Loss-of-function germline GATA2 mutations in patients with MDS/AML or MonoMAC syndrome and primary lymphedema reveal a key role for GATA2 in the lymphatic vasculature


Por: Kazenwadel J., Secker G.A., Liu Y.J., Rosenfeld J.A., Wildin R.S., Cuellar-Rodriguez J., Hsu A.P., Dyack S., Fernandez C.V., Chong C.-E., Babic M., Bardy P.G., Shimamura A., Zhang M.Y., Walsh T., Holland S.M., Hickstein D.D., Horwitz M.S., Hahn C.N., Scott H.S., Harvey N.L.

Publicada: 1 ene 2012
Resumen:
Recent work has established that heterozygous germline GATA2 mutations predispose carriers to familial myelodysplastic syndrome (MDS)/acute myeloid leukemia (AML), "MonoMAC" syndrome, and DCML deficiency. Here, we describe a previously unreported MDS family carrying a missense GATA2 mutation (p.Thr354Met), one patient with MDS/AML carrying a frameshift GATA2 mutation (p.Leu332Thrfs*53), another with MDS harboring a GATA2 splice site mutation, and 3 patients exhibiting MDS or MDS/AML who have large deletions encompassing the GATA2 locus. Intriguingly, 2 MDS/AML or "MonoMAC" syndrome patients with GATA2 deletions and one with a frameshift mutation also have primary lymphedema. Primary lymphedema occurs as a result of aberrations in the development and/or function of lymphatic vessels, spurring us to investigate whether GATA2 plays a role in the lymphatic vasculature. We demonstrate here that GATA2 protein is present at high levels in lymphatic vessel valves and that GATA2 controls the expression of genes important for programming lymphatic valve development. Our data expand the phenotypes associated with germline GATA2 mutations to include predisposition to primary lymphedema and suggest that complete haploinsufficiency or loss of function of GATA2, rather than missense mutations, is the key predisposing factor for lymphedema onset. Moreover, we reveal a crucial role for GATA2 in lymphatic vascular development.

Filiaciones:
Kazenwadel J.:
 Division of Haematology, Centre for Cancer Biology, SA Pathology, PO Box 14, Adelaide, SA 5000, Australia

Secker G.A.:
 Division of Haematology, Centre for Cancer Biology, SA Pathology, PO Box 14, Adelaide, SA 5000, Australia

Liu Y.J.:
 Department of Pathology, University of Washington School of Medicine, Seattle, WA, United States

Rosenfeld J.A.:
 Signature Genomics, PerkinElmer, Spokane, WA, United States

Wildin R.S.:
 St Luke's Children's Hospital, State of Idaho Genetics Program, Department of Health and Welfare, Boise, ID, United States

Cuellar-Rodriguez J.:
 Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health (NIH), Bethesda, MD, United States

Hsu A.P.:
 Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health (NIH), Bethesda, MD, United States

Dyack S.:
 Department of Pediatrics, Maritime Medical Genetics Service, Dalhousie University, Halifax, NS, Canada

Fernandez C.V.:
 Departments of Pediatrics and Bioethics, IWK Health Centre, Dalhousie University, Halifax, NS, Canada

Chong C.-E.:
 Department of Molecular Pathology, Centre for Cancer Biology, SA Pathology, PO Box 14, Adelaide, SA 5000, Australia

 School of Medicine, University of Adelaide, Adelaide, SA, Australia

Babic M.:
 Department of Molecular Pathology, Centre for Cancer Biology, SA Pathology, PO Box 14, Adelaide, SA 5000, Australia

Bardy P.G.:
 Division of Haematology, Centre for Cancer Biology, SA Pathology, PO Box 14, Adelaide, SA 5000, Australia

Shimamura A.:
 Fred Hutchinson Cancer Research Center, Seattle, WA, United States

 Seattle Children's Hospital, Seattle, WA, United States

Zhang M.Y.:
 Fred Hutchinson Cancer Research Center, Seattle, WA, United States

 Department of Genome Sciences, Department of Medicine, University of Washington, Seattle, WA, United States

Walsh T.:
 Department of Genome Sciences, Department of Medicine, University of Washington, Seattle, WA, United States

Holland S.M.:
 Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health (NIH), Bethesda, MD, United States

Hickstein D.D.:
 Experimental Transplantation and Immunology Branch, National Cancer Institute, NIH, Bethesda, MD, United States

Horwitz M.S.:
 Department of Pathology, University of Washington School of Medicine, Seattle, WA, United States

Hahn C.N.:
 Department of Molecular Pathology, Centre for Cancer Biology, SA Pathology, PO Box 14, Adelaide, SA 5000, Australia

 School of Medicine, University of Adelaide, Adelaide, SA, Australia

Scott H.S.:
 Department of Molecular Pathology, Centre for Cancer Biology, SA Pathology, PO Box 14, Adelaide, SA 5000, Australia

 School of Medicine, University of Adelaide, Adelaide, SA, Australia

 School of Molecular and Biomedical Science, University of Adelaide, Adelaide, SA, Australia

Harvey N.L.:
 Division of Haematology, Centre for Cancer Biology, SA Pathology, PO Box 14, Adelaide, SA 5000, Australia

 School of Medicine, University of Adelaide, Adelaide, SA, Australia
ISSN: 00064971
Editorial
AMER SOC HEMATOLOGY, 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA, Estados Unidos America
Tipo de documento: Article
Volumen: 119 Número: 5
Páginas: 1283-1291
WOS Id: 000300400300029
ID de PubMed: 22147895
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