The DOI matches its Crossref record; 55 of the 55 references it cites were found in a registry or an index.
ΔNp63α Is an Oncogene that Targets Chromatin Remodeler Lsh to Drive Skin Stem Cell Proliferation and Tumorigenesis
Open accessAbstract
SUMMARY The p53 homolog p63 is essential for development, yet its role in cancer is not clear. We discovered that p63 deficiency evokes the tumor suppressive mechanism of cellular senescence, causing a striking absence of stratified epithelia such as the skin. Here we identify the predominant p63 isoform, ΔNp63α, as a protein that bypasses oncogene induced senescence to drive tumorigenesis in vivo. Interestingly, bypass of senescence promotes stem-like proliferation and maintains survival of the keratin 15-positive stem cell population. Furthermore, we identify the chromatin remodeling protein Lsh as a new target of ΔNp63α that is an essential mediator of senescence bypass. These findings indicate that ΔNp63α is an oncogene that cooperates with Ras to promote tumor-initiating stem-like proliferation, and suggest that Lsh-mediated chromatin remodeling events are critical to this process.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The cited source says what the claim attributes to it.
In the citing paper
“Specific TFs were also essential, including TP63, the epidermal master regulator and cSCC oncogene (Keyes et al., 2011), as well as the AP1 family TFs, FOSL1 and JUNB.”
From Multimodal Analysis of Composition and Spatial Architecture in Human Squamous Cell Carcinoma (2020) · cites this paper as Keyes et al., 2011
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a
Serrano, M., Lin, A. W., McCurrach, M. E., Beach, D., & Lowe, S. W. (1997) · Cell · doi:10.1016/s0092-8674(00)81902-9 · Cited by 5,218 · cited 1×
“As shown previously, Ras induced features of senescence, including proliferation arrest, a characteristic morphology, and enhanced senescence-associated b-galactosidase (SA-b-gal) activity (Figure 1; Serrano et al., 1997).”
Mice deficient for p53 are developmentally normal but susceptible to spontaneous tumours
Donehower, L. A., Harvey, M., Slagle, B. L., McArthur, M. J., Montgomery, C. A., Butel, J. S., & Bradley, A. (1992) · Nature · doi:10.1038/356215a0 · Cited by 4,649 · cited 1×
“In contrast to the viable and fertile, yet tumor-prone, phenotype of p53-deficient mice (Donehower et al., 1992; Jacks et al., 1994), p63-deficient mice die postnatally from severe developmental anomalies, including a lack of skin and associated derivatives, an absence of glands such as prostate and breast, and trunca…”
p63 is essential for regenerative proliferation in limb, craniofacial and epithelial development
Yang, A., Schweitzer, R., Sun, D., Kaghad, M., Walker, N., Bronson, R. T., Tabin, C. J., Sharpe, A. H., Caput, D., Crum, C. P., et al. (1999) · Nature · doi:10.1038/19539 · Cited by 2,264
Crypt stem cells as the cells-of-origin of intestinal cancer
Barker, N., Ridgway, R. A., van Es, J. H., van de Wetering, M., Begthel, H., van den Born, M., Danenberg, E., Clarke, A. R., Sansom, O. J., & Clevers, H. C. (2008) · Nature · doi:10.1038/nature07602 · Cited by 2,232 · cited 1×
“In some tumors, the cell of origin is suggested to be a normal somatic stem cell that has acquired mutations that allow it to transform (Barker et al., 2009).”
Yang, A., Kaghad, M., Wang, Y., Gillett, E. S., Fleming, M. D., Dötsch, V., Andrews, N. C., Caput, D., & McKeon, F. (1998) · Molecular Cell · doi:10.1016/s1097-2765(00)80275-0 · Cited by 2,118
Tumor spectrum analysis in p53-mutant mice
Jacks, T., Remington, L., Williams, B. O., Schmitt, E. M., Halachmi, S., Bronson, R. T., & Weinberg, R. A. (1994) · Current Biology · doi:10.1016/s0960-9822(00)00002-6 · Cited by 2,051
Defining the Epithelial Stem Cell Niche in Skin
Tumbar, T., Guasch, G., Greco, V., Blanpain, C., Lowry, W. E., Rendl, M., & Fuchs, E. (2004) · Science · doi:10.1126/science.1092436 · Cited by 2,031 · cited 1×
“Genes whose expression is elevated in the keratinocyte stem cell populations of mouse skin have been identified (Blanpain et al., 2004; Mignone et al., 2007; Tumbar et al., 2004).”
