Author

J. L. Yang

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· 3

Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Organism:mouse· 3 Assay:bulk RNA-seq· 2 Research Focus:cancer & tumor microenvironment· 2 Research Focus:cell type annotation· 1 Assay:ChIP-seq· 1 Research Focus:chromatin & epigenetic regulation· 1 Research Focus:differential expression· 1

Frequent Co-Authors

R. Koche· 3 shared A. Dunbar· 2 shared A. Karzai· 2 shared M. Farina· 2 shared W. Xiao· 2 shared Y. Park· 2 shared A. F. Rendeiro· 1 shared A. Grimont· 1 shared

Activity by Year

2021-2022 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 30 mutual co-author links

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3 shared papersCancer Biology

R. Koche

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Author profile →

3 papers

Recent·Most cited

Jak2V617F Reversible Activation Shows an Essential Requirement for Jak2V617F in Myeloproliferative Neoplasms

A. Dunbar, R. L. Bowman, Y. Park, F. Izzo, R. M. Myers, A. Karzai, W. Jun Kim, I. Fernandez Maestre, M. R. Waarts, A. Nazir, W. Xiao, M. Brodsky, M. Farina, L. Cai, S. F. Cai, , R. L. Levine

This study shows that reversible activation of Jak2V617F in a mouse model demonstrates its essential role in myeloproliferative neoplasms and highlights the therapeutic potential of mutant-specific JAK2 inhibition.

bioRxiv · May 18, 2022 · PreprintCancer Biology

CXCL8/CXCR2 signaling mediates bone marrow fibrosis and represents a therapeutic target in myelofibrosis

A. Dunbar, D. Kim, M. Lu, M. Farina, J. L. Yang, Y. Park, F. Gobbo, P. Verachi, F. Martelli, A. Karzai, W. Xiao, L. Xia, N. Elmansy, M. Kleppe, Z. Chen, , R. Hoffman

This study identifies CXCL8/CXCR2 signaling as a driver of bone marrow fibrosis in myelofibrosis and shows its therapeutic potential through genetic and pharmacologic inhibition.

bioRxiv · Dec 8, 2021Cancer Biology

An epigenetic memory of inflammation controls context-dependent lineage plasticity in the pancreas

D. J. Falvo, A. Grimont, P. Zumbo, J. L. Yang, A. Osterhoudt, G. Pan, A. F. Rendeiro, J. E. Wilkinson, F. Dündar, O. Elemento, R. K. Yantiss, D. Betel, R. Koche, R. Chandwani

This study shows that inflammation leaves an epigenetic memory in pancreatic acinar cells, affecting their lineage plasticity and tumorigenesis in response to subsequent stress.

bioRxiv · Nov 1, 2021Cancer Biology