August 5th, 2008. Evasion of Ribonuclease Inhibitor as a Determinant of Ribonuclease Cytotoxicity
In several instances, these engineered ribonucleases exhibit greater cytotoxicity in vitro than does ONC. Herein, we review the biochemical characteristics of RI ribonuclease complexes and progress towards the development of mammalian ribonuclease-based chemotherapeutics through the elicitation of RI-evasion.
August 5th, 2008. Onconase and Amphinase, the Antitumor Ribonucleases from Rana pipiens Oocytes
Onconase and Amphinase are highly cationic molecules and their preferential toxicity towards cancer cells (having distinctly higher negative charge compared to normal cells) may depend on increased binding efficiency to the cell surface by electrostatic interactions. Here we will discuss the structures of Onconase and Amphinase and the molecular basis for their enzymatic and anticancer functions.
August 5th, 2008. Antibody-onconase conjugates: cytotoxicity and intracellular routing
Antibody-onconase conjugates are effective in preclinical models, cause little non-specific toxicities in mice and have favorable formulation properties. Understanding the reason for their potency coupled with understanding novel RNA-based mechanisms of tumor cell death will lead to improved variations of targeted onconase.
August 5th, 2008. Antibody-targeted RNase fusion proteins (immunoRNases) for cancer therapy
Conjugation of RNases to internalizing tumor-targeting monoclonal antibodies was shown to enhance specific cell killing by several orders of magnitude both in vitro and in animal models. In this review we describe the development and current status of genetically engineered 2(nd) generation immunoRNases as promising novel anti-cancer therapeutics.
July 9th, 2008. A novel combination: ranpirnase and rosiglitazone induce a synergistic apoptotic effect by down-regulating Fra-1 and Survivin in cancer cells
The drug combination does not have a synergistic effect on killing in Fra-1 knockdown cells, showing that Fra-1 modulation accounts in part for the synergism. The novel drug combination of ranpirnase and rosiglitazone is a promising combination to treat cancers with increased PI3K-dependent Fra-1 expression or Survivin.
June 4th, 2008. Ranpirnase as a potential antitumor ribonuclease treatment for mesothelioma and other malignancies
Most clinical studies have been conducted in patients with malignant mesothelioma, and a confirmatory Phase IIIb trial is currently underway for the treatment of this disease. Owing to its selective destruction of malignant cells and favorable toxicology profile, ranpirnase is a promising antitumor agent with ideal attributes that are generally lacking in conventional cytotoxic drugs.
Conclusion: In animal studies, improvements in tumour physiology (i.e., increased blood flow, inhibited oxygen consumption, increased oxygenation and decreased tumour hypertension) and selectively enhanced radiation responses (i.e., increased radiation sensitivity and inhibited repair of sublethal and potentially lethal damage) were observed after ranpirnase treatment in preclinical tumour models. Ranpirnase is a promising candidate as an enhancer for radiation- and chemotherapy. Ongoing clinical trials promise to further improve the treatment of mesothelioma and lung cancer.
April 30th, 2008. Remarkable enhancement of cytotoxicity of onconase and cepharanthine when used in combination on various tumor cell lines
The mechanism of the observed synergism is unclear but it may be associated with the Onc activity in targeting microRNAs and/or NFkappaB and Cep activity also targeting NFkappaB. The data suggest that the combination of these two drugs, that individually express a low toxic profile, may have strong antitumor potential.
January 25th, 2008. Ribonucleases as novel chemotherapeutics: the ranpirnase example
The basis for its specific toxicity for cancer cells is not known. This review describes the development of ranpirnase as a cancer chemotherapeutic agent.
March 3rd, 2007. Mild hyperthermia predisposes tumor cells to undergo apoptosis upon treatment with onconase
Although at 41 degrees C in absence of ONC the incidence of apoptosis was elevated compared to 37 degrees C the cytotoxicity of ONC was further enhanced and the overall pro-apoptotic effect was above the level of additive effects of ONC plus that of 41 degrees C-hyperthermia. While the mechanism of the observed enhancement of ONC cytotoxicity is currently under investigation, the findings suggest that a combination of ONC and mild hyperthermia should be explored to increase effectiveness of ONC in cancer treatment.
February 28th, 2007. Ranpirnase: amphibian ribonuclease A, P-30 protein-alfacell.
6 423 515 B1) entitled 'Methods of Making Nucleic Acids Encoding Ribonucleases'. This patent is effective until 2020.
March 27th, 2006. Ranpirnase - an antitumour ribonuclease: its potential role in malignant mesothelioma
Standard first-line treatment for MM has recently been established with an antifolate and cisplatin. At present, a Phase III trial of doxorubicin with or without ranpirnase is nearing completion in MM patients without prior chemotherapy or one prior chemotherapy regimen.
November 28th, 2005. Ribonucleases as a Novel Pro-Apoptotic Anticancer Strategy: Review of the Preclinical and Clinical Data for Ranpirnase
Phase II tumor-specific trials investigated the activity of ranpirnase in malignant mesothelioma, breast cancer, non-small cell lung cancer, and renal cell cancer. A Phase III randomized study in malignant mesothelioma patients compares the combination of ranpirnase plus doxorubicin to doxorubicin monotherapy.
Finally, a cooperative effect was observed between small molecule inhibitors of PI3-K and Onconase in the killing of malignant mesothelioma cells. Our results suggest that kinase screening of individual malignant mesotheliomas for endogenous levels of activated PI3-K/AKT may be predictive of the efficacy of Onconase and possibly other chemotherapeutic agents.
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