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Farres-Casas, J.

Publications and source records attributed to Farres-Casas, J..

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↗

iPSC-derived NF1-CDKN2A-PRC2 deficient neural crest cells mimic glial-to-neuro-mesenchymal transition and form MPNST-like tumors in vivo

Neurofibromatosis Type 1 (NF1) predisposes to peripheral nerve tumor development. Commonly, the progression from a benign plexiform neurofibroma (PNF) towards a deadly malignant peripheral nerve sheath tumor (MPNST) involves a poorly understood glial-to-mesenchymal transition and the sequential loss of NF1, CDKN2A, and polycomb repressive complex 2 (PRC2). Using an iPSC-derived neural crest (NC) model, we reproduced this malignant transformation through gene editing. NF1-CDKN2A double-knockout (2KO) NCs retained glial differentiation capacity and formed neurofibroma-like tumors in vivo, requiring inactivation of p14ARF and p16INK4a. Additional PRC2 loss (3KO) disrupted pluripotency and induced mesenchymal stem cell-like features in iPSCs an NCs. 3KO NCs suffered a global chromatin reprograming that silenced SOX10 preventing gliogenesis and activated neuro-mesenchymal programs. Gene signatures characterizing this glial-to-neuro-mesenchymal transition were recapitulated in human PNF-ANNUBP-MPNST tumors. 3KO NC spheres formed MPNST-like tumors in vivo upon nerve engraftment, genuinely mimicking an early-stage MPNST. We used the developed 3D NC spheroid models for the discovery of drugs targeting MPNSTs by performing a high-throughput screening of an epigenetic compound library. We found that poly(ADP-ribose) polymerase inhibitors (PARPi) exhibit selective efficacy in PRC2-deficient NC spheroids. We confirmed that Olaparib-Selumetinib combination in a MPNST PDX mouse model was well tolerated and significantly suppressed tumor growth.

cancer biology↗