Home  About us  Contact
 

Human Anaplastic Thyroid Cancer Cells (human + anaplastic_thyroid_cancer_cell)

Distribution by Scientific Domains
Medical Sciences100%

Selected Abstracts

Peroxisome Proliferator-activated Receptor Gamma Activation Induces Cell Cycle Arrest via the p53-independent Pathway in Human Anaplastic Thyroid Cancer Cells

CANCER SCIENCE, Issue 12 2002
Sung Hwa Chung
Anaplastic thyroid carcinoma is one of the most aggressive human malignancies. Outcomes of intensive multimodal therapy have been far from satisfactory. Furthermore, p53 gene dysfunction, often found in this type of cancer, is known to impair the efficacy of the therapeutic agents. Specific ligands for peroxisome proliferator activated receptor gamma (PPAR-,) induce growth suppression in some tumor cells. In this study, we investigated the role of PPAR-, in anaplastic thyroid cancer cell lines (OCUT-1, ACT-1). PPAR-, was expressed and functional in both cell lines. Activation of PPAR-, with its specific ligands, troglitazone and 15-deoxy-,12, 14 -prostaglandin J2, inhibited cell growth in a dose-dependent manner through inducing G1 cell cycle arrest. P53 protein expression differed in OCUT-1 and in ACT-1, though the levels stayed constant irrespective of ligand exposure in both cell lines. In contrast, p21 and p27 proteins were induced in a dose-dependent manner in both situations. This study showed that PPAR-, ligands were able to induce growth suppression in anaplastic thyroid cancer cells via a p53-independent, but p21- and p27-dependent cytostatic pathway. These tumor-suppressive effects of PPAR-, may provide a novel approach to the treatment of anaplastic thyroid cancer. [source]

Synthesis and in vitro cytotoxic activity on human anaplastic thyroid cancer cells of lipoamino acid conjugates of gemcitabine

DRUG DEVELOPMENT RESEARCH, Issue 5 2010
Rosario Pignatello
Abstract Lipophilic derivatives of the antitumor drug gemcitabine (GEM) with the potential for improving drug loading in lipid-based colloidal carriers, like liposomes or lipid nanoparticles, are described. GEM free base was conjugated to lipoamino acids bearing an alkyl side chain of different length, by either a carbodiimide-assisted or an ethylchloroformiate-assisted coupling reaction, to obtain N4 -acyl GEM derivatives. These compounds retained the same in vitro cell growth inhibitory activity of the parent drug against two lines of human anaplastic thyroid cancer cells. Stability studies suggested that the observed activity was due mainly to intact derivatives and not to released GEM. Accordingly, these amphiphilic derivatives can be proposed in a further step for the encapsulation in liposomes or lipid nanocarriers, to achieve as a final goal an improvement of the pharmacokinetics and therapeutic activity of GEM. Drug Dev Res 2010. © 2010 Wiley-Liss, Inc. [source]

Thiazolidinediones and antiblastics in primary human anaplastic thyroid cancer cells

CLINICAL ENDOCRINOLOGY, Issue 6 2009
Alessandro Antonelli
Summary Objective, No study has evaluated the antiproliferative effects of thiazolidinediones and antiblastics in ,primary cultured human anaplastic thyroid cancer cells'. Design, Primary anaplastic cells proliferation was evaluated after incubation with increasing concentrations of rosiglitazone or pioglitazone or antiblastics (bleomycin, cisplatin, gemcitabine) by a proliferation assay (WST-1-tetrazolium reaction) and cell counting. Measurements and results, A reduction of proliferation by thiazolidinediones at 1 h (from the start of tetrazolium reaction) [of 11% and 25%, with rosiglitazone, 10 or 20 (P = 0·0001) µM, respectively; of 7% and 17%, with pioglitazone, 10 or 20 (P = 0·0125) µM, respectively], and at 2 h [of 14% and 24%, with rosiglitazone, 10 (P = 0·0043) or 20 (P < 0·0001) µM, respectively; of 9% and 21%, with pioglitazone, 10 (P = 0·0397) or 20 (P = 0·0001) µM, respectively] was shown. No significant thiazolidinediones effect was observed in normal thyroid follicular cells. Bleomycin, cisplatin and gemcitabine significantly (P < 0·0001) inhibited (> 50%) anaplastic cells proliferation. Cell counting confirmed the above mentioned results. Inhibition of proliferation was similar in tumours with or without V600EBRAF mutation, both for thiazolidinediones and antiblastics. Conclusions, Thiazolidinediones exert an antiproliferative effect in primary cultured human anaplastic carcinoma cells in vitro, such as antiblastics. [source]