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There's a time and a place for MYCN.

Cancer cell

Phoenix TN, Gilbertson RJ.
PMID: 22624707
Cancer Cell. 2012 May 15;21(5):593-595. doi: 10.1016/j.ccr.2012.05.001.

Brain tumors display extensive diversity. In this issue of Cancer Cell, Swartling et al. provide evidence that the temporal and spatial transcriptional programs in neural stem cells underlie a diverse response to the MYCN oncogene, potentially contributing to cancer...

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Phoenix TN, Gilbertson RJ. There's a time and a place for MYCN. Cancer Cell. 2012;21(5):593-595doi: 10.1016/j.ccr.2012.05.001.
Phoenix, T. N., & Gilbertson, R. J. (2012). There's a time and a place for MYCN. Cancer cell, 21(5), 593-595. https://doi.org/10.1016/j.ccr.2012.05.001
Phoenix, Timothy N, and Gilbertson, Richard J. "There's a time and a place for MYCN." Cancer cell vol. 21,5 (2012): 593-595. doi: https://doi.org/10.1016/j.ccr.2012.05.001
Phoenix TN, Gilbertson RJ. There's a time and a place for MYCN. Cancer Cell. 2012 May 15;21(5):593-595. doi: 10.1016/j.ccr.2012.05.001. PMID: 22624707.
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A novel, ataxic mouse model of ataxia telangiectasia caused by a clinically relevant nonsense mutation.

eLife

Perez H, Abdallah MF, Chavira JI, Norris AS, Egeland MT, Vo KL, Buechsenschuetz CL, Sanghez V, Kim JL, Pind M, Nakamura K, Hicks GG, Gatti RA, Madrenas J, Iacovino M, McKinnon PJ, Mathews PJ.
PMID: 34723800
Elife. 2021 Nov 01;10. doi: 10.7554/eLife.64695.

Ataxia Telangiectasia (A-T) and Ataxia with Ocular Apraxia Type 1 (AOA1) are devastating neurological disorders caused by null mutations in the genome stability genes, A-T mutated (

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Perez H, Abdallah MF, Chavira JI, et al. A novel, ataxic mouse model of ataxia telangiectasia caused by a clinically relevant nonsense mutation. Elife. 2021;10doi: 10.7554/eLife.64695.
Perez, H., Abdallah, M. F., Chavira, J. I., Norris, A. S., Egeland, M. T., Vo, K. L., Buechsenschuetz, C. L., Sanghez, V., Kim, J. L., Pind, M., Nakamura, K., Hicks, G. G., Gatti, R. A., Madrenas, J., Iacovino, M., McKinnon, P. J., & Mathews, P. J. (2021). A novel, ataxic mouse model of ataxia telangiectasia caused by a clinically relevant nonsense mutation. eLife, 10. https://doi.org/10.7554/eLife.64695
Perez, Harvey, et al. "A novel, ataxic mouse model of ataxia telangiectasia caused by a clinically relevant nonsense mutation." eLife vol. 10 (2021). doi: https://doi.org/10.7554/eLife.64695
Perez H, Abdallah MF, Chavira JI, Norris AS, Egeland MT, Vo KL, Buechsenschuetz CL, Sanghez V, Kim JL, Pind M, Nakamura K, Hicks GG, Gatti RA, Madrenas J, Iacovino M, McKinnon PJ, Mathews PJ. A novel, ataxic mouse model of ataxia telangiectasia caused by a clinically relevant nonsense mutation. Elife. 2021 Nov 01;10. doi: 10.7554/eLife.64695. PMID: 34723800; PMCID: PMC8601662.
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A Chimeric GM-CSF/IL18 Receptor to Sustain CAR T-cell Function.

Cancer discovery

Lange S, Sand LGL, Bell M, Patil SL, Langfitt D, Gottschalk S.
PMID: 33563660
Cancer Discov. 2021 Jul;11(7):1661-1671. doi: 10.1158/2159-8290.CD-20-0896. Epub 2021 Feb 09.

The inability of chimeric antigen receptor (CAR) T cells to sustain their effector function after repeated exposure to tumor cells is a major obstacle to their success in patients with solid tumors. To overcome this limitation, we designed a...

