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18篇 您的检索式:作者名="Gran V"
    题名 作者 年代 出处 被引量
1Transcriptional regulation of the survivin gene显示文摘Boidot R Végran F Lizard-Nacol S 2014Mol Biol Rep2014,41,1:1
2In vitro generation of endothelial microparticles and possible prothrombotic activity in patients with lupus anticoagulant显示文摘Combes V Simon AC Gran GE 1999J Clin Invest1999,104,:1
3Targeting lactate-fueled respiration selectively kills hypoxic tumor cells in mice显示文摘Sonveaux Pierre Végran Frédérique Schroeder Thies Wergin Melanie C Verrax Julien Rabbani Zahid N De Saedeleer Christophe J Kennedy Kelly M Diepart Caroline Jordan Bénédicte F Kelley Michael J Gallez Bernard Wahl Miriam L Feron Olivier Dewhir 2008Journal of Clinical Investigation2008,,12:1
4Denitrification in estuarine sediments in the eastern Gulf of Finland,Baltic Sea显示文摘GRAN V PITK NEN H 1999Hydrobiologia1999,393,10:1
5IL-24 is expressed by rat and Human macrophages 显示文摘Gam H Sehmidt A Gran V 2002Immunobiology2002,205,3:1
6Detection of DNA damage in gametocytes of zebra mussel using comet assay 显示文摘Mirjana Pavlica Gran I V Klobu Nina Moja 2001Mutation Research/Genetic Toxicology and Environmental Mutagenesis2001,490,2:1
7Mechanical properties of superhard TiB2 coatings prepared by DC magnetron sputtering显示文摘MIKULA M GRAN(C)I(C) B BUR(S)(I)KOV(A) V 2007Vacuum2007,82,2:1
8Overexpression of caspase-3s splice variant in locally advanced breast carcinoma is associated with poor response to neoadjuvant chemotherapy显示文摘 Boidot R Oudin C 2006Clin Cancer Res2006,12,:1
9The transcription factor IRF1dictates the IL-21-dependent anticancer functions of TH9 cells显示文摘Végran F Berger H Boidot R 2014Nat Immunol2014,15,8:1
10Transcriptional regulation of the survivin gene显示文摘BOIDOT R VGRAN F LIZARD-NACOL S 2014Mol Biol Rep2014,41,:1
11Targeting lactate-fueled respiration selectively kills hypoxic tumor cells in mice显示文摘Sonveaux P Végran F Schroeder T 2008J Clin Invest2008,118,12:1
12Overexpression of caspase-3ssplice variant in locally advanced breast carcinoma is associated withpoor response to neoadjuvant chemotherapy显示文摘Végran F Boidot R Oudin C 2006Clin Cancer Res2006,12,19:1
13Skin involvement in chronic myelomonocytic leukaemia as a predictor of transformation into acute myeloid leukaemia显示文摘Pont V Miquel FJ Gran TC 2001J Eur Acad Dermatol Venereol2001,15,3:1
14Dacarbazine-mediated upregu-lation of NKG2D ligands on tumor cells activates NK and CD8 T cells and restrains melanoma growth显示文摘Hervieu A Rébé C Végran F 0,,02:1
15Gene expression profile and response to trastuzumab-docetaxel-based treat-ment in breast carcinoma显示文摘Végran F Boidot R Coudert B 2009Br J Cancer2009,101,8:1
16Targeting lactate-fueledrespiration selectively kills hypoxic tumor cells in mice显示文摘Sonveaux P Végran F Schroeder T 2008J Clin In-vest2008,118,12:1
17Human 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 2016OncoImmunology2016,,:1
18Efficiency 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 2016World Journal of Gastroenterology2016,22,48:0
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