Chromosome 11q13 Amplification in Head and Neck Squamous Cell Carcinoma: Association With Poor Prognosis

Meredith, Scott D.; Levine, Paul A.; Burns, James A.; Gaffey, M. J.; Boyd, James C.; Weiss, Lawrence M.; Erickson, Nicholette; Williams, Michael E.

doi:10.1001/archotol.1995.01890070076016

Cited by 122 publications

(86 citation statements)

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“…Thus, human cortactin appears to display a cancer-restricted immunological pro®le and may be considered as a putative cancer antigen. Moreover, the results of screening of the clone MOBr-140 with a panel of breast cancer and head and neck squamous cell carcinoma sera are in good agreement with published data on average frequency of cortactin gene ampli®cation in primary breast carcinoma and head and neck squamous cell carcinoma (Hui et al, 1998;Meredith et al, 1995).Human immune response to oncogenic proteins has been reported in several studies (Disis and Cheever, 1996) and our ®ndings add human cortactin to this list. Further studies using larger panels of sera and tumor specimens is required to determine whether the presence of antibodies against this gene product in sera of cancer patients correlates with the tumor type and prognosis and could be valuable in cancer diagnostics.…”

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confidence: 90%

“…Cortactin is involved in the signaling pathway of mitogenic receptors and adhesion molecules mediating cytoskeletal reorganization (Schuuring et al, 1993(Schuuring et al, , 1998van Damme et al, 1997;Campbell et al, 1999). Human cortactin maps to the chromosomal band 11q13 which is known to be ampli®ed in about 15% of primary breast carcinomas and 30% of head and neck squamous cell carcinoma (Schuuring, 1995;Meredith et al, 1995;Hui et al, 1998). Such ampli®cation has been also reported for other malignancies, including ovarian and bladder cancer (Bringuier et al, 1996).…”

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confidence: 93%

“…Ampli®cation of cortactin in breast and head and neck carcinomas is associated with poor clinical outcome. (Meredith et al, 1995;Schuuring et al, 1992Schuuring et al, , 1995Hui et al, 1998). Additionally, recent studies have shown the overexpression of cortactin in NIH3T3 cells to result in increased cell invasion/migration in vitro (Patel et al, 1998;Huang et al, 1998).…”

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Human cortactin as putative cancer antigen

et al. 2000

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Humoral immune response against overexpressed oncogenic or tumor supressor proteins has been demonstrated for many types of cancer. In this study we report on the detection of the autologous antibody response to putative oncogene, human cortactin using serological analysis of breast carcinoma expression library. Cortactin maps to chromosome 11q13, the region ampli®ed in about 15% of primary breast carcinomas and 30% of head and neck squamous cell carcinomas. Cortactin overexpression due to such ampli®cation might a ect adhesive properties of human cancer cells and is associated with poor disease prognosis. Accordingly, we detected overexpression of cortactin transcript in autologous tumor and ampli®ca-tion/overexpression of cortactin in tumors of breast cancer patients serologically positive for this marker. We demonstrate that 15% of breast cancer patients elicit humoral immune response against human cortactin. Oncogene (2000) 19, 5204 ± 5207.Keywords: breast cancer; cortactin; cancer antigen; tumor markerThe development of cancer vaccines requires the identi®cation and characterization of tumor antigens. In the past decade many tumor antigens have been de®ned (reviewed by Old and Chen, 1998;Rosenberg, 1999).In 1991 T Boon and colleagues discovered the ®rst antigen recognized by cytotoxic T-lymphocytes (CTL) in human melanoma (van der Bruggen et al., 1991). In their study tumor antigens have been identi®ed by the transfection of cDNA libraries into cells expressing the appropriate MHC molecule followed by the identi®ca-tion of transfectant using cytokine release or lysis by human T cells with speci®c antitumor reactivity (Boon et al., 1994).An alternative technique for the identi®cation of tumor antigens has been reported by Sahin et al. (1995). This approach of serological analysis of cDNA expression libraries (SEREX), was based on previously described molecular screening techniques (D'Arpa et al., 1988) and exploited patient's B-cell repertoire for the identi®cation of human tumor antigens that show immunogenicity in the autologous host. Many antigens have been isolated by this technique, demonstrating that most, if not all, human cancers express multiple antigens including ampli®ed/overexpressed proteins with known cancer association (reviewed by Old and Chen, 1998;Disis and Cheever, 1996;Brass et al., 1999).In this study we applied the SEREX method to isolate and characterize candidate tumor antigens expressed in breast carcinoma. A cDNA library in phage expression vector (lambda ZAP Express) was prepared from a surgical tumor specimen of a 56-yearold woman with ER-positive breast carcinoma (T 1 M 0 N 0 ). The library was plated and screened with autologous patient's serum diluted 1 : 200 as previously described (Scanlan et al., 1998). Screening of 3610 5 primary recombinant phage clones yielded a total of 70Oncogene (2000) 19, 5204 ± 5207 ã 2000 Macmillan Publishers Ltd All rights reserved 0950 ± 9232/00 $15.00 www.nature.com/onc The deduced amino acid sequence of MOBr-140 represents human cortactin from a...

