Paola Bruni's research while affiliated with Fondazione IRCCS Istituto Nazionale dei Tumori di Milano and other places

... Additionally, as wide-ranging studies suggest, genome-wide analyses and their integration with the current approach could further augment and inform our understanding of the genetic landscape in OC. These extensive and comprehensive tools can provide insights into genomic variations, epigenetic modifications, and gene-environment interactions, thereby enabling a more holistic view of tumor behavior beyond the scope of individual genes or loci [75][76][77][78]. Also, the other potential confounding factors that might affect the association between the studied lncRNA variants and OC risk or progression should be considered. ...

... Amplification of the PIK3C gene encoding PI3K or the Akt gene lead to the constitutive activation of the PI3K-Akt pathway. PTEN (phosphatase and tensin homologue deleted on chromosome 10) can inhibit the Akt activation and mutation in the PTEN gene also causes the constitutive activation of Akt [29][30][31]. Recent evidence has also suggested that Akt plays an important role in cancer cell migration and invasion [32,33]. This review focuses on the regulatory roles of Akt in cancer cell metastasis including head and neck cancer emphasising cell migration. ...

... Another interesting result of our study is the specific downregulation of cyclin D3, but not cyclin D1, in the cells treated with the combination of CDK4/6 and PI3K/mTOR inhibitors. The role of cyclin D3 in thyroid epithelial cell proliferation has already been established (Motti et al. 2003, Paternot et al. 2006, supporting the hypothesis that cyclin D3 is the key D-type cyclin that is involved in resistance to palbociclib in thyroid cancer. The unexpected upregulation of cyclin D1 upon PI3K/mTOR inhibition might be the effect of relief of a feedback and will need to be addressed in future studies. ...

... As it is known, VEGF is secreted by thyrocytes in response to TSH [39][40][41][42]. Conceivably, it is expected that serum TSH concentrations in HT, which are decreased remarkably after levothyroxine treatment, especially when euthyroid state has been achieved [32,43], might be positively correlated with serum VEGF levels [27,32]. ...

... This variant has been shown in vitro to lead to inactivation of phosphatase activity [21]. This variant is absent from the gnomAD database [22], but has been reported in other individuals with features of PHTS [23,24], and has been reported by multiple commercial laboratories on Clin-Var [25]. Another variant (p.Cys136Arg) at this position has also been reported as pathogenic by multiple laboratories [26]. ...

... Loss of hetreozygosity (LOH) studies have implicated the protein tyrosine phosphatase receptor J (PTPRJ, DEP-1, PTP-η, CD148) gene in the development of human meningioma [1], colon, lung and breast cancers, and quantitative trait analysis in mouse identified the mouse Ptprj orthologue as the sole candidate gene for the murine colon cancer susceptibility locus (Scc1) [2]. A reduction in the proliferation, survival and tumorigenicity of several cell types upon ectopic expression of PTPRJ further suggests a tumor suppressor role for this protein [3], [4], [5], [6], [7], [8]. Typical tumor suppressor gene ‘loss of function’ can result from loss or alteration of protein function, epigenetic silencing, RNA interference or post-translational modifications, or dysregulation by noncoding (nc) RNA [9], [10]. ...

... A multitude of anti-apoptotic proteins aid in regulation of apoptosis, among them Bcell lymphoma 2 (Bcl-2) (Opferman and Kothari, 2018) and Bcl-2 associated athanogene-1 (BAG-1) (Takayama et al., 1995), both of which inhibit the intrinsic pathway (Kinkel et al., 2004). In addition, some proteins play a role in regulation of apoptosis such as thymosin-β 10, a member of a group of actin monomer-sequestering proteins that inhibit actin polymerization (Shiotsuka et al., 2013;Viglietto et al., 1999). ...

... There was significant increase in VEGF level in stage II among patients with CG genotype and patients with GG genotype) compared to patients with genotype CC and significant increase in stage III among patients with CG compared to patients with CC genotype and patients with GG, P = 0.001. Previous study, revealed a relationship between the polymorphisms of the VEGF-pathway and clinical outcome of thyroid cancer which depends upon the clinical stage of the thyroid cancer [42], though the effect of VEGF in the angiogenesis of the tumor is vital, and is associated with effects with other angiogenic factors in late stages [28]. ...

... Protein p27 Kip is mainly known for its nuclear role as a cyclin dependent kinase inhibitor and thus inhibitor of cell cycle progression (72). However, it also plays an important role in the cytoplasm where it interacts with other proteins through its C-terminal domain to modulate cell motility and tumor progression (67,73,74). ...

... Interestingly, there was a marked reduction in p27 Kip1 between the two E2F1null clones when compared to wild-type vector controls (Fig. 1G). p27 Kip1 is a key cell cycle inhibitor and also plays an active antiapoptotic role in some contexts (18)(19)(20)(21). Taken together, these findings suggest a role for E2F1 in facilitating cell survival after oxidative stress insult. ...