Nuclear localization of the caspase-3-cleaved form of p73 in anoikis.

The transcription factor p73 is a homologue of p53 that can be expressed as pro- or anti-apoptotic isoforms. Unlike p53, p73 is rarely mutated or lost in cancers and it is found to replace defective p53 inducing apoptosis. Here, we investigated the p73 involvement in anoikis, a type of apoptosis caused by inadequate cell-matrix interactions.

Retinoic acid receptor alpha amplifications and retinoic acid sensitivity in breast cancers.

Background: Molecular segmentation of breast cancer allows identification of small groups of patients who present high sensitivity to targeted agents. A patient, with chemo- and trastuzumab-resistant HER2-overexpressing breast cancer, who presented concomitant acute promyelocytic leukemia, showed a response in her breast lesions to retinoic acid, arsenic, and aracytin. We therefore investigated whether RARA gene amplification could be associated with sensitivity to retinoic acid derivatives in breast cancers.

P53 family: at the crossroads in cancer therapy.

p53 and its related genes, p73 and p63, are members of the p53 gene family. While p53 is the most frequently mutated gene in human tumors, p73 and p63 are rarely mutated or lost in cancers. Although p53-deficient cancer cells are often less responsive to chemotherapy, they are not completely drug resistant, suggesting that other apoptotic pathways are at work.

Lobular and ductal carcinomas of the breast have distinct genomic and expression profiles.

Invasive ductal carcinomas (IDCs) and invasive lobular carcinomas (ILCs) are the two major pathological types of breast cancer. Epidemiological and histoclinical data suggest biological differences, but little is known about the molecular alterations involved in ILCs. We undertook a comparative large-scale study by both array-compared genomic hybridization and cDNA microarray of a set of 50 breast tumors (21 classic ILCs and 29 IDCs) selected on homogeneous histoclinical criteria.

Involvement of N-terminally truncated variants of p73, deltaTAp73, in head and neck squamous cell cancer: a comparison with p53 mutations.

p73, a p53-related gene, encodes two classes of isoforms with opposing functions: (1) a full-length transactivation-competent p73 protein (TAp73) with tumour suppressor activity; and (2) a group of NH2-terminally truncated, transactivation-deficient p73 proteins, deltaEx2p73, deltaEx2-3p73, deltaNp73 and deltaN'p73 (collectively named deltaTAp73) with oncogenic activity. In this study, for the first time, we analyse the deregulations of TAp73 and deltaTAp73 in head and neck squamous cell cancer (HNSCC) and compare them to p53 status. We found that all the p73 isoforms in HNSCC tissue were upregulated with respect to those in normal adjacent tissue.