Distribution of p63, a novel myoepithelial marker, in fine-needle aspiration biopsies of the breast

Abstract

A novel methodology for the de novo identification of peptides by mixed‐integer optimization and tandem mass spectrometry is presented in this article. The various features of the mathematical model are presented and examples are used to illustrate the key concepts of the proposed approach. Several problems are examined to illustrate the proposed method's ability to address (1) residue‐dependent fragmentation properties and (2) the variability of resolution in different mass analyzers. A preprocessing algorithm is used to identify important m/z values in the tandem mass spectrum. Missing peaks, resulting from residue‐dependent fragmentation characteristics, are dealt with using a two‐stage algorithmic framework. A cross‐correlation approach is used to resolve missing amino acid assignments and to identify the most probable peptide by comparing the theoretical spectra of the candidate sequences that were generated from the MILP sequencing stages with the experimental tandem mass spectrum. © 2006 American Institute of Chemical Engineers AIChE J 2007

Hippo Component TAZ Functions as a Co-repressor and Negatively Regulates ΔNp63 Transcription through TEA Domain (TEAD) Transcription Factor

“…These results are consistent with studies showing ⌬Np63 as an inhibitor of cell migration, invasion, and metastatic progression in breast cells (45,46). Moreover, p63 and particularly ⌬Np63 expression has been specifically observed in normal myoepithelial breast cells, has been proposed as a marker for cell differentiation, and is shown to be down-regulated in non-metaplastic invasive breast carcinomas (33,(53)(54)(55). Importantly, TAZ overexpression is highly correlated with breast cancer invasiveness and dissemination (32).…”

Application of Immunohistochemistry in Breast Pathology: A Review and Update

“…p63, a p53 homologue, detects MECs in breast with a dotlike nuclear staining pattern as illustrated in Figure 1, b. p63 is considered one of the best MEC markers with clean background, for example, no cross-reaction with stromal myofibroblasts or vascular smooth muscle cells; however, it may show focal gaps (discontinuous pattern) around noninvasive epithelial nests (especially with CIS) [5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21] and may also label adenoid cystic CA and metaplastic CA of the squamous component in a diffuse fashion, as illustrated in Figures 3, a through d. In papillary lesions, especially papillary CA, p63 may show focal patchy reactivity in tumor cells in up to 33.3% of cases. 17,18 Because of its dotlike, noncontinuous nuclear-staining pattern, the evaluation may not be very easy in lesions such as sclerosing adenosis and papillary lesions.…”

p63 and p73 in human cancer: defining the network

“…In any event, numerous studies have demonstrated p63 overexpression in up to 80% of primary head and neck squamous cell carcinomas (HNSCCs), and p63 overexpression is also commonly observed in other squamous epithelial cancers, including lung, nasopharyngeal, esophageal and cervical cancers (Wang et al, 2001; p63 and p73 in human cancer: defining the network MP DeYoung and LW Ellisen Hu et al, 2002;Weber et al, 2002;Massion et al, 2003;Sniezek et al, 2004). Reports have varied as to the frequency of p63 expression in invasive breast carcinomas, with studies ranging from 0 to 30% (Wang et al, 2002;Reis-Filho et al, 2003;Koker and Kleer, 2004;Ribeiro-Silva et al, 2005). It now seems clear, however, that p63 is expressed in at least a subset of breast tumors that are known to exhibit a basal epithelial phenotype (Perou et al, 2000).…”