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Your search keyword '"Lilia Cabrera-Cosme"' showing total 5 results
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5 results on '"Lilia Cabrera-Cosme"'

1. HOXA9 has the hallmarks of a biological switch with implications in blood cancers

Author

Laure Talarmain, Matthew A. Clarke, David Shorthouse, Lilia Cabrera-Cosme, David G. Kent, Jasmin Fisher, and Benjamin A. Hall

Subjects
Science
Abstract

HOXA9 plays an important role in acute myeloid leukaemia (AML), but its relevance for other blood malignancies is unclear. Here, the authors show that HOXA9 has a binary switch function that can clinically stratify AML patients, and model how the interactions with JAK2, TET2 and NOTCH impact myeloproliferative neoplasms.

Published
2022
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5. HOXA9 has the hallmarks of a biological switch with implications in blood cancers

Author

Laure Talarmain, Matthew A. Clarke, David Shorthouse, Lilia Cabrera-Cosme, David G. Kent, Jasmin Fisher, and Benjamin A. Hall

Subjects
Homeodomain Proteins, Leukemia, Myeloid, Acute, Multidisciplinary, Myeloproliferative Disorders, Hematologic Neoplasms, Core Binding Factor Alpha 2 Subunit, Mutation, General Physics and Astronomy, Humans, General Chemistry, General Biochemistry, Genetics and Molecular Biology
Abstract

Blood malignancies arise from the dysregulation of haematopoiesis. The type of blood cell and the specific order of oncogenic events initiating abnormal growth ultimately determine the cancer subtype and subsequent clinical outcome. HOXA9 plays an important role in acute myeloid leukaemia (AML) prognosis by promoting blood cell expansion and altering differentiation; however, the function of HOXA9 in other blood malignancies is still unclear. Here, we highlight the biological switch and prognosis marker properties of HOXA9 in AML and chronic myeloproliferative neoplasms (MPN). First, we establish the ability of HOXA9 to stratify AML patients with distinct cellular and clinical outcomes. Then, through the use of a computational network model of MPN, we show that the self-activation of HOXA9 and its relationship to JAK2 and TET2 can explain the branching progression of JAK2/TET2 mutant MPN patients towards divergent clinical characteristics. Finally, we predict a connection between the RUNX1 and MYB genes and a suppressive role for the NOTCH pathway in MPN diseases.

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