p16 mutations/deletions are not frequent events in prostate cancer.

Cyclin-dependent kinase-4 inhibitor gene (p16INK4) has recently been mapped to chromosome 9p21. Homozygous deletions of this gene have been found at high frequency in cell lines derived from different types of tumours. These findings suggested therefore, that p16INK4 is a tumour-suppressor gene involved in a wide variety of human cancers. To investigate the frequency of p16INK mutations/deletions in prostate cancer, we screened 20 primary prostate tumours and four established cell lines by polymerase chain reaction (PCR) and single-strand conformation polymorphism (SSCP) analysis for exon 1 and exon 2. In contrast to most previous reports, no homozygous deletions were found in prostate cancer cell lines, but one cell line (DU145) has revealed to a mutation at codon 76. Only two SSCP shifts were detected in primary tumours: one of them corresponds to a mutation at codon 55 and the other one probably corresponds to a polymorphism. These data suggest that mutation of the p16INK4 gene is not a frequent genetic alteration implicated in prostate cancer development

On the electrodynamics of moving bodies at low velocities

We discuss the seminal article in which Le Bellac and Levy-Leblond have identified two Galilean limits of electromagnetism, and its modern implications. We use their results to point out some confusion in the literature and in the teaching of special relativity and electromagnetism. For instance, it is not widely recognized that there exist two well defined non-relativistic limits, so that researchers and teachers are likely to utilize an incoherent mixture of both. Recent works have shed a new light on the choice of gauge conditions in classical electromagnetism. We retrieve Le Bellac-Levy-Leblond's results by examining orders of magnitudes, and then with a Lorentz-like manifestly covariant approach to Galilean covariance based on a 5-dimensional Minkowski manifold. We emphasize the Riemann-Lorenz approach based on the vector and scalar potentials as opposed to the Heaviside-Hertz formulation in terms of electromagnetic fields. We discuss various applications and experiments, such as in magnetohydrodynamics and electrohydrodynamics, quantum mechanics, superconductivity, continuous media, etc. Much of the current technology where waves are not taken into account, is actually based on Galilean electromagnetism

Central Limit Theorem and Large Deviation Principle for Continuous Time Open Quantum Walks

International audienceOpen Quantum Walks (OQWs), originally introduced in [2], are quantum generalizations of classical Markov chains. Recently, natural continuous time models of OQW have been developed in [24]. These models, called Continuous Time Open Quantum Walks (CTOQWs), appear as natural continuous time limits of discrete time OQWs. In particular they are quantum extensions of continuous time Markov chains. This article is devoted to the study of homogeneous CTOQW on Z^d. We focus namely on their associated quantum trajectories which allow us to prove a Central Limit Theorem for the "position" of the walker as well as a Large Deviation Principle

Genetic aberrations of c-myc and CCND1 in the development of invasive bladder cancer

Detrusor muscle invasive transitional cell carcinoma is associated with poor prognosis and is responsible for the majority of bladder cancer related deaths. Amplifications of c-myc and CCND1 are associated with detrusor-muscle-invasive transitional cell carcinoma, however, their precise role in driving disease progression is unclear. Fluorescence in situ hybridisation on archival tissue from 16 patients with primary diagnosis of ⩾pT2 transitional cell carcinoma and 15 cases with primary pTa/pT1 disease subsequently progressing to detrusor-muscle-invasion was performed, in the latter group both pre and post muscle invasive events were studied. No patients presenting with ⩾pT2 had amplification of c-myc, two out of 16 (12.5%) had CCND1 amplification. Of patients who developed ⩾pT2, two out of 15 (13.3%) had amplification of c-myc, both in ⩾pT2, five out of 15 (33.3%) had CCND1 amplification, two in pTa/pT1 tumours, three in ⩾pT2 transitional cell carcinomas. In total, two out of 31 (6.5%) of patients' ⩾pT2 TCCs were amplified for c-myc and six out of 31 (19%) were amplified for CCND1. Eighty-seven per cent (40 out of 46) of tumours were polysomic for chromosome 8 and 80% (37 out of 46) were polysomic for chromosome 11 and this reflected the high copy numbers of c-myc and CCND1 observed. In almost all cases an increase in c-myc/CCND1 copy number occurred prior to invasion and persisted in advanced disease. Amplification of CCND1 or alterations in c-myc/CCND1 early in bladder cancer may have clinical relevance in promoting and predicting progression to detrusor-muscle-invasive transitional cell carcinoma