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MeSH Review


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Disease relevance of Polyps


Psychiatry related information on Polyps


High impact information on Polyps

  • RESULTS: At base line, the mean (+/-SD) number of polyps in focal areas where polyps were counted was 15.5+/-13.4 in the 15 patients assigned to placebo, 11.5+/-8.5 in the 32 patients assigned to 100 mg of celecoxib twice a day, and 12.3+/-8.2 in the 30 patients assigned to 400 mg of celecoxib twice a day (P=0.66 for the comparison among groups) [1].
  • Tamoxifen-induced endometrial polyp [8].
  • Furthermore, treating Apc delta716 mice with a novel COX-2 inhibitor reduced the polyp number more significantly than with sulindac, which inhibits both isoenzymes [9].
  • Administration of the nonsteroidal antiinflammatory drug sulindac has been followed by regression of polyps in patients with this disorder, but no controlled trial of this drug in patients who have not had surgery has been reported [10].
  • Mucosa from dysplastic polyps showed higher mean ornithine decarboxylase activity than mucosa from polyps that were not dysplastic (P less than 0.05) [11].

Chemical compound and disease context of Polyps

  • Here we show that the adenosine 5'-triphosphate-dependent protease Lon formed a complex with polyP and degraded most of the ribosomal proteins, including S2, L9, and L13 [12].
  • METHODS: This study was conducted in 41 men and 22 women, 42-78 years of age, with a history of polyps, who participated in a randomized clinical trial testing the effects of piroxicam on rectal mucosal PGE2 levels [13].
  • Steady-state serum concentration of alpha tocopherol not altered by supplementation with oral beta carotene. The Polyp Prevention Study 1 Group [14].
  • APC(min-/+) mice overexpressing one of the alternatively processed forms of gastrin, glycine-extended gastrin, show a significant increase in polyp number [15].
  • Letter: Faecal cholesterol conversion and polyp status [16].
  • In analysis of only polypectomized subjects, the numbers of total polyps and adenomas in the sulindac group were even more markedly lower, with P values of 0.014 and 0.034, respectively [17].

Biological context of Polyps

  • We have previously suggested that the APC protein might modulate the frequency of mutations, such as loss of heterozygosity (LOH), necessary for colon polyp formation [18].
  • This phenotype is in agreement with the paucity of mutations in Ras seen in PJS polyps and suggests that loss of Lkb1 function as an early neoplastic event renders cells resistant to subsequent oncogene-induced transformation [19].
  • NSAIDs restore normal apoptosis in human adenomatous colorectal polyps and in various cancer cell lines that have lost adenomatous polyposis coli gene function [4].
  • By comparing the data obtained from polyps deriving from non-CF subjects and a CF patient homozygous for dF508 mutation, it is shown that no reduction of CF gene expression is evident in R1162X respiratory tissue [20].
  • RESULTS: Although sulindac caused a significant decrease in polyp size and number, there was no significant change in cytokinetic variables or cell cycle distribution 3 months after treatment [21].

Anatomical context of Polyps

  • We carefully dissected such microadenomas from nascent polyps by peeling off the normal epithelium and determined their genotype by PCR: all microadenomas had already lost the wild-type Apc allele, whereas the mutant allele remained unchanged [22].
  • Four patients had a germ-line E1317Q missense variant of APC that was not present in controls; one of these individuals had an unusually large number of metaplastic polyps of the colorectum [23].
  • Although the frequency of BOP-induced tumors in the gallbladder (all polyps) was not altered by either SZ or insulin, the frequency of the common duct polyps was significantly lower in the SZ + insulin + BOP group than in the BOP group (P less than 0.005) [24].
  • By PCR genotyping and immunohistochemical staining, the wild-type Smad4 allele has been lost in the polyp epithelial cells, ie., loss of heterozygosity [25].
  • On the basis of these results, we propose that COX-1 expression in the stromal cells secures the basal level of PGE(2) that can support polyp growth to approximately 1 mm, and that simultaneous inductions of COX-2 and mPGES support the polyp expansion beyond approximately 1 mm by boosting the stromal PGE(2) production [26].

