Absence of activating mutations in ras and gsp oncogenes in a cohort of nine patients with sporadic pediatric thyroid tumors

✍ Scribed by Pauws, Erwin ;Tummers, Rob F.H.M. ;Ris-Stalpers, Carrie ;de Vijlder, Jan J.M. ;Voûte, Tom

• Publisher: John Wiley and Sons
• Year: 2001
• Tongue: English
• Weight: 158 KB
• Volume: 36
• Category: Article
• ISSN: 0098-1532
• DOI: 10.1002/mpo.1140

✦ Synopsis

Abstract

Background

Characterization of the genetic background of pediatric thyroid carcinomas could aid in distinguishing between differently staged tumors with respect to treatment and prognosis. Two known genetic factors associated with thyroid carcinoma, the proto‐oncogenes gsp and ras were investigated.

Procedure

DNA was extracted from paraffin sections from both tumor and normal thyroid tissue of nine patients (ages 9–16 years). Of these patients, eight were diagnosed with papillary carcinoma and one with follicular adenoma. The coding exons of gsp and the three known ras genes (H, K, and N‐ras) were screened for mutations using SSCP‐analysis.

Results

There were no mutations present in the ras and gsp proto‐oncogenes hot spots, however, LOH of H‐ras (chromosome location 11p15.5) was found in tumor tissue from one patient and a homozygous mutation in exon 12 of gsp causing a Pro→Ser conversion was present in the thyroid tumor tissue from another patient. Two silent polymorphisms were detected, H‐ras exon1, 86T→C and gsp exon 5, 81T→C.

Conclusions

Our results indicate that the ras/gsp mutations found are probably late events in the tumorigenesis representing general oncogenic stress. In conclusion, it seems that ras/gsp activation is not a factor in the mechanism causing sporadic thyroid carcinoma in children. Med. Pediatr. Oncol. 36:630–634, 2001. © 2001 Wiley‐Liss, Inc.