Publications by authors named "R Navaridas"

Metastasis is responsible for most cancer-related deaths. Different cancers have their own preferential sites of metastases, a phenomenon termed metastatic organotropism. The mechanisms underlying organotropism are multifactorial and include the generation of a pre-metastatic niche (PMN), metastatic homing, colonization, dormancy, and metastatic outgrowth.

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  • - The study investigates how certain mutations in the p53 protein can lead to increased cancer cell invasion, contradicting previous views on mutant p53's role in cancer progression.
  • - Researchers found that mutant p53 enhances the ability of cancer cells to invade their surroundings by modulating the RhoA/ROCK signaling pathway and affecting the organization of the extracellular matrix (ECM).
  • - The findings suggest that the invasive effects of mutant p53 are influenced not just by the cells themselves but also by the mechanical properties of the ECM, highlighting the complex interactions during cancer metastasis.
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  • The Sprouty genes (Spry1-4) inhibit receptor tyrosine kinases and play important roles in embryo development and tumor suppression in adults.* -
  • Research involving adult-onset triple knockout mice for Spry1, Spry2, and Spry4 shows that while these mice experience various health issues, like weight loss and endocrine abnormalities, they do not have an increased incidence of tumors compared to normal mice.* -
  • Findings suggest that the loss of Sprouty genes may impact metabolic and endocrine functions without necessarily leading to tumor development.*
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Metformin is a widespread antidiabetic agent that is commonly used as a treatment against type 2 diabetes mellitus patients. Regarding its therapeutic potential, multiple studies have concluded that Metformin exhibits antineoplastic activity on several types of cancer, including endometrial carcinoma. Although Metformin's antineoplastic activity is well documented, its cellular and molecular anticancer mechanisms are still a matter of controversy because a plethora of anticancer mechanisms have been proposed for different cancer cell types.

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Phosphatase and TENsin homolog (Pten) and p53 are two of the most frequently mutated tumor suppressor genes in endometrial cancer. However, the functional consequences and histopathological manifestation of concomitant p53 and Pten loss of function alterations in the development of endometrial cancer is still controversial. Here, it is demonstrated that simultaneous Pten and p53 deletion is sufficient to cause epithelial to mesenchymal transition phenotype in endometrial organoids.

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