The remarkable diversity of malignant processes underlies the difficulty in elucidating pathophysiology of and treatment for cancer. As eloquently outlined by Hanahan and Weinberg, a number of traits are acquired in the transformation from normal cell to neoplastic process, including sustained growth promoting signaling, circumventing apoptosis, immune evasion, and suppression of tumor suppressor genes, among others [1]. These changes may occur via somatic mutations; alternatively, they can arise from epigenetic modification.
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