(2004) Struttura, natura del legame e proprietà elettroniche di SrTiO3 e Sr1-3x/2LaxTiO3

Th2 cytokines induce chemotherapy resistance in epithelial tumors via PI3K/AKT pathway

Several studies designate apoptosis as the predominant mechanism by which cancer cells die in response to chemotherapeutic drugs. Moreover, it was suggested that anti-apoptotic molecules activation play a pivotal role in the chemotherapeutic drugs resistance. We have recently demonstrated that the presence of Th2 cytokines in thyroid cancer microenvironment increase FLIP, Bcl-2 and Bcl-xl expression levels and protect cancer cells from chemotherapeutic drugs induced apoptosis. Particularly, in this study we demonstrate that IL-4 and IL-10 promote proliferation and chemotherapy resistance activating the PI3K/AKT signal pathway. Therefore, we extensively studied cell survival-related substrat…

BISPHOSPHONATES SENSITIZE OSTEOSARCOMA CELLS TO CHEMOTHERAPEUTIC DRUGS

Autocrine production of interleukin-4 and interleukin-10 is required for survival and growth of thyroid cancer cells.

AbstractAlthough CD95 and its ligand are expressed in thyroid cancer, the tumor cell mass does not seem to be affected by such expression. We have recently shown that thyroid carcinomas produce interleukin (IL)-4 and IL-10, which promote resistance to chemotherapy through the up-regulation of Bcl-xL. Here, we show that freshly purified thyroid cancer cells were completely refractory to CD95-induced apoptosis despite the consistent expression of Fas-associated death domain and caspase-8. The analysis of potential molecules able to prevent caspase-8 activation in thyroid cancer cells revealed a remarkable up-regulation of cellular FLIPL (cFLIPL) and PED/PEA-15, two antiapoptotic proteins whos…

Bisphosphonates sensitize osteosarcoma cells to chemoterapeutic drugs

CANCER STEM CELLS CONTRIBUTE TO THE AGGRESSIVE BEHAVIOUR OF HUMAN EPITHELIAL COLON CANCER.

Bisphosphonates sensitise osteosarcoma cells to chemotherapeutic drugs

Suppressor of cytokine signaling 3 sensitizes anaplastic thyroid cancer to standard chemotherapy

We previously showed that cancer cells from papillary, follicular, and anaplastic thyroid carcinomas produce interleukin-4 and interleukin-10, which counteract the cytotoxic activity of conventional chemotherapy through the up-regulation of antiapoptotic molecules. Here, we identify Janus kinase/signal transducers and activators of transcription (STAT) and phosphatidyl inositol 3-kinase (PI3K)/AKT as the down-stream pathways through which these cytokines confer resistance to cell death in thyroid cancer. We found that the absence of suppressors of cytokine signaling (SOCS) molecules allows the propagation of the survival signaling. Exogenous expression of SOCS1, SOCS3, and SOCS5 in the high…

LYPOXYGENASE INDUCES CHEMORESISTANCE IN THYROID CANCER

Autocrine production of IL-4 confers resistance to chemotherapy and CD-95 induced cell death in cancer cells.

RAPID ANALYSIS OF NEFAs AS METHYL ESTERS FROM SMALL VOLUME OF PLASMA AND OTHERS DIFFERENT BIOLOGICAL SPECIMENS BY GC AND GCMS AFTER ONLY ONE STEP ESTERIFICATION