Author

T. Haferlach

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

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Cancer Biology· 5

Signature Assays, Organisms & Methods

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Assay:bulk RNA-seq· 4 Organism:human· 4 Research Focus:cancer & tumor microenvironment· 3 Approach:experimental assay· 3 Approach:statistical model· 3 Research Focus:cell type annotation· 2 Research Focus:differential expression· 2 Research Focus:gene regulatory network inference· 2

Frequent Co-Authors

F. Grebien· 2 shared T. Eder· 2 shared A. Bagchi· 1 shared A. Boersma· 1 shared A. Deshpande· 1 shared A. G. X. Zeng· 1 shared A. Krippner-Heidenreich· 1 shared A. Mitchell· 1 shared

Activity by Year

2020-2023 · peak 3/yr

Co-Author Collaboration Network

10 top collaborators · 10 mutual co-author links

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2 shared papersCancer Biology

F. Grebien

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5 papers

Recent·Most cited

Cancer BiologybioRxivDec 26, 2023

Single-cell transcriptional mapping reveals genetic and non-genetic determinants of aberrant differentiation in AML

A. G. X. Zeng, I. Iacobucci, S. Shah…·J. E. Dick

The paper constructs a reference atlas of human hematopoiesis and maps AML differentiation patterns, revealing genetic and non-genetic factors driving aberrant differentiation in leukemia.

DOI 10.1158/2643-3230.bcd-24-0342

humanscRNA-seq

Cancer BiologybioRxivPreprintNov 7, 2023

The neuronal homeobox transcription factor HMX3 is a crucial vulnerability factor in MECOM-negative KMT2A::MLLT3 acute myelomonocytic leukemia

S. Arza-Apalategi, B. M. H. Heuts, S. M. Bergevoet…·B. A. van der Reijden

The paper identifies HMX3 as a critical vulnerability in MECOM-negative KMT2A::MLLT3 AML, showing it promotes proliferation and blocks differentiation.

DOI 10.1101/2023.11.07.565950

humanbulk RNA-seq

Cancer BiologybioRxivMar 28, 2023

TET2 lesions enhance the aggressiveness of CEBPA-mutant AML by rebalancing GATA2 expression

E. Heyes, A. S. Wilhelmson, A. Wenzel…·B. T. Porse

This study identifies GATA2 as a target of the CEBPA-TET2 mutational axis in AML, showing how TET2 lesions rebalance GATA2 expression and enhance disease aggressiveness.

DOI 10.1038/s41467-023-41927-x

humanbulk RNA-seq

Cancer BiologybioRxivPreprintDec 21, 2022

STAT5 Gain-of-Function Variants Promote Precursor T-Cell Receptor Activation to Drive T-Cell Acute Lymphoblastic Leukemia

T. Suske, H. Sorger, F. Ruge…·R. Moriggl

This study identifies STAT5 gain-of-function mutations as drivers of T-ALL by promoting pre-TCR signaling and shows therapeutic targeting potential with STAT3/5 or ZAP70 inhibitors.

DOI 10.1101/2022.12.21.519945

humanbulk RNA-seq

Cancer BiologybioRxivAug 31, 2020

A JAK/STAT-Mediated Inflammatory Signaling Cascade Drives Oncogenesis In AF10-Rearranged AML

B. Chen, A. Deshpande, K. O. Barbosa…·A. Deshpande

This study identifies JAK1 as a therapeutic target in AF10-rearranged AML by showing its role in JAK/STAT-mediated inflammatory signaling and oncogenesis.

DOI 10.1182/blood.2020009023

mousebulk RNA-seq