RESUMEN
In the present review article a global approach regarding the usefulness of genomic microarrays in prostate cancer management, is attempted. Cancer is a multistep process of mutations in key regulatory genes and epigenetic alterations that result in loss of balanced gene expression. A complete knowledge of the interaction between the genetic variability of the neoformation (tumor profiling) and the genetic variability of the host (inherited genome profiling), will be able to determine the better strategy against the cancer and the less toxicity for the patient. Alterations in the sequence of the hormone binding domain of the androgen receptor as well as mutations in some genes, determine radioresistance and resistance or sensitivity to some chemotherapeutic drugs. New therapies using monoclonal antibodies directed against specific extracellular binding domains of some receptors are based on molecular alterations observed in tumors.
Asunto(s)
Perfilación de la Expresión Génica , Genoma Humano , Biología Molecular/métodos , Análisis de Secuencia por Matrices de Oligonucleótidos , Neoplasias de la Próstata/genética , Anticuerpos Monoclonales/uso terapéutico , Humanos , Masculino , Mutación , Neoplasias de la Próstata/metabolismo , Receptores Androgénicos/química , Receptores Androgénicos/genética , Receptores Androgénicos/metabolismoRESUMEN
The present review article regarding the kinin system-bradykinin is dealing with the biological effects of the abovementioned entity mediated by specific B1 and B2 receptors as well as with its clinical implications known nowadays. The activation of the kinin system-bradykinin is particularly important in blood pressure regulation and in inflammatory reactions, through bradykinin ability to elevate vascular permeability and to cause vasodilatation in some arteries and veins. Recent data on bradykinin formation and release, synergy with ligands, receptors for bradykinin as well as on bradykinin participation in the mitogenesis process, are given in detail. Therapeutic potentials and future applications in many clinical situations including respiratory allergic reactions, septic shock, hypertension and its treatment, hypotensive transfusion reactions, heart diseases, pancreatitis, hereditary and acquired angioedema, Alzheimer disease and liver cirrhosis with ascites, are discussed in brief. Its role as a neuromediator, regulator of several vascular and renal functions, and its participation in signaling pathways, is also discussed in some detail.
RESUMEN
The intercellular adhesion molecule-1 (ICAM-1) is a member of the immunoglobulin gene superfamily of adhesion molecules expressed in multiple human tissues and participating in various physiologic and pathophysiologic processes of the human body. The alterations in the expression of ICAM-1 in the various types of the cancer of the head and neck are discussed in this mini-review following the existing status from the current literature. Possible applications of this developing knowledge in the diagnosis and prognosis of head and neck cancer are briefly mentioned.
Asunto(s)
Neoplasias de Cabeza y Cuello/metabolismo , Molécula 1 de Adhesión Intercelular/metabolismo , Animales , HumanosRESUMEN
p53 is the main intrinsic factor inducing apoptosis by recognizing the external stimuli and activating the p53 responsive genes to an irreversible series of events. P53 activates the transcription of specific proapoptotic genes called p53 target genes. A growing number of p53 responsive genes have been identified and numerous studies have demonstrated that p53 proapoptotic factors such as Noxa, Puma and Perp play cell type specific roles in p53's mediated response to certain stimuli. Perp (p53 apoptosis effector related to PMP-22) is a direct proapoptotic target gene encoding a tetraspan protein. Perp is highly expressed in cells undergoing apoptosis compared to cells under G1 arrest and its overexpression is sufficient to cause cell death in fibroblasts. Noxa is another member of the preapoptotic p53 genes family. When expressed Noxa acts in a BH3 motif-dependent localization to mitochondria, causing structural changes, activation of caspase 9 and release of cytochrome c from mitochondria to cytosol. Puma (p53 mutant of apoptosis) is another critical mediator of p53-dependent apoptosis. P53 binds to Puma-promoter gene sites, leading to puma production. The mtCLIC, a member of intracellular chloride channels, is a cytoplasmic and mitochondrial protein positively regulated by p53. Caspase 10 is induced in p53-dependent manner leading to cellular apoptosis. Other newly announced factors are also involved in p53-regulated apoptosis such as brain-specific angiogenesis inhibitor-1 (BSAI1), MSOD and GPX genes. A global discussion on this topic is attempted in the present review article.
RESUMEN
In this review article adjuvant and neoadjuvant therapies in patients at high risk for localized prostate cancer are presented in some detail. Adjuvant hormone therapy by antiandrogens as well as antineoplastic chemotherapeutic agents such as estramustine and taxanes are referred. Neoadjuvant therapies in addition to systemic therapy before or after local treatment for prostate cancer may improve the outcome of high risk patients otherwise destined to treatment fail. Data regarding some substances used in neoadjuvant therapies such as androgen deprivation therapy and use of rapamycin with its analogs, as well as some novel therapeutic approach strategies are also discussed.