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A new era in blood and lymphatic cancer biology and therapy

DOI: http://dx.doi.org/10.2147/BLCTT.S16965

Keywords: A new era in blood and lymphatic cancer biology and therapy Editorial (2518) Total Article Views Authors: David Dingli Published Date March 2011 Volume 2011:1 Pages 1 - 3 DOI: http://dx.doi.org/10.2147/BLCTT.S16965 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 incre

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A new era in blood and lymphatic cancer biology and therapy Editorial (2518) Total Article Views Authors: David Dingli Published Date March 2011 Volume 2011:1 Pages 1 - 3 DOI: http://dx.doi.org/10.2147/BLCTT.S16965 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. Post to: Cannotea Citeulike Del.icio.us Facebook LinkedIn Twitter Readers of this article also read: Bone resorption in incompletely impacted mandibular third molars and acute pericoronitis Epigenomics in cancer management Evaluation of in-vitro antibiotic susceptibility of different morphological forms of Borrelia burgdorferi Intercellular cancer collisions generate an ejected crystal comet tail effect with fractal interface embryoid body reassembly transformation Radio electric asymmetric brain stimulation in the treatment of behavioral and psychiatric symptoms in Alzheimer disease Advances in the diagnosis and management of lymphoma Emerging treatment approaches in acute lymphoblastic and acute myeloid leukemias Integrative systems of genomic risk markers for cancer and other diseases: future of predictive medicine Peripheral T cell lymphoma: clinical utility of romidepsin Topical azithromycin or ofloxacin for endophthalmitis

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