Fetal cell carcinogenesis of the thyroid: theory and practice.

A novel hypothesis of thyroid carcinogenesis, the "fetal cell carcinogenesis" hypothesis, in which cancer cells are derived from the remnants of three types of fetal thyroid cells, instead of normal thyroid follicular cells, is proposed. In this hypothesis, thyroid cancer cells are generated from fetal cells by proliferation without differentiation and oncogenes play an oncogenic role by preventing fetal cells from differentiating. This hypothesis explains well the clinical and biological features and recent molecular evidence of thyroid carcinoma.

Fetal cell carcinogenesis: a new hypothesis for better understanding of thyroid carcinoma.

Modern advances in molecular technology have given us the chance to establish a new insight into thyroid carcinogenesis. Gene expression in thyroid malignancies usually reveals highly consistent profiles, which leads to questioning of the classic concept of multistep carcinogenesis, in which cancer cells are produced from well-differentiated benign cells by transformation caused by accumulating damage to their genome. We propose a novel hypothesis of thyroid carcinogenesis, the fetal cell carcinogenesis hypothesis, in which cancer cells are derived from the remnants of three types of fetal thyroid cells, instead of normal thyroid follicular cells.

Fetal cell carcinogenesis of the thyroid: a hypothesis for better understanding of gene expression profile and genomic alternation in thyroid carcinoma.

Since the 1980s, cancer cells have been considered to be generated from well-differentiated benign cells by transformation caused by accumulating damage in their genomes. However, recent progress in gene expression analysis in thyroid malignancies has raised the possibility of another model of thyroid carcinogenesis. We propose a novel hypothesis of thyroid carcinogenesis, the fetal cell carcinogenesis hypothesis, in which cancer cells are derived from the remnants of fetal thyroid cells, instead of from normal thyroid follicular cells.

Autoantibodies against four kinds of neurotransmitter receptors in psychiatric disorders.

There is a hypothesis that autoimmune abnormalities in neurotransmitter receptors might cause some psychiatric disorders. Using a sensitive radioligand assay, we detected serum autoantibodies to recombinant human muscarinic cholinergic receptor 1 (CHRM1, 34.4%), mu-opioid receptor (OPRM1, 13.

Autoantibodies against muscarinic cholinergic receptor in chronic fatigue syndrome.

The disturbance of the central nervous system and immunological abnormalities have been suggested in patients with chronic fatigue syndrome (CFS). We focused on immunological abnormalities against neurotransmitter receptors in CFS. Using a sensitive radioligand assay, we examined serum autoantibodies to recombinant human muscarinic cholinergic receptor 1 (CHRM1), mu-opioid receptor (OPRM1), 5-hydroxytryptamine receptor 1A (HTR1A), and dopamine receptor D2 (DRD2) in patients with CFS (n=60) and results were compared with those in patients with autoimmune disease (n=33) and in healthy controls (n=30).

Detection of autoantibodies against the pituitary-specific proteins in patients with lymphocytic hypophysitis.

Objective: Several reports have described antipituitary antibodies by immunofluorescent or immunoblotting methods in patients with lymphocytic hypophysitis. However, with the exception of the pituitary hormones, individual antigens specific for the pituitary gland have not been studied. To understand the pathogenesis of lymphocytic hypophysitis and to diagnose this disease efficiently, we studied the presence of autoantibodies against three pituitary-specific proteins, GH and two novel pituitary-specific proteins, namely, pituitary gland specific factor 1a (PGSF1a) and PGSF2.