A5087030379- Multiple Myeloma Research and Treatments
- Telomeres, Telomerase, and Senescence
- Angiogenesis and VEGF in Cancer
- Sexual Differentiation and Disorders
- Acute Myeloid Leukemia Research
- Genetic and Clinical Aspects of Sex Determination and Chromosomal Abnormalities
- Adrenal and Paraganglionic Tumors
- Cancer Cells and Metastasis
- Celiac Disease Research and Management
- Epigenetics and DNA Methylation
- Myeloproliferative Neoplasms: Diagnosis and Treatment
- Cancer Research and Treatments
- Cancer-related gene regulation
- Gender Studies in Language
- Diabetes and associated disorders
- LGBTQ Health, Identity, and Policy
- Hematological disorders and diagnostics
- Mitochondrial Function and Pathology
- Eosinophilic Disorders and Syndromes
- Genomics and Chromatin Dynamics
- MicroRNA in disease regulation
- Thyroid Disorders and Treatments
- T-cell and B-cell Immunology
- Systemic Sclerosis and Related Diseases
- Cancer-related Molecular Pathways
European Institute of Oncology
2016
Inserm
2008-2013
Bilkent University
2004-2013
Université Joseph Fourier
2010-2013
Institut pour l'avancée des biosciences
2008
Abstract Objective Scleroderma (SSc) is an autoimmune disease of unknown etiology. The 3–8 times more frequent in women than men. role X chromosome inactivation (XCI) the predisposition to autoimmunity has been questioned. Until now this not illustrated experimentally. This study was undertaken test hypothesis that disturbances XCI mosaicism may be involved pathogenesis female patients with SSc. Methods Seventy SSc and 160 controls were analyzed for androgen receptor locus by Hpa...
Senescence is a permanent proliferation arrest in response to cell stress such as DNA damage. It contributes strongly tissue aging and serves major barrier against tumor development. Most cells are believed bypass the senescence (become "immortal") by inactivating growth control genes TP53 CDKN2A. They also reactivate telomerase reverse transcriptase. Senescence-to-immortality transition accompanied phenotypic biochemical changes mediated genome-wide transcriptional modifications. This...
The Smyd2 protein (Set- and Mynd domain containing 2) is a methyl-transferase that can modify both histones cytoplasmic proteins. over-expressed in several cancer types was shown to be limiting for tumor development the pancreas. However, genetic evidence role of other cancers or mouse missing date. Using germ line-deleted strains, we now show related Smyd3 are dispensable normal development. Ablation did not affect hematopoiesis, but retarded leukemia promoted by MLL-AF9, fusion oncogene...
Background Breast cancer is a remarkably heterogeneous disease. Luminal, basal-like, "normal-like", and ERBB2+ subgroups were identified shown to have different prognoses. The mechanisms underlying this heterogeneity are poorly understood. In our study, we explored the role of cellular differentiation senescence as potential cause heterogeneity. Methodology/Principal Findings A panel breast cell lines, isogenic clones, tumors used. Based on their ability generate senescent progeny under...
Abstract Background: The role of extremely skewed X‐chromosome inactivation (XCI) has been questioned in the pathogenesis recurrent spontaneous abortion (RSA) but results obtained were conflicting. Aims: We therefore investigated XCI patterns peripheral blood DNA from 80 patients who had RSA and 160 age‐matched controls. Methods: Pregnancy history, age, karyotype, disease information was collected all subjects. methylation status a highly polymorphic cytosine‐adenine‐guanine repeat...
Abstract Background In multiple myeloma (MM), increased neoangiogenesis contributes to tumor growth and disease progression. Increased levels of endothelial progenitor cells (EPCs) contribute in MM, and, importantly, covary with activity response treatment. order understand the mechanisms responsible for EPC neoangiogenic function we investigated whether these were clonal by determining X-chromosome inactivation (XCI) patterns female patients a human androgen receptor assay (HUMARA)....