Amplification of 11q13 DNA markers in head and neck squamous cell carcinomas: Correlation with clinical outcome

Muller, Danièle; Millon, Régine; Velten, Michel; Brönner, G.; Jung, G.M.; Engelmann, A.; Flesch, H.; Eber, M.; Methlin, G; Abecassis, Joseph

doi:10.1016/s0959-8049(97)00198-6

Cited by 59 publications

(52 citation statements)

References 20 publications

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“…We confirmed that they are overexpressed in HNSCC compared to N tissue by quantitative RT-PCR, determined the size of the transcripts by Northern blotting and showed that the proteins are expressed in tumour cells by immunohistochemitry (see Results). The TMEM16A gene is located in the CCND1-EMS1 region (11q13), a locus that is frequently amplified in HNSCC (Muller et al, 1997) and is enriched in genes that are differentially expressed in hypopharynx carcinoma (Cromer et al, 2004). TMEM16A is predicted to be associated with the cell membrane.…”

Section: Genes and Processesmentioning

confidence: 99%

Head and neck squamous cell carcinoma transcriptome analysis by comprehensive validated differential display

Millon²,

et al. 2005

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Head and neck squamous cell carcinoma (HNSCC) is common worldwide and is associated with a poor rate of survival. Identification of new markers and therapeutic targets, and understanding the complex transformation process, will require a comprehensive description of genome expression, that can only be achieved by combining different methodologies. We report here the HNSCC transcriptome that was determined by exhaustive differential display (DD) analysis coupled with validation by different methods on the same patient samples. The resulting 820 nonredundant sequences were analysed by high throughput bioinformatics analysis. Human proteins were identified for 73% (596) of the DD sequences. A large proportion (>50%) of the remaining unassigned sequences match ESTs (expressed sequence tags) from human tumours. For the functionally annotated proteins, there is significant enrichment for relevant biological processes, including cell motility, protein biosynthesis, stress and immune responses, cell death, cell cycle, cell proliferation and/or maintenance and transport. Three of the novel proteins (TMEM16A, PHLDB2 and ARH-GAP21) were analysed further to show that they have the potential to be developed as therapeutic targets.

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Section: Genes and Processesmentioning

confidence: 99%

Head and neck squamous cell carcinoma transcriptome analysis by comprehensive validated differential display

Millon²,

et al. 2005

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“…In head and neck squamous cell carcinoma, this amplification is one of the most frequently observed genetic alterations [11][12][13][14][15][16][17][18][19][20] and is reportedly correlated with aggressive tumor growth [9,13,19], the presence of lymph node metastases [17,[21][22][23], and poor prognosis [9,19,24]. The amplified 11q13 region is 3-5 megabases in size and includes four putative oncogenes: CCND1 (PRAD1), FGF3 (INT2), FGF4 (HST1), and EMS1.…”

Section: Introductionmentioning

confidence: 99%

Co-overexpression of cortactin and CRKII increases migration and invasive potential in oral squamous cell carcinoma

