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H. Kantarjian, F. Giles, N. Gattermann, K. Bhalla, et al., “Nilotinib (Formerly AMN 107), a Highly Selective bcrabl Tyrosine Kinase Inhibitor, Is Effective in Patient with Philadelphia Chromosome Positive Chronic Myelogenous Leukemia in Chronic Phase Following Resistance and Intolerance to Imatinib,” Blood, Vol. 110, 2007, pp. 3540-3546. doi:10.1182/blood-2007-03-080689

has been cited by the following article:

• TITLE: Cross Skin Reactivity to Tyrosine Kinase Inhibitors in a Patient with Chronic Myelogenous Leukemia

  AUTHORS: V. Broshtilova, M. Balabanova

  KEYWORDS: Cross Toxicity; Lichenoid Drug Reaction; Hyperpigmentation

  JOURNAL NAME: Journal of Cancer Therapy, Vol.4 No.7, August 16, 2013

  ABSTRACT: Tyrosine kinase inhibitors (TKI) targeting the bcr-abl protein, c-kit and the platelet-derived growth factor receptors, are significant part of the pathogenic therapy of chronic myelogenous leukemia. A broad spectrum of cutaneous side effects has been described with the clinical use of imatinib mesylate, ranging from various acute rashes to toxic epidermal necrolysis. Herein, a case of cross skin toxicity to TKI in a patient with chronic myelogenous leukemia is presented. In the course of imatinib mesylate therapy the patient developed a grade 4 diffuse lichenoid drug eruption. Six months after switching to nilotinib, hyperpigmented macules and patches spread over his trunk and extremities. To date, few cases of cross skin reactivity to imatinib and nilotinib have been described, none of which showing different clinical phenotypes. Further understanding of the underlying mechanisms and leading to the development of skin rashes from different class of TKI is important to highlight new drug targets and modify the current therapies to a level of maximal efficacy.