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- W2280242427 abstract "A180 Malignant melanoma is one of the most highly invasive tumors and melanoma mortality rates are increasing more rapidly than any other cancer indication. Surgical resection and systemic chemotherapy are the major therapeutic approaches for melanoma. However, systemic therapy faces two significant limitations: a priori resistance to therapy and toxicity towards normal tissues. Bcl-2 protein plays a major role in preventing apoptosis and has been linked to chemotherapy resistance in melanoma. G3139 (a bcl-2 antisense oligodeoxynucleotide that selectively targets bcl-2 RNA for degradation by RNase H and thereby decreases Bcl-2 protein production; Genta Inc.), when combined with a glutathione (GSH) depleting strategy, has been shown to facilitate regression of murine B16 melanoma F10 liver metastases by radiochemotherapy (S. Mena et al. Clin Cancer Res.13: 2658-66). However the potential application of this approach to human melanoma remains to be investigated. A375 human melanoma cells, as compare to normal melanocytes, overexpress bcl-2 and have higher GSH content. In addition to its antiapoptotic properties, Bcl-2 also inhibits the release of GSH through the cystic fibrosis transmembrane conductance regulator (CFTR, a MRP1-like member of the ABC family of membrane transport proteins), which facilitates accumulation of GSH and enhance resistance of A375 cells against cytotoxic agents. Selective Bcl-2 and GSH depletion in A375 cells in vivo was achieved by G3139- and verapamil (an MRP1 activator)-induced acceleration of GSH efflux, in combination with acivicin-induced inhibition of γ-glutamyl transpeptidase (which limits GSH synthesis by preventing cysteine generation from extracellular GSH). A375 tumor-bearing mice were also mice fed a L-glutamine-enriched diet (which further promotes depletion of the mitochondrial GSH pool and potentiates the proapoptotic effect of Bcl-2 depletion). This strategy sensitized A375 cells to combined chemotherapy (abraxane + daunorubicin) and tumor-focused radiotherapy (X rays). Albumin-bound paclitaxel (ABP) + daunorubicin (DNR) were selected as the best after screening A375 cells in vitro against most drugs used regularly against human melanoma cells (also including vincristine, vindesine, vinblastine, bleomycin, methotrexate, arsenate, cisplatin, carmustine, paclitaxel, dacarbazine, and temozolomide). Chemotherapy alone was almost useless (≈12% inhibition), whereas combined ABP + DNR and X rays only induced a minor regression (≈33% inhibition) of A375 xenograft growth. However, our full experimental therapy (G3139+ABP+DNR+X rays+diet) led to regression of tumors to non-detectable levels in mice bearing A375 melanoma xenografts." @default.
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- W2280242427 date "2007-11-01" @default.
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- W2280242427 title "Bcl-2 antisense oligodeoxynuleotides- and GSH depletion-induced sensitization to chemoradiotherapy lead to complete regression of A375 melanoma xenogratfs" @default.
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