Objective: To analyze the p53, PKD1, and MAP2K4 expressions in serum of patients with endometrial carcinoma (EC) and their prognostic value.
Methods: A total of 84 patients with EC who were treated in our hospital between January 2018 and January 2020 were enrolled into a research group. There were 50 healthy individuals over the same time who were included in a control group for a retrospective analysis. qRT-PCR was used for quantifying the relative levels of p53, PKD1, and MAP2K4 in the serum of the control group and the research groups (in both cancer and paracancerous tissues). The associations of p53, PKD1, and MAP2K4 with pathological features of EC were analyzed. Patients were followed up for 1 year to observe their death and analyze the associations of p53, PKD1, and MAP2K4 with prognosis of EC.
Results: The patients with EC had low p53 and MAP2K4 levels and high PKD1 levels (P<0.05). The p53, MAP2K4, and PKD1 levels in serum were relevant to EC differentiation, FIGO stage, lymph node metastasis, and deep myometrial invasion (P<0.05). During the follow-up of prognosis, the serum levels of p53 and MAP2K4 in dead patients were lower than those in surviving patients. PKD1 in former patients was higher (P<0.05).
Conclusion: The low expressions of p53 and MAP2K4 and high expression of PKD1 in EC cases were related with disease progression. These expressions can help effectively evaluate the prognosis and survival of patients. They are of crucial research and reference significance for future diagnosis and therapy.
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Biomolecules
September 2024
Department of Internal Medicine, Mayo Clinic, Rochester, MN 55905, USA.
Autosomal dominant polycystic kidney disease (ADPKD) is a predominant genetic disease, which is caused by mutations in PKD genes and is associated with DNA damage in cystic cells. The intrinsic stimulator of interferon genes (STING) pathway is crucial for recognizing damaged DNA in the cytosol, triggering the expression of inflammatory cytokines to activate defense mechanisms. However, the precise roles and mechanisms of STING in ADPKD remain elusive.
View Article and Find Full Text PDFHum Mol Genet
January 2023
Department of Internal Medicine, Mayo Clinic, Rochester, MN 55905, USA.
Am J Transl Res
July 2022
Gynecology Department Ward2, Cangzhou Central Hospital Cangzhou 061000, Hebei Province, P. R. China.
Objective: To analyze the p53, PKD1, and MAP2K4 expressions in serum of patients with endometrial carcinoma (EC) and their prognostic value.
Methods: A total of 84 patients with EC who were treated in our hospital between January 2018 and January 2020 were enrolled into a research group. There were 50 healthy individuals over the same time who were included in a control group for a retrospective analysis.
J Cell Mol Med
October 2021
Division of Nephrology, Kidney Institute of People's Liberation Army (PLA), Changzheng Hospital, Second Military Medical University, Shanghai, China.
Autosomal-dominant polycystic kidney disease (ADPKD) is characterized by uncontrolled renal cyst formation, and few treatment options are available. There are many parallels between ADPKD and clear-cell renal cell carcinoma (ccRCC); however, few studies have addressed the mechanisms linking them. In this study, we aimed to investigate their convergences and divergences based on bioinformatics and explore the potential of compounds commonly used in cancer research to be repurposed for ADPKD.
View Article and Find Full Text PDFCells
March 2021
Centre for Transplant and Renal Research, Westmead Institute for Medical Research, The University of Sydney, Westmead, NSW 2145, Australia.
The DNA damage response (DDR) pathway is upregulated in autosomal dominant polycystic kidney disease (ADPKD) but its functional role is not known. The ataxia-telangiectasia mutated (ATM) and AT and Rad3-related (ATR) protein kinases are key proximal transducers of the DDR. This study hypothesized that reducing either ATM or ATR attenuates kidney cyst formation and growth in experimental ADPKD.
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