p63 is a p53 homologue required for limb and epidermal morphogenesis
Mills, A. A., Zheng, B., Wang, X., Vogel, H. S., Roop, D. R., & Bradley, A. (1999) · Nature · doi:10.1038/19531 · Cited by 2,015 · cited 1×
“, 1994), p63-deficient mice die postnatally from severe developmental anomalies, including a lack of skin and associated derivatives, an absence of glands such as prostate and breast, and truncation of limbs (Mills et al., 1999; Yang et al., 1999).”
Self-citationEpigenetic gene silencing in cancer – a mechanism for early oncogenic pathway addiction?
Baylin, S. B., & Ohm, J. E. (2006) · Nature reviews. Cancer · doi:10.1038/nrc1799 · Cited by 1,657
Granulocyte-macrophage progenitors as candidate leukemic stem cells in blast-crisis CML
Jamieson, C. H. M., Ailles, L. E., Dylla, S. J., Muijtjens, M., Jones, C., Zehnder, J. L., Gotlib, J., Li, K., Manz, M. G., Keating, A., et al. (2004) · New England Journal of Medicine · doi:10.1056/nejmoa040258 · Cited by 1,485
Senescence in premalignant tumours
Collado, M., Gil, J., Efeyan, A., Guerra, C., Schuhmacher, A. J., Barradas, M., Benguría, A., Zaballos, A., Flores, J. M., Barbacid, M., et al. (2005) · Nature · doi:10.1038/436642a · Cited by 1,482 · cited 1×
“Topical treatment of mouse skin with DMBA induces Ras mutations, which facilitate development of premalignant papillomas with markers and features of OIS; inactivation of mediators of OIS facilitates senescence bypass and converts preneoplastic lesions tomalignant SCC (Collado et al., 2005).”
Blanpain, C., Lowry, W. E., Geoghegan, A., Polak, L., & Fuchs, E. (2004) · Cell · doi:10.1016/j.cell.2004.08.012 · Cited by 1,428
p63 identifies keratinocyte stem cells
Pellegrini, G., Dellambra, E., Golisano, O., Martinelli, E., Fantozzi, I., Bondanza, S., Ponzin, D., McKeon, F., & Luca, M. D. (2001) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.061032098 · Cited by 1,359 · cited 1×
“There is accumulating evidence that p63, and in particular the DNp63a isoform, maintains the proliferative capacity of epithelial stem cells of the skin, thymus, prostate, breast, and eye (Pellegrini et al., 2001; Senoo et al., 2007; Xin et al., 2007).”
Capturing and profiling adult hair follicle stem cells
Morris, R. J., Liu, Y., Marles, L., Yang, Z., Trempus, C., Li, S., Lin, J. S., Sawicki, J. A., & Cotsarelis, G. (2004) · Nature Biotechnology · doi:10.1038/nbt950 · Cited by 1,283 · cited 2×
“C which the K15 promoter drives GFP expression in stem cells of the hair follicle bulge that can give rise to all epidermal cell types (Morris et al., 2004).”
p63 Is Essential for the Proliferative Potential of Stem Cells in Stratified Epithelia
Senoo, M., Pinto, F., Crum, C. P., & McKeon, F. (2007) · Cell · doi:10.1016/j.cell.2007.02.045 · Cited by 881 · cited 3×
“There is accumulating evidence that p63, and in particular the DNp63a isoform, maintains the proliferative capacity of epithelial stem cells of the skin, thymus, prostate, breast, and eye (Pellegrini et al., 2001; Senoo et al., 2007; Xin et al., 2007).”