Gene context of Polyps

  • Loss of expression of hMLH1 and MGMT protein has been demonstrated immunohistochemically in serrated polyps [27].
  • Subsequent examination of a large series of human PJS polyps revealed that COX-2 was also highly up-regulated in the majority of these polyps [28].
  • In colonic epithelia, these mutations produce elevated levels of Tcf4-beta-catenin, which stimulates a transcriptional response that initiates polyp formation and eventually malignant growth [29].
  • Surprisingly, the size, expansion, and pathological progression of the polyps appear Egfr-independent [30].
  • Polyp multiplicity in Min mice is greatly influenced by genetic background [31].

Analytical, diagnostic and therapeutic context of Polyps


  1. The effect of celecoxib, a cyclooxygenase-2 inhibitor, in familial adenomatous polyposis. Steinbach, G., Lynch, P.M., Phillips, R.K., Wallace, M.H., Hawk, E., Gordon, G.B., Wakabayashi, N., Saunders, B., Shen, Y., Fujimura, T., Su, L.K., Levin, B. N. Engl. J. Med. (2000) [Pubmed]
  2. Indian Hedgehog is an antagonist of Wnt signaling in colonic epithelial cell differentiation. van den Brink, G.R., Bleuming, S.A., Hardwick, J.C., Schepman, B.L., Offerhaus, G.J., Keller, J.J., Nielsen, C., Gaffield, W., van Deventer, S.J., Roberts, D.J., Peppelenbosch, M.P. Nat. Genet. (2004) [Pubmed]
  3. Multiclonal origin of polyps in Gardner syndrome. Hsu, S.H., Luk, G.D., Krush, A.J., Hamilton, S.R., Hoover, H.H. Science (1983) [Pubmed]
  4. Nonsteroidal anti-inflammatory drugs as anticancer agents: mechanistic, pharmacologic, and clinical issues. Thun, M.J., Henley, S.J., Patrono, C. J. Natl. Cancer Inst. (2002) [Pubmed]
  5. Phenotypic and molecular characteristics of hyperplastic polyposis. Rashid, A., Houlihan, P.S., Booker, S., Petersen, G.M., Giardiello, F.M., Hamilton, S.R. Gastroenterology (2000) [Pubmed]
  6. A new family with periventricular nodular heterotopia and peculiar dysmorphic features. A probable X-linked dominant trait. Musumeci, S.A., Ferri, R., Elia, M., Scuderi, C., Del Gracco, S., Azan, G., Stefanini, M.C. Arch. Neurol. (1997) [Pubmed]
  7. Bacteriocolonic pathway for ethanol oxidation: characteristics and implications. Salaspuro, M. Ann. Med. (1996) [Pubmed]
  8. Tamoxifen-induced endometrial polyp. Neven, P., De Muylder, X., Van Belle, Y. N. Engl. J. Med. (1997) [Pubmed]
  9. Suppression of intestinal polyposis in Apc delta716 knockout mice by inhibition of cyclooxygenase 2 (COX-2). Oshima, M., Dinchuk, J.E., Kargman, S.L., Oshima, H., Hancock, B., Kwong, E., Trzaskos, J.M., Evans, J.F., Taketo, M.M. Cell (1996) [Pubmed]
  10. Treatment of colonic and rectal adenomas with sulindac in familial adenomatous polyposis. Giardiello, F.M., Hamilton, S.R., Krush, A.J., Piantadosi, S., Hylind, L.M., Celano, P., Booker, S.V., Robinson, C.R., Offerhaus, G.J. N. Engl. J. Med. (1993) [Pubmed]
  11. Ornithine decarboxylase as a biologic marker in familial colonic polyposis. Luk, G.D., Baylin, S.B. N. Engl. J. Med. (1984) [Pubmed]
