Tara Barron

All Publications

• GLIOMA SYNAPSES RECRUIT MECHANISMS OF ADAPTIVE PLASTICITY Taylor, K., Barron, T., Zhang, H., Hui, A., Hartmann, G., Ni, L., Venkatesh, H., Du, P., Mancusi, R., Yalcin, B., Chau, I., Ponnuswami, A., Aziz-Bose, R., Monje, M. OXFORD UNIV PRESS INC. 2022: 25

  View details for Web of Science ID 000888571000100

• NF1 MUTATION DRIVES NEURONAL ACTIVITY-DEPENDENT OPTIC GLIOMA INITIATION Pan, Y., Hysinger, J., Barron, T., Schindler, N., Cobb, O., Guo, X., Yalcin, B., Anastasaki, C., Mulinyawe, S., Ponnuswami, A., Scheaffer, S., Ma, Y., Chang, K., Xia, X., Toonen, J., Lennon, J., Gibson, E., Huguenard, J., Liau, L., Goldberg, J., Monje, M., Gutmann, D. OXFORD UNIV PRESS INC. 2021: 212

  View details for Web of Science ID 000757356200853

• EARLY GABAERGIC NEURONAL LINEAGE DEFINES DEPENDENCIES IN HISTONE H3 G34R/V GLIOMA Liu, I., Bjerke, L., Cruzeiro, G., Rogers, R. F., Grabovska, Y., Panditharatna, E., Mackay, A., Barron, T., Shaw, M., Hoffman, S. E., Hack, O. A., Quezada, M. A., Dempster, J., Temelso, S., Englinger, B., Molinari, V., Mire, H. M., Jiang, L., Madlener, S., Mayr, L., Dorfer, C., Geyeregger, R., Rota, C., Ricken, G., Alexandrescu, S., Braun, E., Danan-Gotthold, M., Hu, L., Siletti, K., Sundstroem, E., Hodge, R., Lein, E., Agnihotri, S., Eisenstat, D. D., Carceller, F., Stapleton, S., Bleil, C., Mastronuzzi, A., Cole, K. A., Waanders, A. J., Montero Carcaboso, A., Vinci, M., Hargrave, D., Haberler, C., Gojo, J., Slavc, I., Linnarsson, S., Monje, M., Jones, C., Filbin, M. G. OXFORD UNIV PRESS INC. 2021: 18

  View details for DOI 10.1093/neuonc/noab090.072

  View details for Web of Science ID 000671540600073

• TARGETING GABAERGIC NEURON-GLIOMA SYNAPSES IN DIFFUSE INTRINSIC PONTINE GLIOMA (DIPG) THROUGH ANTI-EPILEPTIC DRUG REPURPOSING Barron, T., Mehta, V., Woo, P., Monje, M. OXFORD UNIV PRESS INC. 2021: 17-18

  View details for DOI 10.1093/neuonc/noab090.070

  View details for Web of Science ID 000671540600071

• MALIGNANT SYNAPTIC PLASTICITY IN PEDIATRIC HIGH-GRADE GLIOMAS Taylor, K., Barron, T., Hartmann, G., Zhang, H., Hui, A., Gillespie, S., Monje, M. OXFORD UNIV PRESS INC. 2021: 21

  View details for DOI 10.1093/neuonc/noab090.085

  View details for Web of Science ID 000671540600086

• NF1 mutation drives neuronalactivity-dependent initiation of optic glioma. Nature Pan, Y., Hysinger, J. D., Barron, T., Schindler, N. F., Cobb, O., Guo, X., Yalcin, B., Anastasaki, C., Mulinyawe, S. B., Ponnuswami, A., Scheaffer, S., Ma, Y., Chang, K., Xia, X., Toonen, J. A., Lennon, J. J., Gibson, E. M., Huguenard, J. R., Liau, L. M., Goldberg, J. L., Monje, M., Gutmann, D. H. 2021

  Abstract

  Neurons have recently emerged as essential cellular constituents of the tumour microenvironment, and their activity has been shown to increase the growth of a diverse number of solid tumours1. Although the role of neurons in tumour progression has previously been demonstrated2, the importance of neuronal activity to tumour initiation is less clear-particularly in the setting of cancer predisposition syndromes. Fifteen per cent of individuals with theneurofibromatosis1 (NF1) cancer predisposition syndrome (in which tumours arise in close association with nerves) develop low-grade neoplasms of the optic pathway (known as optic pathway gliomas (OPGs)) during early childhood3,4, raising the possibility that postnatal light-induced activity of the optic nerve drives tumour initiation. Here we use an authenticated mouse model of OPG driven by mutations in the neurofibromatosis1 tumour suppressor gene (Nf1)5 to demonstrate that stimulation of optic nerve activity increases optic glioma growth, and that decreasing visual experience via light deprivation prevents tumour formation and maintenance. We show that the initiation of Nf1-driven OPGs (Nf1-OPGs) depends on visual experience during a developmental period in which Nf1-mutant mice are susceptible to tumorigenesis. Germline Nf1 mutation in retinal neurons results in aberrantly increased shedding of neuroligin3 (NLGN3) within the optic nerve in response to retinal neuronal activity. Moreover, genetic Nlgn3 loss or pharmacological inhibition of NLGN3 shedding blocks the formation and progression of Nf1-OPGs. Collectively, our studies establish an obligate role for neuronal activity in the development of some types of brain tumours, elucidate a therapeutic strategy to reduce OPG incidence or mitigate tumour progression, and underscore the role of Nf1mutation-mediated dysregulation of neuronal signalling pathways in mouse models of the NF1 cancer predisposition syndrome.

  View details for DOI 10.1038/s41586-021-03580-6

  View details for PubMedID 34040258