Loss of heterozygosity (LOH) studies have been used to identify sites harbo
uring tumour suppressor genes (TSGs) involved in tumour initiation or progr
ession. To further elucidate the genetic mechanism; for follicular and papi
llary thyroid tumours development, we studied the frequency of LOH in 36 th
yroid tumours (21 follicular thyroid adenomas (FAs) and 15 papillary thyroi
d carcinomas (PTCs)) on 10 specific genomic areas: 3p22. 3p25. 7q21, 7q31,
10q23, 10q25-26. 11q13, 11q23, 13q13 and 17p13.3-13.2 using 20 polymorphic
markers. We have selected these areas for two reasons: (a) Even though LOH
in thyroid neoplasms has been described in some of these areas, results are
controversial, and (b) we have also studied areas described as involved in
other epithelial or endocrine tumour types. but not studied up to now in t
hyroid neoplasms. Two areas showed a high percentage of LOH: 7q31 and 11q23
. A 62% LOH was found at 7q31 in the FAs, suggesting. as other authors have
proposed, that at least one TSG must be present in the vicinity of the c-m
et locus. The second area in frequency was at the 11q23 locus. with a 45% L
OH in the FAs. This area wits studied because it has been described as bein
g involved in the development of epithelial and endocrine cancers. This loc
us had not been studied before in thyroid neoplasms. This result is interes
ting because the LOH11CR2A gene is localised at this locus. We suggest that
this gene and;or an other TSG nearby may be involved in the progression to
FA. In our study, a low percentage of LOH was found in the PTC samples. in
dicating that TSGs present in the areas we have studied are not significant
ly involved in their progression. Our data also suggest that TSGs located i
n areas where no LOH was detected (PTEN. MEN1, Cyclin DI. BRCA2 and RFC3) a
re not involved or do not have an important role in tumour progression. (C)
2001 Elsevier Science Ltd. All rights reserved.