A Mutant-p53/Smad Complex Opposes p63 to Empower TGFβ-Induced Metastasis
Adorno, M., Cordenonsi, M., Montagner, M., Dupont, S., Wong, C., Hann, B. C., Solari, A., Bobisse, S., Rondina, M. B., Guzzardo, V., et al. (2009) · Cell · doi:10.1016/j.cell.2009.01.039 · Cited by 794
Dai, C., Celestino, J., Okada, Y., Louis, D. N., Fuller, G. N., & Holland, E. C. (2001) · Genes & Development · doi:10.1101/gad.903001 · Cited by 708 · cited 1×
“In contrast with tumors such as pancreatic intraepithelial neoplasia and malignant astrocytomas, in which Nestin-positive stem/progenitor cells are the source of malignancy after oncogene activation or tumor-suppressor loss (Alcantara Llaguno et al., 2009; Carrière et al., 2007; Dai et al., 2001), our data suggest tha…”
Neural stem and progenitor cells in nestin‐GFP transgenic mice
Mignone, J., Kukekov, V. G., Chiang, A., Steindler, D. A., & Enikolopov, G. (2004) · The Journal of Comparative Neurology · doi:10.1002/cne.10964 · Cited by 707
Self-citationHeterozygous Germline Mutations in the p53 Homolog p63 Are the Cause of EEC Syndrome
Celli, J., Duijf, P. H. G., Hamel, B. C. J., Bamshad, M. J., Kramer, B., Smits, A., Newbury-Ecob, R. A., Hennekam, R. C. M., Buggenhout, G. V., van Haeringen, A., et al. (1999) · Cell · doi:10.1016/s0092-8674(00)81646-3 · Cited by 707 · cited 1×
“The R279H mutation within the DNA binding domain of p63 causes EEC syndrome in humans and corresponds to one of the most prevalent p53 point mutations found in human cancer (Celli et al., 1999).”
Alcantara Llaguno, S., Chen, J., Kwon, C.-H., Jackson, E. L., Li, Y., Burns, D. K., Alvarez-Buylla, A., & Parada, L. F. (2009) · Cancer Cell · doi:10.1016/j.ccr.2008.12.006 · Cited by 694
Isolation and Characterization of Multipotent Skin‐Derived Precursors from Human Skin
Toma, J. G., McKenzie, I. A., Bägli, D., & Miller, F. D. (2005) · Stem Cells · doi:10.1634/stemcells.2004-0134 · Cited by 678 · cited 1×
“, 2009)—a progenitor population that gives rise to neuronal and mesenchymal cell types, but not to epithelial cell types such as keratinocytes (Fernandes et al., 2008; Toma et al., 2005).”
Probing tumor phenotypes using stable and regulated synthetic microRNA precursors
Dickins, R., Hemann, M., Zilfou, J. T., Simpson, D. R., Ibarra, I., Hannon, G., & Lowe, S. (2005) · Nature Genetics · doi:10.1038/ng1651 · Cited by 561 · cited 1×
“html) website, cloned into LMP vectors (Dickins et al., 2005), evaluated for efficiency in mouse embryonic fibroblasts (mefs), and assessed by western blotting 2 days after drug selection.”
p63 expression profiles in human normal and tumor tissues.
Como, C. J. D., Urist, M. J., Babayan, I., Drobnjak, M., Hedvat, C. V., Teruya‐Feldstein, J., Kamal, P., Hoos, A., & Cordon‐Cardo, C. (2002) · PubMed · Cited by 511
Flores, E. R., Sengupta, S., Miller, J. B., Newman, J. J., Bronson, R. T., Crowley, D. G., Yang, A., McKeon, F., & Jacks, T. (2005) · Cancer Cell · doi:10.1016/j.ccr.2005.02.019 · Cited by 499 · cited 1×
“The tumorigenic potential of p63-deficient mice has surprisingly not helped to clarify the role of p63 in cancer, because different groups have reported disparate results (Flores et al., 2005; Keyes et al., 2006).”
AIS is an oncogene amplified in squamous cell carcinoma
Hibi, K., Trink, B., Patturajan, M., Westra, W. H., Caballero, O. L., Hill, D. E., Ratovitski, E. A., Jen, J., & Sidransky, D. (2000) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.97.10.5462 · Cited by 464 · cited 3×
“In further contrast to p53, the predominant p63 isoform detectable in proliferating epithelia, DNp63a, is frequently overexpressed in a variety of human tumors, particularly SCC of the skin, head and neck, and lung (Hibi et al., 2000; Tonon et al., 2005), although an oncogenic role for DNp63a had not”
Influentialp63 mediates survival in squamous cell carcinoma by suppression of p73-dependent apoptosis
Rocco, J. W., Leong, C., Kuperwasser, N., DeYoung, M. P., & Ellisen, L. W. (2006) · Cancer Cell · doi:10.1016/j.ccr.2005.12.013 · Cited by 435 · cited 1×
“shown to rely on enhanced DNp63a expression (Rocco et al., 2006).”
