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A new era in blood and lymphatic cancer biology and therapy

Authors Dingli D

Published 8 March 2011 Volume 2011:1 Pages 1—3


Review by Single anonymous peer review

Peer reviewer comments 5

David Dingli
Division of Hematology and Department of Internal Medicine, Mayo Clinic, Rochester, MN, USA

Tumors derived from the transformation of hematopoietic or lymphoid cells are increasing in incidence1 and with improvements in therapy, their prevalence is also growing. The increasing availability of more sophisticated molecular tools is refining the definition of these diseases2 and now more than ever, we are on the verge of ‘personalized medicine’. No disease is as personal as cancer. The current view of tumorigenesis is that somatic cells serially acquire mutations that lead to the malignant phenotype,3,4 a state characterized by loss of cell cycle regulation, resistance to apoptosis, unbridled cellular proliferation, angiogenesis, evasion of the immune response, and ultimately, invasion of other tissues.5,6 Although many somatic mutations probably do not provide a reproductive advantage to cells or can even be deleterious, some mutations enhance the reproductive fitness of the cell enabling it to expand into a clone where additional mutations may lead to the full malignant phenotype. Given that evolution is the result of reproduction, mutation and selection, cancer is a natural consequence, especially in large multicellular organisms that can live for many years.7 Exposure to genotoxic agents (chemicals, viruses, radiation) or the response to chronic injury increases the risk of transformation since at some level, the risk is related to the number of cells that are dividing and how often they divide. It is not yet clear how many mutations are required to lead to the cancer phenotype but perhaps with very few exceptions, one mutation is not enough to lead to neoplastic transformation and disease.

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