Christian-Jacques Larsen

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The p16(INK4A-ARF) locus plays a crucial role in the control of cellular proliferation via both the Rb and P53 pathways. We previously demonstrated that this locus is altered in human skin carcinomas. In the present study we have studied the expression of the p16(INK4A-ARF) locus following UVB irradiation of normal human keratinocytes both at the mRNA(More)
Recent studies suggest that loss of heterozygosity may play an important role in various human neoplasia. Cytogenetic abnormalities detected in primary breast tumors led us to examine breast tumor DNAs for deletions. In the present study, we demonstrate, using restriction fragment length polymorphism (RFLP) analysis at the L-myc proto-oncogene (chromosome(More)
The tumor suppressor Arf (Alternative Reading Frame) protein (p14ARF in human and p19ARF in mouse) is mainly located in the nucleolus consistent with its subcellular localization, the protein has been shown to specifically interact with 5.8S rRNA and with B23/Nucleophosmin and to regulate ribosome biogenesis. Here, we show that the p14ARF protein interacts(More)
We recently reported an interaction between the p14(ARF) protein and human topoisomerase I (Topo I) resulting in the stimulation of the relaxation activity of Topo I. Our data showed that the complex between the two proteins was located within the nucleolus. In the present work, we have investigated the regions of p14(ARF) involved in this interaction by(More)
We previously reported the presence of circulating autoantibodies to hnRNPG protein in dogs with systemic lupus erythematosus (Soulard et al. 1993, 1994). These antibodies appeared to be specifically limited to German shepherd dog species. In the present report, we have analysed the nature of the hnRNPG epitopes responsible for autoantibody specificity. By(More)
Recent works aimed at clarifying the respective roles of p16INKa and p14ARF (both located on the same INK4a locus on chromosome 9p21 in man) in malignant transformation come to the conclusion that p16INK4a is the true tumor suppressor gene in man. In mouse, it is the p19ARF knockout that suppresses the barrier protecting cells from malignant transformation.(More)
The nucleolar Arf protein has initially been shown to regulate cell cycle through the so-called Arf-mdm2-p53 pathway. In addition to this well characterized pathway, convergent data published since 2000 indicate that Arf can inhibit cell proliferation in absence of p53, suggesting the existence of a p53-independent pathway. Several partners have recently(More)
This presentation reports a series of data dealing with recurrent genetic abnormalities and gene expression profiles that characterize primary glioblastomas and secondary glioblastomas resulting from the transformation of low grade tumors (grade II and III astrocytomas and oligodendrogliomas). The most recent aspects of the concept of tumor stem cells that(More)