Dr Mary Scott

  • Research Fellow (Paul O'Gorman Leukaemia Research Centre)

telephone: 01413302606
email: Mary.Scott@glasgow.ac.uk

Wolfson Wohl Cancer Research Centre, Garscube Estate, Glasgow, Uk, G61 1QH

Import to contacts

ORCID iDhttps://orcid.org/0000-0002-7177-6960

Publications

List by: Type | Date

Jump to: 2024 | 2023 | 2021 | 2020 | 2019 | 2018 | 2016 | 2015 | 2014 | 2013 | 2011 | 2010 | 2009 | 2008 | 2007 | 2004 | 2003 | 2002 | 2000 | 1996
Number of items: 28.

2024

Khalaf, A. et al. (2024) Nutrient-sensitizing drug repurposing screen identifies lomerizine as a mitochondrial metabolism inhibitor of chronic myeloid leukemia. Science Translational Medicine, 16(751), eadi5336. (doi: 10.1126/scitranslmed.adi5336) (PMID:38865484)

Dawson, A. et al. (2024) Leukaemia exposure alters the transcriptional profile and function of BCR::ABL1 negative macrophages in the bone marrow niche. Nature Communications, 15, 1090. (doi: 10.1038/s41467-024-45471-0) (PMID:38316788) (PMCID:PMC10844594)

Scott, M. T. et al. (2024) Activating p53 abolishes self-renewal of quiescent leukaemic stem cells in residual CML disease. Nature Communications, 15, 651. (doi: 10.1038/s41467-024-44771-9) (PMID:38246924) (PMCID:PMC10800356)

2023

Zarou, M. M. et al. (2023) Leukaemia Exposure Alters the Transcriptional Profile and Function of Macrophages in the Bone Marrow Niche. 65th ASH Annual Meeting and Exposition, San Diego, California, USA, 09-12 Dec 2023. (doi: 10.1182/blood-2023-181630)

Rattigan, K. M. et al. (2023) Arginine dependency is a therapeutically exploitable vulnerability in chronic myeloid leukaemic stem cells. EMBO Reports, 24, e56279. (doi: 10.15252/embr.202256279) (PMID:37489735) (PMCID:PMC10561355)

Rattigan, K. M. et al. (2023) Pyruvate anaplerosis is a targetable vulnerability in persistent leukaemic stem cells. Nature Communications, 14, 4634. (doi: 10.1038/s41467-023-40222-z) (PMID:37591854) (PMCID:PMC10435520)

2021

Ianniciello, A. et al. (2021) ULK1 inhibition promotes oxidative stress–induced differentiation and sensitizes leukemic stem cells to targeted therapy. Science Translational Medicine, 13(613), eabd5016. (doi: 10.1126/scitranslmed.abd5016) (PMID:34586834)

2020

Kinstrie, R. et al. (2020) CD93 is expressed on chronic myeloid leukemia stem cells and identifies a quiescent population which persists after tyrosine kinase inhibitor therapy. Leukemia, 34(6), pp. 1613-1625. (doi: 10.1038/s41375-019-0684-5) (PMID:31896780) (PMCID:PMC7272220)

2019

Bugler, J., Kinstrie, R., Scott, M. T. and Vetrie, D. (2019) Epigenetic reprogramming and emerging epigenetic therapies in CML. Frontiers in Cell and Developmental Biology, 7, 136. (doi: 10.3389/fcell.2019.00136) (PMID:31380371) (PMCID:PMC6652210)

Baquero, P. et al. (2019) Targeting quiescent leukemic stem cells using second generation autophagy inhibitors. Leukemia, 33(4), pp. 981-994. (doi: 10.1038/s41375-018-0252-4) (PMID:30185934) (PMCID:PMC6292500)

2018

Pellicano, F. et al. (2018) Hsa-mir183/EGR1-mediated regulation of E2F1 is required for CML stem/progenitor cell survival. Blood, 131(14), pp. 1532-1544. (doi: 10.1182/blood-2017-05-783845) (PMID:29437554) (PMCID:PMC6027092)

2016

Scott, M. T. et al. (2016) Epigenetic reprogramming sensitizes CML stem cells to combined EZH2 and tyrosine kinase inhibition. Cancer Discovery, 6(11), pp. 1248-1257. (doi: 10.1158/2159-8290.CD-16-0263) (PMID:27630125) (PMCID:PMC6538532)

Abraham, S. A. et al. (2016) Dual targeting of P53 and C-MYC induces selective elimination of leukemic stem cells. Nature, 534(7607), pp. 341-346. (doi: 10.1038/nature18288) (PMID:27281222) (PMCID:PMC4913876)