Isolation and functional characterization of murine prostate stem cells
Lawson, D. A., Xin, L., Lukacs, R. U., Cheng, D., & Witte, O. N. (2006) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0609684104 · Cited by 406
Lsh, a member of the SNF2 family, is required for genome-wide methylationPreprint
Dennis, K., Fan, T., Geiman, T. M., Yan, Q., & Muegge, K. (2001) · Genes & Development · doi:10.1101/gad.929101 · Cited by 381
Assou, S., Carrour, T. L., Tondeur, S., Ström, S., Gabelle, A., Marty, S., Nadal, L., Pantesco, V., Reme, T. X., Hugnot, J., et al. (2007) · Stem Cells · doi:10.1634/stemcells.2006-0352 · Cited by 348 · cited 1×
“Our identification of Lsh, a chromatin-remodeling protein robustly expressed in human embryonic stem cells (Assou et al., 2007), as a DNp63a target suggests that p63 plays a role in epigenetic regulation of stemness.”
Missero, C., Cunto, F. D., Kiyokawa, H., Koff, A., & Dotto, G. P. (1996) · Genes & Development · doi:10.1101/gad.10.23.3065 · Cited by 311
p63 deficiency activates a program of cellular senescence and leads to accelerated agingPreprint
Keyes, W. M., Wu, Y., Vogel, H. S., Guo, X., Lowe, S. W., & Mills, A. A. (2005) · Genes & Development · doi:10.1101/gad.342305 · Cited by 305 · cited 10×
“To assess whether DNp63a is required for Lsh expression, we ablated p63 in primary keratinocytes obtained from the p63 conditional mouse model that we described previously (Keyes et al., 2005; Mills et al., 2002).”
InfluentialSelf-citationCao, L., Li, W., Kim, S., Brodie, S. G., & Deng, C.-X. (2003) · Genes & Development · doi:10.1101/gad.1050003 · Cited by 293 · cited 1×
“, 2007), and Brca1 (Cao et al., 2003).”
Self-citationYang, A., Zhu, Z., Kapranov, P., McKeon, F., Church, G. M., Gingeras, T., & Struhl, K. (2006) · Molecular Cell · doi:10.1016/j.molcel.2006.10.018 · Cited by 285
TAp63 induces senescence and suppresses tumorigenesis in vivo
Guo, X., Keyes, W. M., Papazoglu, C., Zuber, J. A., Li, W., Lowe, S. W., Vogel, H. S., & Mills, A. A. (2009) · Nature Cell Biology · doi:10.1038/ncb1988 · Cited by 251 · cited 2×
“, 2005) and more recently found that TAp63 isoforms are essential inducers of OIS that halt both the initiation and progression of Ras-driven p53-deficient tumors in vivo (Guo et al., 2009).”
Self-citationTAp63 Prevents Premature Aging by Promoting Adult Stem Cell Maintenance
Su, X., Paris, M., Gi, Y. J., Tsai, K. Y., Cho, M. S., Lin, Y.-L., Biernaskie, J., Sinha, S., Prives, C. L., Pevny, L., et al. (2009) · Cell stem cell · doi:10.1016/j.stem.2009.04.003 · Cited by 251 · cited 1×
“A recent report suggests that the TAp63 isoforms also function to regulate senescence within a different stem cell niche, inhibiting cellular senescence in skin-derived progenitor cells (SKPs) (Su et al., 2009)—a progenitor population that gives rise to neuronal and mesenchymal cell types, but not to epithelial cell t…”
Aranda, V., Haire, T., Nolan, M. E., Calarco, J. P., Rosenberg, A. Z., Fawcett, J. P., Pawson, T. J., & Muthuswamy, S. K. (2006) · Nature Cell Biology · doi:10.1038/ncb1485 · Cited by 247 · cited 2×
“For immunofluorescence, cultures were fixed and stained as described (Aranda et al., 2006), with antiK14 polyclonal antibody AF64 (Covance Research Products Inc.”
