English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

To date, more than 500 fusion genes have been described in hematological malignancies, yet only a small fraction of these are sufficiently common, and with a known clinical impact, to justify routine clinical analysis.1 For this small subgroup, however, their presence can provide crucial information for diagnosis, prognosis and treatment. For example, the presence of fusion genes such as BCR/ABL1 in chronic myeloid leukemia (CML) and PML/RARA in acute promyelocytic leukemia warrants treatment specifically targeting the fusion proteins. Other gene fusions, for which there might not exist targeted therapies, are used to risk stratify leukemias into different treatment groups; for example, ETV6/RUNX1, TCF3/PBX1 and various MLL fusions in childhood B-cell acute lymphoblastic leukemia (ALL). The proportion of cases harboring known clinically relevant fusion genes varies substantially between hematological malignancies, but in ALL and acute myeloid leukemia (AML) 25–45% of the cases are positive for any of the clinically relevant fusion genes. To what extent the remaining cases harbor novel fusions, perhaps also suitable for targeted treatment, is not known, largely because the process of identifying new gene fusions has been laborious.

RNA-seq identifies clinically relevant fusion genes in leukemia including a novel MEF2D/CSF1R fusion responsive to imatinib