One more thing. Another work led by the dedicated and talented scientists @DiqiuR and Shangshang Wang, stemming from our long-standing collaboration with Rahul Kohli and @andyjminn’s labs at Penn.
https://t.co/3YrjJQ5nwE
Very excited to get this new work by Shin Ngiow up on #bioRxiv. We may be blocking PD-1 too long causing detrimental effects on Tpex cells. A drug holiday approach may be beneficial. Also some cool new Tpex biology here. #immunopharmacology https://t.co/TjkOE423Gu
Have been missing twitter. Excited to share our new study. This was a close collaboration with Kathrin Bernt's and @KaiTanLab1 labs, led by the talented and unstoppable @TomZhendong and Sixiang Yu
https://t.co/iq30DVhpiK
Our improved, inducible base editing system (seBE) provides controllable and robust genome editing to systematically identify functionally relevant key residues for cancer functional genomics.
One more thing. Another work led by the dedicated and talented scientists @DiqiuR and Shangshang Wang, stemming from our long-standing collaboration with Rahul Kohli and @andyjminn’s labs at Penn.
https://t.co/3YrjJQ5nwE
A high-resolution tiling base editing mutagenesis screen targeting Adar1, an adenosine deaminase associated with tumor immunity, identified both loss-of-function and gain-of-function alleles.
This robust and general CRISPR-based functional genomics approach in primary AML patient samples opens up new opportunities to prioritize/identify therapeutic targets and understand resistance mechanisms in AML.
CRISPR knockout screens reveal both shared and distinct AML dependencies in primary samples. CRISPRi screens identify essential cis-regulatory elements in PDXs. We further used Perturb-seq to dissect regulatory networks and cellular heterogeneity in primary AML cells.
Healthy blood cells can live without ARHGAP45—but acute myeloid leukemia cells can’t. 🩸 Junwei Shi, PhD, Associate Professor of Cancer Biology (@junwei_s) and team show a CAR T + CDC42 inhibition strategy could target AML with minimal side effects. https://t.co/2mD0DW5rQs
Systematic evaluation of GAPs and GEFs identifies a targetable dependency for hematopoietic malignancies ft. Yuqiao Liu & @junwei_s (@Penn_CBIO) @CD_AACR https://t.co/gnC1Am9Lh4
@AbdelWahablab@DaniyanMd@PuZhang09980432@TomZhendong Even more exciting: CDC42 inhibition not only synergizes with ARHGAP45 loss intrinsically in leukemia cells, but also enhances TCR-CAR T cell function. A dual strategy to target cancer cells and augment immune responses.