Self-citationSelf-Renewal and Multilineage Differentiation In Vitro from Murine Prostate Stem Cells
Xin, L., Lukacs, R. U., Lawson, D. A., Cheng, D., & Witte, O. N. (2007) · Stem Cells · doi:10.1634/stemcells.2007-0355 · Cited by 202
Gemenetzidis, E., Bose, A., Riaz, A., Chaplin, T., Young, B. D., Ali, M., Sugden, D., Thurlow, J. K., Cheong, S., Teo, S., et al. (2009) · PLoS ONE · doi:10.1371/journal.pone.0004849 · Cited by 189 · cited 1×
“Although the mechanism by which DNp63a-driven Lsh expression facilitates senescence bypass and tumor development remain to be elucidated, a recent report that Lsh is overexpressed in human HNSCC (Gemenetzidis et al., 2009) supports our finding that DNp63a promotes tumorigenesis via induction of Lsh-mediated bypass of…”
Sun, L.-Q., Lee, D. W., Zhang, Q., Xiao, W., Raabe, E. H., Meeker, A. K., Miao, D., Huso, D. L., & Arceci, R. J. (2004) · Genes & Development · doi:10.1101/gad.1176104 · Cited by 186 · cited 6×
“Interestingly, mouse models deficient for three of these candidates have phenotypes of cellular senescence or organismal aging: Lsh (Sun et al., 2004), Exo1 (Schaetzlein et al.”
InfluentialThe p63 gene in EEC and other syndromes
Brunner, H. G., Hamel, B. C. J., & van Bokhoven, H. (2002) · Journal of Medical Genetics · doi:10.1136/jmg.39.6.377 · Cited by 179 · cited 1×
“Unlike p53, point mutations in p63 are rarely associated with cancer, but cause a spectrum of developmental birth defects (Brunner et al., 2002).”
Narita, M., & Lowe, S. W. (2005) · Nature Medicine · doi:10.1038/nm0905-920 · Cited by 153 · cited 1×
“OIS is a tumor-suppressive mechanism that curtails aberrant proliferation of cells responding to DNA damage or oncogenic signaling, a program mediated predominantly by tumor suppressors such as p53, p16, and Rb (Narita and Lowe, 2005).”
Lsh, an epigenetic guardian of repetitive elements
Huang, J. (2004) · Nucleic Acids Research · doi:10.1093/nar/gkh821 · Cited by 148 · cited 1×
“In particular, Lsh is required for methylation-induced silencing of repeat elements and transposons in the pericentromeric regions (Huang et al., 2004; Sun et al., 2004) and also causes transcriptional silencing of individual loci including Cdkn1c/p57 (Sun et al.”
Schaetzlein, S., Nalapareddy, K., Ju, Z., Lechel, A., Stępczyńska, A., Lilli, D. R., Clark, A. B., Rudolph, C., Kühnel, F., Wei, K., et al. (2007) · Cell · doi:10.1016/j.cell.2007.08.029 · Cited by 146 · cited 1×
“, 2004), Exo1 (Schaetzlein et al., 2007), and Brca1 (Cao et al.”
LSH Cooperates with DNA Methyltransferases To Repress Transcription
Myant, K., & Stancheva, I. (2007) · Molecular and Cellular Biology · doi:10.1128/mcb.01073-07 · Cited by 142 · cited 1×
“Lsh functions by recruiting DNAmethyltransferases (Myant and Stancheva, 2008) or through direct interaction withmembers of the Polycomb repressive complex 1 (Xi et al.”
The Nestin progenitor lineage is the compartment of origin for pancreatic intraepithelial neoplasia
Carrière, C., Seeley, E. S., Goetze, T., Longnecker, D. S., & Korc, M. (2007) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0701117104 · Cited by 138 · cited 1×
“In contrast with tumors such as pancreatic intraepithelial neoplasia and malignant astrocytomas, in which Nestin-positive stem/progenitor cells are the source of malignancy after oncogene activation or tumor-suppressor loss (Alcantara Llaguno et al., 2009; Carrière et al., 2007; Dai et al., 2001), our data suggest tha…”
Fernandes, K. J. L., Toma, J. G., & Miller, F. D. (2007) · Philosophical Transactions of the Royal Society B Biological Sciences · doi:10.1098/rstb.2006.2020 · Cited by 129 · cited 1×
“, 2009)—a progenitor population that gives rise to neuronal and mesenchymal cell types, but not to epithelial cell types such as keratinocytes (Fernandes et al., 2008; Toma et al., 2005).”
