Pallis M, Grundy M, Turzanski J, Kofler R, Russell N: Mitochondrial membrane sensitivity to depolarization in acute myeloblastic leukemia is associated with spontaneous in vitro apoptosis, wild-type TP53, and vicinal thiol/disulfide status. Blood 2001, 98:405?13. 53. Fulda S, Debatin KM: Extrinsic versus intrinsic apoptosis pathways in anticancer chemotherapy. Oncogene 2006, 25:4798?11.doi:10.1186/1472-6882-13-230 Cite this article as: Saha et al.: Calcarea carbonica induces apoptosis in cancer cells in p53-dependent manner through an immuno-modulatory circuit. BMC Complementary and Alternative Medicine 2013 13:230.Submit your subsequent manuscript to BioMed Central and take full benefit of:?Hassle-free on the web submission ?Thorough peer assessment ?No space constraints or color figure charges ?Immediate publication on acceptance ?Inclusion in PubMed, CAS, Scopus and Google Scholar ?Study that is freely obtainable for redistributionSubmit your manuscript at biomedcentral/submit
Regardless of significant advances in early diagnosis and also the development of molecularly targeted drugs, cancer remains the top result in of mortality in the Western world (1). Chemoprevention applying pharmaceuticals or by dietary intervention represents a well-Corresponding Author: Gary A. Piazza, Ph.D., Chief of Drug Discovery, Professor of Oncologic Sciences and Pharmacology, Abraham A. Mitchell Distinguished Investigator, Mitchell Cancer Institute, University of South Alabama 1660 Springhill Avenue, Suite 3029, Mobile AL 36604, 251-445-8412, [email protected]. Disclosure of Possible Conflicts of Interest: The authors have no disclosures.4-Bromo-1,2,3,5,6,7-hexahydro-s-indacene structure Author Contributions: Conception and Style: E.Price of 175281-76-2 G., W.E.G., G.A.P.; Writing, evaluation and/or revision of the manuscript: E.G., W.E.G., G.A.P.; Administrative, Technical and or Material Assistance: E.PMID:24324376 G., W.E.G., G.A.P.; Study Supervision: W.E.G., G.A.P.Gurpinar et al.Pageaccepted method to inhibit illness progression in men and women with precancerous lesions, and in high-risk populations with genetic predispositions or long-term exposure to environmental carcinogens which include cigarette smoke. Even so, the implementation of chemoprevention methods mandates exceptional security and efficacy. Over the past 3 decades, epidemiological, clinical and experimental research have established that nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit carcinogenesis in several tissues and at different stages of progression. Despite the strong proof of activity, the usage of NSAIDs for cancer chemoprevention is just not advised due to the fact of potentially serious gastrointestinal, renal, and cardiovascular side effects that result from cyclooxygenase (COX) inhibition and also the suppression of physiologically vital prostaglandins. Additionally, the chemopreventive efficacy of NSAIDs is incomplete, even though it is actually unclear if this shortfall is resulting from dosage limitations or resistance elements. The molecular and cellular mechanisms accountable for the cancer chemopreventive properties of NSAIDs are complex and probably involve a number of effects on cancer cells and their microenvironment. Inhibition of COX is frequently thought to become the main mechanism responsible for their antineoplastic activity, even though a lot of research have concluded that option targets can be involved, as reviewed previously (2?). Provided that the usage of NSAIDs for cancer chemoprevention is limited by COX-dependent toxicities, identifying the relevant targets that mediate their antitumor propertie.
