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1.
Arch Razi Inst ; 77(1): 229-234, 2022 02.
Artigo em Inglês | MEDLINE | ID: mdl-35891746

RESUMO

Endometrial hyperplasia is defined as a common clinical disorder caused by the increased levels of estrogens with low levels of progesterone; therefore, this hormonal imbalance leads to an increase in the proliferation rate of the endometrial cells. Endometrial carcinoma is one of the most important malignancies affecting women all over the world "accounting for 37.7% of all other disorders affecting the female reproductive system". The expression of the Ki-67 protein is related to the proliferative behavior of malignant tumor cell populations of their own, allowing it to be used as a marker of tumor aggressiveness. The present study was conducted to examine the expression of the proliferation marker, Ki-67 in various endometrial lesions. Ki-67 expression was evaluated in 60 endometrial samples that resulted as either endometrial curetting or hysterectomy specimens, diagnosed with simple hyperplasia (n=10), complex hyperplasia (n=20), atypical hyperplasia (n=6), and endometrial carcinoma (n=24). In patients with endometrial carcinoma, there was an increased expression of Ki-67, compared to proliferative endometrium and simple hyperplasia (P-value=0.0001). There was no such discrepancy between atypical hyperplasia and endometrial carcinoma cases. The expression of Ki-67 showed a positive association with the degree of endometrial cancer (P-value=0.0013), however, not with the age of the patients (P-value>0.05). There is a wide range of variations in the proliferation rate within the development of different endometrial lesions, including benign and malignant lesions. Our findings may be of value in differential diagnosis and prognosis of endometrial hyperplasia and endometrial carcinoma.


Assuntos
Hiperplasia Endometrial , Neoplasias do Endométrio , Antígeno Ki-67 , Hiperplasia Endometrial/diagnóstico , Hiperplasia Endometrial/metabolismo , Neoplasias do Endométrio/diagnóstico , Neoplasias do Endométrio/metabolismo , Neoplasias do Endométrio/patologia , Endométrio/metabolismo , Endométrio/patologia , Feminino , Humanos , Hiperplasia/metabolismo , Hiperplasia/patologia , Antígeno Ki-67/metabolismo
2.
Arch Razi Inst ; 76(6): 1639-1643, 2021 12.
Artigo em Inglês | MEDLINE | ID: mdl-35546982

RESUMO

Inflammatory bowel disease (ulcerative colitis and Crohn's disease) is a remitting and relapsing disease that affects millions of people worldwide. In the intestine, homeostasis between repair and signaling of the proinflammatory of the immune system is needful for the upkeep of intestinal balance. The recent evidence has highlighted the dysfunction of the immune system, particularly toll-like receptors (TLRs)-mediated immune system dysfunction, in the ulcerative colitis pathogenesis. The main objective of the current study was to analyze the expression level of TLR5 at the mRNA in ulcerative colitis patients and investigate the impacts of the TLR5 gene as genetic factors that contribute to the development of ulcerative colitis. The paraffin-embedded blocks were retrospectively collected from 25 patients diagnosed with ulcerative colitis and 25 cases with normal colonic tissue. The quantitative real-time polymerase chain reaction method was employed for the estimation of TLR5at the mRNA level. The analysis of the data of TLR5 gene expression revealed that the expression of this gene is downregulated in ulcerative colitis cases, as compared to that in normal colonic tissue. As evidenced by the results of this study, TLR5 may play a role in the development of ulcerative colitis; therefore, it should be introduced in the management of ulcerative colitis.


Assuntos
Colite Ulcerativa , Receptor 5 Toll-Like , Colite Ulcerativa/genética , Colite Ulcerativa/patologia , Humanos , RNA Mensageiro , Estudos Retrospectivos , Receptor 5 Toll-Like/genética
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