Τίτλος:
Genes’ interactions: A major contributor to the malignant transformation of endometriosis
Γλώσσες Τεκμηρίου:
Αγγλικά
Περίληψη:
The genetic and epigenetic factors that contribute to the malignant transformation of endometriosis are still under investigation. The objective of the present study was to investigate the genetic link between endometriosis and cancer by examining and correlating the latest clinical observations with biological experimental data. We collected updated evidence about the genetic relationship between endometriosis and cancers by conducting a comprehensive search of PubMed and Scopus databases, focusing on the papers published between January 2018 and January 2019. New insights into the mechanism of the malignant transformation of endometriosis have been published recently. The use of state-of-the-art techniques and methods, such as the genome-wide association study analysis and the weighted gene co-expression analysis, have significantly altered our understanding of the association between endometriosis and endometriosis-associated cancer development. Interestingly, the interactions formed between genes seem to play a pivotal role in the phenotypic expression of mutations. Therefore, the effect of single nucleotide polymorphisms and the function of the expression quantitative trait loci on genes’ expression have been the subject of many recent works. In addition, it has been discovered that genes, the mutations of which have been related to the development of endometriosis, play a role as hub genes. This may lead to new areas of research for understanding the mechanism of malignant transformation of the disease. Significant steps forward have been made towards the identification of factors that control the malignant transformation of endometriosis. Still, due to rarity of the event, a better-organized scheme for sampling on a global level should be adopted. © 2019 by the authors. Licensee MDPI, Basel, Switzerland.
Συγγραφείς:
Sapalidis, K.
Machairiotis, N.
Zarogoulidis, P.
Vasilakaki, S.
Sardeli, C.
Koimtzis, G.
Pavlidis, E.
Katsaounis, A.
Giannakidis, D.
Michalopoulos, N.
Mantalobas, S.
Alexandrou, V.
Koulouris, C.
Amaniti, A.
Kesisoglou, I.
Περιοδικό:
International Journal of Molecular Sciences
Λέξεις-κλειδιά:
creatine kinase; estrogen; gelatinase B; heme oxygenase 1; homeobox protein Nkx 2.1; inflammasome; interleukin 18; long untranslated RNA; microRNA; phosphatidylinositol 3,4,5 trisphosphate 3 phosphatase; protein p53; toll like receptor 1; toll like receptor 7; biological marker, carcinogenesis; cell survival; clear cell carcinoma; copy number variation; cystectomy; endometriosis; endometrium cancer; endometrium tumor; epigenetics; epithelial mesenchymal transition; gene expression; gene interaction; gene mutation; genome-wide association study; human; in vitro fertilization; malignant transformation; menstrual cycle; mismatch repair; missense mutation; molecular phylogeny; next generation sequencing; oxidative stress; phenotype; pleiotropy; quantitative trait locus; Review; tumor growth; tumor microenvironment; unfolded protein response; upregulation; uterus myoma; whole exome sequencing; cell transformation; complication; endometriosis; female; genetics; metabolism; ovary tumor; pathology; single nucleotide polymorphism, Biomarkers; Cell Transformation, Neoplastic; Endometriosis; Female; Humans; Ovarian Neoplasms; Polymorphism, Single Nucleotide; Quantitative Trait Loci
DOI:
10.3390/ijms20081842
