Somatic Mutations in Prostate Cancer: Closer to Personalized Medicine
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REVIEW ARTICLE
Somatic Mutations in Prostate Cancer: Closer to Personalized Medicine M. J. Alvarez-Cubero1,2 • L. J. Martinez-Gonzalez2 • I. Robles-Fernandez2 J. Martinez-Herrera2 • G. Garcia-Rodriguez2 • M. Pascual-Geler3 • J. M. Cozar3 • J. A. Lorente1,2
•
Ó Springer International Publishing Switzerland 2016
Abstract The molecular cause of prostate cancer (PCa) is still unclear; however, its progression involves androgen, PI3K/Akt, and PTEN signaling, as cycle and apoptotic pathways. Alterations in oncogenes and tumor suppressor genes as PIK3CA, BRAF, KRAS and TP53 are not very common. Recently, somatic mutations have been discovered in relation to cancer progression mainly in genes such as PIK3CA; however, little data has been described in PCa. Nowadays genetic tools allow us to investigate multiple details about the biological heterogeneity of PCa, to better understand the mechanisms of disease progression and treatment resistance. Therefore, if the most relevant somatic mutations were included during screening, we could identify the best treatment for the right patient, bringing us closer to personalized medicine. The main objective of this article is to provide a review of the principal somatic mutations that appear to have a relevant role in hormonal cancers, like prostate cancer.
Key Points This review covers the principal somatic mutations that may have an important role in PCa. Somatic mutations in androgen, PI3K/Akt, and PTEN signaling, like cycle and apoptotic pathways, can provide biomarkers useful for the prognosis and some treatment strategies in PCa.
1 Introduction A high percentage of PCa is considered sporadic, while a minority of cases are considered familial and hereditary PCa [1]. Sporadic PCa is caused mainly by somatic mutations, that, according to the NCI dictionary of cancer terms, are ‘‘alterations in DNA that occurs after conception
& M. J. Alvarez-Cubero [email protected] & L. J. Martinez-Gonzalez [email protected] I. Robles-Fernandez [email protected]
J. A. Lorente [email protected] 1
Laboratory of Genetic Identification, Legal Medicine and Toxicology Department, Faculty of Medicine, Universidad de Granada, Granada, Spain
2
GENYO (Pfizer-University of Granada-Andalusian Government Centre for Genomics and Oncological Research), P. T. Ciencias de la Salud. Avda. de la Ilustracio´n 114, 18007 Granada, Spain
3
Urology Department, University Hospital Virgen de las Nieves, Granada, Spain
J. Martinez-Herrera [email protected] G. Garcia-Rodriguez [email protected] M. Pascual-Geler [email protected] J. M. Cozar [email protected]
M. J. Alvarez-Cubero et al.
and it can occur in any of the cells of the body except the germ cells (sperm and egg) and therefore are not passed on to children’’. In the context of somatic mutation, the difference between hereditary and familial is that the familial PCa may be due to germline mutations (they are hereditary) and/or to somatic mutations caused by shared environmental and lifestyle factors by family
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