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Vincent Laville Sigrid Le Clerc Khaled Ezzedine Randa Jdid Lieng Taing Toufik Labib Cdric Coulonges Damien Ulveling Pilar Galan Christiane Guinot Leopold Fezeu Frdrique Morizot Julie Latreille Denis Malvy Erwin Tschachler Jean‐Franois Zagury 《Experimental dermatology》2019,28(8):892-898
Sagging eyelid is considered as an outward of skin ageing and may cause medical issues. However, little is known about the factors involved in sagging eyelid. The study, which aims at determining genetic risk factors for eyelid sagging, was conducted in a cohort of 502 unrelated Caucasian women living in the Paris region. All included participants were aged between 44 and 70 years old (mean age, 57.6 years old). The severity of sagging eyelid was graded in 6 categories by a dermatologist using standardized photographs of the face. A genome wide association study adjusted on potential risk factors (including age and smoking habits) was conducted to identify genetic associations. Two single nucleotide polymorphisms in total linkage disequilibrium on chromosome 10, rs16927253 (P = 7.07 × 10‐10) and rs4746957 (P = 1.06 × 10‐8), were significantly associated with eyelid sagging severity. The rs16927253‐T and rs4746957‐A alleles showed a dominant protective effect towards eyelid sagging. These polymorphisms are located in intronic parts of the H2AFY2 gene which encodes a member of the H2A histone family and very close to the AIFM2 gene that induces apoptosis. Additionally, single nucleotide polymorphisms with a false discovery rate below 0.25 were located nearby the type XIII collagen COL13A1 gene on chromosome 10 and in the ADAMTS18 gene on chromosome 16. Several relevant genes were identified by the genome wide association study for their potential role in the sagging eyelid severity. 相似文献
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Cross‐sectional survey and surveillance for influenza viruses and MERS‐CoV among Egyptian pilgrims returning from Hajj during 2012‐2015 下载免费PDF全文
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Małek LA Labib S Mazurkiewicz L Saj M Płoski R Tesson F Bilińska ZT 《Journal of human genetics》2011,56(1):83-86
Mutations in the lamin A/C gene (LMNA) are established causes of familial dilated cardiomyopathy (DCM) with atrio-ventricular block although relatively little is known about genotype-phenotype correlations. We describe a 23-year-old patient who presented with inferolateral wall thinning and akinesis with evidence of mid-myocardial fibrosis on cardiac magnetic resonance. Molecular analysis driven by clinical similarities with a previously described case harboring the p.R541C LMNA mutation revealed a novel c.1621 C > G, p.R541G substitution whose pathogenicity was confirmed by transfection of mouse myoblasts. Our results emphasize the role of LMNA mutations at position R541 in DCM cases with segmental LV wall motion akinesis/dyskinesis. 相似文献
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Soares DG Machado MS Rocca CJ Poindessous V Ouaret D Sarasin A Galmarini CM Henriques JA Escargueil AE Larsen AK 《Molecular cancer therapeutics》2011,10(8):1481-1489
PM01183 is a novel marine-derived covalent DNA binder in clinical development. PM01183 is structurally similar to trabectedin (yondelis, ecteinascidin-743) except for the C subunit, and this modification is accompanied by different pharmacokinetics in cancer patients. We here characterize the interaction of PM01183 with the nucleotide excision repair (NER) pathway in comparison with trabectedin. Our results show for the first time that although neither PM01183 nor trabectedin is repaired by NER, both compounds are able to interfere with the NER machinery thereby attenuating the repair of specific NER substrates. We further show that the NER activity is increased in 3 of 4 cellular models with acquired resistance to cisplatin or oxaliplatin, confirming the involvement of NER in the resistance to platinum derivatives. Importantly, both PM01183 and trabectedin show unchanged or even enhanced activity toward all 4 cisplatin- and oxaliplatin-resistant cell lines. We finally show that combinations of PM01183 and cisplatin were mostly synergistic toward both parental and cisplatin-resistant ovarian carcinoma cells as indicated by Chou and Talalay analysis. These data show that the C subunit of trabectedin can be subjected to at least some structural modifications without loss of activity or NER interaction. While PM01183 and trabectedin appear functionally similar in cellular models, it is likely that the differences in pharmacokinetics may allow different dosing and scheduling of PM01183 in the clinic that could lead to novel and/or increased antitumor activity. Taken together, our results provide a mechanistic basis to support clinical trials of PM01183 alone or in combination with cisplatin. 相似文献
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Le Scodan R Massard C Jouanneau L Coussy F Gutierrez M Kirova Y Lerebours F Labib A Mouret-Fourme E 《Journal of neuro-oncology》2012,106(1):169-176
To develop a specific prognostic score for patients with brain metastases (BM) from breast cancer (BC), including the BC molecular
subtype and treatment parameters, we analyzed the outcome of 130 patients with BM from BC who received whole-brain radiotherapy.
We identified hierarchical risk groups for estimated survival by using recursive partitioning analysis (RPA). Seven prognostic
factors, namely performance status, age, trastuzumab-based therapy for HER-2-overexpressing tumors, a triple-negative phenotype,
Scarff-Bloom-Richardson grade, the serum LDH level and the lymphocyte count at BM diagnosis, were incorporated in the RPA.
The final RPA nodes were grouped according to the survival time. The RPA tree showed that survival was best (median 19.5 months)
among patients with HER2-overexpressing tumors who received trastuzumab-based therapy. The worst survival (median 3.5 months)
was observed among patients who did not receive trastuzumab and who had lymphopenia at BM diagnosis, or KPS <70 and age over
50 years, or KPS ≥70 and a triple-negative tumor (HR− & HER-2−). The other patients had a median survival of 12.5 months (P < 0.001). This 3-class specific prognostic score successfully predicted the outcomes of a heterogeneous group of patients
with brain metastases from BC. 相似文献
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