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Introduction and objective: E74-like transcription factor 3 (ELF3) is mainly expressed in epithelial tissue, being responsible for differentiation and regeneration. Furthermore, it plays a role in inflammation, remodeling, allergy regulation and apoptosis. Various studies on ELF3 conducted since 1997 have also proved its connection with carcinogenesis and metastasis. This review summarizes recent advances in understanding the role of ELF3 in the following cancers: ampullary, bladder, breast, gastric, hepatocellular, nasopharyngeal, thyroid, lung and ovarian ones. State of knowledge: There are still many unresolved and undiscovered issues regarding ELF3 mutations, however, based on research since 2016, a link to many signaling pathways important for carcinogenesis has been shown. There is no simple correlation between a specific ELF3 mutation and effect on cancer cells. In various types of cancers, ELF3 is associated with other pathways, and modifications exerted by silencing or amplifying its or associated genes, cause different effects in patient prediction. An example of the effect of ELF3 on tumor progression is achieved by negatively regulating the ZEB1 transcription factor responsible for metastasis. WNT, RAS, Akt, mTOR, HER2, Cyclin D, IRF6 are other ELF3-related factors that affects pathways crucial for tumorigenesis. Conclusions: Further research and attempts to use ELF3 in the treatment and prognosis of cancer appear to be beneficial.
EN
Introduction: Vestibular schwannomas (VS) are benign tumors developing from the myelin-producing Schwann cells, which surround the vestibular branches of the auditory nerve. The vast majority occur sporadically and a small proportion are associated with neurofibromatosis type 2 (NF2). Most sVS are slow-growing neoplasms; however some have a cystic structure, show more rapid growth, cause more frequently paralysis of the facial nerve, and brainstem compression. The molecular hallmark of both sporadic and NF-2 associated VS is the inactivation of the tumor-suppressor gene NF2, also called merlin gene. Purpose: The paper presents the current knowledge on the molecular biology of VS, including: information on genetic and epigenetic aberrations, changes in gene expression and specific microRNA expression profiles.
EN
Cholesteatoma is described as cystic lesion consisting of keratinizing squamous cell epithelium, filed with keratin debris, surrounded by inflammatory fibrous tissue, gradually expanding in the middle ear and causing destruction of neighboring bones. This paper presents brief review of existing hypotheses explaining its etiology in the light of the researches using high throughput, “omics”, technologies of molecular biology. Classic theories of pathogenesis of acquired cholesteatoma as: immigration, squamous metaplasia, basal cell hyperplasia or invagination theory have not been able to explain fully all pathological processes observed in cholesteatoma tissue. This also concerns the newer concepts that cholesteatoma is a result of mucosal traction generated by interaction of migrating opposing surfaces, a natural attempt by the body to cure the underlying inflammation in the cavity or chronic wound healing process triggered by micro defects in the basement membrane of the epithelium in the retraction pocket. Introduction of high-throughput, “omics”, technologies of molecular biology to the studies under cholesteatoma pathogenesis allowed identification of cholesteatoma-related gene expression signatures using full-genome microarrays as well as proteomic analysis of cholesteatoma. Those studies confirmed known pathological processes observed in cholesteatoma tissue such as: high proliferative activity, decreased signal transduction, active immunological response, alterations in the extracellular matrix, increased expression of proinflammatory cytokines, neovascularization and may others. This technique allows precise and complete insight into molecular mechanisms in those processes. However, it is still unknown what is the cause that trigger epithelial hyperplasia, inhibited migration and inflammatory response in the preexisting retraction pocket.
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