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MeSH Review

Papilloma

 
 
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Disease relevance of Papilloma

 

Psychiatry related information on Papilloma

 

High impact information on Papilloma

  • The K5-SOS-F papillomas and primary keratinocytesfrom wa2 mice display increased apoptosis, reduced Akt phosphorylation and grafting experiments imply a cell-autonomous requirement for EGFR in keratinocytes [7].
  • However, c-fos-deficient papillomas quickly became very dry and hyperkeratinized, taking on an elongated, horny appearance [8].
  • The number, size, and growth rate of benign papillomas were not increased in the p53 heterozygous mice in comparison with wild type [9].
  • One of these genes, hMT-IA, was found to encode a functional protein that confers heavy metal resistance to NIH 3T3 cells after transfer on a bovine papilloma virus-derived vector [10].
  • These isolates were highly potent when evaluated for inhibition of chemically induced preneoplastic lesions in mammary organ culture and inhibition of papillomas in the two-stage mouse skin model, and they appear to function by a unique mechanism at the level of ODC messenger RNA expression [11].
 

Chemical compound and disease context of Papilloma

  • The mice carry in the germline a mutant ras oncogene that has an arginine at codon 12 instead of glycine present in the wild-type, and after physical (wounding) or chemical promotion, these mice have a high probability for developing papillomas that progress to cancer [12].
  • The mode of action of an aromatic analogue of retinoic acid, ethyl all-trans-9-(4-methoxy-2,3,6-trimethyl-phenyl)-3,7-dimethyl-2,4,6,8-nonatetraenoate (Ro 10-9359), a compound known to possess a considerable prophylactic and therapeutic effect on skin papillomas and carcinomas, was investigated with autoradiographic and histopathologic methods [13].
  • A dose-dependent inhibition of carcinogenic expression, as determined by a decreased number of papillomas per animal, was observed in each mouse stock with the use of both FA and Ro 10-9359 when given alone [14].
  • Papillomas of the forestomach developed in 20 and 100% of the rats given diets containing 1 and 2% BHA, respectively [15].
  • Papilloma multiplicity increased from subgroup A to subgroup C in the MNAN plus B. pilosa group but not in the MNAN plus catechol group [16].
 

Biological context of Papilloma

  • The papilloma virus E2 transcriptional trans-activator is representative of a class of transcriptional modulators that activate transcription through direct binding to cis-acting DNA sequences [17].
  • The approximately 1000 nucleotide long upstream regulatory region (URR) of bovine papilloma virus-1 (BPV-1) contains a cis element which responds to trans-activation by a diffusible factor encoded in the viral E2 open reading frame (ORF) [18].
  • The same DNA segment, that does not contain the consensus sequences of all papilloma viruses relevant for E2 protein-mediated transcription enhancement, functions in an enhancer-like fashion in addition to its glucocorticoid responsive action [19].
  • Cell proliferation induced by uracil-calculi and subsequent development of reversible papillomatosis in the rat urinary bladder [20].
  • Although the rate of apoptosis in papillomas was unaffected by acute DFMO treatment, tumor cell proliferation was rapidly decreased after drug treatment [21].
 

Anatomical context of Papilloma

 

Gene context of Papilloma

  • Pten heterozygous (Pten+/-) mice develop increased papilloma numbers and show decreased carcinoma latency time in comparison with controls after skin treatment with dimethyl benzanthracene (DMBA) and tetradecanoyl-phorbol acetate (TPA) [27].
  • Finally, Ptprv loss enhances the formation of epidermal papillomas after exposure to chemical carcinogens, suggesting that Ptprv acts to suppress tumor formation in vivo [28].
  • Importantly, MDM2 increases papilloma formation induced by chemical carcinogenesis and predisposes to the appearance of premalignant lesions and squamous cell carcinomas. p53 has a natural role in the protection against UV damage in the basal layer of the epidermis [29].
  • We report here that, similarly to loss of p53, disruption of the p21(WAF1/Cip1) gene results in a markedly increased susceptibility to chemically induced skin carcinoma formation, whereas the number of papillomas is reduced [30].
  • A large body of evidence indicates that in this model, activation of Ha-ras is the critical event in papilloma formation, a process that involves epidermal proliferation and stroma remodeling, which includes angiogenesis [31].
 

