%0 Journal Article
%T Potential therapeutic application of gold nanoparticles in B-chronic lymphocytic leukemia (BCLL): enhancing apoptosis
%A Priyabrata Mukherjee
%A Resham Bhattacharya
%A Nancy Bone
%A Yean K Lee
%A Chitta Patra
%A Shanfeng Wang
%A Lichun Lu
%A Charla Secreto
%A Pataki C Banerjee
%A Michael J Yaszemski
%A Neil E Kay
%A Debabrata Mukhopadhyay
%J Journal of Nanobiotechnology
%D 2007
%I BioMed Central
%R 10.1186/1477-3155-5-4
%X There is increasing evidence that angiogenesis plays a critical role in the pathogenesis of human malignancies [1,2]. Angiogenesis is an event that relies on the formation of vessels from preexisting vasculature that occurs in health and disease. Initially it was found that without new capillary formation there could not be significant tumor growth or metastasis to other organ sites. While the original evidence for this was based on the finding of tissue neovascularization, there have been significant advances delineating the presence of autocrine and/or paracrine pathways in both solid tumors and human leukemias [3,4]. Hematological diseases with aberrant vascularization include; multiple myeloma, acute myeloid leukemia and more recently B-chronic lymphocytic leukemia (CLL). These findings have led to the exciting possibility that strategies that undermine the angiogenic pathways could be used as non-overlapping methods of treatment for these diseases [5].Initially the secretion of VEGF from malignant tumors was believed to be of primary importance in the development of neovascularization of the tumor involved tissue sites. This important biologic event was associated with more aggressive disease status. However more recently the paracrine role of VEGF has been modified to include autocrine pathway(s) that increase survival of malignant cells in both mouse and human tumor types [6]. Interruption/blockade of the VEGF pathway in those tumor cells has been shown to lead to cell death. To a great extent the level of interruption/blockade has been either to bind VEGF or to inhibit VEGFR-1 or VEGFR-2 [7,8]. Importantly, ourselves and others have found that CLL B cells secrete VEGF and express the VEGF receptors; VEGFR-1, VEGFR-2 and Neuropilin-1 (NRP-1) [9]. The VEGF based pathway appears to be important in the apoptosis resistance of CLL B cells. Thus we have found that culturing CLL B cells with receptor tyrosine kinase inhibitors or anti-VEGF antibodies (Avastin; beva
%U http://www.jnanobiotechnology.com/content/5/1/4