MYC Amplification in Squamous Cell Carcinomas of the Head and Neck

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

doi:10.1001/archotol.1996.01890170038008

Cited by 42 publications

(30 citation statements)

References 13 publications

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“…On the other hand, c-myc was correlated with tumor stage and lymphatic permeation, while in our study the expression was practically the same. Rodrigo et al (35) found no relationship between c-myc overexpression and tumor prognosis, similar to Hayry et al (33). Baral et al (27) found that tumors with positive p53 and c-myc were in the advanced stages of the disease (poorly differentiated, stage III), while OSCCs in early stages did not show positive immonoreactivity for p53 and c-myc.…”

Section: Discussionmentioning

confidence: 74%

Quantitative determination of c-myc facilitates the assessment of prognosis of OSCC patients

et al. 2014

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Abstract.Myc genes are a family of proto-oncogenes whose proteins are implicated in the regulation of cell proliferation, differentiation and apoptosis, and in regulating the activity of genes involved in cell division. The aim of the present study was to establish a quantitative description of the expression of c-myc and evaluate its relationship with other clinical and prognostic factors, as well as to establish a multivariate survival prediction model. This is a retrospective study of 68 patients diagnosed with oral squamous cell carcinoma (OSCC). We constructed a tissue microarray for investigating the expression of c-myc by immunohistochemistry. Statistical analyses were carried out, and a multivariate model that predicts survival was established. The average expression of c-myc was 50.32 (SD, 26.05) with a range from 6.60 to 99.

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Section: Discussionmentioning

confidence: 74%

Quantitative determination of c-myc facilitates the assessment of prognosis of OSCC patients

et al. 2014

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“…Recently, Kasugai et al (13) identified CCND3 and BYSL as the targets for the 6p21 amplification in diffuse large cell lymphoma. Similarly, co-overexpression of EMS1 gene with CCND1 with 11q13 amplification has been reported in several tumor types (15)(16)(17)(18)(19). Runx2 is a transcription factor that regulates bone development and belongs to one of three members (Runx1/AML and Runx3) of the runt family (20).…”

Section: Discussionmentioning

confidence: 89%

“…Our expression data revealed a consistent overexpression of CCND3, CDC5L, and RUNX2 in primary tumors and cell lines. Of these three genes, CCND3 has been previously implicated in several tumor types (13,(15)(16)(17)(18)(19). CCND3 is a member of a family with cyclin D, which encodes a protein involved in the regulation of the G 1 -S phase of cell cycle regulation.…”

Section: Discussionmentioning

confidence: 99%

Cell Cycle Regulator GeneCDC5L, a Potential Target for 6p12-p21 Amplicon in Osteosarcoma

Lu²,

Zhao³

et al. 2008

Molecular Cancer Research

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Osteosarcoma is a primary malignant tumor of bone arising from primitive bone-forming mesenchymal cells and accounts for f60% of malignant bone tumors. Our comparative genomic hybridization (CGH) studies have identified frequent amplification at 6p12-p21, 12q13-q15, and 17p11.2 in osteosarcoma. Of these amplified regions, 6p12-p21 is particularly interesting because of its association with progression and poor prognosis in patients with osteosarcoma. In an attempt to identify aberrantly expressed gene(s) mapping to the 6p12-p21 amplicon, a region-specific array was generated using 108 overlapping BAC and P1 clones covering a 28.8-Mb region at 0.26-Mb intervals. Based on array CGH analysis, the 6p amplicon was refined to 7.9 Mb between the clones RP11-91E11 and RP1-244F2 and 10 amplified clones, with possible target genes, were identified. To study the expression pattern of the target genes from the hotspot amplicon and known candidate genes from 6p12-21, we did quantitative reverse transcription-PCR analysis of MAPK14, MAPK13, CDKN1A, PIM1, MDGA1, BTB9, DNAH8, CCND3, PTK7, CDC5L, and RUNX2 on osteosarcoma patient samples and seven cell lines. The combined array CGH and quantitative reverse transcription-PCR analysis identified amplification and overexpression of CDC5L, CCND3, and RUNX2. We screened these three genes for protein expression by Western blotting and immunohistochemistry and detected overexpression of CDC5L. Furthermore, we used an in vivo assay to show that CDC5L possesses potential oncogenic activity. These results indicate that CDC5L, a cell cycle regulator important for the G 2 -M transition, is the most likely candidate oncogene for the 6p12-p21 amplicon found in osteosarcoma. (Mol Cancer Res 2008;6(6):937 -46)

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“…The expression pattern of genes down-regulated in HNSCC compared with NOM is relatively uniform, although a few clusters of functionally relevant genes can be defined. A cluster of genes mapping to a region of chromosome 1q21 (involucrin, SPRR 1A, 1B, 2B, 3, NICE-1, S100 A1, 6,8,9,14), termed the epidermal differentiation complex, is down-regulated in the majority of HNSCC samples. Genes located in this region are highly expressed in terminally differentiated squamous epithelium and have been shown to play an important role in maintenance of the epithelial phenotype (39).…”

Section: Resultsmentioning

confidence: 99%

Identification of a Gene Expression Signature Associated with Recurrent Disease in Squamous Cell Carcinoma of the Head and Neck

et al. 2004

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Molecular studies of squamous cell carcinoma of the head and neck (HNSCC) have demonstrated multiple genetic abnormalities such as activation of various oncogenes (Ras, Myc, epidermal growth factor receptor, and cyclin D1), tumor suppressor gene inactivation (TP53 and p16), and loss of heterozygosity at numerous chromosomal locations. Despite these observations, accurate and reliable biomarkers that predict patients at highest risk for local recurrence have yet to be defined. In an effort to identify gene expression signatures that may serve as biomarkers, we studied 41 squamous cell carcinoma tumors (25 primary and 16 locally recurrent) from various anatomical sites and 13 normal oral mucosal biopsy samples from healthy volunteers with microarray analysis using Affymetrix U133A GeneChip arrays. Differentially expressed genes were identified by calculating generalized t tests (P < 0.001) and applying a series of filtering criteria to yield a highly discriminant list of 2890 genes. Hierarchical clustering and image generation using standard software were used to visualize gene expression signatures. Several gene expression signatures were readily identifiable in the HNSCC tumors, including signatures associated with proliferation, extracellular matrix production, cytokine/chemokine expression, and immune response. Of particular interest was the association of a gene expression signature enriched for genes involved in tumor invasion and metastasis with patients experiencing locally recurrent disease. Notably, these tumors also demonstrated a marked absence of an immune response signature suggesting that modulation of tumor-specific immune responses may play a role in local treatment failure. These data provide evidence for a new gene expression-based biomarker of local treatment failure in HNSCC.

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MYC Amplification in Squamous Cell Carcinomas of the Head and Neck

Cited by 42 publications

References 13 publications

Quantitative determination of c-myc facilitates the assessment of prognosis of OSCC patients

Quantitative determination of c-myc facilitates the assessment of prognosis of OSCC patients

Cell Cycle Regulator GeneCDC5L, a Potential Target for 6p12-p21 Amplicon in Osteosarcoma

Identification of a Gene Expression Signature Associated with Recurrent Disease in Squamous Cell Carcinoma of the Head and Neck

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