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Lange S, Sand LGL, Bell M, et al. A Chimeric GM-CSF/IL18 Receptor to Sustain CAR T-cell Function. Cancer Discov. 2021;11(7):1661-1671doi: 10.1158/2159-8290.CD-20-0896.
Lange, S., Sand, L. G. L., Bell, M., Patil, S. L., Langfitt, D., & Gottschalk, S. (2021). A Chimeric GM-CSF/IL18 Receptor to Sustain CAR T-cell Function. Cancer discovery, 11(7), 1661-1671. https://doi.org/10.1158/2159-8290.CD-20-0896
Lange, Shannon, et al. "A Chimeric GM-CSF/IL18 Receptor to Sustain CAR T-cell Function." Cancer discovery vol. 11,7 (2021): 1661-1671. doi: https://doi.org/10.1158/2159-8290.CD-20-0896
Lange S, Sand LGL, Bell M, Patil SL, Langfitt D, Gottschalk S. A Chimeric GM-CSF/IL18 Receptor to Sustain CAR T-cell Function. Cancer Discov. 2021 Jul;11(7):1661-1671. doi: 10.1158/2159-8290.CD-20-0896. Epub 2021 Feb 09. PMID: 33563660; PMCID: PMC8292158.
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Exome sequencing analysis of murine medulloblastoma models identifies WDR11 as a potential tumor suppressor in Group 3 tumors.

Oncotarget

Wei L, Murphy BL, Wu G, Parker M, Easton J, Gilbertson RJ, Zhang J, Roussel MF.
PMID: 29029386
Oncotarget. 2017 Jul 27;8(39):64685-64697. doi: 10.18632/oncotarget.19642. eCollection 2017 Sep 12.

Mouse models of human cancers are widely used in cancer research, yet questions frequently arise regarding their faithfulness in recapitulating their human counterparts. To compare the somatic mutations of murine models with human medulloblastoma (MB), we performed whole-exome sequencing...

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Wei L, Murphy BL, Wu G, et al. Exome sequencing analysis of murine medulloblastoma models identifies WDR11 as a potential tumor suppressor in Group 3 tumors. Oncotarget. 2017;8(39):64685-64697doi: 10.18632/oncotarget.19642.
Wei, L., Murphy, B. L., Wu, G., Parker, M., Easton, J., Gilbertson, R. J., Zhang, J., & Roussel, M. F. (2017). Exome sequencing analysis of murine medulloblastoma models identifies WDR11 as a potential tumor suppressor in Group 3 tumors. Oncotarget, 8(39), 64685-64697. https://doi.org/10.18632/oncotarget.19642
Wei, Lei, et al. "Exome sequencing analysis of murine medulloblastoma models identifies WDR11 as a potential tumor suppressor in Group 3 tumors." Oncotarget vol. 8,39 (2017): 64685-64697. doi: https://doi.org/10.18632/oncotarget.19642
Wei L, Murphy BL, Wu G, Parker M, Easton J, Gilbertson RJ, Zhang J, Roussel MF. Exome sequencing analysis of murine medulloblastoma models identifies WDR11 as a potential tumor suppressor in Group 3 tumors. Oncotarget. 2017 Jul 27;8(39):64685-64697. doi: 10.18632/oncotarget.19642. eCollection 2017 Sep 12. PMID: 29029386; PMCID: PMC5630286.
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Medulloblastoma: advances and challenges.

F1000 biology reports

Roussel MF, Robinson G.
PMID: 21655335
F1000 Biol Rep. 2011;3:5. doi: 10.3410/B3-5. Epub 2011 Mar 01.

Medulloblastoma, a cancer of the posterior fossa, is the most common malignant brain tumor in children. Although 80% of patients with average-risk medulloblastoma are cured, their quality of life is often compromised by treatment-related side effects. Recently, molecular and...

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Roussel MF, Robinson G. Medulloblastoma: advances and challenges. F1000 Biol Rep. 2011;3:5doi: 10.3410/B3-5.
Roussel, M. F., & Robinson, G. (2011). Medulloblastoma: advances and challenges. F1000 biology reports, 35. https://doi.org/10.3410/B3-5
Roussel, Martine F, and Robinson, Giles. "Medulloblastoma: advances and challenges." F1000 biology reports vol. 3 (2011): 5. doi: https://doi.org/10.3410/B3-5
Roussel MF, Robinson G. Medulloblastoma: advances and challenges. F1000 Biol Rep. 2011;3:5. doi: 10.3410/B3-5. Epub 2011 Mar 01. PMID: 21655335; PMCID: PMC3100785.
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Correction to: H3.3 K27M depletion increases differentiation and extends latency of diffuse intrinsic pontine glioma growth in vivo.

