Ily require local administration [83], although this is controversial since it has only been demonstrated in mice. Dosage could begin based on the standard protocol for superficial basal cell carcinoma of 5 times per week on a 25 cm2 area of skin. Monitoring of therapy would most likely involve ex vivo analysis of cytokine production, as well as in more advanced clinical research settings tetramer analysis for BCR-ABL specific T cells. A potential concern for clinical implementation of AldaraTM treatment for CML may be the possibility of activation of immunity that targets not only hematopoietic stem cells of leukemic origin, but also non-leukemic hematopoietic stem cells. Indeed the graft versus leukemia effect observed after donor lymphocyte infusions is correlated with a period of aplasia in which normal hematopoietic stem cells are also targeted [107]. This is in agreement PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/27488460 with other studies of immune stimulation to cancer antigens in which autoimmunity arises as an unintended adverse event [108]. Given that AldaraTM treatment as used clinically today is not associated with induction autoimmunity towards hematological targets, the authors do not anticipate this to be a major concern, however the experimental use of AldaraTM in CML patients will need to be monitored by hematological assessment to ensure that
Journal of Translational MedicineResearchBioMed CentralOpen AccessDiagnosis of drug-induced renal tubular toxicity using global gene expression profilesYing Jiang*1, David L Gerhold1, Daniel J Holder2, David J Figueroa1, Wendy J Bailey1, Ping Guan1, Thomas R Skopek1, Frank D Sistare1 and Joseph F SinaAddress: 1Safety Assessment, Merck Research Laboratories, Merck Co., Inc, 770 Sumneytown Pike, West Point, PA 19486, USA and 2Biometric Research, Merck Research Laboratories, Merck Co., Inc, 770 Sumneytown Pike, West Point, PA 19486, USA Email: Ying Jiang* – [email protected]; David L Gerhold – [email protected]; Daniel J Holder – [email protected]; David J Figueroa – [email protected]; Wendy J Bailey – [email protected]; Ping Guan – [email protected]; Thomas R Skopek – [email protected]; Frank D Sistare – [email protected]; Joseph F Sina – [email protected] * Corresponding authorPublished: 1 October 2007 Journal of Translational Medicine 2007, 5:47 doi:10.1186/1479-5876-5-Received: 10 July 2007 Accepted: 1 OctoberThis article is available from: http://www.translational-medicine.com/content/5/1/47 ?2007 Jiang et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, Mangafodipir (trisodium)MedChemExpress Mangafodipir (trisodium) provided the original work is properly cited.AbstractToxicogenomics can measure the expression of thousands of genes to identify changes associated with drug induced toxicities. It is expected that toxicogenomics can be an alternative or complementary approach in preclinical drug safety evaluation to identify or predict drug induced toxicities. One of the major concerns in applying toxicogenomics to diagnose or predict drug induced organ toxicity, is how generalizable the statistical classification model is when derived from small datasets? Here we presented that a diagnosis of kidney proximal tubule toxicity, measured by pathology, can successfully be achieved even with a study design of limited number of training studies or.
