Publications by authors named "D D'Aliberti"

Article Synopsis
  • Protocadherins, especially Protocadherin 9 (PCDH9), are important for cell-cell interactions and have been linked to Autism Spectrum Disorder (ASD) and Major Depressive Disorder (MDD).
  • Knockout (KO) of PCDH9 in mice leads to abnormal neuronal development, characterized by larger presynaptic terminals and increased excitatory synapse activity in the hippocampus.
  • The findings suggest that PCDH9 plays a critical role in regulating excitatory synapse morphology and function, influencing glutamatergic transmission and potentially contributing to neurodevelopmental disorders.
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Background: Anaplastic Large Cell Lymphoma (ALCL) is a rare and aggressive T-cell lymphoma, classified into ALK-positive and ALK-negative subtypes, based on the presence of chromosomal translocations involving the ALK gene. The current standard of treatment for ALCL is polychemotherapy, with a high overall survival rate. However, a subset of patients does not respond to or develops resistance to these therapies, posing a serious challenge for clinicians.

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Article Synopsis
  • * The study found that MSCs influence microglia, the brain's immune cells, to adopt pro-regenerative functions by altering the extracellular matrix in response to inflammation.
  • * Key findings showed that MSC secretome leads to changes in microglial behavior, enhancing their mobility and cellular structures, which are important for promoting healing in the brain.
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Polycythemia Vera (PV) is typically caused by V617F or exon 12 JAK2 mutations. Little is known about Polycythemia cases where no JAK2 variants can be detected, and no other causes identified. This condition is defined as idiopathic erythrocytosis (IE).

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Article Synopsis
  • SETBP1 mutations are associated with various clonal myeloid disorders, but their role in initiating leukemia is uncertain, as they usually occur later in the progression of the disease.
  • Researchers created a mouse model with SETBP1 mutations in blood-forming tissue, which resulted in significant changes in cell differentiation and the development of a serious myeloid neoplasm.
  • In a study of triple-negative primary myelofibrosis patients, two groups were identified—those with SETBP1 mutations, who experienced more aggressive disease, and those without mutations, suggesting that SETBP1 mutations may act earlier in some clonal disorders than previously thought.
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