Stéphanie Larrivée-Vanier1,2, Fabien Magne1,2, Natalie Patey3, Jean-Pierre Chanoine4, Jean-Marc Vuissoz5, Guy Van Vliet1,2, Johnny Deladoëy1,2. 1. 1 Endocrinology Service and Research Center, Centre Hospitalier Universitaire Sainte-Justine, University of Montreal , Montreal, Canada . 2. 2 Department of Pediatrics, Centre Hospitalier Universitaire Sainte-Justine, University of Montreal , Montreal, Canada . 3. 3 Department of Pathology, Centre Hospitalier Universitaire Sainte-Justine, University of Montreal , Montreal, Canada . 4. 4 Endocrinology and Diabetes Unit, Department of Pediatrics, British Columbia Children's Hospital, University of British Columbia , Vancouver, Canada . 5. 5 Division of Pediatric Endocrinology, University Children's Hospital Basel (UKBB), University of Basel , Basel, Switzerland .
Abstract
BACKGROUND: In humans, the cause of arrested migration of the median thyroid anlage resulting in an ectopic sublingual gland is unknown. These ectopic glands have a normal follicular architecture but their thyrotropin-induced growth is insufficient, leading to congenital hypothyroidism in the vast majority of affected subjects. We hypothesized that arrested migration is due to premature differentiation [reflected by decreased telomere length (TL)], as observed in neural tube defects in mice. METHODS: Absolute TL and telomerase reverse transcriptase (hTERT) expression was measured in four ectopic and six orthotopic thyroids. TL was measured by quantitative polymerase chain reaction of genomic DNA, whereas hTERT expression was measured by quantitative polymerase chain reaction of total RNA. RESULTS: The mean±standard deviation TL (in kilobases per diploid genome) was 140.45±40.07 in ectopic and 97.50±30.48 in orthotopic thyroids (p=0.12). Expression of hTERT was quiescent in both ectopic and orthotopic thyroids. CONCLUSIONS: Compared with orthotopic thyroids, TL shortening is not observed in ectopic thyroid tissues and, consequently, no compensatory hTERT expression was measured. This makes premature differentiation an unlikely cause of arrested migration and it suggests, indirectly, that ectopic thyroids are not at higher risk of cancer than orthotopic thyroids.
BACKGROUND: In humans, the cause of arrested migration of the median thyroid anlage resulting in an ectopic sublingual gland is unknown. These ectopic glands have a normal follicular architecture but their thyrotropin-induced growth is insufficient, leading to congenital hypothyroidism in the vast majority of affected subjects. We hypothesized that arrested migration is due to premature differentiation [reflected by decreased telomere length (TL)], as observed in neural tube defects in mice. METHODS: Absolute TL and telomerase reverse transcriptase (hTERT) expression was measured in four ectopic and six orthotopic thyroids. TL was measured by quantitative polymerase chain reaction of genomic DNA, whereas hTERT expression was measured by quantitative polymerase chain reaction of total RNA. RESULTS: The mean±standard deviation TL (in kilobases per diploid genome) was 140.45±40.07 in ectopic and 97.50±30.48 in orthotopic thyroids (p=0.12). Expression of hTERT was quiescent in both ectopic and orthotopic thyroids. CONCLUSIONS: Compared with orthotopic thyroids, TL shortening is not observed in ectopic thyroid tissues and, consequently, no compensatory hTERT expression was measured. This makes premature differentiation an unlikely cause of arrested migration and it suggests, indirectly, that ectopic thyroids are not at higher risk of cancer than orthotopic thyroids.