A5039742852- Thyroid Cancer Diagnosis and Treatment
- Thyroid Disorders and Treatments
- Cancer-related Molecular Pathways
- Congenital heart defects research
- Wnt/β-catenin signaling in development and cancer
- Animal Genetics and Reproduction
- TGF-β signaling in diseases
- Cell Image Analysis Techniques
- Ion channel regulation and function
- Erythrocyte Function and Pathophysiology
- Barrier Structure and Function Studies
- Ion Transport and Channel Regulation
- Cancer-related gene regulation
- Cancer Cells and Metastasis
- Renal and related cancers
- Developmental Biology and Gene Regulation
- S100 Proteins and Annexins
- Cancer, Hypoxia, and Metabolism
- Medical Imaging Techniques and Applications
- Connexins and lens biology
- Radiopharmaceutical Chemistry and Applications
- Protein Kinase Regulation and GTPase Signaling
- Pancreatic function and diabetes
- Estrogen and related hormone effects
- Neonatal Health and Biochemistry
University of Gothenburg
2014-2025
Institute for Biomedicine
2024
Sahlgrenska University Hospital
2013-2023
Applied Natural Sciences
2009
Cargotec (Poland)
2009
Uppsala University Hospital
1990-1995
Uppsala University
1991
Enhancement of tumor cell growth and invasiveness by transforming factor-β (TGF-β) requires constitutive activation the ras/MAPK pathway. Here we have investigated how MEK epidermal factor (EGF) influences response fully differentiated growth-arrested pig thyroid epithelial cells in primary culture to TGF-β1. The tightness was maintained after single stimulation with EGF or TGF-β1 (both 10 ng/ml) for 48 hours. In contrast, co-stimulation abolished transepithelial resistance increased...
Current understanding infers a neural crest origin of thyroid C cells, the major source calcitonin in mammals and ancestors to neuroendocrine tumors. The concept is primarily based on investigations quail-chick chimeras involving fate-mapping cells ultimobranchial glands that regulate Ca2+ homeostasis birds, reptiles, amphibians fishes, but whether mammalian cell development implicates homologous ontogenetic trajectory has not been experimentally verified. With lineage tracing we now provide...
Abstract Normal mouse thyroid development has been revised to identify critical morphogenetic events. The early primordium associates with the aortic sac endothelium at time of specification and budding. vascular contact is lost after buds from pharyngeal endoderm, but resumed before gland divides form two lobes. Lateral expansion parenchyma takes place along course third arch arteries. Thyroid precursor cells expressing Titf1/Nkx2.1 do not proliferate until migration stage, implicating that...
Transforming growth factor beta (TGF-β) plays major roles in tumorigenesis by regulating cell growth, epithelial-to-mesenchymal transition (EMT), migration/invasion and metastasis. The epithelial markers E-cadherin, claudin-3 claudin-4, commonly decreased human adenocarcinomas are actually up regulated during ovarian carcinogenesis. In cancer TGF-β1 may either suppress or promote tumor progression, but whether other TGF-β isoforms (TGF-β2 TGF-β3) exert similar effects is not known.In this...
Differentiated thyroid cancer primarily classified by tumor histology comprises follicular carcinoma (FTC) and papillary (PTC), which represent distinct malignancies regarding pattern of spreading, responsiveness to radioiodine treatment clinical outcome. As FTC PTC also differ genetically i.e. RAS mutations predominate in whereas mutant BRAF is much more frequent PTC, it assumed although yet unproven that the archetypical growth - versus depends on mutation identity potentially graded...
<p>Oligoclonal growth of BRAF-induced thyroid tumors revealed by clonal tracing. Images obtained from 6-month-old noninduced <i>Tg-CreER</i><sup><i>T2</i></sup>;<i>Braf</i><sup><i>CA/+</i></sup>;<i>mTmG</i> mice. Separate green (<b>A′–D′</b>) and red channels (<b>A″–D″</b>) are shown for clarity. <b>A</b> <b>B,</b> Coordinated contiguous...
<p>Clonal folliculogenesis in response to <i>Braf</i><sup><i>CA</i></sup> activation. Images from serially sectioned thyroid specimen the same <i>Tg-CreER</i><sup><i>T2</i></sup>;<i>Braf</i><sup><i>CA/+</i></sup>;<i>mTmG</i> mouse which individual tumor clones are identified and numbered as outlined <a href="#fig4" target="_blank">Fig. 4</a>....
<p>IF images Figure S2. Clonal tracing of BRAF mutant thyroid carcinoma that displays a follicular tumor phenotype.</p>
<p>Clonal tracing of thyroid tumor development in noninduced <i>Tg-CreER</i><sup><i>T2</i></sup>;<i>Braf</i><sup><i>CA/+</i></sup>;<i>mTmG</i> mice. Reporter gene activation designated by switch from mTomato (mT<sup>+</sup>) to mGFP (mG<sup>+</sup>) expression was monitored fluorescence microscopy. Induced Cre-mediated recombination served as controls for comparison....
<p>Papillary–follicular transition in <i>Braf</i><sup><i>CA</i></sup>-induced PTC. Advanced tumor stage of a 12-month-old noninduced <i>Tg-CreER</i><sup><i>T2</i></sup>;<i>Braf</i><sup><i>CA/+</i></sup>;<i>mTmG</i> mouse. Both thyroid lobes were serially sectioned from pole to for comprehensive evaluation. <b>A–C,</b> Overview tumors present the left lobe...
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<p>Comparison of tamoxifen-induced and noninduced thyroid tumorigenesis in <i>Tg-CreER</i><sup><i>T2</i></sup>;<i>Braf</i><sup><i>CA/+</i></sup> mice. Representative images histology IHC staining <i>Tg</i> CRE recombinase. <b>A</b> <b>B,</b> Thyroid lobe wild-type (WT) animals. Normal follicular tissue (<b>A</b>) uniform accumulation follicle lumina...
<p>IF images Figure S1. Clonal tracing of sporadically developed BRAF mutant neoplasia in mouse thyroid.</p>
<div>Abstract<p>Differentiated thyroid cancer primarily classified by tumor histology comprises follicular carcinoma (FTC) and papillary (PTC), which represent distinct malignancies regarding the pattern of spreading, responsiveness to radioiodine treatment, clinical outcome. As FTC PTC also differ genetically i.e., <i>RAS</i> mutations predominate in whereas mutant <i>BRAF</i> is much more frequent PTC, it assumed although yet unproven that archetypical...
Thyroid dysgenesis is the major cause of congenital hypothyroidism in humans. The underlying molecular mechanism most cases unknown, but frequent co-incidence cardiac anomalies suggests that thyroid morphogenetic process may depend on proper cardiovascular development. T-box transcription factor TBX1, which probable gene for 22q11 deletion syndrome (22q11DS/DiGeorge syndrome/velo-cardio-facial syndrome), has emerged as a central player coordinated formation organs and tissues derived from...