Yamada

Yanamoto

Rokutanda

et al. 2014

Journal of Oral and Maxillofacial Surgery, Medicine, and Pathol

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Cortactin stimulates cell migration, invasion, and experimental metastasis. Overexpression of cortactin has been reported in several human cancers. CRK was originally identified as an oncogene product of v-CRK in a CT10 chicken retrovirus system. Overexpression of CRKII has been reported in several human cancers. CRKII regulates cell migration, morphogenesis, invasion, phagocytosis, and survival; however, the underlying mechanisms are not well understood. We evaluated the possibility of the combination of cortactin and CRKII as an appropriate molecular target for cancer gene therapy. The expression of cortactin and CRKII in 70 primary oral squamous cell carcinomas and 10 normal oral mucosal specimens was determined immunohistochemically, and the correlation of cortactin and CRKII co-overexpression with clinicopathological factors was evaluated. Co-overexpression of cortactin and CRKII was detected in 31 of 70 oral squamous cell carcinomas, the frequency being significantly greater than in normal oral mucosa. In addition, cortactin and CRKII co-overexpression was more frequent in higher-grade cancers according to 3 the T classification, N classification, and invasive pattern. RNAi-mediated co-suppression of cortactin and CRKII expression reduced the migration and invasion potential of an oral squamous cell carcinoma cell line, OSC20. Downregulation of cortactin and CRKII expression also reduced the expression of vimentin, fibronectin, and N-cadherin. These results indicate that the co-overexpression of cortactin and CRKII may be tightly associated with an aggressive phenotype of oral squamous cell carcinoma. Therefore, we propose that the combination of cortactin and CRKII could be a potential molecular target of gene therapy by RNAi-targeting in oral squamous cell carcinoma. 4 1.IntroductionOral squamous cell carcinoma (OSCC) is the most common malignant tumor of the head and neck region and accounts for more than 90% of cancers of the oral cavity [1]. The primary therapeutic modality for OSCC is surgery. Although recent advances in surgical techniques and anticancer agents have improved tumor regression and survival for patients with OSCC, wide surgical resection of OSCC inevitably causes various oral dysfunctions. Therefore, new treatment strategies are urgently needed.The presence of neck lymph node metastasis is strongly related to a poor prognosis in squamous cell carcinoma of the head and neck [2][3][4]. Moreover, it has been reported that an alteration in the expression of adhesion-related molecules is associated with poor prognosis in OSCC patients [5][6][7][8].Chromosomal band 11q13 is a frequently amplified genomic segment in a large number of malignant neoplasms, and is thought of as a potential biomarker for diagnosis and prognosis [9,10]. In head and neck squamous cell carcinoma, this amplification is one of the most frequently observed genetic alterations [11][12][13][14][15][16][17][18][19][20] and is reportedly correlated with aggressive tumor growth [9,13,19], the presence of lymph node ...

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“…genomic segment in a large number of malignant neoplasms, and is thought of as a potential biomarker for diagnosis and prognosis 12,13 .In head and neck squamous cell carcinoma, this amplification is one of the most frequently observed genetic alterations [14][15][16][17][18][19][20][21][22][23] and is reportedly correlated with aggressive tumor growth, 12,16,22 the presence of lymph node metastases, 20,[24][25][26] and poor prognosis. 12,22,27 The amplified 11q13 region is 3-5 megabases in size and includes four putative oncogenes: CCND1 (PRAD1), FGF3…”

Section: Introductionmentioning

confidence: 99%

Overexpression of Cortactin Increases Invasion Potential in Oral Squamous Cell Carcinoma

Yamada

Yanamoto

Kawasaki

et al. 2010

Pathol. Oncol. Res.

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Cortactin stimulates cell migration, invasion, and experimental metastasis. However, the underlying mechanism is not still understood. In the present study, we therefore evaluated the possibility that cortactin could be appropriate as a molecular target for cancer gene therapy. In 70 primary oral squamous cell carcinomas and 10 normal oral mucosal specimens, cortactin expression was evaluated by immunological analyses, and the correlations of the overexpression of cortactin with clinicopathologic factors were evaluated. Overexpression of cortactin was detected in 32 of 70 oral squamous cell carcinomas; significantly more frequently than in normal oral mucosa. Cortactin overexpression was more frequent in higher grade cancers according to T classification, N classifications, and invasive pattern. Moreover, RNAi-mediated decrease in cortactin expression reduced invasion. Downregulation of cortactin expression 4 increased the expression levels of E-cadherin, β-catenin, and EpCAM. The siRNA of cortactin also reduced PTHrP expression via EGF signaling. These results consistently indicate that the overexpression of cortactin is strongly associated with an aggressive phenotype of oral squamous cell carcinoma. In conclusion, we propose that cortactin could be a potential molecular target of gene therapy by RNAi targeting in oral squamous cell carcinoma. 5

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Amplification of 11q13 DNA markers in head and neck squamous cell carcinomas: Correlation with clinical outcome

Cited by 59 publications

References 20 publications

Head and neck squamous cell carcinoma transcriptome analysis by comprehensive validated differential display

Head and neck squamous cell carcinoma transcriptome analysis by comprehensive validated differential display

Co-overexpression of cortactin and CRKII increases migration and invasive potential in oral squamous cell carcinoma

Overexpression of Cortactin Increases Invasion Potential in Oral Squamous Cell Carcinoma

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