Paclitaxel in the Treatment of Retinal Tumors of LH beta-Tag Murine Transgenic Model of Retinoblastoma

Abstract

Subconjunctival delivery of paclitaxel effectively inhibits intraocular tumor burden in the LH beta-Tag model of retinoblastoma. This treatment modality may represent a novel strategy for the clinical management of retinoblastoma.

A Phase I Study of Periocular Topotecan in Children with Intraocular Retinoblastoma

“…Periocular chemotherapy has been recently investigated as a way to increase the ocular bioavailability of various drugs such as carboplatin and more recently etoposide and paclitaxel. 8,22,23 To our knowledge, no other drug besides carboplatin has been widely used periocularly in children with retinoblastoma. Therefore, our study may add significant information of a new treatment modality for the treatment of this malignancy.…”

Progress in Small Molecule Therapeutics for the Treatment of Retinoblastoma

“…The primary impediments to pursuing paclitaxel as a retinoblastoma therapeutic appear to be toxicity [157–158] and formulation (to overcome its poor water solubility, paclitaxel is commonly formulated in Cremaphor which can induce side effects). [159] However, the formulation concerns can potentially be overcome.…”

“…Tumor burden determined by taking the ratio of tumor area to total globe area of the histology cross-section with the largest tumor focus. Reductions in tumor burden for saline- and DMSO-treated control eyes were not statistically significant (reproduced with permission from Suárez et al [157] ) (b-c) representative histopathologic examination of enucleated globes of transgenic retinoblastoma mice (b) left untreatedor (c) treated with 0.25 mg paclitaxel administered via subconjunctival injection (reproduced with permission from Suárez et al [157] )…”

Vitamin D: Implications for ocular disease and therapeutic potential

“…Y79 and Weri-RB1 cells also expressed the CYP24A1 gene (Morrison et al, 2011). Human retinoblastoma tissue and tumors from LH beta-Tag transgenic mice, a model in which the overexpression of the SV40 T antigen induces retinal tumors similar to human disease (Suárez et al, 2007; Windle et al, 1990), also expressed the receptor, suggesting that these tumors would be responsive to vitamin D treatment (Albert et al, 2002; Wagner et al, 2003). 1,25D 3 treatment did inhibit Y79 cell growth in vitro , inducing G0/G1 cell cycle arrest, and apoptosis, or programmed cell death, of the tumor cells.…”