Hostname: page-component-78c5997874-mlc7c Total loading time: 0 Render date: 2024-11-05T03:58:25.707Z Has data issue: false hasContentIssue false

Allelic imbalance on chromosomes 3p, 9p and 17p in malignant progression of laryngeal mucosa

Published online by Cambridge University Press:  14 May 2007

T Guo*
Affiliation:
Department of Otorhinolaryngology Head and Neck Surgery, An Hui Province Hospital, An Hui Medical University, Hefei City, An Hui Province, China
J W Sun
Affiliation:
Department of Otorhinolaryngology Head and Neck Surgery, An Hui Province Hospital, An Hui Medical University, Hefei City, An Hui Province, China
Q P Lv
Affiliation:
Department of Otorhinolaryngology Head and Neck Surgery, An Hui Province Hospital, An Hui Medical University, Hefei City, An Hui Province, China
X G Li
Affiliation:
Department of Otorhinolaryngology Head and Neck Surgery, An Hui Province Hospital, An Hui Medical University, Hefei City, An Hui Province, China
*
Address for correspondence: Dr JingWu Sun, Dept of Otorhinolaryngology, An Hui Province Hospital, Hefei City 230001, China. E-mail: [email protected]

Abstract

Objectives/hypothesis:

To evaluate the character and significance of microsatellite deoxyribonucleic acid allelic imbalance in laryngeal squamous cell carcinogenesis.

Methods:

We investigated the frequency of expression and clinical relationships of loss of heterozygosity and microsatellite instability in 49 laryngeal premalignant and malignant lesions. Allelic imbalance was analysed using six polymorphic markers (D3S1234, D9S171, D9S1748, D9S162, D9SINFA and D17S796), via polymerase chain reaction – single sequence length polymorphism – silver staining.

Results:

Allelic loss was seen in 3.7 per cent of the six markers in hyperplastic lesions, 10.81 per cent in mild dysplasia, 26.03 per cent in moderate to severe dysplasia, and 38.67 per cent in laryngeal squamous cell carcinoma. Significant associations were found between allelic loss and clinical pathological grades (χ2 = 17.686, p = 0.000). No statistically significant difference was found in the frequency of microsatellite instability (χ2 = 0.314, p > 0.05). In the early stages of neoplastic change, the incidence of microsatellite instability was higher than that of loss of heterozygosity.

Conclusions:

Allelic imbalance was associated with the carcinogenesis and progression of laryngeal squamous cell carcinoma. Microsatellite analysis might provide new approaches to early genetic detection for patients with premalignant laryngeal lesions.

Type
Main Articles
Copyright
Copyright © JLO (1984) Limited 2007

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

1Parkin, DM, Pisani, P, Ferlay, J. Estimates of the worldwide incidence of eighteen major cancers in 1985. Int J Cancer 1993;54:594600CrossRefGoogle ScholarPubMed
2Ah-See, KW, Cooke, TG, Pickford, IR, Soutar, D, Balmain, A. An allelotype of squamous carcinoma of the head and neck using microsatellite markers. Cancer Res 1994;54:1617–21Google ScholarPubMed
3Califano, J, van der Riet, P, Westra, W, Nawroz, H, Clayman, G, Piantadosi, S et al. Genetic progression model for head and neck cancer: implications for field cancerization. Cancer Res 1996;56:2488–92Google ScholarPubMed
4Tabor, MP, Brakenhoff, RH, van Houten, VM, Kummer, JA, Snel, MH, Snijders, PJ et al. Persistence of genetically altered fields in head and neck cancer patients: biological and clinical implications. Clinical Cancer Research 2001;7:1523–32Google ScholarPubMed
5Yoo, WJ, Cho, SH, Lee, YS, Park, GS, Kim, MS, Kim, BK et al. Loss of heterozygosity on chromosomes 3p, 8p, 9p and 17p in the progression of squamous cell carcinoma of the larynx. J Korean Med Sci 2004;19:345–51CrossRefGoogle ScholarPubMed
6Sudbo, J, Kildal, W, Risberg, B, Koppang, HS, Danielsen, HE, Reith, A. DNA content as a prognostic marker in patients with oral leukoplakia. N Engl J Med 2001;344:1270–8CrossRefGoogle ScholarPubMed
7Zhou, X, Jordan, RC, Li, Y, Huang, BL, Wong, DT. Frequent allelic imbalances at 8p and 11q22 in oral and oropharyngeal epithelial dysplastic lesions. Cancer Genet Cytogenet 2005;161:86–9CrossRefGoogle ScholarPubMed
8Shiga, K, Matsuura, K, Tateda, M, Saijo, S, Ogawa, T, Miyagi, T et al. Allelic loss correlated with tissue specificity in head and neck squamous cell carcinomas and the clinical features of patients. [J] Tohoku J Exp Med 2004;2:163–72CrossRefGoogle Scholar
9Rogowski, M, Walenczak, I, Pepinski, W, Skawronska, M, Sieskiewicz, A, Klatka, J. Loss of heterozygosity in laryngeal cancer. Rocz Akad Med Bialymst 2004;49:262–4Google ScholarPubMed
10Joseph, C, William, HW, Glenn, M, Russel, C, Wayne, MK, David, S. Genetic progression and clonal relationship of recurrent premalignant head and neck lesions. Clinical Cancer Research 2000;6:347–52Google Scholar
11Kakinuma, N, Kohu, K, Sato, M, Yamada, T, Nakajima, M, Akiyama, T et al. Candidate regions of tumor suppressor gene by loss of heterozygosity analysis on chromosome 8p11.1-q13.3 in gastric cancer. Cancer Lett 2004;213:111–16CrossRefGoogle ScholarPubMed
12Ha, PK, Pilkington, TA, Westra, WH, Sciubba, J, Sidransky, D, Califano, JA. Progression of microsatellite instability from premalignant lesions to tumors of the head and neck. Int J Cancer 2002;102:615–17CrossRefGoogle ScholarPubMed
13Simoneau, AR, Jones, PA. Bladder cancer: the molecular progression to invasive disease. World J Urol 1994;12:8995CrossRefGoogle ScholarPubMed
14Braakhuis, BJM, Tabor, MP, Kummer, JA, Leemans, CR, Brakenhoff, RH. A genetic explanation of Slaughter's concept of field cancerization: evidence and clinical implications. Cancer Res 2003;63:1727–30Google ScholarPubMed
15Rizos, E, Sourvinos, G, Spandidos, DA. Loss of heterozygosity at 8P, 9P and 17P in laryngeal cytological specimens. Oral Oncol 1998;34:519–23CrossRefGoogle Scholar