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Biology subjects

Salvador, H.

Publications and source records attributed to Salvador, H..

2 recordsLinked to original sources

Identification of Malignant Peripheral Nerve Sheath Tumor subtypes with distinct genomic identities

Malignant peripheral nerve sheath tumors (MPNSTs) are aggressive soft-tissue sarcomas arising sporadically or in people with neurofibromatosis type 1 (NF1). Their marked heterogeneity challenges diagnosis and has hampered an integrative view of MPNST molecular pathogenesis. Here, a thorough whole-genome and transcriptome analysis of MPNSTs and the re-analysis of a large independent cohort allowed us to identify three molecular subtypes of MPNSTs (G1-G3) with distinct genomic identities and clinicopathological features. Furthermore, it provided a simple and unifying model of MPNST development, defining a distinct progression path for each group. This work uncovers new genomic aspects of MPNSTs, including the identification of recurrent copy-neutral loss of heterozygosity regions, distinct copy-number profiles among G1-G3, and CDKN2A-inactivating translocations in pre-malignant lesions (ANNUBPs). Altogether, these analyses overcome the dominant influence of PRC2 status in MPNST classification and provide a framework for their differential diagnosis and potential precision oncology treatment. SIGNIFICANCEMPNST is a highly heterogeneous soft-tissue sarcoma with difficult clinical management and no effective systemic therapies. This work defines three molecular subtypes of MPNSTs with distinct development paths and histological and clinical characteristics with potential impact on translational studies and subtype-tailored treatments.

cancer biology↗

Antisense oligonucleotides targeting exon 11 are able to partially rescue the Neurofibromatosis Type 2 phenotype in vitro

Neurofibromatosis type 2 (NF2) is an autosomal dominant condition caused by loss of function variants in the NF2 gene, which codes for the protein Merlin, and characterized by the development of multiple tumours of the nervous system. The clinical presentation of the disease is variable and related to the type of the inherited germline variant. Here, we tested if PMOs could be used to correct the splice signalling caused by variants at +/-13 within the intron-exon boundary region. Here we show that the PMOs designed for these variants do not constitute a therapeutic approach. Furthermore, we evaluated the use of phosphorodiamidate morpholino oligomers (PMOs) to reduce the severity of the effects of NF2 truncating variants with the aim of generating milder hypomorphic isoforms in vitro through the induction of the in-frame deletion of the exon-carrying variant. We were able to specifically induce the skipping of exons 4, 8 and 11 maintaining the NF2 gene reading frame at cDNA level. Only the skipping of exon 11 produced a hypomorphic Merlin (Merlin-e11), able to partially rescue the observed phenotype in primary fibroblast cultures from NF2 patients, being encouraging for the treatment of patients harbouring truncating variants located in exon 11.

genetics↗