Glioblastoma, also referred to as glioblastoma multiforme (GBM), is grade IV astrocytoma characterized by being fast-growing and the most aggressive brain tumor. In adults, it is the most prevalent type of malignant brain tumor. Despite the advancements in both diagnosis tools and therapeutic treatments, GBM is still associated with poor survival rate without any statistically significant improvement in the past three decades.
View Article and Find Full Text PDFGenetic alterations drive tumor onset and progression. However, the cross‑talk between tumor cells and the benign components of the surrounding stroma can also promote the initiation, progression and metastasis of solid tumors. These cellular and non‑cellular stromal components form the tumor microenvironment (TME), which co‑evolves with tumor cells.
View Article and Find Full Text PDFCancer still ranks as one of the top causes of morbidity and mortality despite recent improvements in standard chemotherapy, radiotherapy, and surgery. This underlines some of the difficulties in creating successful therapeutic strategies, but it also highlights the shortcomings of conventional methods. In order to enhance the standard treatment of cancer patients, biology‑driven therapies are emerging towards more specific and effective clinical options.
View Article and Find Full Text PDFMotivation: Leucine-aspartic acid (LD) motifs are short linear interaction motifs (SLiMs) that link paxillin family proteins to factors controlling cell adhesion, motility and survival. The existence and importance of LD motifs beyond the paxillin family is poorly understood.
Results: To enable a proteome-wide assessment of LD motifs, we developed an active learning based framework (LD motif finder; LDMF) that iteratively integrates computational predictions with experimental validation.
Focal adhesion kinase (FAK) and its close paralogue, proline-rich tyrosine kinase 2 (PYK2), are key regulators of aggressive spreading and metastasis of cancer cells. While targeted small-molecule inhibitors of FAK and PYK2 have been found to have promising antitumor activity, their clinical long-term efficacy may be undermined by the strong capacity of cancer cells to evade anti-kinase drugs. In healthy cells, the expression and/or function of FAK and PYK2 is tightly controlled via modulation of gene expression, competing alternatively spliced forms, non-coding RNAs, and proteins that directly or indirectly affect kinase activation or protein stability.
View Article and Find Full Text PDFAdult neural stem cells (aNSCs) are relatively quiescent populations that give rise to distinct neuronal subtypes throughout life, yet, at a very low rate and restricted differentiation potential. Thus, identifying the molecular mechanisms that control their cellular expansion is critical for regeneration after brain injury. Loss of the Retinoblastoma protein, Rb, leads to several defects in cell cycle as well as neuronal differentiation and migration during brain development.
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