Lab
Jane Zhu Lab
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Statement of Research Interest
Dr. Zhu's laboratory utilizes functional genomics approach and robust zebrafish model system to explore the contributions of findings emerging from integrative genomic studies to the pathogenesis of neuroblastoma and different types of cancers, and to translate the knowledge gained from experimental studies into effective therapy for these devastating malignancies.
Focus areas
1. Neuroblastoma pathogenesis. Dr. Zhu's laboratory focuses on i) exploring the in vivo contributions of new genetic findings emerging from integrative genomic studies to neuroblastoma pathogenesis, ii) uncovering molecular mechanisms that underlie the tumor initiation and progression, and iii) developing novel targeted therapies for this devastating childhood malignancy.
2. Tumor metastasis. By taking the advantage of an innovative zebrafish model of neuroblastoma metastasis, Dr. Zhu is particularly interested in defining the mechanisms underlying the metastasis of neuroblastoma cells in vivo and identifying novel genes and pathways are critical for this metastatic disease using novel forward and reverse genetic approaches.
3. Phosphatase signaling in tumorigenesis. An additional area of focus is to understand the role of aberrantly regulated phosphatases signaling, including the SHP2 and the PTPRD tyrosine phosphatases and their pathways, in malignant transformation and progression of neuroblastoma and different types of cancers.
Focus areas
1. Neuroblastoma pathogenesis. Dr. Zhu's laboratory focuses on i) exploring the in vivo contributions of new genetic findings emerging from integrative genomic studies to neuroblastoma pathogenesis, ii) uncovering molecular mechanisms that underlie the tumor initiation and progression, and iii) developing novel targeted therapies for this devastating childhood malignancy.
2. Tumor metastasis. By taking the advantage of an innovative zebrafish model of neuroblastoma metastasis, Dr. Zhu is particularly interested in defining the mechanisms underlying the metastasis of neuroblastoma cells in vivo and identifying novel genes and pathways are critical for this metastatic disease using novel forward and reverse genetic approaches.
3. Phosphatase signaling in tumorigenesis. An additional area of focus is to understand the role of aberrantly regulated phosphatases signaling, including the SHP2 and the PTPRD tyrosine phosphatases and their pathways, in malignant transformation and progression of neuroblastoma and different types of cancers.
Lab Members
Dong, Zhiwei Post-Doc | Zhang, Xiaoling Post-Doc |
- Lawrence, J.M., Tan, S.H., Kim, D.C., Tan, K.E., Schroeder, S.E., Yeo, K.S., Schaefer, M.A., Sosic, A.M., Zhu, S. (2024) Diverse Engraftment Capability of Neuroblastoma Cell Lines in Zebrafish Larvae. Zebrafish. 21(6):385-393
- Weichert-Leahey, N., Shi, H., Tao, T., Oldridge, D.A., Durbin, A.D., Abraham, B.J., Zimmerman, M.W., Zhu, S., Wood, A.C., Reyon, D., Joung, J.K., Young, R.A., Diskin, S.J., Maris, J.M., Look, A.T. (2023) Genetic predisposition to neuroblastoma results from a regulatory polymorphism that promotes the adrenergic cell state. The Journal of Clinical Investigation. 133(10):
- Anderson, N.M., Qin, X., Finan, J.M., Lam, A., Athoe, J., Missiaen, R., Skuli, N., Kennedy, A., Saini, A.S., Tao, T., Zhu, S., Nissim, I., Look, A.T., Qing, G., Simon, M.C., Feng, H. (2021) Metabolic Enzyme DLST Promotes Tumor Aggression and Reveals a Vulnerability to OXPHOS Inhibition in High-Risk Neuroblastoma. Cancer research. 81(17):4417-4430
- Dong, Z., Yeo, K.S., Lopez, G., Zhang, C., Dankert Eggum, E.N., Rokita, J.L., Ung, C.Y., Levee, T.M., Her, Z.P., Howe, C.J., Hou, X., van Ree, J.H., Li, S., He, S., Tao, T., Fritchie, K., Torres-Mora, J., Lehman, J.S., Meves, A., Razidlo, G.L., Rathi, K.S., Weroha, S.J., Look, A.T., van Deursen, J.M., Li, H., Westendorf, J.J., Maris, J.M., Zhu, S. (2021) GAS7 Deficiency Promotes Metastasis in MYCN-driven Neuroblastoma. Cancer research. 81(11):2995-3007
- Koach, J., Holien, J.K., Massudi, H., Carter, D.R., Ciampa, O.C., Herath, M., Lim, T., Seneviratne, J.A., Milazzo, G., Murray, J.E., McCarroll, J.A., Liu, B., Mayoh, C., Keenan, B., Stevenson, B.W., Gorman, M.A., Bell, J.L., Doughty, L., Hüttelmaier, S., Oberthuer, A., Fischer, M., Gifford, A.J., Liu, T., Zhang, X., Zhu, S., Gustafson, W.C., Haber, M., Norris, M.D., Fletcher, J.I., Perini, G., Parker, M.W., Cheung, B.B., Marshall, G.M. (2019) Drugging MYCN Oncogenic Signaling through the MYCN-PA2G4 Binding Interface. Cancer research. 79:5652-5667
- Zimmerman, M.W., Liu, Y., He, S., Durbin, A.D., Abraham, B.J., Easton, J., Shao, Y., Xu, B., Zhu, S., Zhang, X., Li, Z., Weichert-Leahey, N., Young, R.A., Zhang, J., Look, A.T. (2018) MYC Drives a Subset of High-Risk Pediatric Neuroblastomas and Is Activated through Mechanisms Including Enhancer Hijacking and Focal Enhancer Amplification. Cancer discovery. 8:320-335
- Tao, T., Sondalle, S.B., Shi, H., Zhu, S., Perez-Atayde, A.R., Peng, J., Baserga, S.J., Look, A.T. (2017) The pre-rRNA processing factor DEF is rate limiting for the pathogenesis of MYCN-driven neuroblastoma. Oncogene. 36(27):3852-3867
- Zhang, X., Dong, Z., Zhang, C., Ung, C.Y., He, S., Tao, T., Oliveira, A.M., Meves, A., Ji, B., Look, A.T., Li, H., Neel, B.G., Zhu, S. (2017) Critical Role for GAB2 in Neuroblastoma Pathogenesis through the Promotion of SHP2/MYCN Cooperation. Cell Reports. 18:2932-2942
- Zhu, S., Zhang, X., Weichert-Leahey, N., Dong, Z., Zhang, C., Lopez, G., Tao, T., He, S., Wood, A.C., Oldridge, D., Ung, C.Y., van Ree, J.H., Khan, A., Salazar, B.M., Lummertz da Rocha, E., Zimmerman, M.W., Guo, F., Cao, H., Hou, X., Weroha, S.J., Perez-Atayde, A.R., Neuberg, D.S., Meves, A., McNiven, M.A., van Deursen, J.M., Li, H., Maris, J.M., Look, A.T. (2017) LMO1 Synergizes with MYCN to Promote Neuroblastoma Initiation and Metastasis. Cancer Cell. 32(3):310-323.e5
- He, S., Mansour, M.R., Zimmerman, M.W., Ki, D.H., Layden, H.M., Akahane, K., Gjini, E., de Groh, E.D., Perez-Atayde, A.R., Zhu, S., Epstein, J.A., Look, A.T. (2016) Synergy between loss of NF1 and overexpression of MYCN in neuroblastoma is mediated by the GAP-related domain. eLIFE. 5
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