Analytical, diagnostic and therapeutic context of Papilloma

References

  1. Malignant conversion of mouse skin tumours is increased by tumour initiators and unaffected by tumour promoters. Hennings, H., Shores, R., Wenk, M.L., Spangler, E.F., Tarone, R., Yuspa, S.H. Nature (1983) [Pubmed]
  2. Activation of BPV-1 replication in vitro by the transcription factor E2. Yang, L., Li, R., Mohr, I.J., Clark, R., Botchan, M.R. Nature (1991) [Pubmed]
  3. Carcinogenicity of butylated hydroxyanisole in F344 rats. Ito, N., Fukushima, S., Hagiwara, A., Shibata, M., Ogiso, T. J. Natl. Cancer Inst. (1983) [Pubmed]
  4. Detection of mutant Ha-ras genes in chemically initiated mouse skin epidermis before the development of benign tumors. Nelson, M.A., Futscher, B.W., Kinsella, T., Wymer, J., Bowden, G.T. Proc. Natl. Acad. Sci. U.S.A. (1992) [Pubmed]
  5. Inhibitory effects of dietary curcumin on forestomach, duodenal, and colon carcinogenesis in mice. Huang, M.T., Lou, Y.R., Ma, W., Newmark, H.L., Reuhl, K.R., Conney, A.H. Cancer Res. (1994) [Pubmed]
  6. Epidermal growth factor enhancement of skin tumor induction in mice. Rose, S.P., Stahn, R., Passovoy, D.S., Herschman, H. Experientia (1976) [Pubmed]
  7. The EGF receptor provides an essential survival signal for SOS-dependent skin tumor development. Sibilia, M., Fleischmann, A., Behrens, A., Stingl, L., Carroll, J., Watt, F.M., Schlessinger, J., Wagner, E.F. Cell (2000) [Pubmed]
  8. c-fos is required for malignant progression of skin tumors. Saez, E., Rutberg, S.E., Mueller, E., Oppenheim, H., Smoluk, J., Yuspa, S.H., Spiegelman, B.M. Cell (1995) [Pubmed]
  9. Reduction of p53 gene dosage does not increase initiation or promotion but enhances malignant progression of chemically induced skin tumors. Kemp, C.J., Donehower, L.A., Bradley, A., Balmain, A. Cell (1993) [Pubmed]
  10. Structural and functional analysis of the human metallothionein-IA gene: differential induction by metal ions and glucocorticoids. Richards, R.I., Heguy, A., Karin, M. Cell (1984) [Pubmed]
  11. Rotenoids mediate potent cancer chemopreventive activity through transcriptional regulation of ornithine decarboxylase. Gerhäuser, C., Mar, W., Lee, S.K., Suh, N., Luo, Y., Kosmeder, J., Luyengi, L., Fong, H.H., Kinghorn, A.D., Moriarty, R.M. Nat. Med. (1995) [Pubmed]
  12. Enhanced growth of primary tumors in cancer-prone mice after immunization against the mutant region of an inherited oncoprotein. Siegel, C.T., Schreiber, K., Meredith, S.C., Beck-Engeser, G.B., Lancki, D.W., Lazarski, C.A., Fu, Y.X., Rowley, D.A., Schreiber, H. J. Exp. Med. (2000) [Pubmed]
  13. Autoradiographic and histopathologic studies on the mode of action of an aromatic retinoid (Ro 10-9359) on chemically induced epithelial tumors in Swiss mice. Frigg, M., Torhorst, J. J. Natl. Cancer Inst. (1977) [Pubmed]
  14. Inhibition of phorbol ester-induced tumor promotion in mice by vitamin A analog and anti-inflammatory steroid. Weeks, C.E., Slaga, T.J., Hennings, H., Gleason, G.L., Bracken, W.M. J. Natl. Cancer Inst. (1979) [Pubmed]
  15. Dose response in butylated hydroxyanisole induction of forestomach carcinogenesis in F344 rats. Ito, N., Fukushima, S., Tamano, S., Hirose, M., Hagiwara, A. J. Natl. Cancer Inst. (1986) [Pubmed]
  16. Test of catechol, tannic acid, Bidens pilosa, croton oil, and phorbol for cocarcinogenesis of esophageal tumors induced in rats by methyl-n-amylnitrosamine. Mirvish, S.S., Salmasi, S., Lawson, T.A., Pour, P., Sutherland, D. J. Natl. Cancer Inst. (1985) [Pubmed]
  17. Functional analysis of the papilloma virus E2 trans-activator in Saccharomyces cerevisiae. Lambert, P.F., Dostatni, N., McBride, A.A., Yaniv, M., Howley, P.M., Arcangioli, B. Genes Dev. (1989) [Pubmed]
  18. Trans-activation of an upstream early gene promoter of bovine papilloma virus-1 by a product of the viral E2 gene. Haugen, T.H., Cripe, T.P., Ginder, G.D., Karin, M., Turek, L.P. EMBO J. (1987) [Pubmed]
