Chromosomal Deletion Involving ANKRD26 Leads to Expression of a Fusion Protein Responsible for ANKRD26-Related Thrombocytopenia.

涉及 ANKRD26 的染色体缺失导致融合蛋白的表达,该融合蛋白是 ANKRD26 相关血小板减少症的罪魁祸首

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作者:Dell'Orso Gianluca, Passarella Tommaso, Cappato Serena, Cappelli Enrico, Regis Stefano, Maffei Massimo, Balbi Matilde, Ravera Silvia, Di Martino Daniela, Viaggi Silvia, Davì Sabrina, Corsolini Fabio, Giarratana Maria Carla, Arcuri Luca, Mariani Eugenia, Morini Riccardo, Massaccesi Erika, Guardo Daniela, Calvillo Michaela, Palmisani Elena, Coviello Domenico, Fioredda Francesca, Dufour Carlo, Bocciardi Renata, Miano Maurizio
ANKRD26-related thrombocytopenia (ANKRD26-RT) is characterized by lifelong mild to moderate thrombocytopenia. Patients suffer from an increased susceptibility to acute or chronic myeloid leukemia, myelodysplastic syndrome, or chronic lymphocytic leukemia. We described here a patient with inherited thrombocytopenia initially misdiagnosed as immune thrombocytopenic purpura. A chromosomal deletion involving the ANKRD26 gene was identified. Gene and protein expression analyses suggest an alternative pathogenic mechanism of altered megakaryopoiesis: the synthesis of a chimeric protein with aberrant expression due to the unregulated action of a promoter from a gene located upstream of ANKRD26. This study highlights the importance of advanced genetic testing and functional analysis of patients' primary cells in the case of the detection of previously unrecognized structural variants in order to understand pathogenic mechanisms. These investigations provided a definitive diagnosis for the patient and facilitated the development of a tailored clinical management strategy, especially concerning the potential for myeloid transformation.

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