Article Data

  • Views 951
  • Dowloads 119

Original Research

Open Access

Genetic imbalance and human papillomavirus states in vulvar squamous cell carcinomas

  • O. Yangling1,*,
  • Z. Shulang1
  • C. Rongli1
  • L. Bo1
  • C. Lili1
  • W. Xin1

1Department of Obstetrics and Gynecology, Shengjing Hospital of China Medical University, Shenyang, China

DOI: 10.12892/ejgo200706442 Vol.28,Issue 6,November 2007 pp.442-446

Published: 10 November 2007

*Corresponding Author(s): O. Yangling E-mail:

Abstract

Purpose of investigation: Vulvar squamous cell carcinoma (VSCC) is a disease of significant clinical importance, which arises in the presence or absence of human papillomavirus (HPV). Methods: We used comparative genomic hybridization (CGH) to document non-random chromosomal gains and losses with HPV positive and negative VSCCs. Results: Gains of 3q and 12q were significantly more common in HPV-positive cancers compared to HPV-negative cancers where chromosome 8q was more commonly gained in HPV-negative compared to HPV-positive cancer chromosomes and, 4p and 3p were lost in both categories of VSCCs. Conclusions: The data indicate that one or more oncogenes important in the development and progression of HPV-induced carcinomas are located on 3q and 12q.

Keywords

Vulvar squamous cell carcinomas (VSCC); Comparative genomic hybridization (CGH); Human papillomavirus (HPV)

Cite and Share

O. Yangling,Z. Shulang,C. Rongli,L. Bo,C. Lili,W. Xin. Genetic imbalance and human papillomavirus states in vulvar squamous cell carcinomas. European Journal of Gynaecological Oncology. 2007. 28(6);442-446.

References

[1] Le Jie. Obstetric Science, 6th edn., People's Health Press, Beijing, 2003, 310.

[2] Flowers L.C., Wistuba I.I., Scurry J., Muller C.Y., Ashfaq R., Miller D.S. et al.: "Genetic changes during the multistage pathogenesis of human papillomavirus positive and negative vulvar carcinomas". J. Soc. Gynecol. Invest., 1999, 6, 213.

[3] Hording U., Junge J., Daugaard S., Lundvall F., Poulsen H., Bock J.E. et al.: "Vulvar squamous cell carcinoma and papillomaviruses: indication for two different etiologies". Gynecol. Oneal., 1994, 52, 241.

[4] Bryndorf T., Kirchhoff M., Larsen J., Andreasson B., Bjerregaard B., Westh H. et al.: "The most common chromosome aberration detected by high-resolution comparative genomic hybridization in vulvar intraepithelial neoplasia is not seen in vulvar squmaous cell carcinoma". Cytogenet. Genome Res., 2004, 106, 43.

[5] Allen D.G., Hutchins A.-M., Hammet F., White D.J., Scuny J.P., Tabrizi S.N. et al.: "Genetic aberrations detected by comparative genomic hybridisation in vulvar cancers". Br. J. Cancer., 2002, 86, 924.

[6] Jee K.J.,Kim Y.T., Kim K.R., Kim H.S., Yan A., Knuutila S.: "Loss in 3p and 4p and gain of 3q are concomitant aberrations in squamous cell carcinoma of the vulva". Mod. Pathol., 2001, 14, 377.

[7] Raitanen M., Worsham M.J., Lakkala T., Carey T.E., Van Dyke D.L., Grenman R. et al.: "Characterization of IO vulvar carcinoma cell lines by karyotyping, comparative genomic hybridization and flow cytometry". Gynecol. Oneal., 2004, 93, 155.

[8] Huang F.Y., Kwok Y.K., Lau E.T., Tang M.H., Ng Y.Y., Ngan H.Y.: "Genetic abnormalities and HPV status in cervical and vulvar squamous cell carcinomas". Cancer Genet. Cytogenet., 2005, 157, 42.

[9] Allen D.G.,White D.J., Hutchins A.M., Scu巧J.P., Tabrizi S.N., Garland S.M. et al.: "Progressive genetic aberrations detected by comparative genomic hybridization in squamous cell cervival cancer". Br. J. Cancer., 2000, 83, 1659.

[10] Haga T., Kim S.H., Jensen R.H., Darragh T., Palefsky J.M.: "Detection of genetic changes in anal intraepithelial neoplasia (AIN) of HIV-pos山ve and HIV-negative men". J. Acquir. Immune Defic Syndr., 2001, 26, 256.

[11] Yen C.C., Chen Y.J.. Chen J.T., Hsia J.Y., Chen P.M.. Liu J.H. et al.: "Comparative genomic hybridization of esophageal squamous cell carcinoma: correlations between chromosomal aberrations and disease progression/prognosis". Cancer, 2001, 92, 2769.

[12] Kirchhoff M.. Rose H.. Petersen B.L.. Maahr J.. Gerdes T., Lundsteen C. et al.: "Comparative genomic hybridization reveals a recurrent pattern of chromosomal aberrations in severe dysplasia/ carcinoma in situ of the cervix and in advanced-stage cervical carcinoma". Genes Chrom. Cancer, 1999, 24, 144.

