Siar, C.H. and Nagatsuka, H. and Chuah, K.S. and Rivera, R.S. and Nakano, K. and Ng, K.H. and Kawakami, T. (2010) Notch4 overexpression in ameloblastoma correlates with the solid/multicystic phenotype. Oral Surgery Oral Medicine Oral Pathology Oral Radiology and Endodontology, 110 (2). pp. 224-233. ISSN 1079-2104, DOI https://doi.org/10.1016/j.tripleo.2010.03.009.
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Abstract
Objective. Notch signaling has been implicated in cell fate decisions during odontogenesis and tumorigenesis of some odontogenic neoplasms; however, its role in solid/multicystic (SA), unicystic (UA), and recurrent (RA) ameloblastoma remains unclear. The aim of this study was to determine Notch receptor and ligand expressions in these subtypes and to speculate on their significance. Methods. Notch receptors (Notch1, 2, 3, 4) and ligands (Jagged1, 2, and Delta1) were examined immunohistochemically in SA (n = 23), UA (n = 22), and RA (n = 19). Results. Notch4 overexpression in SA (n = 19/23; 82.6) compared with UA (n = 1/22; 4.5) or RA (n = 10/19; 52.6) (P < .05) suggests positive correlation between Notch4 signaling and ameloblastomas with a solid/multicystic phenotype. Ligand (Jagged1 and Delta1) underexpression compared with their receptors (Notch1, 3, 4) (P < .05) and nonreactivity for Notch2 and Jagged2 in all 3 subsets suggests that ameloblastoma epithelium belongs to an earlier stage of differentiation (equivalent to inner enamel epithelium of developing tooth germ) before lineage commitment. Conclusion. Present findings suggest that Notch signaling molecules may play differing roles in the acquisition of different ameloblastoma phenotypes. (Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2010; 110: 224-233)
| Item Type: | Article |
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| Funders: | UNSPECIFIED |
| Additional Information: | ISI Document Delivery No.: 631GE Times Cited: 5 Cited Reference Count: 32 Cited References: Artavanis-Tsakonas S, 1999, SCIENCE, V284, P770, DOI 10.1126/science.284.5415.770 Borkosky SS, 2008, BIOCELL, V32, P251 Callahan R, 2004, J MAMMARY GLAND BIOL, V9, P145, DOI 10.1023/B:JOMG.0000037159.63644.81 Escande C, 2009, J CRANIO MAXILL SURG, V37, P363, DOI 10.1016/j.jcms.2009.05.001 Fiuza UM, 2007, J ENDOCRINOL, V194, P459, DOI 10.1677/JOE-07-0242 Fortini ME, 2009, DEV CELL, V16, P633, DOI 10.1016/j.devcel.2009.03.010 Gardner DG, 2005, WHO CLASSIFICATION T, P296 Harper JA, 2003, CLIN GENET, V64, P461, DOI 10.1046/j.1399-0004.2003.00194.x Kumamoto H, 2008, J ORAL PATHOL MED, V37, P228, DOI 10.1111/j.1600-0714.2007.00629.x Leong KG, 2006, BLOOD, V107, P2223, DOI 10.1182/blood-2005-08-3329 Miele L, 2006, CLIN CANCER RES, V12, P1074, DOI 10.1158/1078-0432.CCR-05-2570 MITSIADIS TA, 1995, J CELL BIOL, V130, P407, DOI 10.1083/jcb.130.2.407 Mitsiadis TA, 1998, DEV BIOL, V204, P420, DOI 10.1006/dbio.1998.9092 Mitsiadis TA, 2003, EXP CELL RES, V282, P101, DOI 10.1016/S0014-4827(02)00012-5 Mitsiadis TA, 2005, ARCH ORAL BIOL, V50, P137, DOI 10.1016/j.archoralbio.2004.10.006 Mitsiadis TA, 1997, DEVELOPMENT, V124, P1473 Miyamoto Y, 2003, CANCER CELL, V3, P565, DOI 10.1016/S1535-6108(03)00140-5 Nagatsuka H, 2005, ORAL ONCOL, V41, P542, DOI 10.1016/j.oraloncology.2005.01.004 Nakano K, 2008, EUR J MED RES, V13, P476 Nakano K, 2008, ORAL MED PATHOL, V12, P53, DOI 10.3353/omp.12.53 Nakano K, 2002, J ORAL PATHOL MED, V31, P494, DOI 10.1034/j.1600-0714.2002.00162.x NEVILLE BW, 2008, DIAGNOSTIC SURG PATH, P785 NG KH, 1990, ORAL SURG ORAL MED O, V70, P210, DOI 10.1016/0030-4220(90)90121-8 Nickoloff BJ, 2003, ONCOGENE, V22, P6598, DOI 10.1038/sj.onc.1206758 O'Neill CF, 2007, AM J PATHOL, V171, P1023, DOI 10.2353/ajpath.2007.061029 ROBINSON L, 1977, CANCER, V40, P2278, DOI 10.1002/1097-0142(197711)40:5<2278::AID-CNCR2820400539>3.0.CO;2-L SIAR CH, 2006, ORAL MED PATHOL, V11, P35 Siar C. H., 1993, Annals Academy of Medicine Singapore, V22, P856 Tsujigiwa H, 2005, ORAL ONCOL, V41, P843, DOI 10.1016/j.oraloncology.2005.04.005 WENIG BM, 2008, ATLAS HEAD NECK PATH, P131 Wu J, 2005, MOL CELL BIOL, V25, P1458, DOI 10.1128/MCB.25.4.1458-1474.2005 Xu P, 2009, PATHOL ONCOL RES, V15, P703, DOI 10.1007/s12253-009-9173-x Siar, Chong Huat Nagatsuka, Hitoshi Chuah, Kee Seng Rivera, Rosario Santos Nakano, Keisuke Ng, Kok Han Kawakami, Toshiyuki University of MalayaFS170/2008C; Japan Society for the Promotion of Science21592326C]] This study was jointly supported by the University of Malaya Research Grant (No. FS170/2008C) and Grant-in-Aid for Scientific Research (C) (21592326C) from the Japan Society for the Promotion of Science. Mosby-elsevier New york |
| Uncontrolled Keywords: | Epithelial-mesenchymal interactions cell fate expression tooth mouse differentiation tumorigenesis pathway growth gene |
| Subjects: | R Medicine > RK Dentistry |
| Divisions: | Faculty of Dentistry > Dept of Oral Pathology & Oral Medicine & Periodontology |
| Depositing User: | Ms Nursyafiqah Abd Malek |
| Date Deposited: | 10 Jan 2013 00:08 |
| Last Modified: | 10 Jan 2013 00:08 |
| URI: | http://eprints.um.edu.my/id/eprint/4327 |
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