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Human cortactin as putative cancer antigen

et al. 2000

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“…Amplification of the 11q13.3 region has been related to a worse prognosis (Meredith et al, 1995;Xie et al, 2006). Furthermore, expression of cortactin, cyclin D1 and more recently FADD (Gibcus et al, 2007b), have been described separately as potential predictors for increased disease-related mortality, for lymph node metastasis and poor prognosis.…”

Section: Discussion Cortactin Predicts Poor Survival In Late Stage Lamentioning

confidence: 99%

“…Amplification of this region in HNSCC has been associated with decreased survival (Akervall et al, 1995;Meredith et al, 1995), increased distant metastasis (Namazie et al, 2002) and lymph node metastasis (Chen et al, 2004;Hermsen et al, 2005;Xia et al, 2007). It is believed that amplification increases gene dosage and expression of genes within the amplified region (amplicon) (Albertson, 2006).…”

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Cortactin expression predicts poor survival in laryngeal carcinoma

et al. 2008

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Amplification of the 11q13 region is one of the most frequent aberrations in squamous cell carcinomas of the head and neck region (HNSCC). Amplification of 11q13 has been shown to correlate with the presence of lymph node metastases and decreased survival. The 11q13.3 amplicon carries numerous genes including cyclin D1 and cortactin. Recently, we reported that FADD becomes overexpressed upon amplification and that FADD protein expression predicts for lymph node positivity and disease-specific mortality. However, the gene within the 11q13.3 amplicon responsible for this correlation is yet to be identified. In this paper, we compared, using immunohistochemical analysis for cyclin D1, FADD and cortactin in a series of 106 laryngeal carcinomas which gene correlates best with lymph node metastases and increased disease-specific mortality. Univariate Cox regression analysis revealed that high expression of cyclin D1 (P ¼ 0.016), FADD (P ¼ 0.003) and cortactin (P ¼ 0.0006) predict for increased risk to disease-specific mortality. Multivariate Cox analysis revealed that only high cortactin expression correlates with disease-specific mortality independent of cyclin D1 and/or FADD. Of genes located in the 11q13 amplicon, cortactin expression is the best predictor for shorter diseasespecific survival in late stage laryngeal carcinomas. Current methods to predict the outcome of head and neck squamous cell carcinoma (HNSCC) patients mainly involve clinicopathological parameters such as tumour size, differentiation grade and presence of lymph node metastasis. Patients with laryngeal squamous cell carcinomas (LSCC) have not shown an increase in 5-year survival rates over the last 30 years (Almadori et al, 2005). Therefore, other parameters such as molecular markers that are able to more accurately predict the outcome of disease, are needed.A frequent molecular event in HNSCC is amplification of the 11q13 region (36%) (Schuuring, 1995;Freier et al, 2006). Amplification of this region in HNSCC has been associated with decreased survival (Akervall et al, 1995;Meredith et al, 1995), increased distant metastasis (Namazie et al, 2002) and lymph node metastasis (Chen et al, 2004;Hermsen et al, 2005;Xia et al, 2007). It is believed that amplification increases gene dosage and expression of genes within the amplified region (amplicon) (Albertson, 2006). Recently, we reported that the commonly amplified region is located at 11q13.3 and contains at least six genes (cyclin D1, TAOS1, FGF19, FADD, PPFIA1 and cortactin) that are overexpressed when amplified (Gibcus et al, 2007b). We concluded that the selection for tumour cells with the 11q13.3 amplicon during tumorigenesis could be based on the increased doses of one or more of these genes. We proposed FADD as a possible candidate for this selection, since FADD showed the best correlation between DNA amplification and increased expression (Gibcus et al, 2007b). Furthermore, FADD protein expression correlated with disease specific mortality (DSM) in a series of late stage laryngeal carcinom...

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