[13] Rosenthal A.N., Ryan A., Hopster D., Surentheran T., Jacobs I.J. "High frequency of loss of heterozygosity in vulva! intraepithelial neoplasia (VIN) is associated with invasive vulva! squamous cell carcinoma (VSCC)". Int. J. Cancer, 2001, 94, 896.

[14] Heselmeyer K., Macville M., Schrock E., Blegen H., Hellstrom A.C., Shah K.: "Advanced-stage cervical carcinomas are defined by a recurrent pattern of chromosomal aberrations revealing high genetic instability and a consistent gain of chromosome arm 3q". Genes Chrom. Cancer, 1997, 19, 233.

[15] Jin Y., Jin C., Wennerberg J., Hoglund M., Mertens F.: "Cytogenetic and fluorescence in situ hybridization characterization of chromosome 8 rearrangement in head and neck squamous cell carcinomas". Cancer Genet. Cytogenet., 2001, 130, 111.

[16] Yang J., Qin L.X.,Ye S.L., Liu Y.K.,归Y., Gao D.M. et al.: "The abnormalities of chromosome 8 in two hepatocellular carcinoma cell clones with the same genetic background and different metastatic potential". J. Cancer Res. Clin. Oneal., 2003, 129, 303.

[ 17] Tsarouha H., Pandis N., Bardi G., Teixeira M.R., Andersen J.A., Heim S.: "Karyotypic evolution in breast carcinomas with

i(l)(q!O) and der(l;16)(q10;p l 0) as the primary chromosome abnormality". Cancer Genet. Cytogenet., 1999, 113, 156.

[18] Aalto Y., Eriksson L., Seregard S., Larsson 0., Knuutila S.: "Concomitant loss of chromosome 3 and whole arm losses and gains of chromosome 1,6,or 8 in metastasizing primary uveal melanoma". Invest. Ophthalmol. Vis. Sci., 2001, 42, 313.

[19] Higashiyama M., Doi 0., Kodama K., Yokouchi H., Kasugai T., Ishiguro S. et al.: "MDM2 gene amplication and expression in non-small-cell lung cancer: immunohistochemical expression of its protein is a favourable prognostic marker in patients without p53 protein accumulation". Br. J. Cancer, 1997, 75, 1302.

[20] Marchetti A., Buttitta F., Girlando S., Dalla Palma P., Pellegrini S., Fina P. et al.: "MDM2 gene alterations and MDM2 protein expression in breast carcinomas". J. Pathol., 1995, 175, 31.

[21] Inoue H., Ishii H., Alder H., Snyder E., Druck T., Huebner K "Sequence of the FRA3B common fragile region: implications for the mechanism of FHIT deletion". Proc. Natl. Acad. Sci. USA , 1997, 94, 14584.

[22] W istuba I.I., Montellano F.D., Milchqrub S., Virmani A.K., Behrens C., Chen H. et al.: "Deletions of chromosome 3p are frequent and early events in the pathogenesis of uterine cervical carcinoma". Cancer. Res., 1997, 57, 3154.

[23] Muller C.Y., O'Boyle J.D., Fong K.M., Wistuba I.I., Biesterveld E., Ahmadian M. et al.: "Abnomalities of fragile hisidine triad genomic and complementary DNAs in cervical cancer: association with human papillomavirus type". J. Natl. Cancer Inst., 1998, 90, 433.

[24] Shayesteh L., Lu Y., Kuo W.L., Baldocchi R., Godfrey T., Collins C. et al.: "P IK3CA is implicated as an oncogene in ovarian cancer". Nat. Genet., 1999, 21, 99.

[25] Vivanco I., Sawyers C.L.: "The phosphatidylinositol 3-kinase AKT pathway in human cancer". Nat. Rev. Cancer, 2002, 2, 489.

[26] Cantley L.C.: "The phosphoinositide 3-kinase pathway". Science, 2002, 296, 1655.

[27] Katso R., Okkenhaug K., Ahmadi K., White S., Timms J., Waterfield M.D. et al.: "Cellular function of phosphoinositide 3-kinases: implications for development ,homeostasis, and cancer". Ann. Rev. Cell. Dev. Biol., 2001, 17, 615.

[28] Macville M., Schrock E., Padilla-Nash H., Keck C., Ghadim1 B.M., Zimonjic D. et al.: "Comprehensive and definitive molecular cytogenetic characterization of Hela cells by spectral karyotyping". Cancer Res., 1999, 59, 141.

[29] Zhang A., Maner S., Betz R., Angstrom T., Stendahl U., Bergman F. et al.: "Genetic alterations in cervical carcinomas: frequent lowlevel amplifications of oncogenes are associated with human papillomavirus infection". Int. J. Cancer, 2002, 101, 427.

[30] Shayesteh L., Lu Y., Kuo W.L., Baldocchi R., Godfrey T., Collins C. et al.: "P IK 3CA is implicated as an oncogene in ovarian cancer". Nat. Genet., 1999, 21, 64.

Abstracted / indexed in

Web of Science (WOS) (On Hold)

Journal Citation Reports/Science Edition

Google Scholar

JournalSeek

Submission Turnaround Time

Top