A new era in blood and lymphatic cancer biology and therapy

David DingliDivision of Hematology and Department of Internal Medicine, Mayo Clinic, Rochester, MN, USATumors 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 availabilit...

Descripción completa

Guardado en:

Detalles Bibliográficos
Autor principal:	David Dingli
Formato:	article
Lenguaje:	EN
Publicado:	Dove Medical Press 2011
Materias:	Diseases of the blood and blood-forming organs RC633-647.5
Acceso en línea:	https://doaj.org/article/5e50a58f82d344c4a927cbc79ab987b4
Etiquetas:	Agregar Etiqueta Sin Etiquetas, Sea el primero en etiquetar este registro!

id	oai:doaj.org-article:5e50a58f82d344c4a927cbc79ab987b4
record_format	dspace
spelling	oai:doaj.org-article:5e50a58f82d344c4a927cbc79ab987b42021-12-02T01:15:53ZA new era in blood and lymphatic cancer biology and therapy1179-9889https://doaj.org/article/5e50a58f82d344c4a927cbc79ab987b42011-03-01T00:00:00Zhttp://www.dovepress.com/a-new-era-in-blood-and-lymphatic-cancer-biology-and-therapy-a6593https://doaj.org/toc/1179-9889David DingliDivision of Hematology and Department of Internal Medicine, Mayo Clinic, Rochester, MN, USATumors 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 &lsquo;personalized medicine&rsquo;. 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.David DingliDove Medical PressarticleDiseases of the blood and blood-forming organsRC633-647.5ENBlood and Lymphatic Cancer: Targets and Therapy, Vol 2011, Iss default, Pp 1-3 (2011)
institution	DOAJ
collection	DOAJ
language	EN
topic	Diseases of the blood and blood-forming organs RC633-647.5
spellingShingle	Diseases of the blood and blood-forming organs RC633-647.5 David Dingli A new era in blood and lymphatic cancer biology and therapy
description	David DingliDivision of Hematology and Department of Internal Medicine, Mayo Clinic, Rochester, MN, USATumors 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 &lsquo;personalized medicine&rsquo;. 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.
format	article
author	David Dingli
author_facet	David Dingli
author_sort	David Dingli
title	A new era in blood and lymphatic cancer biology and therapy
title_short	A new era in blood and lymphatic cancer biology and therapy
title_full	A new era in blood and lymphatic cancer biology and therapy
title_fullStr	A new era in blood and lymphatic cancer biology and therapy
title_full_unstemmed	A new era in blood and lymphatic cancer biology and therapy
title_sort	new era in blood and lymphatic cancer biology and therapy
publisher	Dove Medical Press
publishDate	2011
url	https://doaj.org/article/5e50a58f82d344c4a927cbc79ab987b4
work_keys_str_mv	AT daviddingli anewerainbloodandlymphaticcancerbiologyandtherapy AT daviddingli newerainbloodandlymphaticcancerbiologyandtherapy
_version_	1718403201307246592

A new era in blood and lymphatic cancer biology and therapy

Ejemplares similares