Publications by authors named "F De Amicis"

Regulated cell death, a regulatory form of cell demise, has been extensively studied in multicellular organisms. It plays a pivotal role in maintaining organismal homeostasis under normal and pathological conditions. Although alterations in various regulated cell death modes are hallmark features of tumorigenesis, they can have divergent effects on cancer cells.

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The biological activity of structural HIV-1 proteins is not limited to ensuring a productive viral infection but also interferes with cellular homeostasis through intra- and extracellular signaling activation. This interference induces genomic instability, increases the lifespan of the infected cell by inhibiting apoptosis, and subverts cell senescence, resulting in unrestricted cell proliferation. HIV structural proteins are present in a soluble form in the lymphoid tissues and blood of infected individuals, even without active viral replication.

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  • - The study investigates hexanucleotide repeat expansions (RE) in genes associated with amyotrophic lateral sclerosis (ALS), particularly focusing on their frequency within the Italian population and their potential link to the disorder's clinical features.
  • - Researchers screened 302 ALS patients and compared their RE distribution with that of 167 healthy controls, finding similar distributions but a moderate correlation between longer repeat lengths and certain clinical features such as age of onset and family history.
  • - This research is the first of its kind in southern Italy, revealing that while REs are present, the rare pathogenic repeats do not show a significant association with ALS, contributing valuable insights to the genetic understanding of the disorder.
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Prostate cancer (PCa) is the second most common male cancer. Its incidence derives from the interaction between modifiable and non-modifiable factors. The progression of prostate cancer into a more aggressive phenotype is associated with chronic inflammation and increased ROS production.

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  • Glioblastoma multiforme (GBM) is a highly aggressive cancer with poor treatment outcomes, largely due to the presence of cancer stem cells that drive recurrence and resistance to therapy.
  • A study found that using a combination of the γ-secretase inhibitor RO4929097 (to block the Notch signaling pathway) and resveratrol can transform GBM cells back to a less aggressive, epithelial-like state, which impacts their invasive properties and stemness.
  • The involvement of cyclin D1 and CDK4 was crucial in this process, as altering these factors affected cell migration and could help develop new therapeutic strategies targeting CDK4 in treating GBM.
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