Immunohistochemical Analysis of BRAF (V600E) Mutation and P16 Expression in Malignant Melanoma in Lagos, Nigeria: A 10-Year Retrospective Study

被引:4
作者
Obadofin, O. [1 ]
Badmos, K. [1 ]
Orsi, N. [2 ]
Bipin, M. [3 ]
Rotimi, O. [3 ]
Banjo, A. [1 ]
机构
[1] Lagos Univ, Dept Anat & Mol Pathol, Teaching Hosp, Lagos 100254, Nigeria
[2] St James Univ Hosp, Leeds Inst Canc & Pathol, Leeds, W Yorkshire, England
[3] St James Univ Hosp, Dept Histopathol, Leeds, W Yorkshire, England
关键词
GENE;
D O I
10.1155/2019/1628247
中图分类号
R75 [皮肤病学与性病学];
学科分类号
100206 ;
摘要
Background. In Blacks, malignant melanoma (MM) is associated with greater morbidity and mortality compared to Caucasians. MMs with BRAF V600E mutation as well as those with loss of p16 protein expression are associated with aggressive behavior and worse prognosis. Objectives. We determined BRAF (V600E) mutation status and loss of p16 expression in MM cases in Lagos, Nigeria, and correlated these with histopathologic parameters and patients' age. Methods. Forty-five cases of MM received between January 2005 and December 2014 in the Anatomic and Molecular Pathology Department of Lagos University Teaching Hospital were subjected to immunohistochemical studies to determine BRAF V600E mutation and p16 protein expression. These included cutaneous (n=37), musosal (n=3), and ocular MM (n=2) as well as lymph node metastatases (n=3). Results. BRAF (V600E) mutations were detected in 5/45 (11%) while 31/45 (69%) of the cases had loss of p16 expression. No statistically significant association was found between the BRAF (V600E) mutation, loss of p16 expression, and histologic parameters such as histologic variant, Clark level, Breslow thickness, and ulceration. Conclusion. BRAF (V600E) mutation was detected only in a small proportion of cases while loss of p16 expression occurred in most cases which also had high Clark level, high Breslow thickness, and ulceration.
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页数:6
相关论文
共 26 条
[1]  
Adeyi O, 1998, NIGERIAN Q J HOSP ME, V8, P99, DOI DOI 10.4314/nqjhm.v8i2.12607
[2]  
[Anonymous], 2010, CANCER
[3]  
[Anonymous], 2014, SEER CANC STAT REV 1
[4]  
BYRD K, 2002, JOURNAL OF THE AMERI, V50, P21, DOI DOI 10.1016/S0192-9622(03)02091-7
[5]  
Calder C. K., 2010, MECH ONCOGENESIS UPD, P151
[6]  
Cancer Research UK, 2014, SKIN CANC INC STAT
[7]  
Chalya PL, 2012, TANZANIA JOURNAL OF, V14, P1
[8]  
CHAPMAN P, 2002, THE NEW ENGLAND JOUR, V364, P2507, DOI DOI 10.1056/NEJMoa1103782
[9]  
CURTIN J, 2002, THE NEW ENGLAND JOUR, V353, P2135, DOI DOI 10.1056/NEJMoa050092
[10]   Mutations of the BRAF gene in human cancer [J].
Davies, H ;
Bignell, GR ;
Cox, C ;
Stephens, P ;
Edkins, S ;
Clegg, S ;
Teague, J ;
Woffendin, H ;
Garnett, MJ ;
Bottomley, W ;
Davis, N ;
Dicks, N ;
Ewing, R ;
Floyd, Y ;
Gray, K ;
Hall, S ;
Hawes, R ;
Hughes, J ;
Kosmidou, V ;
Menzies, A ;
Mould, C ;
Parker, A ;
Stevens, C ;
Watt, S ;
Hooper, S ;
Wilson, R ;
Jayatilake, H ;
Gusterson, BA ;
Cooper, C ;
Shipley, J ;
Hargrave, D ;
Pritchard-Jones, K ;
Maitland, N ;
Chenevix-Trench, G ;
Riggins, GJ ;
Bigner, DD ;
Palmieri, G ;
Cossu, A ;
Flanagan, A ;
Nicholson, A ;
Ho, JWC ;
Leung, SY ;
Yuen, ST ;
Weber, BL ;
Siegler, HF ;
Darrow, TL ;
Paterson, H ;
Marais, R ;
Marshall, CJ ;
Wooster, R .
NATURE, 2002, 417 (6892) :949-954