C-myc PROTO-ONCOGENE EXPRESSION AND PROGNOSIS IN EARLY CARCINOMA OF THE UTERINE CERVIX

Riou, G; Le, M. H.; Doussal, V. Le; Barrois, Michel; George, Mercy; Haie, C.

doi:10.1016/s0140-6736(87)92795-4

Cited by 140 publications

(45 citation statements)

References 7 publications

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“…Since the c-myc protooncogene is present on chromosome 8 (Neel et al, 1982) and alterations of this gene have been associated with HPV-16 and transformation (Riou et al, 1987;Durst et al, 1987 a;Crook et al, 1990) (Jariwalla et al, 1983), it could not immortalize R-30 cells by itself. This suggests that requirements for immortalizing human cells are unique with respect to primary rodent cells.…”

Section: Comparison Of N-16 and R-30 Cellsmentioning

confidence: 99%

Characterization of primary human fibroblasts transformed by human papilloma virus type 16 and herpes simplex virus type 2 DNA sequences

Dhanwada

Veerisetty

Zhu

et al. 1992

Journal of General Virology

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Human papilloma virus type 16 (HPV-16) and herpes simplex virus type 2 (HSV-2) are human viruses implicated in the development of cancer, in particular cervical cancer. The ability of HSV-2 and HPV-16 to transform early passage human cells was examined in this report. For these studies, gingival fibroblasts were utilized. One gingival cell strain was derived from a normal individual (N-16). The second cell strain was derived from hyperplastic gingival tissue of an epileptic individual (R-30) treated with phenytoin, an antiseizure drug. A common side effect of phenytoin is the induction of gingival overgrowth. R-30 cells contained a stable chromosomal translocation between chromo-

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Section: Comparison Of N-16 and R-30 Cellsmentioning

confidence: 99%

Characterization of primary human fibroblasts transformed by human papilloma virus type 16 and herpes simplex virus type 2 DNA sequences

Dhanwada

Veerisetty

Zhu

et al. 1992

Journal of General Virology

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“…The c-myc protein acts as a transcription factor (10), and ectopic expression of this protein is sufficient to induce the progression of the cell cycle. c-myc is also related to a poor tumor prognosis (11)(12)(13)(14) as well as the self-renewal of tumor stem cells (15)(16)(17)(18).…”

Section: Introductionmentioning

confidence: 99%

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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“…Little data have been published concerning differences in genetic abnormalities between CIN and invasive carcinoma. Activation of FGFR3 (Cappellen et al, 1999;Rosty et al, 2005a), KRAS (Crook et al, 1988;Jiko et al, 1994), HRAS (Riou et al, 1988), MYB (Nurnberg et al, 1995) and MYC (Riou et al, 1987;Zhang et al, 2002) has been reported in invasive carcinoma of the cervix. The integration of viral DNA into the host genome is seen in a minority of cervical intraepithelial neoplasia compared to a majority of invasive cancers (Cullen et al, 1991;Klaes et al, 1999;Kalantari et al, 2001) and corresponds thus to a crucial step in oncogenesis.…”

Section: Introductionmentioning

confidence: 99%

MYC activation associated with the integration of HPV DNA at the MYC locus in genital tumors

et al. 2006

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To determine whether integration of human papillomavirus (HPV) DNA sequences could lead to the deregulation of genes implied in oncogenesis, we analysed the HPV integration sites in a series of nine cell lines derived from invasive genital carcinomas. Using in situ hybridization, HPV16 or 18 sequences were found at chromosome band 8q24, the localization of MYC, in IC1, IC2, IC3, IC6 and CAC-1 cells and at other sites in IC4, IC5, IC7 and IC8 cells. We then localized viral sequences at the molecular level and searched for alterations of MYC structure and expression in these cells. MYC genomic status and viral integration sites were also analysed in primary tumors from which IC1, IC2, IC3 and IC6 cells were derived. In IC1, IC2 and CAC-1 cells, HPV DNA was located within 58 kb of MYC, downstream, upstream, or within MYC. In IC3 and IC6 cells, HPV DNA was located 400-500 kb upstream of MYC. Amplification studies showed that, in IC1, IC2 and IC3, viral and MYC sequences were coamplified in an amplicon between less than 50 and 800 kb in size. MYC amplification was also observed in primary tumors, indicating that this genetic alteration, together with viral insertion at the MYC locus, had already taken place in vivo. MYC was not amplified in the other cell lines. MYC mRNA and protein overexpression was observed in the five cell lines in which the HPV DNA was inserted close to the MYC locus, but in none of the lines where the insertion had occurred at other sites. MYC activation, triggered by the insertion of HPV DNA sequences, can be an important genetic event in cervical oncogenesis.

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C-myc PROTO-ONCOGENE EXPRESSION AND PROGNOSIS IN EARLY CARCINOMA OF THE UTERINE CERVIX

Cited by 140 publications

References 7 publications

Characterization of primary human fibroblasts transformed by human papilloma virus type 16 and herpes simplex virus type 2 DNA sequences

Characterization of primary human fibroblasts transformed by human papilloma virus type 16 and herpes simplex virus type 2 DNA sequences

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

MYC activation associated with the integration of HPV DNA at the MYC locus in genital tumors

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