A photo of Jianqiang Wu.

Jianqiang Wu, MD, MS

  • Member, Division of Experimental Hematology & Cancer Biology
  • Cancer Biology and Neural Tumors Program
  • Associate Professor, UC Department of Pediatrics



I have been a researcher for more than 25 years, and I started working at Cincinnati Children’s in 2003. My research areas of interest include transcriptional factors and microRNA in neurofibromatosis type 1 (NF1) related plexiform neurofibroma (PNF) formation, the influence of microenvironment on PNF formation and pre-clinical testing of PNF.

There is no effective therapy for PNF. Surgery remains the mainstay of treatment, but sometimes surgery is impossible due to the invasive nature of PNFs, their large size and their association with critical anatomic structures.

The Food and Drug Administration (FDA) approved Selumetinib (Koselugo™), a cytostatic MEK inhibitor that shrinks about 70 percent of tumors in Nf1fl/fl; DhhCre neurofibroma-bearing mice and in inoperable PNF patients. Unfortunately, tumors regrow after stopping drug treatment. Therefore, new therapeutic strategies and MEK-independent targets for the treatment of PNFs are urgently needed. My goal is to find a cure for PNF.

One of my lab’s groundbreaking discoveries is developing a PNF mouse model and a method to monitor the drug efficacy for pre-clinical testing on this mouse’s PNFs by measuring tumor volumes on MRI images.

My research has been published in respected journals, such as Cancer Cell, Cell Stem Cell, Science Advances, New England Journal of Medicine, Acta Neuropathologica, Journal of Clinical Investigation, Cancer Research and Oncogene.


Multiple Nf1 Schwann cell populations reprogram the plexiform neurofibroma tumor microenvironment. Kershner, LJ; Choi, K; Wu, J; Zhang, X; Perrino, M; Salomonis, N; Shern, JF; Ratner, N. JCI insight. 2022; 7.

P2RY14 cAMP signaling regulates Schwann cell precursor self-renewal, proliferation, and nerve tumor initiation in a mouse model of neurofibromatosis. Cram, JP; Wu, J; Coover, RA; Rizvi, TA; Chaney, KE; Ravindran, R; Cancelas, JA; Spinner, RJ; Ratner, N. eLife. 2022; 11.

Cdkn2a Loss in a Model of Neurofibroma Demonstrates Stepwise Tumor Progression to Atypical Neurofibroma and MPNST. Chaney, KE; Perrino, MR; Kershner, LJ; Patel, AV; Wu, J; Choi, K; Rizvi, TA; Dombi, E; Szabo, S; Largaespada, DA; et al. Cancer Research. 2021; 80:4720-4730.

Mechanisms of stearoyl CoA desaturase inhibitor sensitivity and acquired resistance in cancer. Oatman, N; Dasgupta, N; Arora, P; Choi, K; Gawali, MV; Gupta, N; Parameswaran, S; Salomone, J; Reisz, JA; Lawler, S; et al. Science advances. 2021; 7.

MicroRNA-155 contributes to plexiform neurofibroma growth downstream of MEK. Na, Y; Hall, A; Choi, K; Hu, L; Rose, J; Coover, RA; Miller, A; Hennigan, RF; Dombi, E; Kim, MO; et al. Oncogene. 2021; 40:951-963.

The Role of RUNX1 in NF1-Related Tumors and Blood Disorders. Na, Y; Huang, G; Wu, J. Molecules and Cells. 2020; 43:153-159.

The Clinical, Molecular, and Mechanistic Basis of RUNX1 Mutations Identified in Hematological Malignancies. Yokota, A; Huo, L; Lan, F; Wu, J; Huang, G. Molecules and Cells. 2020; 43:145-152.

NF1 patient missense variants predict a role for ATM in modifying neurofibroma initiation. Yu, Y; Choi, K; Wu, J; Andreassen, PR; Dexheimer, PJ; Keddache, M; Brems, H; Spinner, RJ; Cancelas, JA; Martin, LJ; et al. Acta Neuropathologica. 2020; 139:157-174.

CBMT-05. GENETIC AND EPIGENETIC MECHANISMS REGULATING SCD INHIBITOR SENSITIVITY IN GLIOBLASTOMA. Oatman, N; Dasgupta, N; Choi, K; Gawali, M; Gupta, N; Parameswaran, S; Lawler, S; Brennan, C; Wu, J; Sallans, L; et al. Neuro-Oncology. 2019; 21:vi33-vi33.

The evolution and multi-molecular properties of NF1 cutaneous neurofibromas originating from C-fiber sensory endings and terminal Schwann cells at normal sites of sensory terminations in the skin. Rice, FL; Houk, G; Wymer, JP; Gosline, SJ C; Guinney, J; Wu, J; Ratner, N; Jankowski, MP; La Rosa, S; Dockum, M; et al. PLoS ONE. 2019; 14.