Signal Transduction Pathways Controlling the Switch Between Keratinocyte Growth and Differentiation
Dotto, G. P. (1999) · Critical Reviews in Oral Biology & Medicine · doi:10.1177/10454411990100040201 · Cited by 101 · cited 1×
“We askedwhether RDN cells have this capacity by taking advantage of the ability of primary keratinocytes to terminally differentiate and to withdraw from the cell cycle in the presence of elevated calcium (Dotto, 1999).”
Lsh, a SNF2 family member, is required for normal murine development
Geiman, T. M., Tessarollo, L., Anver, M. R., Kopp, J. B., Ward, J. M., & Muegge, K. (2001) · Biochimica et Biophysica Acta (BBA) - General Subjects · doi:10.1016/s0304-4165(01)00129-5 · Cited by 91 · cited 2×
“Lsh plays a key role in senescence and aging, with Lsh-deficient mice exhibiting either postnatal lethality (Geiman et al., 2001) or aberrant aging and enhanced cellular senescence (Sun et al.”
p63 heterozygous mutant mice are not prone to spontaneous or chemically induced tumors
Keyes, W. M., Vogel, H. S., Koster, M. I., Guo, X., Qi, Y., Petherbridge, K. M., Roop, D. R., Bradley, A., & Mills, A. A. (2006) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0602477103 · Cited by 88
Self-citationNeural Potential of a Stem Cell Population in the Hair Follicle
Mignone, J., Roig-López, J. L., Fedtsova, N. G., Schones, D. E., Manganas, L. N., Maletić‐Savatić, M., Keyes, W. M., Mills, A. A., Gleiberman, A. S., Zhang, M. Q., et al. (2007) · Cell Cycle · doi:10.4161/cc.6.17.4593 · Cited by 80 · cited 2×
“Genes whose expression is elevated in the keratinocyte stem cell populations of mouse skin have been identified (Blanpain et al., 2004; Mignone et al., 2007; Tumbar et al., 2004).”
Self-citationLsh controls Hox gene silencing during development
Xi, S., Zhu, H., Xu, H., Schmidtmann, A., Geiman, T. M., & Muegge, K. (2007) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0703669104 · Cited by 71 · cited 2×
“Lsh functions by recruiting DNAmethyltransferases (Myant and Stancheva, 2008) or through direct interaction withmembers of the Polycomb repressive complex 1 (Xi et al., 2007).”
Ortt, K., & Sinha, S. (2006) · FEBS Letters · doi:10.1016/j.febslet.2006.07.004 · Cited by 65 · cited 1×
“p63 consensus-binding sitesWDDCNDGHHD {1-25}WDDCNDGHHDwere identified with modifications of previously published motifs (Ortt and Sinha, 2006; Yang et al., 2006).”
Lsh, a guardian of heterochromatin at repeat elements
Muegge, K. (2005) · Biochemistry and Cell Biology · doi:10.1139/o05-119 · Cited by 63 · cited 2×
“Lsh regulates DNA methylation and transcriptional silencing (Muegge, 2005), as indicated by the fact that its deficiency causes DNA hypomethylation, altered histone modification, and alterations in heterochromatin (Dennis et al.”
Conditional inactivation of p63 by Cre‐mediated excision
Mills, A. A., Qi, Y., & Bradley, A. (2002) · genesis · doi:10.1002/gene.10067 · Cited by 46 · cited 2×
“To assess whether DNp63a is required for Lsh expression, we ablated p63 in primary keratinocytes obtained from the p63 conditional mouse model that we described previously (Keyes et al., 2005; Mills et al., 2002).”
