ABSTRACT
The different pathologies of the prostate, involve the presence of a new microenvironment where inflammatory cells are actively recruited. This research explores the presence of mast cells and eosinophils associated with age and the evaluation of prostate cancer progress (Gleason Index). Forty two biopsies of anonymized patients, with confirmed prostate cancer, were used for histological analysis for eosinophils and mast cells and subsequent determination of Gleason index according to age. The results of the histological analyzes show the presence of eosinophils and mast cells in prostate biopsies with confirmed cancer. In the multiple correlation studies, a high correlation was observed between the presence of lymphocytes and the age of the patient diagnosed with prostate cancer, same correlation was observed between the patient's age and higher Gleason Index (Pearson and Spearman p< 0.05). It is concluded that in prostate biopsies from Chilean patients with confirmed cancer, eosinophilia and tissue mastocytosis were observed. Correlation analyzes show a direct correlation between older patients, higher Gleason index and presence of mast cell. Regarding eosinophilia, only a correlation between age and Gleason index was observed Further studies are suggested to determine that the presence of eosinophils and mast cells can be used as early bioindicators of prostate cancer.
Las diferentes patologías de próstata, involucran la presencia de un nuevo microambiente donde las células inflamatorias son activamente reclutadas. La presente investigación explora la presencia de mastocitos y eosinófilos asociadas a la edad y la evaluación del progreso del cáncer de próstata según índice de Gleason. Cuarenta y dos biopsias de pacientes anonimizados, con cáncer prostático confirmados, fueron utilizadas para su análisis histológico para eosinófilos y mastocitos y posterior determinación del índice de Gleason según edad. Los resultados de los análisis histológicos, muestran la presencia de eosinófilos y mastocitos en biopsias de próstata con cáncer confirmado. En los estudios de correlación múltiple, se observó una alta correlación entre la presencia de linfocitos, mastocitos y la edad del paciente diagnosticado con cáncer prostático, igual correlación se observó entre la edad del paciente y mayor índice de Gleason (Pearson y Spearman p<0,05). Se concluyó que en las biopsias de próstata de pacientes chilenos con cáncer confirmado, se observó eosinofilia y mastocitosis tisular. Los análisis de correlación muestran una correlación directa entre pacientes de mayor edad, índice de Gleason más alto y la presencia de mastocitos. Con respecto a la eosinofilia, solo se observó una correlación entre la edad y el índice de Gleason. Se sugieren estudios adicionales para determinar que la presencia de eosinófilos y mastocitos puede usarse como bioindicadores tempranos del cáncer de próstata.
Subject(s)
Humans , Male , Prostatic Neoplasms/pathology , Prostate/pathology , Prostatic Neoplasms/diagnosis , Biopsy , Mastocytosis/pathology , Biomarkers, Tumor/analysis , Chile , Age Factors , Eosinophilia/pathology , Early Detection of Cancer , Neoplasm GradingABSTRACT
Classical protein kinase C (cPKC) enzymes are ser/thr protein kinases that have been an important factor in regulating a variety of cellular functions required for both in terms of health and disease. Therefore, precise control of cPKC-mediated signal is necessary for cellular homeostasis; however, their dysregulation leads to the development of several pathophysiological conditions including cancer. In cellular microenvironment, cPKC-mediated signaling is accompanied by multiple molecular mechanisms including phosphorylation, second messenger binding, and scaffold proteins. Functional cPKC interacts with a number of cellular proteins involved in the regulation of multiple biological functions such as cell growth, survival, migration, and adhesion. Further, the role of cPKC varies from cell to cell, substrate to substrate and, therefore, it is plausible to assume that the dysregulation of cPKC activity causes cellular transformation. Currently, there is no sufficient literature available to provide better understating to develop an effective therapeutic regimen to reverse pathophysiological condition caused by functionally dysregulated cPKC. Therefore, in the present review, we have focused on to provide a better and detail information on the various aspects of cPKC such as structure, mode of activation, regulation, and distinct cellular functions useful for the development of an effective therapeutic regimen against the breast cancer.
Subject(s)
Breast Neoplasms/enzymology , Protein Kinase C/metabolism , Female , HumansABSTRACT
Amyotrophic Lateral Sclerosis (ALS) is a paradigmatic neurodegenerative disease, characterized by progressive paralysis of skeletal muscles associated with motor neuron degeneration. It is well-established that glial cells play a key role in ALS pathogenesis. In transgenic rodent models for familial ALS reactive astrocytes, microglia and oligodendrocyte precursors accumulate in the degenerating spinal cord and appear to contribute to primary motor neuron death through a non-cell autonomous pathogenic mechanism. Furthermore in rats expressing the ALS-linked SOD1G93A mutation, rapid spread of paralysis coincides with emergence of neurotoxic and proliferating aberrant glia cells with an astrocyte-like phenotype (AbA cells) that are found surrounding damaged motor neurons. AbAs simultaneously express astrocytic markers GFAP, S100ß and Connexin-43 along with microglial markers Iba-1, CD11b and CD163. Studies with cell cultures have shown that AbAs originate from inflammatory microglial cells that undergo phenotypic transition. Because AbAs appear only after paralysis onset and exponentially increase in parallel with disease progression, they appear to actively contribute to ALS progression. While several reviews have been published on the pathogenic role of glial cells in ALS, this review focuses on emergence and pro-inflammatory activity of AbAs as part of an increasingly complex neurodegenerative microenvironment during ALS disease development.