Acta neuropathologica

Silveira AB, Kasper LH, Fan Y, Jin H, Wu G, Shaw TI, Zhu X, Larson JD, Easton J, Shao Y, Yergeau DA, Rosencrance C, Boggs K, Rusch MC, Ding L, Zhang J, Finkelstein D, Noyes RM, Russell BL, Xu B, Broniscer A, Wetmore C, Pounds SB, Ellison DW, Zhang J, Baker SJ.
PMID: 30976974
Acta Neuropathol. 2019 Jun;137(6):1021. doi: 10.1007/s00401-019-02006-y. Epub 2019 Apr 11.

The original article can be found online.

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Silveira AB, Kasper LH, Fan Y, et al. Correction to: H3.3 K27M depletion increases differentiation and extends latency of diffuse intrinsic pontine glioma growth in vivo. Acta Neuropathol. 2019;137(6):1021doi: 10.1007/s00401-019-02006-y.
Silveira, A. B., Kasper, L. H., Fan, Y., Jin, H., Wu, G., Shaw, T. I., Zhu, X., Larson, J. D., Easton, J., Shao, Y., Yergeau, D. A., Rosencrance, C., Boggs, K., Rusch, M. C., Ding, L., Zhang, J., Finkelstein, D., Noyes, R. M., Russell, B. L., Xu, B., Broniscer, A., Wetmore, C., Pounds, S. B., Ellison, D. W., Zhang, J., & Baker, S. J. (2019). Correction to: H3.3 K27M depletion increases differentiation and extends latency of diffuse intrinsic pontine glioma growth in vivo. Acta neuropathologica, 137(6), 1021. https://doi.org/10.1007/s00401-019-02006-y
Silveira, André B, et al. "Correction to: H3.3 K27M depletion increases differentiation and extends latency of diffuse intrinsic pontine glioma growth in vivo." Acta neuropathologica vol. 137,6 (2019): 1021. doi: https://doi.org/10.1007/s00401-019-02006-y
Silveira AB, Kasper LH, Fan Y, Jin H, Wu G, Shaw TI, Zhu X, Larson JD, Easton J, Shao Y, Yergeau DA, Rosencrance C, Boggs K, Rusch MC, Ding L, Zhang J, Finkelstein D, Noyes RM, Russell BL, Xu B, Broniscer A, Wetmore C, Pounds SB, Ellison DW, Zhang J, Baker SJ. Correction to: H3.3 K27M depletion increases differentiation and extends latency of diffuse intrinsic pontine glioma growth in vivo. Acta Neuropathol. 2019 Jun;137(6):1021. doi: 10.1007/s00401-019-02006-y. Epub 2019 Apr 11. PMID: 30976974; PMCID: PMC6999025.
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A Chimeric GM-CSF/IL18 Receptor to Sustain CAR T-cell Function.

Cancer discovery

Lange S, Sand LGL, Bell M, Patil SL, Langfitt D, Gottschalk S.
PMID: 33563660
Cancer Discov. 2021 Jul;11(7):1661-1671. doi: 10.1158/2159-8290.CD-20-0896. Epub 2021 Feb 09.

The inability of chimeric antigen receptor (CAR) T cells to sustain their effector function after repeated exposure to tumor cells is a major obstacle to their success in patients with solid tumors. To overcome this limitation, we designed a...

Cite
Lange S, Sand LGL, Bell M, et al. A Chimeric GM-CSF/IL18 Receptor to Sustain CAR T-cell Function. Cancer Discov. 2021;11(7):1661-1671doi: 10.1158/2159-8290.CD-20-0896.
Lange, S., Sand, L. G. L., Bell, M., Patil, S. L., Langfitt, D., & Gottschalk, S. (2021). A Chimeric GM-CSF/IL18 Receptor to Sustain CAR T-cell Function. Cancer discovery, 11(7), 1661-1671. https://doi.org/10.1158/2159-8290.CD-20-0896
Lange, Shannon, et al. "A Chimeric GM-CSF/IL18 Receptor to Sustain CAR T-cell Function." Cancer discovery vol. 11,7 (2021): 1661-1671. doi: https://doi.org/10.1158/2159-8290.CD-20-0896
Lange S, Sand LGL, Bell M, Patil SL, Langfitt D, Gottschalk S. A Chimeric GM-CSF/IL18 Receptor to Sustain CAR T-cell Function. Cancer Discov. 2021 Jul;11(7):1661-1671. doi: 10.1158/2159-8290.CD-20-0896. Epub 2021 Feb 09. PMID: 33563660; PMCID: PMC8292158.
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Deleting DNMT3A in CAR T cells prevents exhaustion and enhances antitumor activity.

