rss
J Clin Pathol 2003;56:512-518 doi:10.1136/jcp.56.7.512
  • Original article

Allelic imbalance at chromosome 11 in head and neck squamous cell carcinoma in an Indian patient population

  1. G Mondal1,
  2. A Tripathi2,
  3. N Bhattacharya2,
  4. N Sikdar5,
  5. A Roy3,
  6. A Sengupta4,
  7. B Roy5,
  8. C K Panda2,
  9. S Roychoudhury1
  1. 1Human Genetics and Genomics Division, Indian Institute of Chemical Biology, Kolkata 700 032, India
  2. 2Department of Oncogene Regulation, Chittaranjan National Cancer Institute, Kolkata 700 026, India
  3. 3Department of Pathology, Medical College and Hospital, Kolkata 700 073, India
  4. 4Cancer Centre and Welfare Home, Kolkata 700 063, India
  5. 5Anthropology and Human Genetics Unit, Indian Statistical Institute, Kolkata 700 035, India
  1. Correspondence to:
 Dr S Roychoudhury, Human Genetics and Genomics Division, Indian Institute of Chemical Biology, 4, Raja S. C. Mullick Road, Kolkata 700 032, India; 
 susantar{at}hotmail.com
  • Accepted 27 February 2003

Abstract

Background: Genetic instability of chromosome 11 is a frequent event in many solid tumours, including head and neck squamous cell carcinoma (HNSCC).

Aims: To perform allelic imbalance analysis of cytogenetically mapped altered regions of human chromosome 11 in patients with HNSCC from eastern India.

Methods: Genomic alterations were investigated using highly polymorphic microsatellite markers in both HNSCC and leukoplakia tissues.

Results: Microsatellite markers D11S1758 from 11p13–15 and D11S925 from 11q23.3–24 had the highest frequency (38% and 32%, respectively) of loss of heterozygosity among all the markers analysed. Allelic loss at the marker D11S925 was seen in both leukoplakia and in all stages of HNSCC tumour tissues suggesting that it is an early event in HNSCC tumorigenesis. Microsatellite size alteration was also found to be high (> 20%) in several markers. In leukoplakia samples microsatellite instability was seen at a higher frequency than loss of the allele, indicating such alterations might initiate the process of tumorigenesis in HNSCC.

Conclusions: The high rate of chromosomal alterations at 11q21–24 in HNSCC suggests the presence of a putative tumour suppressor gene in this region.

Footnotes

    This Article

    1. Abstract
    2. Full text
    3. PDF

    Responses

    1. Submit a response
    2. No responses published

    Register for free content

    The full back archive is now available for all BMJ Journals. Institutional subscribers may access the entire archive as part of their subscription. Personal subscribers will also have access to all content when logged in. Non-subscribers who register have free access to all articles published before 2006 right back to volume 1 issue 1. Register here to access the free archive of all BMJ Journals.

    Don't forget to sign up for content alerts so you keep up to date with all the articles as they are published.