  12. Role of inorganic polyphosphate in promoting ribosomal protein degradation by the Lon protease in E. coli. Kuroda, A., Nomura, K., Ohtomo, R., Kato, J., Ikeda, T., Takiguchi, N., Ohtake, H., Kornberg, A. Science (2001) [Pubmed]
  13. Physical activity, body mass index, and prostaglandin E2 levels in rectal mucosa. Martínez, M.E., Heddens, D., Earnest, D.L., Bogert, C.L., Roe, D., Einspahr, J., Marshall, J.R., Alberts, D.S. J. Natl. Cancer Inst. (1999) [Pubmed]
  14. Steady-state serum concentration of alpha tocopherol not altered by supplementation with oral beta carotene. The Polyp Prevention Study 1 Group. Nierenberg, D.W., Stukel, T.A., Mott, L.A., Greenberg, E.R. J. Natl. Cancer Inst. (1994) [Pubmed]
  15. Gastrin is a target of the beta-catenin/TCF-4 growth-signaling pathway in a model of intestinal polyposis. Koh, T.J., Bulitta, C.J., Fleming, J.V., Dockray, G.J., Varro, A., Wang, T.C. J. Clin. Invest. (2000) [Pubmed]
  16. Letter: Faecal cholesterol conversion and polyp status. Hackman, A.S., Wilkins, T.D., Finegold, S.M., Sutter, V.L. Lancet (1976) [Pubmed]
  17. Randomized double-blind trial of sulindac and etodolac to eradicate aberrant crypt foci and to prevent sporadic colorectal polyps. Takayama, T., Nagashima, H., Maeda, M., Nojiri, S., Hirayama, M., Nakano, Y., Takahashi, Y., Sato, Y., Sekikawa, H., Mori, M., Sonoda, T., Kimura, T., Kato, J., Niitsu, Y. Clin. Cancer Res. (2011) [Pubmed]
  18. Alleles of APC modulate the frequency and classes of mutations that lead to colon polyps. Spirio, L.N., Samowitz, W., Robertson, J., Robertson, M., Burt, R.W., Leppert, M., White, R. Nat. Genet. (1998) [Pubmed]
  19. Loss of the Lkb1 tumour suppressor provokes intestinal polyposis but resistance to transformation. Bardeesy, N., Sinha, M., Hezel, A.F., Signoretti, S., Hathaway, N.A., Sharpless, N.E., Loda, M., Carrasco, D.R., DePinho, R.A. Nature (2002) [Pubmed]
  20. Nonsense mutation R1162X of the cystic fibrosis transmembrane conductance regulator gene does not reduce messenger RNA expression in nasal epithelial tissue. Rolfini, R., Cabrini, G. J. Clin. Invest. (1993) [Pubmed]
  21. The effects of sulindac on colorectal proliferation and apoptosis in familial adenomatous polyposis. Pasricha, P.J., Bedi, A., O'Connor, K., Rashid, A., Akhtar, A.J., Zahurak, M.L., Piantadosi, S., Hamilton, S.R., Giardiello, F.M. Gastroenterology (1995) [Pubmed]
  22. Loss of Apc heterozygosity and abnormal tissue building in nascent intestinal polyps in mice carrying a truncated Apc gene. Oshima, M., Oshima, H., Kitagawa, K., Kobayashi, M., Itakura, C., Taketo, M. Proc. Natl. Acad. Sci. U.S.A. (1995) [Pubmed]
  23. The APC variants I1307K and E1317Q are associated with colorectal tumors, but not always with a family history. Frayling, I.M., Beck, N.E., Ilyas, M., Dove-Edwin, I., Goodman, P., Pack, K., Bell, J.A., Williams, C.B., Hodgson, S.V., Thomas, H.J., Talbot, I.C., Bodmer, W.F., Tomlinson, I.P. Proc. Natl. Acad. Sci. U.S.A. (1998) [Pubmed]