  19. The upstream regulatory region of the human papilloma virus-16 contains an E2 protein-independent enhancer which is specific for cervical carcinoma cells and regulated by glucocorticoid hormones. Gloss, B., Bernard, H.U., Seedorf, K., Klock, G. EMBO J. (1987) [Pubmed]
  20. Cell proliferation induced by uracil-calculi and subsequent development of reversible papillomatosis in the rat urinary bladder. Shirai, T., Fukushima, S., Tagawa, Y., Okumura, M., Ito, N. Cancer Res. (1989) [Pubmed]
  21. Polyamines regulate expression of the neoplastic phenotype in mouse skin. Peralta Soler, A., Gilliard, G., Megosh, L., George, K., O'Brien, T.G. Cancer Res. (1998) [Pubmed]
  22. Enhanced degradation of p53 protein in HPV-6 and BPV-1 E6-immortalized human mammary epithelial cells. Band, V., Dalal, S., Delmolino, L., Androphy, E.J. EMBO J. (1993) [Pubmed]
  23. cDNA cloning of a serotonin 5-HT1C receptor by electrophysiological assays of mRNA-injected Xenopus oocytes. Lübbert, H., Hoffman, B.J., Snutch, T.P., van Dyke, T., Levine, A.J., Hartig, P.R., Lester, H.A., Davidson, N. Proc. Natl. Acad. Sci. U.S.A. (1987) [Pubmed]
  24. Translation of bicistronic viral mRNA in transfected cells: regulation at the level of elongation. Fajardo, J.E., Shatkin, A.J. Proc. Natl. Acad. Sci. U.S.A. (1990) [Pubmed]
  25. Squamous cell tumors in mice heterozygous for a null allele of Atp2a2, encoding the sarco(endo)plasmic reticulum Ca2+-ATPase isoform 2 Ca2+ pump. Liu, L.H., Boivin, G.P., Prasad, V., Periasamy, M., Shull, G.E. J. Biol. Chem. (2001) [Pubmed]
  26. Uracil-induced calculi and proliferative lesions of the mouse urinary bladder. Sakata, T., Masui, T., St John, M., Cohen, S.M. Carcinogenesis (1988) [Pubmed]
  27. Mutually exclusive mutations of the Pten and ras pathways in skin tumor progression. Mao, J.H., To, M.D., Perez-Losada, J., Wu, D., Del Rosario, R., Balmain, A. Genes Dev. (2004) [Pubmed]
  28. G1 checkpoint failure and increased tumor susceptibility in mice lacking the novel p53 target Ptprv. Doumont, G., Martoriati, A., Beekman, C., Bogaerts, S., Mee, P.J., Bureau, F., Colombo, E., Alcalay, M., Bellefroid, E., Marchesi, F., Scanziani, E., Pelicci, P.G., Marine, J.C. EMBO J. (2005) [Pubmed]
  29. MDM2 induces hyperplasia and premalignant lesions when expressed in the basal layer of the epidermis. Ganguli, G., Abecassis, J., Wasylyk, B. EMBO J. (2000) [Pubmed]
  30. p21(WAF1/Cip1) functions as a suppressor of malignant skin tumor formation and a determinant of keratinocyte stem-cell potential. Topley, G.I., Okuyama, R., Gonzales, J.G., Conti, C., Dotto, G.P. Proc. Natl. Acad. Sci. U.S.A. (1999) [Pubmed]
  31. A critical role for ras-mediated, epidermal growth factor receptor-dependent angiogenesis in mouse skin carcinogenesis. Casanova, M.L., Larcher, F., Casanova, B., Murillas, R., Fernández-Aceñero, M.J., Villanueva, C., Martínez-Palacio, J., Ullrich, A., Conti, C.J., Jorcano, J.L. Cancer Res. (2002) [Pubmed]
  32. Multiple cutaneous papillomas and carcinomas that develop spontaneously in a mouse mutant, the repeated epilation heterozygote Er/+. Lutzner, M.A., Guenet, J.L., Breitburd, F. J. Natl. Cancer Inst. (1985) [Pubmed]
  33. Elevation of the epidermal growth factor receptor and dependent signaling in human papillomavirus-infected laryngeal papillomas. Johnston, D., Hall, H., DiLorenzo, T.P., Steinberg, B.M. Cancer Res. (1999) [Pubmed]
  34. Epidermal growth factor receptor-mediated activation of Stat3 during multistage skin carcinogenesis. Chan, K.S., Carbajal, S., Kiguchi, K., Clifford, J., Sano, S., DiGiovanni, J. Cancer Res. (2004) [Pubmed]
  35. Human papillomavirus DNA in respiratory papillomatosis detected by in situ hybridization and the polymerase chain reaction. Levi, J.E., Delcelo, R., Alberti, V.N., Torloni, H., Villa, L.L. Am. J. Pathol. (1989) [Pubmed]
  36. Latent infection induced with cottontail rabbit papillomavirus. A model for human papillomavirus latency. Amella, C.A., Lofgren, L.A., Ronn, A.M., Nouri, M., Shikowitz, M.J., Steinberg, B.M. Am. J. Pathol. (1994) [Pubmed]
 
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