Science translational medicine

Prinzing B, Zebley CC, Petersen CT, Fan Y, Anido AA, Yi Z, Nguyen P, Houke H, Bell M, Haydar D, Brown C, Boi SK, Alli S, Crawford JC, Riberdy JM, Park JJ, Zhou S, Velasquez MP, DeRenzo C, Lazzarotto CR, Tsai SQ, Vogel P, Pruett-Miller SM, Langfitt DM, Gottschalk S, Youngblood B, Krenciute G.
PMID: 34788079
Sci Transl Med. 2021 Nov 17;13(620):eabh0272. doi: 10.1126/scitranslmed.abh0272. Epub 2021 Nov 17.

[Figure: see text].

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Prinzing B, Zebley CC, Petersen CT, et al. Deleting DNMT3A in CAR T cells prevents exhaustion and enhances antitumor activity. Sci Transl Med. 2021;13(620):eabh0272doi: 10.1126/scitranslmed.abh0272.
Prinzing, B., Zebley, C. C., Petersen, C. T., Fan, Y., Anido, A. A., Yi, Z., Nguyen, P., Houke, H., Bell, M., Haydar, D., Brown, C., Boi, S. K., Alli, S., Crawford, J. C., Riberdy, J. M., Park, J. J., Zhou, S., Velasquez, M. P., DeRenzo, C., Lazzarotto, C. R., Tsai, S. Q., Vogel, P., Pruett-Miller, S. M., Langfitt, D. M., Gottschalk, S., Youngblood, B., & Krenciute, G. (2021). Deleting DNMT3A in CAR T cells prevents exhaustion and enhances antitumor activity. Science translational medicine, 13(620), eabh0272. https://doi.org/10.1126/scitranslmed.abh0272
Prinzing, Brooke, et al. "Deleting DNMT3A in CAR T cells prevents exhaustion and enhances antitumor activity." Science translational medicine vol. 13,620 (2021): eabh0272. doi: https://doi.org/10.1126/scitranslmed.abh0272
Prinzing B, Zebley CC, Petersen CT, Fan Y, Anido AA, Yi Z, Nguyen P, Houke H, Bell M, Haydar D, Brown C, Boi SK, Alli S, Crawford JC, Riberdy JM, Park JJ, Zhou S, Velasquez MP, DeRenzo C, Lazzarotto CR, Tsai SQ, Vogel P, Pruett-Miller SM, Langfitt DM, Gottschalk S, Youngblood B, Krenciute G. Deleting DNMT3A in CAR T cells prevents exhaustion and enhances antitumor activity. Sci Transl Med. 2021 Nov 17;13(620):eabh0272. doi: 10.1126/scitranslmed.abh0272. Epub 2021 Nov 17. PMID: 34788079.
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A Chimeric GM-CSF/IL18 Receptor to Sustain CAR T-cell Function.

Cancer discovery

Lange S, Sand LGL, Bell M, Patil SL, Langfitt D, Gottschalk S.
PMID: 33563660
Cancer Discov. 2021 Jul;11(7):1661-1671. doi: 10.1158/2159-8290.CD-20-0896. Epub 2021 Feb 09.

The inability of chimeric antigen receptor (CAR) T cells to sustain their effector function after repeated exposure to tumor cells is a major obstacle to their success in patients with solid tumors. To overcome this limitation, we designed a...