Self-citationCommon and Contrasting Genomic Profiles among the Major Human Lung Cancer SubtypesPreprint
Tonon, G., Brennan, C. W., Protopopov, A. I., Maulik, G., Feng, B., ZHANG, Y., Khatry, D., You, M. J., Aguirre, A. J., Martin, E. S., et al. (2005) · Cold Spring Harbor Symposia on Quantitative Biology · doi:10.1101/sqb.2005.70.021 · Cited by 19
Flagged first, then by citations
Cited by
Sorted by citations
Multimodal Analysis of Composition and Spatial Architecture in Human Squamous Cell Carcinoma
Ji, A. L., Rubin, A. J., Thrane, K., Jiang, S., Reynolds, D. L., Meyers, R. M., Guo, M. G., George, B. M., Mollbrink, A., Bergenstråhle, J., et al. (2020) · Cell · doi:10.1016/j.cell.2020.05.039 · Cited by 1,117
“Specific TFs were also essential, including TP63, the epidermal master regulator and cSCC oncogene (Keyes et al., 2011), as well as the AP1 family TFs, FOSL1 and JUNB.”
BackgroundSenescence and aging: the critical roles of p53
Rufini, A., Tucci, P., Celardo, I., & Melino, G. (2013) · Oncogene · doi:10.1038/onc.2012.640 · Cited by 798
Wang, M., Mao, C., Ouyang, L., Liu, Y., Lai, W., Liu, N., Shi, Y., Chen, L., Xiao, D., Yu, F., et al. (2019) · Cell Death and Differentiation · doi:10.1038/s41418-019-0304-y · Cited by 530
Nowell, C. S., & Radtke, F. (2017) · Nature reviews. Cancer · doi:10.1038/nrc.2016.145 · Cited by 379
Andricovich, J., Perkail, S., Kai, Y., Casasanta, N., Peng, W., & Tzatsos, A. (2018) · Cancer Cell · doi:10.1016/j.ccell.2018.02.003 · Cited by 320
“A molecular hallmark of the “C2-squamous-like” subtype is strong upregulation of the ΔNp63 isoform which has been linked to squamous identity (Hoadley et al., 2014; Keyes et al., 2011).”
Background
Metadata
- Authors
- Keyes, W. M., Pecoraro, M., Aranda, V., Vernersson-Lindahl, E., Li, W., Vogel, H., Guo, X., Garcia, E. L., Michurina, T. V., Enikolopov, G., Muthuswamy, S. K., & Mills, A. A.
- Affiliations
- Cold Spring Harbor Laboratory (US)
- Universitat Pompeu Fabra (ES)
- Stanford Medicine (US)
- University of Toronto (CA)
- Corresponding author
- Keyes, William M.
- Mills, Alea A.
- ORCID
- Venue
- Cell Stem Cell
- Publisher
- Elsevier BV
- Published
- 2011-02
- Volume
- 8
- Issue
- 2
- Pages
- 164-176
- ISSN
- 1875-9777 (ISSN-L)
- 1934-5909
- PMC
- PMC4373450
- OpenAlex
- W2005062632
- Semantic Scholar
- c1f79d43c5cb2d63b4b44bf6992e804b60c11dd7
- Cited by
- 193
- References
- 53
- Citations by year
- 2026: 6 · 2025: 3 · 2024: 11 · 2023: 8 · 2022: 5 · 2021: 14 · 2020: 12 · 2019: 14 · 2018: 13 · 2017: 17 · 2016: 18 · 2015: 6 · 2014: 18 · 2013: 18 · 2012: 17
- FWCI
- 14.39
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell stem cell (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Cold Spring Harbor Laboratory Institutional Repository (Cold Spring Harbor Laboratory) (acceptedVersion)
- Repositori digital de la UPF (Universitat Pompeu Fabra) (submittedVersion, other-oa)
- Funders
- National Cancer Institute (R01CA098830)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Chromatin Remodeling and Cancer
- Keywords
- ΔNp63α, p63 isoforms, LSH, chromatin remodeling, oncogenes, senescence bypass, oncogene-induced senescence, skin stem cells, keratin 15, stem cell proliferation, carcinogenesis, stratified epithelium, skin cancer
- MeSH terms
- Animals, Cells, Cultured, DNA Helicases, Flow Cytometry, Humans, Mice, Nude, Phosphoproteins, Protein Binding, Skin, Stem Cells, Trans-Activators, Keratinocytes, Polymerase Chain Reaction, Chromatin Immunoprecipitation, Cell Proliferation, Mice
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
