Publications by authors named "Irati Hervas-Corpion"

Article Synopsis
  • Pediatric high-grade gliomas (pHGGs), particularly diffuse midline gliomas (DMGs), are highly aggressive tumors with low survival rates, yet the combination of Delta-24-RGD and ONC201 has shown potential for enhanced treatment efficacy.
  • In laboratory and mouse model studies, the combination treatment did not alter virus replication but demonstrated a synergistic or additive cytotoxic effect, leading to increased DNA damage and metabolic disruptions in tumor cells.
  • Additionally, the combination treatment improved survival rates in mice models and led to a shift in the tumor microenvironment towards a more proinflammatory state, indicating a stronger immune response against the tumors.
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Huntington's disease (HD) is caused by an aberrant expansion of CAG repeats in the HTT gene that mainly affects basal ganglia. Although striatal dysfunction has been widely studied in HD mouse models, other brain areas can also be relevant to the pathology. In this sense, we have special interest on the retina as this is the most exposed part of the central nervous system that enable health monitoring of patients using noninvasive techniques.

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Article Synopsis
  • Diffuse intrinsic pontine glioma (DIPG) is a serious brain tumor and is the most common cause of cancer deaths in kids.
  • Scientists found that a protein called TIM-3 is present in both the tumor cells and nearby cells, which may help the tumor grow.
  • By blocking TIM-3, they noticed that it helped some mice live longer and fight off the tumor, showing it could be a good target for new treatments for DIPG.
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High-grade gliomas (HGGs) are the most common and aggressive primary brain tumors in both adult and pediatric populations. Despite the multimodal treatment modality currently available for HGG, the prognosis is dismal, with a low overall survival rate at two years after diagnosis. In the last decade, oncolytic virotherapy has emerged as a promising and feasible therapeutic tool in management of these tumors due to its oncolytic and immunostimulatory properties.

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Glioblastoma (GB) is the most prevalent primary brain cancer and the most aggressive form of glioma because of its poor prognosis and high recurrence. To confirm the importance of epigenetics in glioma, we explored The Cancer Gene Atlas (TCGA) database and we found that several histone/DNA modifications and chromatin remodeling factors were affected at transcriptional and genetic levels in GB compared to lower-grade gliomas. We associated these alterations in our own cohort of study with a significant reduction in the bulk levels of acetylated lysines 9 and 14 of histone H3 in high-grade compared to low-grade tumors.

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Glioblastoma (GB) is the most aggressive form of glioma and is characterized by poor prognosis and high recurrence despite intensive clinical interventions. To retrieve the key factors underlying the high malignancy of GB with potential diagnosis utility, we combined the analysis of The Cancer Gene Atlas and the REMBRANDT datasets plus a molecular examination of our own collection of surgical tumor resections. We determined a net reduction in the levels of the non-canonical histone H3 variant H3.

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Abnormal trinucleotide expansions cause rare disorders that compromise quality of life and, in some cases, lifespan. In particular, the expansions of the CGG-repeats stretch at the 5'-UTR of the Fragile X Mental Retardation 1 () gene have pleiotropic effects that lead to a variety of Fragile X-associated syndromes: the neurodevelopmental Fragile X syndrome (FXS) in children, the late-onset neurodegenerative disorder Fragile X-associated tremor-ataxia syndrome (FXTAS) that mainly affects adult men, the Fragile X-associated primary ovarian insufficiency (FXPOI) in adult women, and a variety of psychiatric and affective disorders that are under the term of Fragile X-associated neuropsychiatric disorders (FXAND). In this review, we will describe the pathological mechanisms of the adult "gain-of-function" syndromes that are mainly caused by the toxic actions of CGG RNA and FMRpolyG peptide.

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Glioblastoma (GBM) is the most frequent and aggressive primary brain tumor and is associated with a poor prognosis. Despite the use of combined treatment approaches, recurrence is almost inevitable and survival longer than 14 or 15 months after diagnosis is low. It is therefore necessary to identify new therapeutic targets to fight GBM progression and recurrence.

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Glioma stem cells (GSCs) are crucial in the formation, perpetuation and recurrence of glioblastomas (GBs) due to their self-renewal and proliferation properties. Although GSCs share cellular and molecular characteristics with neural stem cells (NSCs), GSCs show unique transcriptional and epigenetic features that may explain their relevant role in GB and may constitute druggable targets for novel therapeutic approaches. In this review, we will summarize the most important findings in GSCs concerning epigenetic-dependent mechanisms.

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Huntington disease (HD) is a fatal neurodegenerative disorder without a cure that is caused by an aberrant expansion of CAG repeats in exon 1 of the huntingtin (HTT) gene. Although a negative correlation between the number of CAG repeats and the age of disease onset is established, additional factors may contribute to the high heterogeneity of the complex manifestation of symptoms among patients. This variability is also observed in mouse models, even under controlled genetic and environmental conditions.

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Transcriptional dysregulation in Huntington's disease (HD) affects the expression of genes involved in survival and neuronal functions throughout the progression of the pathology. In recent years, extensive research has focused on epigenetic and chromatin-modifying factors as a causative explanation for such dysregulation, offering attractive targets for pharmacological therapies. In this work, we extensively examined the gene expression profiles in the cortex, striatum, hippocampus and cerebellum of juvenile R6/1 and N171-82Q mice, models of rapidly progressive HD, to retrieve the early transcriptional signatures associated with this pathology.

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