Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0079731 (B-cell lymphoma)
 16,671 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

TSH is the primary physiological regulator of thyroid gland function. The effects of TSH on thyroid cells are mediated via activation of its membrane receptor [TSH receptor (TSHR)]. In this study, we examined functional thyroid differentiation in zebrafish and characterized the role of TSHR signaling during thyroid organogenesis. Cloning of a cDNA encoding zebrafish Tshr showed conservation of primary structure and functional properties between zebrafish and mammalian TSHR. In situ hybridization confirmed that the thyroid is the major site of tshr expression during zebrafish development. In addition, we identified tpo, iyd, duox, and duoxa as novel thyroid differentiation markers in zebrafish. Temporal analyses of differentiation marker expression demonstrated the induction of an early thyroid differentiation program along with thyroid budding, followed by a delayed onset of duox and duoxa expression coincident with thyroid hormone synthesis. Furthermore, comparative analyses in mouse and zebrafish revealed for the first time a thyroid-enriched expression of cell death regulators of the B-cell lymphoma 2 family during early thyroid morphogenesis. Knockdown of tshr function by morpholino microinjection into embryos did not affect early thyroid morphogenesis but caused defects in later functional differentiation. The thyroid phenotype observed in tshr morphants at later stages comprised a reduction in number and size of functional follicles, down-regulation of differentiation markers, as well as reduced thyroid transcription factor expression. A comparison of our results with phenotypes observed in mouse models of defective TSHR and cAMP signaling highlights the value of zebrafish as a model to enhance the understanding of functional differentiation in the vertebrate thyroid.
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PMID:TSH receptor function is required for normal thyroid differentiation in zebrafish. 2173 42

Radiation-induced thyroid dysfunction following oncologic treatment is not uncommon, however limited literature data has been found on patients that underwent chemotherapy only. A change in thyrometabolic autoimmune status is also a rare entity. We present a case of newly diagnosed Graves' thyrotoxicosis following a successful R-CHOP (Rituximab, Cyclophosphamide, Doxorubicine, Vincristine and Prednisone) treatment in a patient with concurrent abdominal and thyroid diffuse large B-cell lymphoma (DLBCL). Following chemotherapy, PET CT showed resolution of FDG-avid thyroid nodule as well as no evidence of the thyroid mass on repeat ultrasound. Her thyroid function also normalized. During her follow-up visit, patient reported significant unintentional weight loss and persistent fatigue over the past couple months. Repeat laboratory evaluation revealed TSH 0.005 mIU/mL, FT4 6.73 ng/dL and thyroid stimulating immunoglobulin (TSI) 535 (ref <140%). She was started on methimazole followed by radioactive iodine therapy. This unique case of Graves' disease following R-CHOP treatment in patients with known Hashimoto's and thyroid lymphoma is one of the first to be reported in the literature. The swing of pendulum from Hashimoto's to Graves' disease is very uncommon. As clinicians, we need to continue monitoring for clinical and biochemical thyroid dysfunction in this subset of population.
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PMID:R-CHOP-Associated Graves' Hyperthyroidism. 3154 72