Publications by authors named "A Malinova"
Article Synopsis
- The study examines the role of SEMA3A, an axon guidance cue, in pancreatic ductal adenocarcinoma (PDAC) progression, highlighting its expression in different PDAC cell types and its impact on cellular behaviors.
- Researchers combined transcriptomic data and experimental approaches to demonstrate that SEMA3A contributes to aggressive cancer traits, including enhanced cell migration and resistance to cell death.
- Findings suggest that SEMA3A promotes a tumor-favorable environment by attracting macrophages and skewing them towards a pro-tumor, M2-like state, while potentially inhibiting effective immune responses from T cells.
Purpose: The identification of pancreatic ductal adenocarcinoma (PDAC) dysregulated genes may unveil novel molecular targets entering inhibitory strategies. Laminins are emerging as potential targets in PDAC given their role as diagnostic and prognostic markers. Here, we investigated the cellular, functional, and clinical relevance of LAMC2 and its regulated network, with the ultimate goal of identifying potential therapies.
View Article and Find Full Text PDFAims: Atrial fibrillation (AF) is the most common cardiac arrhythmia. Pathogenic variants in genes encoding ion channels are associated with familial AF. The point mutation M1875T in the SCN5A gene, which encodes the α-subunit of the cardiac sodium channel Nav1.
View Article and Find Full Text PDFArticle Synopsis
- Transcriptomic analyses have identified two main types of pancreatic ductal adenocarcinoma (PDAC), each with different biology and clinical outcomes, emphasizing the need to understand the roles of FGFR1 and FGFR4 in aggressive PDAC forms.
- FGFR4 expression is high in the classical PDAC subtype, correlating with better patient outcomes, while its downregulation in aggressive basal-like/squamous PDAC is linked to gene hypermethylation and decreased transcription marks.
- In contrast, FGFR1 is widely expressed in various pancreatic tissues and associated with the epithelial-mesenchymal transition (EMT) but not with the aggressive subtype, suggesting that FGFR4 can be a key marker for classifying PD
Cell Lineage Infidelity in PDAC Progression and Therapy Resistance.
Front Cell Dev Biol
December 2021
Infidelity to cell fate occurs when differentiated cells lose their original identity and either revert to a more multipotent state or transdifferentiate into a different cell type, either within the same embryonic lineage or in an entirely different one. Whilst in certain circumstances, such as in wound repair, this process is beneficial, it can be hijacked by cancer cells to drive disease initiation and progression. Cell phenotype switching has been shown to also serve as a mechanism of drug resistance in some epithelial cancers.
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