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Moreover, TNBC is highly aggressive, prone to metastasis, and has a narrow therapeutic window [4]

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Molecular analysis revealed a homozygous deletion of exons 4 and 5 of the IGF1 gene

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According to this scenario, a catalytically inactive SOD1 mutant may act as a prion-like transmitter of the misfolding signal to efficiently spread the pathology, whereas the neurotoxic effect per se is caused by the ubiquitous SOD1 WT , the structural and catalytic properties of which compromised by its interaction with the misfolded SOD1 mutant