  24. Inhibition of streptozotocin-induced islet cell tumors and N-nitrosobis(2-oxopropyl)amine-induced pancreatic exocrine tumors in Syrian hamsters by exogenous insulin. Pour, P.M., Kazakoff, K., Carlson, K. Cancer Res. (1990) [Pubmed]
  25. Gastric and duodenal polyps in Smad4 (Dpc4) knockout mice. Takaku, K., Miyoshi, H., Matsunaga, A., Oshima, M., Sasaki, N., Taketo, M.M. Cancer Res. (1999) [Pubmed]
  26. Cooperation of cyclooxygenase 1 and cyclooxygenase 2 in intestinal polyposis. Takeda, H., Sonoshita, M., Oshima, H., Sugihara, K., Chulada, P.C., Langenbach, R., Oshima, M., Taketo, M.M. Cancer Res. (2003) [Pubmed]
  27. Emerging concepts in colorectal neoplasia. Jass, J.R., Whitehall, V.L., Young, J., Leggett, B.A. Gastroenterology (2002) [Pubmed]
  28. Induction of cyclooxygenase-2 in a mouse model of Peutz-Jeghers polyposis. Rossi, D.J., Ylikorkala, A., Korsisaari, N., Salovaara, R., Luukko, K., Launonen, V., Henkemeyer, M., Ristimaki, A., Aaltonen, L.A., Makela, T.P. Proc. Natl. Acad. Sci. U.S.A. (2002) [Pubmed]
  29. Structure of a human Tcf4-beta-catenin complex. Poy, F., Lepourcelet, M., Shivdasani, R.A., Eck, M.J. Nat. Struct. Biol. (2001) [Pubmed]
  30. Importance of epidermal growth factor receptor signaling in establishment of adenomas and maintenance of carcinomas during intestinal tumorigenesis. Roberts, R.B., Min, L., Washington, M.K., Olsen, S.J., Settle, S.H., Coffey, R.J., Threadgill, D.W. Proc. Natl. Acad. Sci. U.S.A. (2002) [Pubmed]
  31. Identification of the modifier of Min 2 (Mom2) locus, a new mutation that influences Apc-induced intestinal neoplasia. Silverman, K.A., Koratkar, R., Siracusa, L.D., Buchberg, A.M. Genome Res. (2002) [Pubmed]
  32. Multiple hyperplastic polyps in the stomach: evidence for clonality and neoplastic potential. Dijkhuizen, S.M., Entius, M.M., Clement, M.J., Polak, M.M., Van den Berg, F.M., Craanen, M.E., Slebos, R.J., Offerhaus, G.J. Gastroenterology (1997) [Pubmed]
  33. Ligand activation of peroxisome proliferator-activated receptor beta inhibits colon carcinogenesis. Marin, H.E., Peraza, M.A., Billin, A.N., Willson, T.M., Ward, J.M., Kennett, M.J., Gonzalez, F.J., Peters, J.M. Cancer Res. (2006) [Pubmed]
  34. Prostaglandin E2 Stimulates the beta-catenin/T cell factor-dependent transcription in colon cancer. Shao, J., Jung, C., Liu, C., Sheng, H. J. Biol. Chem. (2005) [Pubmed]
  35. Explaining variation in familial adenomatous polyposis: relationship between genotype and phenotype and evidence for modifier genes. Crabtree, M.D., Tomlinson, I.P., Hodgson, S.V., Neale, K., Phillips, R.K., Houlston, R.S. Gut (2002) [Pubmed]
  36. Tumor-associated down-regulation of 15-lipoxygenase-1 is reversed by celecoxib in colorectal cancer. Heslin, M.J., Hawkins, A., Boedefeld, W., Arnoletti, J.P., Frolov, A., Soong, R., Urist, M.M., Bland, K.I. Ann. Surg. (2005) [Pubmed]
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