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BIO 300, a Nanosuspension of Genistein, Mitigates Radiation-Induced Erectile Dysfunction and Sensitizes Human Prostate Cancer Xenografts to Radiation Therapy.
Jackson IL, Pavlovic R, Alexander AA, Connors CQ, Newman D, Mahmood J, Eley J, Harvey AJ, Kaytor MD, Vujaskovic Z
(2019) Int J Radiat Oncol Biol Phys 105: 400-409
MeSH Terms: Animals, Blood Pressure, Disease Models, Animal, Drugs, Investigational, Erectile Dysfunction, Fibrosis, Genistein, Male, Mice, Mice, Nude, Nanoparticles, Penile Erection, Penis, Prostate, Radiation Injuries, Experimental, Radiation-Protective Agents, Random Allocation, Rats, Rats, Sprague-Dawley, Regional Blood Flow, Suspensions, Transplantation, Heterologous
Show Abstract · Added March 30, 2020
PURPOSE - To assess whether BIO 300, a synthetic genistein nanosuspension, improves the therapeutic index in prostate cancer treatment by preventing radiation-induced erectile dysfunction (ED) without reducing tumor radiosensitivity.
METHODS AND MATERIALS - Male Sprague-Dawley rats were exposed to 25 Gy of 220-kV prostate-confined x-rays. Animals were randomized to receive sham radiation therapy (RT), RT alone, RT with daily BIO 300 at 2 experimental dosing regimens, or RT with daily genistein. Erectile response was evaluated over time. Penile shaft tissue was harvested for histologic analyses. Murine xenograft studies using prostate cancer cell lines determined the effects of BIO 300 dosing on RT efficacy.
RESULTS - Prostate-confined RT significantly decreased apomorphine-induced erectile response (P < .05 vs sham RT). Erection frequency in animals receiving prophylactic treatment with BIO 300 starting 3 days before RT was similar to sham controls after RT. Treatment with synthetic genistein did not mitigate loss in erectile frequency. At week 14, post-RT treatment with BIO 300 resulted in significantly higher quality of erectile function compared with both the RT arm and the RT arm receiving genistein starting 3 days before irradiation (P < .05). In hormone-sensitive and insensitive prostate tumor-bearing mice, BIO 300 administration did not negatively affect radiation-induced tumor growth delay.
CONCLUSIONS - BIO 300 prevents radiation-induced ED, measured by erection frequency, erectile function, and erection quality, when administered 3 days before RT and continued daily for up to 14 weeks. Data also suggest that BIO 300 administered starting 2 hours after RT mitigates radiation-induced ED. Data provide strong nonclinical evidence to support clinical translation of BIO 300 for mitigation of ED while maintaining treatment response to RT.
Copyright © 2019. Published by Elsevier Inc.
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MeSH Terms
Update on new drugs in small cell lung cancer.
Horn L, Castellanos EL, Johnson DH
(2011) Expert Opin Investig Drugs 20: 441-5
MeSH Terms: Angiogenesis Inhibitors, Antineoplastic Agents, Antineoplastic Combined Chemotherapy Protocols, Clinical Trials as Topic, Drugs, Investigational, Enzyme Inhibitors, Humans, Lung Neoplasms, Nitrogen Mustard Compounds, Organoplatinum Compounds, Small Cell Lung Carcinoma
Show Abstract · Added June 26, 2014
INTRODUCTION - Small cell lung cancer (SCLC) will account for 25,000 to 32,000 new lung cancer cases in the USA in 2010. Current treatmenta pproaches include platinum-based chemotherapy and etoposide with or without radiation therapy depending on stage and performance status. Five-year survival is approximately 25% for patients with limited stage disease and 1 -- 2% for patients with extensive stage disease and has noti mproved in almost two decades.
AREAS COVERED - This article reviews the results of recent clinical trials that have evaluated targeted agents and novel cytotoxic agents alone or in combination with standard chemotherapy in the treatment of patients with SCLC.
EXPERT OPINION - The lack of a targeted approach to the treatment of patients with SCLC has led investigators to evaluate a multitude of agents with overwhelmingly negative results. A more systematic approach to clinical trials in patients is needed to improve outcomes for patients with this disease.
