Publications by authors named "Triada Doulgeraki"

Background: Persistent infection by oncogenic human papillomavirus (HPV) is necessary although not sufficient for development of cervical cancer. Behavioural, environmental, or comorbid exposures may promote or protect against malignant transformation. Randomised evidence is limited and the validity of observational studies describing these associations remains unclear.

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Introduction: Human papillomavirus (HPV) is necessary but not sufficient for cervical cancer development. During cervical carcinogenesis, methylation levels increase across host and HPV DNA. DNA methylation has been proposed as a test to diagnose cervical intraepithelial neoplasia (CIN); we present a protocol to evaluate the accuracy of methylation markers to detect high-grade CIN and cervical cancer.

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Purpose Of Review: Reproductive function is the interplay between environmental factors and the genetic footprint of each individual. The development in genetic analysis has strengthened its role in the investigation of female reproductive disorders, potential treatment options and provision of personalized care. Despite the increasing requirement of genetic testing, the evidence of the gene-disease relationships (GDR) is limited.

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Article Synopsis
  • A study was conducted to investigate the genetic factors associated with cervical cancer and cervical intraepithelial neoplasia (CIN) by comparing women with these conditions to healthy controls using data from the UK Biobank and FinnGen datasets.
  • The researchers performed a genome-wide association study (GWAS) analyzing nearly 9.6 million genetic variants and identified six significant single-nucleotide polymorphisms (SNPs) linked to the diseases, including novel and previously reported genetic loci.
  • The findings highlight the potential hereditary risk factors for cervical cancer, which can help in understanding the disease's etiology and developing prevention strategies.
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Aim: To study whether mismatch repair (MMR) status is related to the expression of programmed cell death-ligand 1 (PD-L1) and CD8 counts in a series of grade 3 endometrial carcinomas.

Materials And Methods: The expression of MMR protein PD-L1 and CD8 cell count were evaluated by immunohistochemistry and related to several clinicopathological parameters.

Results: Among 105 endometrial carcinomas, 40% were of endometrioid and 60% of non-endometrioid histology.

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Purpose: To evaluate mismatch repair (MMR) status in a series of high-grade endometrial carcinomas and correlate it with several clinicopathological characteristics and with survival.

Methods: One hundred and one patients with high-grade endometrial carcinoma, both of endometrioid and of non-endometrioid type were included in the study. The expression of MLH1, MSH2, MSH6 and PMS2 was evaluated by immunohistochemistry.

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Background: To evaluate the expression of programmed cell death-ligand 1 (PD-L1) and CD8 in high-grade endometrial carcinomas and relate it to several clinicopathological parameters.

Methods: One hundred and one (101) patients with high-grade endometrial carcinomas who were completely surgically staged were included in this study. PD-L1 and CD8 + expression was evaluated by immunohistochemistry.

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Aim: To compare distinct clinicopathological features between atypical proliferative serous tumors and non-invasive low-grade ovarian serous carcinomas.

Methods: Our study group comprised 203 cases of serous borderline tumors sub-classified as atypical proliferative serous tumors or as non-invasive low-grade serous carcinomas. All pathological features related to borderline tumors were re-evaluated by two gynecological pathologists.

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Unlabelled: Five days following the 3rd cycle of nivolumab, a monoclonal antibody, which acts as immune checkpoint inhibitor against the programmed cell death protein-1, for metastatic lung adenocarcinoma, a 56-year-old woman presented at the hospital critically ill. On admission, she had severe diabetic ketoacidosis (DKA), as evidenced by venous glucose of 47 mmol/L, blood ketones of 7.5 mmol/L, pH of 6.

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