Tumor restenosis

Nanoparticles formulated with PLGA have been shown to be rapidly uptaken by the endothelial cells, the uptake was shown to depend on the nanoparticle concentration and the particles where mainly shown to localize in the cytoplasm (207). These nanoparticles were also shown to be biocompatible with the cells with no effect on cell viability (207). This is important due to the fact that endothelium is an important target for gene therapy in a number of disorders including angiogenesis, atherosclerosis, tumor growth, myocardial infarction, limb and cardiac ischemia, restenosis (207). 

Vascular proliferative diseases (i.e., atherosclerosis and restenosis) and cancer are associated with excessive cell growth. The cmcial role of CDK/cychn holoenzymes in the control of cell proliferation has prompted great interest in the development of chemical inhibitors of CDK activity that would be expected to inhibit cellular proliferation and, therefore, may attenuate the development of vascular occlusive lesions and tumor progression. 

Neointimal proliferation inside the stent usually causes only limited reduction in the caval diameter and does not usually lead to significant caval restenosis or thrombosis. When obstruction of a stent occurs and does not respond to local thrombolysis, the likely cause is tumor infiltration the diagnosis can be confirmed by endovascular biopsy. 

A naturally occurring therapeutic-diol, 17-P-estradiol is an endogenous hormone, useful in preventing restenosis and tumor growth (17,18), Steroid-diol 17p-estradiol was introduced in a PEA backbone via the di-TFA salt of the new monomer bis-(L-Leu)-l7p-estradiol-diester (IL5). This monomer was prepared in ca. 70% yield, followed by the reaction in scheme 6 and then directly introduced into the APC reaction. 

While the study off the effectiveness of NCT for treating malignant brain tumors has been a primary focus, this technology has tremendous potential for inhibiting the cell proliferation that leads to restenosis. A study was undertaken to test the effectiveness of GdNCT in inhibiting intimal hyperplasia or thrombosis of vascular wall and whether or not it caused collateral tissue damage. 

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