MODEL OF RISK STRATIFICATION THROUGH EVALUATION OF BLOODY METABOLIC BIOMARKERS AS INDICATORS OF MITOCHONDRIAL DYSFUNCTION GREATER IN PATIENTS WITH THYROID CANCER.
Thyroid World Congress ePoster Library. Vivas López A. 06/20/19; 271994; 196
Dr. Alfredo Vivas López
Dr. Alfredo Vivas López
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Abstract
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INTRODUCTION

Metabolic syndrome is a determining factor in the development of cancer. The mechanisms that connect metabolism and cancer are the suppression of oxidative metabolism and the increase of the glycolytic pathway. A fact poorly studied in the thyroid



MATERIAL AND METHODS

Forty-five patients with thyroid disease who underwent total or partial thyroidectomy (18 carcinomas and 27 hyperplasia) were selected. A histological analysis of the central tissue as well as the periphery was performed. The degree of proliferation by IHC with Ki67, the degree of cell death by TUNEL and the activation of the glycolytic pathways by phosphorylated AKT were evaluated.

For oxidative metabolism, mitochondrial distribution was assessed by IF against TOMM22.



RESULTS

Increased proliferation and apoptosis were observed in the carcinoma samples with respect to those of hyperplasia without reaching statistical significance. The degree of proliferation was found to be significantly greater in the central zone than in the periphery in both carcinomas and hyperplasia.

Greater activation of the glycolytic pathway was observed in carcinomas against hyperplasia.

The assessment of the mitochondrial distribution by staining with TOMM22 showed statistically significant differences for perinuclear distribution and asymmetry, indicating a lower oxidative metabolism in the tumor tissue.



CONCLUSIONS

We can conclude that tumor cells have a higher degree of histological proliferation and higher levels of apoptosis. Probably due to increased metabolic activity.

According to the distribution of the phosphorylated AKT in the tumor cells, we conclude that these present a greater activation of AKT and therefore of the glycolytic pathway.



 


INTRODUCTION

Metabolic syndrome is a determining factor in the development of cancer. The mechanisms that connect metabolism and cancer are the suppression of oxidative metabolism and the increase of the glycolytic pathway. A fact poorly studied in the thyroid



MATERIAL AND METHODS

Forty-five patients with thyroid disease who underwent total or partial thyroidectomy (18 carcinomas and 27 hyperplasia) were selected. A histological analysis of the central tissue as well as the periphery was performed. The degree of proliferation by IHC with Ki67, the degree of cell death by TUNEL and the activation of the glycolytic pathways by phosphorylated AKT were evaluated.

For oxidative metabolism, mitochondrial distribution was assessed by IF against TOMM22.



RESULTS

Increased proliferation and apoptosis were observed in the carcinoma samples with respect to those of hyperplasia without reaching statistical significance. The degree of proliferation was found to be significantly greater in the central zone than in the periphery in both carcinomas and hyperplasia.

Greater activation of the glycolytic pathway was observed in carcinomas against hyperplasia.

The assessment of the mitochondrial distribution by staining with TOMM22 showed statistically significant differences for perinuclear distribution and asymmetry, indicating a lower oxidative metabolism in the tumor tissue.



CONCLUSIONS

We can conclude that tumor cells have a higher degree of histological proliferation and higher levels of apoptosis. Probably due to increased metabolic activity.

According to the distribution of the phosphorylated AKT in the tumor cells, we conclude that these present a greater activation of AKT and therefore of the glycolytic pathway.



 


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