an exacerbated p53/p21 DNA damage response that impairs hematopoietic stem and progenitor cells.
Raphael Ceccaldi,Raphael Ceccaldi,Kalindi Parmar,Enguerran Mouly,Marc Delord,Jung Min Kim,Marie Regairaz,Marie Regairaz,Marika Pla,Marika Pla,Nadia Vasquez,Qing Shuo Zhang,Corinne Pondarré,Régis Peffault de Latour,Eliane Gluckman,Marina Cavazzana-Calvo,Thierry Leblanc,Jérôme Larghero,Jérôme Larghero,Markus Grompe,Gérard Socié,Alan D. D'Andrea,Jean Soulier +22 more
TL;DR: It is found that FA patients exhibit a profound defect in hematopoietic stem and progenitor cells (HSPCs) that is present before the onset of clinical BMF, and an exacerbated p53/p21 "physiological" response to cellular stress and DNA damage accumulation as a central mechanism for progressive HSPC elimination in FA patients.