D. G. Tenen

The paper identifies a compound that degrades both SALL4 isoforms, overcoming IMiD limitations in liver cancer treatment.

The paper identifies E4F1 and ZNF148 as transcriptional activators of the A57C and wildtype TERT promoter, respectively, and shows their role in upregulating TERT transcription and telomerase activity.

This study identifies the cellular origin of aberrant SALL4 expression in MDS using mass cytometry, showing it is mainly in HSPC and myeloid lineages, with SALL4/p53 co-expression linked to TP53 mutations.

The paper shows C/EBPα binds RNA via novel domains, recruits to enhancer sites, and promotes Macrophage differentiation by regulating PU.1 expression.

This study identifies ADAR2 downregulation in t(8;21) AML and shows its role in suppressing leukemogenesis through RNA editing.

The paper shows that CBF fusions in AML activate the PU.1 antisense promoter, reducing sense PU.1 transcription and blocking myeloid differentiation, similar to T-cell differentiation.

The paper identifies the long noncoding RNA LOUP as a mediator of RUNX1 and RUNX1-ETO effects in t(8;21) AML, showing it promotes myeloid differentiation and inhibits cell growth by regulating PU.1 expression.

This study identifies a mechanism by which pseudogene 5 induces DNA demethylation and reactivates the oncogene SALL4 in hepatocellular carcinoma, linking HBV infection to HCC progression.

This study shows chronic IL-1β exposure selects for Cebpa-deficient HSPC by promoting myeloid differentiation and repressing stem cell programs, linking chronic inflammation to hematologic disorders.