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• W1619662783 abstract "Here we report on a child with Li–Fraumeni syndrome with a de novo TP53 mutation c.818G > A, who developed three malignancies at the age of 4 months, 4 and 5 years, respectively. We show that (i) in the choroid plexus carcinoma, the germline mutation was detected in a homozygous state due to copy‐neutral LOH/uniparental disomy, (ii) in the secondary AML, a complex karyotype led to loss of the wild‐type TP53 allele, (iii) in the Wilms tumor, the somatic mutation c.814G > A led to compound heterozygosity. The findings show that the complete inactivation of TP53 by different mechanisms is an important step towards tumorigenesis. Pediatr Blood Cancer 2015;62:1481–1484. © 2015 Wiley Periodicals, Inc." @default.
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• W1619662783 date "2015-03-18" @default.
• W1619662783 modified "2023-10-16" @default.
• W1619662783 title "A child with Li–Fraumeni syndrome: Modes to inactivate the second allele of <i>TP53</i> in three different malignancies" @default.
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• W1619662783 doi "https://doi.org/10.1002/pbc.25486" @default.
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