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5篇 您的检索式：作者名="Ghiringhelli D"

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		题名	作者	年代	出处	被引量
	1	CD4 ( + ) CD25 ( + ) regulatory T eells suppress tumor immunity but are sensitive to cyclophosphamide which allows immunotherapy of established tumors to be curative 显示文摘	Ghiringhelli F Larmonier N Schmitt E Parcellier A Cathelin D Garrido C	2004	Eur J hnmunol2004，34，2：	1
	2	Human ectonucleotidase-expressing CD25high Th17 cells accumulate in breast cancer tumors and exert immunosuppressive functions显示文摘	Marion Thibaudin Marie Chaix Romain Boidot Frédérique Végran Valentin Derangère Emeric Limagne Hélène Berger Sylvain Ladoire Lionel Apetoh Fran?ois Ghiringhelli	2016	OncoImmunology2016，，：	1
	3	Pederinae pseud opederina 显示文摘	Quilico A Cardani C Ghiringhelli D	1961	Chim lnd1961，43，：	1
	4	The structure of pederin 显示文摘	Cardani C Ghiringhelli D Mondelli R	1965	TetrahedronLett1965，29，：	1
	5	Efficiency of olaparib in colorectal cancer patients with an alteration of the homologous repair protein显示文摘Precision medicine is defined by the administration of drugs based on the tumor's particular genetic characteristics. It is developing quickly in the field of cancer therapy. For example, KRAS, NRAS and BRAF genetic testing demonstrates its efficiency for precision medicine in colorectal cancer(CRC). Besides for these well-known mutations, the purpose of performing larger genetic testing in this pathology is unknown. Recent reports have shown that using the poly ADP ribose polymerase(PARP) inhibitor olaparib in patients with homologous repair enzyme deficiency gave positive clinical results in breast, ovarian and prostate cancers. We have reported here the cases of 2 patients with multi-treated metastatic CRC who underwent somatic and constitutional exome analyses. The analyses revealed a loss of function mutation in a homologous repair enzyme resulting in the loss of heterozygosity for both patients(Check2 for the first patient and RAD51 C for the second one). Both patients were treated with off-label usage of olaparib. While the first patient showed clinical benefit, reduction of carcinoembryonic antigen tumor marker and radiologic response, the second patient quickly presented a progression of the tumor. Additional genetic analyses revealed a frameshift truncating mutation of the TP53BP1 gene in the patient who progressed. Interestingly, deficiency in TP53BP1 was previously described to confer resistance to olaparib in mice breast cancer models. Our findings suggest that exome analysis may be a helpful tool to highlight targetable mutations in CRC and that olaparib may be efficient in patients with a homologous repair deficiency.	Francois Ghiringhelli Corentin Richard Sandy Chevrier Frédérique Végran Romain Boidot	2016	World Journal of Gastroenterology2016，22，48：	0

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