Peng Ji
@PengJi_lab
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Physician scientist, Hematopathologist, Vice Chair of Research, Director of Pathology Physician Scientist Training Program
Chicago, IL
Joined August 2019
Congratulations to Dr. Pan Wang who will present two oral abstracts in this year’s ASH meeting! #ASH2025
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Congratulations to our pediatric path fellow, Dr. Lydia Du, for winning the Harry B. Neustein Memorial Award for her platform presentation at the Fall Society for Pediatric Pathology meeting. We’re very proud of her! #PurplePath
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Honored to be recognized!
We are fortunate to provide Endowed Chairs to two of our phenomenal faculty, Drs. Lee Cooper and Peng Ji. Both are world-class investigators and highly deserving! #PurplePath
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Ever wondered what our residency application review process is like? Program Director @JaredAhrendsen is here to give a behind the scenes look! #PurplePath #PathMatch26
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Many thanks to @PengJi_Lab of @NUFeinbergMed for presenting today’s #Pathology Grand Rounds on “The Role of Inflammation in the Evolution from Clonal Hematopoiesis to MDS & AML” Here’s Dr. Ji, center, w/hosts, @gcai1978, left, & @MinaXu7, both Professors of Pathology @YaleMed
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Congratulations to Dr. Barina Aqil, featured in the PathologyOutlines September Newsletter: “What’s New in Hematopathology 2025: Myeloid Neoplasms in the WHO 5th Edition and ICC” #PurplePath
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A study led by @PengJi_lab revealed how a common inherited mutation disrupts red blood cell development and sparks inflammation that can lead to #leukemia, per findings in @NatureComms
https://t.co/LWKYwMBMZV
#LeukemiaAwarenessMonth #BloodCancerAwarenessMonth @NU_Pathology
news.feinberg.northwestern.edu
A new Northwestern Medicine study has revealed how a common inherited mutation disrupts red blood cell development and sparks inflammation that may lead to leukemia, according to findings published...
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Interested in a residency at Northwestern Pathology? Join our current residents for a Q&A on Thursday, September 11, 2025 from 4-5pm CST. Register here: https://t.co/0921VCNG7v
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A new study led by Lurie Cancer Center’s @PengJi_lab revealed how a common inherited mutation disrupts red blood cell development and sparks inflammation that can lead to #leukemia, per findings in @NatureComms #leusm
news.feinberg.northwestern.edu
A new Northwestern Medicine study has revealed how a common inherited mutation disrupts red blood cell development and sparks inflammation that may lead to leukemia, according to findings published...
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Our department cruised down the Chicago River for some well-deserved socializing and R&R. A bit of rain did not get in the way of a fun time for all! Big thanks to @citycruises for the great experience🚢
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Our study establishes DDX41 as a G4 resolvase, essential for erythroid genome stability and suppressing the cGAS-STING pathway.
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In parallel, genome instability also activates the cGas-Sting pathway, impairing survival, as cGas deficiency rescues the lethality of hematopoietic-specific Ddx41 knock-out mice.
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G4 accumulation induces erythroid genome instability, ribosomal defects, and p53 upregulation. However, p53 deficiency does not rescue the embryonic death of Ddx41 hematopoietic-specific knockout mice.
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DX41 deficiency induces a significant upregulation of G-quadruplexes (G4), which co-distribute with DDX41 on the erythroid genome. DDX41 directly binds to and resolves G4, which is significantly compromised in MN-associated DDX41 mutants.
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In this work, we show that DDX41 is essential for erythropoiesis but dispensable for other hematopoietic lineages. Ddx41 knockout in early erythropoiesis is embryonically lethal, while knockout in late-stage terminal erythropoiesis allows mice to survive with normal blood counts
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Deleterious germline DDX41 variants constitute the most common inherited predisposition disorder linked to myeloid neoplasms (MNs), yet their role in MNs remains unclear.
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Delighted to share our recently published work on the role of DDX41 in resolving G-quadruplexes to maintain erythroid genome integrity and prevent cGAS-mediated cell death. https://t.co/7gVvx087Fe
@NatureComms
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We had a great time at the annual Association for Academic Pathology meeting in Denver this past weekend🔬 Nice to see some familiar faces! #AAPath
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ICYMI: Ameliorating myeloproliferative neoplasms with cyclosporin A in preclinical models— @PengJi_lab & team @NUFeinbergMed discover PPIL2 as a target of the JAK2/STAT5 pathway that promotes myeloproliferation through p53 degradation: https://t.co/oT8J1qRr3V
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