Sunitinib inhibits MEK/ERK and SAPK/JNK pathways and increases sodium/iodide symporter expression in papillary thyroid cancer.

Background: Sunitinib malate (Sutent, Pfizer, Inc.; SU11248) is a selective, multitargeted inhibitor of receptor tyrosine kinases and has been shown to inhibit receptors for VEGF, PDGF, KIT, FLT3, and RET. The objective of this study was to determine the effects of sunitinib on signal transduction pathways and on gene expression of iodide-metabolizing proteins in papillary cancer cells with the RET/PTC1 rearrangement.

Indomethacin inhibits cell growth of medullary thyroid carcinoma by reducing cell cycle progression into S phase.

Indomethacin, a non-steroidal anti-inflammatory drug (NSAID), has been reported to inhibit the growth of medullary thyroid carcinoma (MTC) cells in vitro. However, the mechanism of inhibition of MTC cell growth by indomethacin and its potency have yet to be revealed. We examined the effect of indomethacin on three different MTC cell lines (TT cells, DRO 81-1 cells and HRO 85-1 cells) and two non-MTC cells.

Comparison of bone marrow aspirates and biopsies in pediatric patients with ALL at days 7 and 14 of induction therapy.

The percentage of blasts in the bone marrow aspirates at day 7 or 14 of induction therapy in pediatric ALL patients is an indicator of rapid early response and an independent prognostic factor for long term outcome. Discrepancies between the percentages of blasts in bone marrow aspirates compared to biopsies have been reported. In a retrospective study on 44 consecutive patients diagnosed with ALL between 1998 and 2001, important differences were observed in the percentage of blasts between bone marrow aspirates and biopsies at days 7 and 14 of induction therapy.

TCL-1, MTCP-1 and TML-1 gene expression profile in non-leukemic clonal proliferations associated with ataxia-telangiectasia.

We analyzed the role of 4 genes, TCL-1, MTCP-1, TML-1 and ATM, in the early pathogenesis of T cell leukemia, with particular interest in the characteristics of long-standing non-leukemic clonal proliferations in ataxia-telangiectasia (A-T) patients. Five patients were studied: 4 patients had A-T (2 of whom had non-leukemic clonal proliferations [ATCP]), 1 had B cell lymphoma and 1 had T-ALL; a fifth patient with T-PLL did not have A-T. We measured the levels of expression for TCL-1, MTCP-1 and TML-1.