Cite
Lange S, Sand LGL, Bell M, et al. A Chimeric GM-CSF/IL18 Receptor to Sustain CAR T-cell Function. Cancer Discov. 2021;11(7):1661-1671doi: 10.1158/2159-8290.CD-20-0896.
Lange, S., Sand, L. G. L., Bell, M., Patil, S. L., Langfitt, D., & Gottschalk, S. (2021). A Chimeric GM-CSF/IL18 Receptor to Sustain CAR T-cell Function. Cancer discovery, 11(7), 1661-1671. https://doi.org/10.1158/2159-8290.CD-20-0896
Lange, Shannon, et al. "A Chimeric GM-CSF/IL18 Receptor to Sustain CAR T-cell Function." Cancer discovery vol. 11,7 (2021): 1661-1671. doi: https://doi.org/10.1158/2159-8290.CD-20-0896
Lange S, Sand LGL, Bell M, Patil SL, Langfitt D, Gottschalk S. A Chimeric GM-CSF/IL18 Receptor to Sustain CAR T-cell Function. Cancer Discov. 2021 Jul;11(7):1661-1671. doi: 10.1158/2159-8290.CD-20-0896. Epub 2021 Feb 09. PMID: 33563660; PMCID: PMC8292158.
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Deleting DNMT3A in CAR T cells prevents exhaustion and enhances antitumor activity.

Science translational medicine

Prinzing B, Zebley CC, Petersen CT, Fan Y, Anido AA, Yi Z, Nguyen P, Houke H, Bell M, Haydar D, Brown C, Boi SK, Alli S, Crawford JC, Riberdy JM, Park JJ, Zhou S, Velasquez MP, DeRenzo C, Lazzarotto CR, Tsai SQ, Vogel P, Pruett-Miller SM, Langfitt DM, Gottschalk S, Youngblood B, Krenciute G.
PMID: 34788079
Sci Transl Med. 2021 Nov 17;13(620):eabh0272. doi: 10.1126/scitranslmed.abh0272. Epub 2021 Nov 17.

[Figure: see text].

Cite
Prinzing B, Zebley CC, Petersen CT, et al. Deleting DNMT3A in CAR T cells prevents exhaustion and enhances antitumor activity. Sci Transl Med. 2021;13(620):eabh0272doi: 10.1126/scitranslmed.abh0272.
Prinzing, B., Zebley, C. C., Petersen, C. T., Fan, Y., Anido, A. A., Yi, Z., Nguyen, P., Houke, H., Bell, M., Haydar, D., Brown, C., Boi, S. K., Alli, S., Crawford, J. C., Riberdy, J. M., Park, J. J., Zhou, S., Velasquez, M. P., DeRenzo, C., Lazzarotto, C. R., Tsai, S. Q., Vogel, P., Pruett-Miller, S. M., Langfitt, D. M., Gottschalk, S., Youngblood, B., & Krenciute, G. (2021). Deleting DNMT3A in CAR T cells prevents exhaustion and enhances antitumor activity. Science translational medicine, 13(620), eabh0272. https://doi.org/10.1126/scitranslmed.abh0272
Prinzing, Brooke, et al. "Deleting DNMT3A in CAR T cells prevents exhaustion and enhances antitumor activity." Science translational medicine vol. 13,620 (2021): eabh0272. doi: https://doi.org/10.1126/scitranslmed.abh0272
Prinzing B, Zebley CC, Petersen CT, Fan Y, Anido AA, Yi Z, Nguyen P, Houke H, Bell M, Haydar D, Brown C, Boi SK, Alli S, Crawford JC, Riberdy JM, Park JJ, Zhou S, Velasquez MP, DeRenzo C, Lazzarotto CR, Tsai SQ, Vogel P, Pruett-Miller SM, Langfitt DM, Gottschalk S, Youngblood B, Krenciute G. Deleting DNMT3A in CAR T cells prevents exhaustion and enhances antitumor activity. Sci Transl Med. 2021 Nov 17;13(620):eabh0272. doi: 10.1126/scitranslmed.abh0272. Epub 2021 Nov 17. PMID: 34788079; PMCID: PMC8733956.
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Temporal activation of XRCC1-mediated DNA repair is essential for muscle differentiation.

Cell discovery

Al-Khalaf MH, Blake LE, Larsen BD, Bell RA, Brunette S, Parks RJ, Rudnicki MA, McKinnon PJ, Jeffrey Dilworth F, Megeney LA.
PMID: 27462438
Cell Discov. 2016 Jan 12;2:15041. doi: 10.1038/celldisc.2015.41. eCollection 2016.

Transient DNA strand break formation has been identified as an effective means to enhance gene expression in living cells. In the muscle lineage, cell differentiation is contingent upon the induction of caspase-mediated DNA strand breaks, which act to establish...

