PMID- 20662834
OWN - NLM
STAT- MEDLINE
DCOM- 20110110
LR  - 20181201
IS  - 1365-2133 (Electronic)
IS  - 0007-0963 (Linking)
VI  - 163
IP  - 5
DP  - 2010 Nov
TI  - Multiple genetic copy number alterations in oral squamous cell carcinoma: study 
      of MYC, TP53, CCDN1, EGFR and ERBB2 status in primary and metastatic tumours.
PG  - 1028-35
LID - 10.1111/j.1365-2133.2010.09947.x [doi]
AB  - BACKGROUND: Oncogenesis in the oral cavity is believed to result from genetic 
      alterations that cause a stepwise transformation of the mucosa to invasive 
      carcinoma. In oral squamous cell carcinoma (OSCC) multiple cytogenetic 
      abnormalities have been reported, but their practical significance remains 
      uncertain. OBJECTIVE: To evaluate the usefulness of the assessment of CCND1, MYC, 
      EGFR, ERBB2 and TP53 in OSCC and lymph node metastases. METHODS: Fifty-one 
      consecutive samples of OSCC, nine lymph node biopsies showing metastatic spread 
      from OSCC, 16 biopsies diagnosed as oral leucoplakia (OLK), 13 samples 
      corresponding to oral lichen planus (OLP) and 14 samples from normal oral mucosa 
      were included in the study. Clinical and histopathological characteristics were 
      reviewed. The genetic and protein status of the CCND1, MYC, EGFR, ERBB2 oncogenes 
      and the TP53 tumour suppressor gene were assessed by fluorescence in situ 
      hybridization (FISH) and immunohistochemistry (IHC). The obtained results were 
      compared with the clinical characteristics and the outcome of the OSCCs. RESULTS: 
      TP53 gene losses and MYC, ERBB2, CCND1 and EGFR copy number gains and 
      amplifications were detected in a higher proportion in OSCC and lymph node 
      samples than in OLK and OLP samples (P < 0.005). Overexpression of p53, Myc, 
      Cyclin D1, c-erbB-2 and epidermal growth factor receptor (EGFR) was more 
      prevalent in malignant samples than benign samples (P < 0.05). Correlation 
      between FISH and IHC results was demonstrated in MYC, EGFR and CCND1 studies. The 
      presence of two or more genetic abnormalities in the studied loci was exclusively 
      detected in primary and metastatic OSCC. CONCLUSIONS: In our series, genetic 
      abnormalities in TP53, MYC, CCND1, ERBB2 and EGFR detected by FISH were absent in 
      inflammatory lesions, infrequent in precursor lesions and common in tumoral 
      lesions. Evaluation of the genetic status of TP53, MYC, CCND1, ERBB2 and EGFR may 
      be an additional diagnostic tool in distinguishing benign from malignant oral 
      lesions in histopathologically challenging cases.
CI  - (c) 2010 The Authors. BJD (c) 2010 British Association of Dermatologists.
FAU - Martin-Ezquerra, G
AU  - Martin-Ezquerra G
AD  - Department of Medicina i Dermatologia, Universitat Autonoma de Barcelona, 
      Hospital del Mar, Parc de Salut Mar, Passeig Maritim 25-29, 08003 Barcelona, 
      Spain. gmartin@parcdesalutmar.cat
FAU - Salgado, R
AU  - Salgado R
FAU - Toll, A
AU  - Toll A
FAU - Gilaberte, M
AU  - Gilaberte M
FAU - Baro, T
AU  - Baro T
FAU - Alameda Quitllet, F
AU  - Alameda Quitllet F
FAU - Yebenes, M
AU  - Yebenes M
FAU - Sole, F
AU  - Sole F
FAU - Garcia-Muret, M
AU  - Garcia-Muret M
FAU - Espinet, B
AU  - Espinet B
FAU - Pujol, R M
AU  - Pujol RM
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Br J Dermatol
JT  - The British journal of dermatology
JID - 0004041
RN  - 0 (Biomarkers, Tumor)
RN  - 0 (CCND1 protein, human)
RN  - 0 (MYC protein, human)
RN  - 0 (Proto-Oncogene Proteins c-myc)
RN  - 136601-57-5 (Cyclin D1)
RN  - EC 2.7.10.1 (ERBB2 protein, human)
RN  - EC 2.7.10.1 (ErbB Receptors)
RN  - EC 2.7.10.1 (Receptor, ErbB-2)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - Biomarkers, Tumor/genetics/metabolism
MH  - Biopsy
MH  - Carcinoma, Squamous Cell/*genetics
MH  - Cyclin D1/genetics/metabolism
MH  - ErbB Receptors/genetics/metabolism
MH  - Female
MH  - *Gene Dosage
MH  - Genes, p53/genetics
MH  - Humans
MH  - Lymph Nodes
MH  - Male
MH  - Middle Aged
MH  - Mouth Neoplasms/*genetics
MH  - Neoplasm Metastasis/genetics
MH  - Oncogenes/*genetics
MH  - Proto-Oncogene Proteins c-myc/genetics/metabolism
MH  - Receptor, ErbB-2/genetics/metabolism
EDAT- 2010/07/29 06:00
MHDA- 2011/01/11 06:00
CRDT- 2010/07/29 06:00
PHST- 2010/07/29 06:00 [entrez]
PHST- 2010/07/29 06:00 [pubmed]
PHST- 2011/01/11 06:00 [medline]
AID - BJD9947 [pii]
AID - 10.1111/j.1365-2133.2010.09947.x [doi]
PST - ppublish
SO  - Br J Dermatol. 2010 Nov;163(5):1028-35. doi: 10.1111/j.1365-2133.2010.09947.x.