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11 MeSH Terms
Emerging anticancer therapeutic targets and the cardiovascular system: is there cause for concern?
Peng X, Pentassuglia L, Sawyer DB
(2010) Circ Res 106: 1022-34
MeSH Terms: Animals, Antineoplastic Agents, Apoptosis, Cardiovascular Diseases, Cardiovascular System, DNA Repair, Drugs, Investigational, Epigenesis, Genetic, Extracellular Matrix, Focal Adhesions, Humans, Integrins, Molecular Chaperones, Paracrine Communication, Proteasome Endopeptidase Complex, Risk Assessment, Signal Transduction
Show Abstract · Added May 28, 2014
The race for a cure to cancer continues, fueled by unprecedented discoveries of fundamental biology underlying carcinogenesis and tumorigenesis. The expansion of the target list and tools to approach them is moving the oncology community extraordinarily rapidly to clinical trials, bringing new hope for cancer patients. This effort is also propelling biological discoveries in cardiovascular research, because many of the targets being explored in cancer play fundamental roles in the heart and vasculature. The combined efforts of cardiovascular and cancer biologists, along with clinical investigators in these fields, will be needed to understand how to safely exploit these efforts. Here, we discuss a few of the many research foci in oncology where we believe such collaboration will be particularly important.
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Nonantiarrhythmic drug therapy for atrial fibrillation.
Murray KT, Mace LC, Yang Z
(2007) Heart Rhythm 4: S88-90
MeSH Terms: Angiotensin II Type 1 Receptor Blockers, Angiotensin-Converting Enzyme Inhibitors, Animals, Anti-Arrhythmia Agents, Anti-Inflammatory Agents, Antioxidants, Atrial Fibrillation, Calcium Channel Blockers, Connexins, Drugs, Investigational, Fatty Acids, Omega-3, Gap Junctions, Humans, Hydroxymethylglutaryl-CoA Reductase Inhibitors, Mineralocorticoid Receptor Antagonists, Oligopeptides, Oxidative Stress, Receptors, Serotonin, 5-HT4, Renin-Angiotensin System, Serotonin 5-HT4 Receptor Antagonists, Serotonin Antagonists
Show Abstract · Added January 20, 2015
Recent studies have begun to elucidate the molecular mechanisms that promote the generation and progressive nature of atrial fibrillation. Evidence from both experimental and clinical investigations has implicated an important role for the renin-angiotensin-aldosterone system, inflammation, and oxidative stress, with data that suggest a potential beneficial effect for angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, aldosterone receptor antagonists, antiinflammatory agents, 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins), and omega-3 polyunsaturated fatty acids. In addition, compounds that increase gap junctional conductance or that block 5-hydroxytryptamine-4 receptors have also shown promise in the experimental setting. Large-scale, prospective clinical trials will clarify the utility of these new therapeutic approaches to prevent atrial fibrillation in specific clinical settings.
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21 MeSH Terms
Diflomotecan. Ipsen.
Osheroff N
(2004) IDrugs 7: 257-63
MeSH Terms: Animals, Antineoplastic Agents, Camptothecin, Clinical Trials as Topic, DNA Topoisomerases, Type I, Drugs, Investigational, Enzyme Inhibitors, Humans, Neoplasms, Topoisomerase I Inhibitors
Added March 5, 2014
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CMT-3. CollaGenex.
Fingleton B
(2003) Curr Opin Investig Drugs 4: 1460-7
MeSH Terms: Animals, Clinical Trials as Topic, Drugs, Investigational, Enzyme Inhibitors, Humans, Matrix Metalloproteinase Inhibitors, Matrix Metalloproteinases, Neoplasms, Technology, Pharmaceutical, Tetracyclines
Show Abstract · Added March 5, 2014
CMT-3 is an orally active matrix metalloprotease inhibitor, and one of a series of inhibitors of multiple proteases and cytokines, under development by CollaGenex. The compound is currently undergoing phase II trials for the potential treatment of cancer, in particular metastatic cancer and HIV-related Kaposi's sarcoma.
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10 MeSH Terms