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Gerulf Hänel on Muck Rack

Gerulf Hänel

As seen in: Nature
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Articles

TP53 deficiency in AML induces resistance to T-cell engagers through an immunosuppressive secretome

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By Lea Pawlowsky, Amelie Muth, Kieron White, Maryam Kazerani, Daniel Nixdorf, Bettina Brauchle, Gerulf Hänel, Agnese Petrera, Eva Briem, Gordon Hoffmann, Emanuele Carlini, Adrian Gottschlich, Karsten Spiekermann, Tobias Straub, Sebastian Kobold, Michael Andreeff, Veit L. Buecklein, Marion Subklewe, Anne-Sophie Neumann, Lisa Rohrbacher, Thomas Janert, Roman Kischel
| Nature Verified
Abstract Bispecific T-cell engagers (BiTE® molecules) have transformed the treatment of B-cell malignancies, yet clinical activity in AML has been modest. Resistance is driven in part by the genetic heterogeneity of AML, most notably TP53 mutations, present in 10–15% of de novo and up to 25% of therapy-related AML. Thus, we hypothesized that TP53 aberrations in AML contribute to cell-intrinsic and extrinsic resistance against T-cell-based immunotherapy.
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Combining venetoclax and azacytidine with T-cell bispecific antibodies for treatment of acute myeloid leukemia: a preclinical assessment - Leukemia

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By Veit Bücklein, Pablo Umaña, Christian D. Klein, Gerulf Hänel, Daniel Nixdorf, Nora Philipp
| Nature Verified
To the Editor The development of Venetoclax (Ven) and Azacytidine (Aza) as treatment option in Acute Myeloid Leukemia (AML) has been a breakthrough especially for patients unfit for intensive chemotherapy (IC). Ven/Aza induced complete remission (CR) in 36.7% of newly diagnosed elderly AML patients [1].
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