Supplementary Figure S2 from Schlafen 12 Modulation and Targeting in Acute Myeloid Leukemia

Guillen Magaña, Jamie N.; Zannikou, Markella; Baran, Aneta; Small, Sara; Schieber, Michael; Schipma, Matthew J.; Bartom, Elizabeth T.; Kocherginsky, Masha; Saleiro, Diana; Beauchamp, Elspeth M.; Eckerdt, Frank; Platanias, Leonidas C.

doi:10.1158/2767-9764.30635829

Supplementary Figure S2 from Schlafen 12 Modulation and Targeting in Acute Myeloid Leukemia

https://doi.org/10.1158/2767-9764.30635829

journal contribution

posted on 2025-11-17, 08:40 authored by Jamie N. Guillen Magaña, Markella Zannikou, Aneta Baran, Sara Small, Michael Schieber, Matthew J. Schipma, Elizabeth T. Bartom, Masha Kocherginsky, Diana Saleiro, Elspeth M. Beauchamp, Frank Eckerdt, Leonidas C. Platanias

<p>Figure S2. PCA of tumor samples and Heatmap of DEGs.</p>

Funding

National Cancer Institute (NCI)

United States Department of Health and Human Services

Find out more...

U.S. Department of Veterans Affairs (VA)

History

Related Materials

1.
DOI - Is supplement to Schlafen 12 Modulation and Targeting in Acute Myeloid Leukemia

ARTICLE ABSTRACT

We examined the role of SLFN12, a member of the Schlafen (SLFN) family of interferon-regulated genes and proteins in leukemogenesis, and its potential as a therapeutic target in acute myeloid leukemia (AML). We explored the effects of velcrins, a class of small molecules able to modulate SLFN12 biological activity, on AML cells. Velcrin treatment of AML cells stabilized SLFN12 and promoted SLFN12 complex formation with phosphodiesterase 3A or phosphodiesterase 3B. Such effects were associated with growth-inhibitory and proapoptotic responses, as well as potent suppressive effects on leukemic cell growth. In addition, velcrin treatment suppressed clonogenic capacity of primitive leukemic progenitors and significantly extended survival in a mouse AML xenograft model. Taken together, these findings establish an important role of SLFN12 in leukemogenesis and raise the potential for the use of velcrins as a therapeutic strategy for AML. Our studies identify SLFN12 as a potential target in AML with important clinical–translational implications.

Supplementary Figure S2 from Schlafen 12 Modulation and Targeting in Acute Myeloid Leukemia

Funding

National Cancer Institute (NCI)

U.S. Department of Veterans Affairs (VA)

History

Related Materials

ARTICLE ABSTRACT

Usage metrics

Categories

Keywords

Licence

Exports