Thyroid dysgenesis and cancer are the most common developmental defects and tumors of the endocrine system. We investigate basic mechanisms of pathogenesis with the long-term attempt to identify new biomarkers and potential novel treatment strategies of these diseases. Particular interest is paid to inductive and supporting signals that regulate progenitor cell commitment, propagation of endocrine cell lineages, and differentiation of epithelial and hormonogenic phenotypes in normal cells, and the corresponding aberrations recognized in diseased cells.
Current work on embryos concerns expression and functional analysis of transcription factors (e.g. FoxA2) and morphogens (e.g. Sonic hedgehog) implicated in endoderm and neuroendocrine development of the thyroid gland; the potential role of candidate genes for the biology of thyroid cancer with different ancestral cell origins are coordinately addressed. The involvement of ephrin-Eph receptor bidirectional signaling in post-natal thyroid growth is investigated in a model of experimental goitrogenesis. The DNA damage responses of the fetal and young thyroid to potentially carcinogenic levels of 131-I are characterized in mouse models under the influence of modifying genetic and environmental factors. The potential use of kinase inhibitors to restitute iodide transport in thyroid tumors with blocked radioiodine uptake (e.g. by exaggerated/constitutive activation of the EGFR-Ras-MAPK pathway) is studied in cultured cells expressing the sodium/iodide symporter (NIS).
A combination of 3D-organotypic cell culture techniques and animal models is employed for cell and molecular biology and genetic studies. An isotope laboratory is at hand for investigation of radiobiology effects of radioiodine and other nuclides of interest.
Mikael Nilsson, MD, PhD, Professor
Henrik Fagman, MD, PhD
Elin Schoultz, MD, PhD student
Shawn Liang, PhD student
Ellen Johansson, MD, PhD student
Therese Carlsson, Technicia