Molecular cytogenetic analysis of head and neck squamous cell carcinoma: By comparative genomic hybridization, spectral karyotyping, and expression array analysis

Squire, Jeremy A.; Bayani, Jane; Luk, Catherine; Unwin, Lianne; Tokunaga, Jason; MacMillan, Christina; Irish, Jonathan C.; Brown, Dale; Gullane, Patrick; Kamel‐Reid, Suzanne

doi:10.1002/hed.10122

Cited by 83 publications

(58 citation statements)

References 43 publications

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“…Studies on oral cancer and HNSCC have shown that a number of chromosomal regions are consistently altered, such as gains on 3q, 5p, 8q, and 11q13 and losses on 3p and 9p among others. [20][21][22][23]32 Array CGH analysis of oral cancer cases in this study found that the most frequent alterations were mapped to chromosome 3, with gain of the q arm often occurring simultaneously with loss of the p arm. The ''older group'' in this study showed a profile similar to that of the ''classic'' patient with oral cancer in the literature, including deletions on 3p and 9p and gains of 3q, 5q, 7p, and 11q 13.…”

Section: Discussionmentioning

confidence: 64%

“…In concordance with the literature on oral cancer, gain of the q arm was a less frequent event than loss of the p arm. 22 Having established that the profile of the older group resembled closely that found in the literature, our second aim was to compare the genomic profile of the younger group with the older group. The changes occurring most frequently are tabulated in Table 3.…”

Section: Discussionmentioning

confidence: 89%

“…The age limit is problematic, because youth is defined arbitrarily; however, most studies use 40 or 45 years old as the cutoff. [16][17][18][19] Previous studies have analyzed chromosomal alterations in oral cancer [20][21][22][23][24][25] ; however, few have applied array CGH technology. [26][27][28] All CGH work on oral cancer so far in the literature has been directed at the typical patient with oral cancer (ie, the 60-to 70-year-old male smoker) and to date there are no references to array CGH studies of younger patients with oral cancer.…”

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Distinct array comparative genomic hybridization profiles in oral squamous cell carcinoma occurring in young patients

et al. 2006

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Background. Oral cancer typically affects smokers older than 50 years of age. Recently, however, a marked increase in the number of patients 40 years old and younger, many with no history of tobacco smoking, has been noted. Studies in this age group have so far been restricted to genomic areas well recognized as abnormal in typical patients with oral cancer. The aim of this study was to assess genomic aberrations in oral cancer, using comparative genomic hybridization (CGH) microarray technology, and to compare the genomic aberration profile of patients older than 40 years old with those 40 years old and younger.Methods. Tumor samples from 20 patients with oral cancer (age range, 21-78; 10 smokers and 10 nonsmokers) were laser microdissected, and array CGH was used to identify genomic imbalances in these two cohorts.Results. The older cohort showed high numbers of gains and losses in contrast to very few copy number changes in the younger nonsmoker cohort. In concurrence with the literature, tumors from the older cohort manifested deletions involving 3p and 9p21 and gains involving 3q, 5q, 7p, 8q, 11q, and 20q. The younger group, particularly the nonsmokers, showed very few changes overall, and the aberrations were not in the sites classically associated with oral cancer. Deletion of CDKN2A (p16) was completely absent in the younger group but was present in 50% of the older cohort.Conclusions. We have demonstrated that there is far less genomic instability in young nonsmokers with oral cancer than found in typical patients with oral cancer. These observations indicate that oral cancer presenting at a younger age, particularly in nonsmokers, has a genomic profile different from the classically described oral cancer.

