p63 is a prostate basal cell marker and is required for prostate development.
By S. Signoretti, D. Waltregny, J. Dilks, Beth M. Isaac, D. Lin, Levi A. Garraway, A. Yang, R. Montironi, F. McKeon, M. Loda. American Journal of Pathology, 2000
637 citations recorded by the source corpus.
Subfields: Molecular Biology, Oncology, Urology
View Paper: https://www.semanticscholar.org/paper/6f57107aa1d2c82a75911c5e549c3796c162a6fa
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Citations in the corpus
- Positive and negative regulation of ΔN-p63 promoter activity by p53 and ΔN-p63-α contributes to differential regulation of p53 target genes (2003, background): “In luminal epithelial structures such as the mammary gland or prostate, the number of cell layers is reduced, making the decline of p63 more pronounced (Signoretti et al., 2000; DiRenzo et al., 2002).”
- Highly purified CD44+ prostate cancer cells from xenograft human tumors are enriched in tumorigenic and metastatic progenitor cells (2006, background): “Basal cells express cytokeratin 5 (CK5), CK14, Bcl-2 (McDonnell et al., 1992), Her-2/neu (Reiter and Sawyers, 2001), p63 (Signoretti et al., 2000), and CD44 (Liu et al., 1997), whereas differentiated luminal cells express CK8, CK18, AR (androgen receptor), prostate-specific antigen (PSA), prostatic…”
- Prospective identification of tumorigenic prostate cancer stem cells. (2005, background): “It has been suggested that prostate cancers arise from the terminally differentiated luminal cells (21) because the bulk population of tumor cells, in the most common form of prostate cancer, express luminal cell-specific markers (cytokeratins 8 and 18, androgen receptor, prostate-specific antigen, ”
- Molecular characterization of human prostate carcinoma cell lines (2003, background): “Basal cells express keratins 5 and 14 (K5, K14) [13] and p63 [14], while luminal cells express K8 and K18 [13], androgen receptor (AR), and prostate-specific antigen (PSA) [15].”
- Androgen-Induced Differentiation and Tumorigenicity of Human Prostate Epithelial Cells (2004, background): “Because virtually all of the prostate cancers display a secretory phenotype characterized in part by the expression of AR and absence of p63 expression (39), we introduced AR in these immortalized (LHS-AR) and tumorigenic (LHSR-AR) PrECs (Fig.”