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Al-Khalaf MH, Blake LE, Larsen BD, et al. Temporal activation of XRCC1-mediated DNA repair is essential for muscle differentiation. Cell Discov. 2016;2:15041doi: 10.1038/celldisc.2015.41.
Al-Khalaf, M. H., Blake, L. E., Larsen, B. D., Bell, R. A., Brunette, S., Parks, R. J., Rudnicki, M. A., McKinnon, P. J., Jeffrey Dilworth, F., & Megeney, L. A. (2016). Temporal activation of XRCC1-mediated DNA repair is essential for muscle differentiation. Cell discovery, 215041. https://doi.org/10.1038/celldisc.2015.41
Al-Khalaf, Mohammad H, et al. "Temporal activation of XRCC1-mediated DNA repair is essential for muscle differentiation." Cell discovery vol. 2 (2016): 15041. doi: https://doi.org/10.1038/celldisc.2015.41
Al-Khalaf MH, Blake LE, Larsen BD, Bell RA, Brunette S, Parks RJ, Rudnicki MA, McKinnon PJ, Jeffrey Dilworth F, Megeney LA. Temporal activation of XRCC1-mediated DNA repair is essential for muscle differentiation. Cell Discov. 2016 Jan 12;2:15041. doi: 10.1038/celldisc.2015.41. eCollection 2016. PMID: 27462438; PMCID: PMC4860966.
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Highlights of Children with Cancer UK's Workshop on Drug Delivery in Paediatric Brain Tumours.

Ecancermedicalscience

Nailor A, Walker DA, Jacques TS, Warren KE, Brem H, Kearns PR, Greenwood J, Penny JI, Pilkington GJ, Carcaboso AM, Fleischhack G, Macarthur D, Slavc I, Meijer L, Gill S, Lowis S, van Vuurden DG, Pearl MS, Clifford SC, Morrissy S, Ivanov DP, Beccaria K, Gilbertson RJ, Straathof K, Green JJ, Smith S, Rahman R, Kilday JP.
PMID: 27110286
Ecancermedicalscience. 2016 Mar 31;10:630. doi: 10.3332/ecancer.2016.630. eCollection 2016.

The first Workshop on Drug Delivery in Paediatric Brain Tumours was hosted in London by the charity Children with Cancer UK. The goals of the workshop were to break down the barriers to treating central nervous system (CNS) tumours...

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Nailor A, Walker DA, Jacques TS, et al. Highlights of Children with Cancer UK's Workshop on Drug Delivery in Paediatric Brain Tumours. Ecancermedicalscience. 2016;10:630doi: 10.3332/ecancer.2016.630.
Nailor, A., Walker, D. A., Jacques, T. S., Warren, K. E., Brem, H., Kearns, P. R., Greenwood, J., Penny, J. I., Pilkington, G. J., Carcaboso, A. M., Fleischhack, G., Macarthur, D., Slavc, I., Meijer, L., Gill, S., Lowis, S., van Vuurden, D. G., Pearl, M. S., Clifford, S. C., Morrissy, S., Ivanov, D. P., Beccaria, K., Gilbertson, R. J., Straathof, K., Green, J. J., Smith, S., Rahman, R., & Kilday, J. P. (2016). Highlights of Children with Cancer UK's Workshop on Drug Delivery in Paediatric Brain Tumours. Ecancermedicalscience, 10630. https://doi.org/10.3332/ecancer.2016.630
Nailor, Audrey, et al. "Highlights of Children with Cancer UK's Workshop on Drug Delivery in Paediatric Brain Tumours." Ecancermedicalscience vol. 10 (2016): 630. doi: https://doi.org/10.3332/ecancer.2016.630
Nailor A, Walker DA, Jacques TS, Warren KE, Brem H, Kearns PR, Greenwood J, Penny JI, Pilkington GJ, Carcaboso AM, Fleischhack G, Macarthur D, Slavc I, Meijer L, Gill S, Lowis S, van Vuurden DG, Pearl MS, Clifford SC, Morrissy S, Ivanov DP, Beccaria K, Gilbertson RJ, Straathof K, Green JJ, Smith S, Rahman R, Kilday JP. Highlights of Children with Cancer UK's Workshop on Drug Delivery in Paediatric Brain Tumours. Ecancermedicalscience. 2016 Mar 31;10:630. doi: 10.3332/ecancer.2016.630. eCollection 2016. PMID: 27110286; PMCID: PMC4817522.
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Showing 1 to 12 of 23 entries