Publications by authors named "Elena Valentino"

Chromatin organization plays a crucial role in tissue homeostasis. Heterochromatin relaxation and consequent unscheduled mobilization of transposable elements (TEs) are emerging as key contributors of aging and aging-related pathologies, including Alzheimer's disease (AD) and cancer. However, the mechanisms governing heterochromatin maintenance or its relaxation in pathological conditions remain poorly understood.

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Objectives: Coronavirus disease 2019 (COVID-19) carries a high risk for malnutrition owing to the state of debilitation that results from acute respiratory failure symptoms. The aim of this study was to provide an approach to reduce the risk for malnutrition and improve patients' clinical outcomes.

Methods: Short age-adjusted Nutritional Risk Screening was performed with 94 non-intensive care unit (ICU) patients admitted to the Giovanni Borea Civil Hospital in Sanremo.

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Missense mutations in the TP53 gene are frequent in human cancers, giving rise to mutant p53 proteins that can acquire oncogenic properties. Gain of function mutant p53 proteins can enhance tumour aggressiveness by promoting cell invasion, metastasis and chemoresistance. Accumulating evidences indicate that mutant p53 proteins can also modulate cell homeostatic processes, suggesting that missense p53 mutation may increase resistance of tumour cells to intrinsic and extrinsic cancer-related stress conditions, thus offering a selective advantage.

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Breast cancer is the most frequently diagnosed malignancy in women, and mutations in the tumor suppressor p53 are commonly detected in the most aggressive subtypes. The majority of gene alterations are missense substitutions, leading to expression of mutant forms of the p53 protein that are frequently detected at high levels in cancer cells. P53 mutants not only lose the physiological tumor-suppressive activity of the wild-type p53 protein but also acquire novel powerful oncogenic functions, referred to as gain of function, that may actively confer a selective advantage during tumor progression.

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Article Synopsis
  • The tumor suppressor DAB2IP plays a crucial role in regulating the communication between cancer cells and their surrounding environment, and its inactivation is linked to the progression of various cancers.
  • High-throughput screening identified miR-149-3p as a key inhibitor of DAB2IP, which increases cancer cell mobility and invasiveness by activating NF-kB signaling.
  • Additionally, miR-149-3p released by prostate cancer cells can downregulate DAB2IP in nearby blood vessel cells, promoting their growth and movement, while its inhibition can restore DAB2IP function and reduce tumor growth.
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Obesity and type 2 diabetes are significant risk factors for malignancies, being associated with chronic inflammation and hyperinsulinemia. In this context, insulin can synergize with inflammation to promote proliferation, survival, and dissemination of cancer cells. Point mutation of p53 is a frequent event and a significant factor in cancer development and progression.

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Non-Hodgkin lymphomas (NHLs) include a heterogeneous group of diseases, which differ in both cellular origin and clinical behavior. Among the aggressive malignancies of this group, the diffuse large B-cell lymphomas (DLBCLs) are the most frequently observed. They are themselves clinically and molecularly heterogeneous and have been further sub-divided in three sub-types according to different cell of origin, mechanisms of oncogenesis and clinical outcome.

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Molecular etiology of thyroid cancers has been widely studied, and several molecular alterations have been identified mainly associated with follicular and papillary histotypes. However, the molecular bases of the complex pathogenesis of thyroid carcinomas remain poorly understood. HOX genes regulate normal embryonic development, cell differentiation and other critical processes in eukaryotic cell life.

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