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Section: Discussionmentioning

confidence: 64%

Section: Discussionmentioning

confidence: 89%

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confidence: 99%

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Distinct array comparative genomic hybridization profiles in oral squamous cell carcinoma occurring in young patients

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“…16 In addition, 4 matched primary normal epithelial and squamous cell carcinoma samples were used to identify genes associated with head and neck carcinogenesis. 17 Squire et al 18 identified and correlated recurrent gains of 3q and 8q with differentially expressed genes located in these chromosomal regions, as detected by CGH, SKY and expression array analysis, in 7 head and neck cancer cell lines and 5 primary tongue tumors.…”

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Molecular classification of oral cancer by cDNA microarrays identifies overexpressed genes correlated with nodal metastasis

Warner

Reis

Jurišica

et al. 2004

Intl Journal of Cancer

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“…Microarrays have recently been used to understand the molecular basis of tumor initiation and progression in breast cancer, 3 meningiomas, 4 soft tissue tumors 5 and head and neck squamous cell carcinomas. [6][7][8][9][10] Earlier reports of genetic alterations in human salivary gland malignancy focused on cytogenetic abnormalities, molecular changes involving large chromosomal regions, or a few selected genes. [11][12][13][14][15][16] However, little is known about genome-wide expression changes and their correlation with the development and progression of human salivary gland tumors.…”

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Molecular characterization of salivary gland malignancy using the Smgb-Tag transgenic mouse model

Mäkitie

Reis

Arora

et al. 2005

Laboratory Investigation

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The molecular mechanisms underlying salivary gland tumorigenesis remain unclear. In order to identify genetic changes that occur during the development of invasive adenocarcinoma from normal salivary gland, we used the Smgb-Tag transgenic mouse model. This transgene induces the progressive development of dysplasia to invasive adenocarcinoma in the submandibular salivary gland. Gene expression patterns from 20 submandibular glands (two normal, nine dysplasia and nine adenocarcinoma samples) were assessed using a mouse 15 K cDNA array. Unsupervised hierarchical clustering was used to group gene expression based on 157 differentially expressed genes distinguishing between dysplasias and adenocarcinomas. Further analysis identified 25 significantly overexpressed and 28 underexpressed cDNA sequences in adenocarcinoma as compared to dysplasia. Differential expression of five genes (Lcn2, Ptn, Cd24a, Mapk6 and Rnps1) was validated by quantitative real-time RT-PCR in a total of 48 mouse salivary gland tissues (seven histologically normal, 13 dysplasias and 28 adenocarcinomas), including the 20 samples analyzed by cDNA arrays. Immunohistochemical analysis was used to validate the expression of Ptn and Cd24a at the protein level in a subset of 16 mouse salivary glands (four normal, five dysplasia and seven adenocarcinoma samples), as well as in 23 human submandibular gland tumors (16 pleomorphic adenomas, three adenoid cystic carcinomas, one acinic cell carcinoma, one adenocarcinoma NOS, one myoepithelial and one mucoepidermoid carcinoma). We thus demonstrated that the Smgb-Tag transgenic mouse model is a useful tool for the identification of genes that are deregulated in salivary gland adenocarcinomas. Our data suggest that Ptn and Cd24a may be genetic markers associated with salivary gland tumorigenesis and/or progression. Keywords: salivary gland; adenocarcinoma; transgenic mouse; carcinogenesis; gene expression; microarrays Salivary gland tumors are a heterogeneous and relatively rare class of head and neck cancer, with several histologically diverse subtypes, such as carcinoma ex-pleomorphic adenomas, adenoid cystic carcinomas (ACC), mucoepidermoid carcinomas (MECA) and acinic cell carcinomas (AcCA). 1 Risk factors may include external radiation to the head and neck, viral infection, and exposure to carcinogens. 2 The morphological origin and clinical behavior of these tumors differ from the majority of other head and neck tumors, which are squamous cell carcinomas; their genetic origins remain to be elucidated.

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Molecular cytogenetic analysis of head and neck squamous cell carcinoma: By comparative genomic hybridization, spectral karyotyping, and expression array analysis

Cited by 83 publications

References 43 publications

Distinct array comparative genomic hybridization profiles in oral squamous cell carcinoma occurring in young patients

Distinct array comparative genomic hybridization profiles in oral squamous cell carcinoma occurring in young patients

Molecular classification of oral cancer by cDNA microarrays identifies overexpressed genes correlated with nodal metastasis

Molecular characterization of salivary gland malignancy using the Smgb-Tag transgenic mouse model

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