Widening the spectrum of deletions and molecular mechanisms underlying alpha-thalassemia

Annals of Hematology - Tập 96 - Trang 1921-1929 - 2017
José Ferrão1, Marisa Silva1, Lúcia Gonçalves1, Susana Gomes1, Pedro Loureiro1, Andreia Coelho1, Armandina Miranda2, Filomena Seuanes2, Ana Batalha Reis3, Francisca Pina4, Raquel Maia5, Paula Kjöllerström5, Estela Monteiro6,7, João F. Lacerda6,8, João Lavinha1,9, João Gonçalves1,10, Paula Faustino1,11
1Departamento de Genética Humana, Instituto Nacional de Saúde Doutor Ricardo Jorge (INSA), Lisbon, Portugal
2Departamento de Promoção da Saúde e Prevenção de Doenças não Transmissíveis, INSA, Lisbon, Portugal
3Serviço de Patologia Clínica, Hospital São Francisco Xavier, Centro Hospitalar de Lisboa Ocidental, Lisbon, Portugal
4Serviço de Hemato-Oncologia, Hospital do Espírito Santo de Évora, Évora, Portugal
5Unidade de Hematologia, Hospital D. Estefânia, Centro Hospitalar de Lisboa Central, Lisbon, Portugal
6Faculdade de Medicina, Universidade de Lisboa, Lisbon, Portugal
7Serviço de Gastroenterologia, Hospital de Santa Maria, Centro Hospitalar de Lisboa Norte (CHLN), Lisbon, Portugal
8Serviço de Hematologia, Hospital de Santa Maria, CHLN, Lisbon, Portugal
9BioISI, Faculdade de Ciências, Universidade de Lisboa, Lisbon, Portugal
10ToxOmics, Faculdade de Ciências Médicas, Universidade Nova de Lisboa, Lisbon, Portugal
11ISAMB, Faculdade de Medicina, Universidade de Lisboa, Lisbon, Portugal

Tóm tắt

Inherited deletions of α-globin genes and/or their upstream regulatory elements (MCSs) give rise to α-thalassemia, an autosomal recessive microcytic hypochromic anemia. In this study, multiplex ligation-dependent probe amplification performed with commercial and synthetic engineered probes, Gap-PCR, and DNA sequencing were used to characterize lesions in the sub-telomeric region of the short arm of chromosome 16, possibly explaining the α-thalassemia/HbH disease phenotype in ten patients. We have found six different deletions, in heterozygosity, ranging from approximately 3.3 to 323 kb, two of them not previously described. The deletions fall into two categories: one includes deletions which totally remove the α-globin gene cluster, whereas the other includes deletions removing only the distal regulatory elements and keeping the α-globin genes structurally intact. An indel was observed in one patient involving the loss of the MCS-R2 and the insertion of 39 bp originated from a complex rearrangement spanning the deletion breakpoints. Finally, in another case, no α-globin gene cluster deletion was found and the patient revealed to be a very unusual case of acquired α-thalassemia-myelodysplastic syndrome. This study further illustrates the diversity of genomic lesions and underlying molecular mechanisms leading to α-thalassemia.

Tài liệu tham khảo

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