Amplification of ERBB oncogenes in squamous cell carcinomas of the head and neck

Rodrigo, Juan P.; Ramos, Sofı́a; Lazo, Pedro S.; Alvarez, Ignacio; Suárez, Carlos

doi:10.1016/0959-8049(96)00223-7

Cited by 45 publications

(32 citation statements)

References 20 publications

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“…We have not found samples showing 2F51/ 6FX (CCND1) amplification alone. These data indicated that CCND1 amplification is not necessarily associated with EMS1 amplification and thus supports earlier work by Rodrigo et al (2000) indicating that EMS1 and CCND1 amplification could occur separately. Interestingly, the authors found that not CCND1 amplification but EMS1 predicts early recurrence and reduced survival in HNSCC.…”

Section: Dna Amplification In Hnsccsupporting

confidence: 89%

“…Furthermore, 6G27 represents a NotI site found in the promoter of EMS1. Both CCND1 and EMS1 are HNSCC protooncogenes described in previous studies (Rodrigo et al, 2000;Arai et al, 2003). Among 41 patient samples, both 2F51 and 6FX always showed the same levels of enhancement (enhanced in 10 cases; 24%), while 2F63 was observed in nine cases (22%), and 6G27 was enhanced in 11 cases (27%).…”

Section: Dna Amplification In Hnsccmentioning

confidence: 54%

“…Interestingly, the authors found that not CCND1 amplification but EMS1 predicts early recurrence and reduced survival in HNSCC. Therefore, the prognostic significance previously attributed to CCND1 amplification may be attributable to its colocalization with EMS1 on the same amplicon (Rodrigo et al, 2000).…”

Section: Dna Amplification In Hnsccmentioning

confidence: 97%

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DNA copy number gains in head and neck squamous cell carcinoma

et al. 2005

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Gene amplification, a common mechanism for oncogene activation in cancer, has been used as a tag for the identification of novel oncogenes. DNA amplification is frequently observed in head and neck squamous cell carcinoma (HNSCC) and potential oncogenes have already been reported. We applied restriction landmark genome scanning (RLGS) to study gene amplifications and low-level copy number changes in HNSCC in order to locate previously uncharacterized regions with copy number gains in primary tumor samples. A total of 63 enhanced RLGS fragments, indicative of DNA copy number changes, including gains of single alleles, were scored. Enhanced sequences were identified from 33 different chromosomal regions including those previously reported (e.g. 3q26.3 and 11q13.3) as well as novel regions (e.g. 3q29, 8q13.1, 8q22.3, 9q32, 10q24.32, 14q32.32, 17q25.1 and 20q13.33). Furthermore, our data suggest that amplicons 11q13.3 and 3q26.3-q29 may be divided into possibly two and three independent amplicons, respectively, an observation supported by published microarray expression data.

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Section: Dna Amplification In Hnsccsupporting

confidence: 89%

Section: Dna Amplification In Hnsccmentioning

confidence: 54%

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DNA copy number gains in head and neck squamous cell carcinoma

et al. 2005

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“…Cyclin D1 is a cell cycle regulatory protein that is essential for passage through G 1 (Baldin et al, 1993), and overexpression in human tumors is thought to lead to a loss of cell cycle regulation (Schuuring, 1995). Ampli®cation of the cortactin locus can occur with or without cyclin D1 ampli®cation, and elevated cortactin gene levels correlate with poor patient prognosis (Rodrigo et al, 2000), suggesting that ampli®cation of the cortactin gene directly contributes to tumor severity. Cell lines isolated from patients with 11q13 ampli®cation exhibit increased cortactin mRNA and protein levels (Patel et al, 1996;Campbell et al, 1996), providing strong circumstantial evidence that cortactin overexpression plays an important role in tumors with 11q13 ampli®cation.…”

Section: Overexpression and Role Of Cortactin In Human Tumorsmentioning

confidence: 99%

Cortactin: coupling membrane dynamics to cortical actin assembly

2001

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Exposure of cells to a variety of external signals causes rapid changes in plasma membrane morphology. Plasma membrane dynamics, including membrane ru e and microspike formation, fusion or ®ssion of intracellular vesicles, and the spatial organization of transmembrane proteins, is directly controlled by the dynamic reorganization of the underlying actin cytoskeleton. Two members of the Rho family of small GTPases, Cdc42 and Rac, have been well established as mediators of extracellular signaling events that impact cortical actin organization. Actin-based signaling through Cdc42 and Rac ultimately results in activation of the actin-related protein (Arp) 2/3 complex, which promotes the formation of branched actin networks. In addition, the activity of both receptor and non-receptor protein tyrosine kinases along with numerous actin binding proteins works in concert with Arp2/3-mediated actin polymerization in regulating the formation of dynamic cortical actin-associated structures. In this review we discuss the structure and role of the cortical actin binding protein cortactin in Rho GTPase and tyrosine kinase signaling events, with the emphasis on the roles cortactin plays in tyrosine phosphorylation-based signal transduction, regulating cortical actin assembly, transmembrane receptor organization and membrane dynamics. We also consider how aberrant regulation of cortactin levels contributes to tumor cell invasion and metastasis. Oncogene (2001) 20, 6418 ± 6434.

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“…This lack of understanding is the primary factor hindering the effective use of these agents. In HNSCC, classical driver mutations of the pathway, such as PTEN and EGFR mutations, are rare, as are mutations in ERBB2-4 and members of the RAS pathway (23)(24)(25)(26)(27). To resolve this question, we undertook a detailed genomic dissection of the EGFR/PI3K pathway in oral cancer, the most common subsite of HNSCC.…”

mentioning

confidence: 99%

Genomic dissection of the epidermal growth factor receptor (EGFR)/PI3K pathway reveals frequent deletion of the EGFR phosphatase PTPRS in head and neck cancers

Morris¹,

Taylor²,

Bivona³

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

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Activation of the PI3K and epidermal growth factor receptor (EGFR) pathway is able to drive oncogenesis in multiple human cancers, including head and neck squamous cell carcinoma. Targeted agents such as cetuximab and erlotinib are currently used in patients with head and neck squamous cell carcinoma, but, in this disease, the genomic alterations that cause pathway activation and determine response to pharmacologic inhibition remain ill-defined. Here, we present a detailed dissection of the EGFR/PI3K pathway, composed of sequencing of the core pathway components, and high-resolution genomic copy number assessment. Mutations were found in PIK3CA (6%), but no point mutations were observed in other pathway genes such as PTEN and EGFR . In contrast, we observed frequent copy number alterations of genes in the pathway, including PIK3CA , EGFR , protein tyrosine phosphatase receptor S ( PTPRS ), and RICTOR . In total, activating genetic pathway alterations were identified in 74% of head and neck tumors. Importantly, intragenic microdeletions of the EGFR phosphatase PTPRS were frequent (26%), identifying this gene as a target of 19p13 loss. PTPRS loss promoted EGFR/PI3K pathway activation, modulated resistance to EGFR inhibition, and strongly determined survival in lung cancer patients with activating EGFR mutations. These findings have important implications for our understanding of head and neck cancer tumorigenesis and for the use of targeted agents for this malignancy.

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Amplification of ERBB oncogenes in squamous cell carcinomas of the head and neck

Cited by 45 publications

References 20 publications

DNA copy number gains in head and neck squamous cell carcinoma

DNA copy number gains in head and neck squamous cell carcinoma

Cortactin: coupling membrane dynamics to cortical actin assembly

Genomic dissection of the epidermal growth factor receptor (EGFR)/PI3K pathway reveals frequent deletion of the EGFR phosphatase PTPRS in head and neck cancers

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