2015

Aspinall-O'Dea, M., Pierce, A., Pellicano, F., Williamson, A. J., Scott, M. T. , Walker, M. J., Holyoake, T. L. and Whetton, A. D. (2015) Antibody-based detection of protein phosphorylation status to track the efficacy of novel therapies using nanogram protein quantities from stem cells and cell lines. Nature Protocols, 10(1), pp. 149-168. (doi: 10.1038/nprot.2015.007) (PMID:25521791)

2014

Pellicano, F. et al. (2014) The antiproliferative activity of kinase inhibitors in chronic myeloid leukemia cells is mediated by FOXO transcription factors. Stem Cells, 32(9), pp. 2324-2337. (doi: 10.1002/stem.1748) (PMID:24806995) (PMCID:PMC4282530)

2013

Scott, M. T. et al. (2013) Misregulation of the PRC2 Complex in CML Stem Cells Confers Sensitivity to an EZH2 Inhibitor. American Society of Hematology 55th Annual Meeting, New Orleans, LA, USA, 7-10 Dec 2013.

Griaud, F., Pierce, A., Gonzalez Sanchez, M.B., Scott, M. , Abraham, S.A., Holyoake, T.L., Tran, D.D.H., Tamura, T. and Whetton, A.D. (2013) A pathway from leukemogenic oncogenes and stem cell chemokines to RNA processing via THOC5. Leukemia, 27(4), pp. 932-940. (doi: 10.1038/leu.2012.283)

2011

Pang, L. Y., Scott, M. , Hayward, R. L., Mohammed, H., Whitelaw, C. B. A., Smith, G. C.M. and Hupp, T. R. (2011) p21WAF1 is component of a positive feedback loop that maintains the p53 transcriptional program. Cell Cycle, 10(6), pp. 932-950. (doi: 10.4161/cc.10.6.15012) (PMID:21368573)

2010

Xu, N., Hegarat, N., Black, E. J., Scott, M. , Hochegger, H. and Gillespie, D.A. (2010) Akt/PKB suppresses DNA damage processing and checkpoint activation in late G2. Journal of Cell Biology, 190(3), pp. 297-305. (doi: 10.1083/jcb.201003004)

2009

Walker, M., Black, E.J., Oehler, V., Gillespie, D.A. and Scott, M.T. (2009) Chk1 C-terminal regulatory phosphorylation mediates checkpoint activation by de-repression of Chk1 catalytic activity. Oncogene, 28(24), pp. 2314-2323. (doi: 10.1038/onc.2009.102) (PMID:19421147) (PMCID:PMC2857325)

2008

Scorah, J., Dong, M.-Q., Yates, J.R., Scott, M. , Gillespie, D. and McGowan, C.H. (2008) A conserved proliferating cell nuclear antigen-interacting protein sequence in Chk1 is required for checkpoint function. Journal of Biological Chemistry, 283(25), pp. 17250-17259. (doi: 10.1074/jbc.M800369200)

2007

Craig, A. L., Chrystal, J. A., Fraser, J. A., Sphyris, N., Lin, Y., Harrison, B. J., Scott, M. T. , Dornreiter, I. and Hupp, T. R. (2007) The MDM2 ubiquitination signal in the DNA-binding domain of p53 forms a docking site for calcium calmodulin kinase superfamily members. Molecular and Cellular Biology, 27(9), pp. 3542-3555. (doi: 10.1128/MCB.01595-06) (PMID:17339337) (PMCID:PMC1899961)

Zachos, G., Black, E. J., Walker, M., Scott, M. T. , Vagnarelli, P., Earnshaw, W. C. and Gillespie, D. A.F. (2007) Chk1 is required for spindle checkpoint function. Developmental Cell, 12(2), pp. 247-260. (doi: 10.1016/j.devcel.2007.01.003) (PMID:17276342)

2004

Burch, L. R., Scott, M. , Pohler, E., Meek, D. and Hupp, T. (2004) Phage-peptide display identifies the Interferon-responsive, death-activated protein kinase family as a novel modifier of MDM2 and p21WAF1. Journal of Molecular Biology, 337(1), pp. 115-128. (doi: 10.1016/j.jmb.2003.10.081) (PMID:15001356)

2003

Craig, A., Scott, M. , Burch, L., Smith, G., Ball, K. and Hupp, T. (2003) Allosteric effects mediate CHK2 phosphorylation of the p53 transactivation domain. EMBO Reports, 4(8), pp. 787-792. (doi: 10.1038/sj.embor.embor901) (PMID:12897801) (PMCID:PMC1326341)

2002

Scott, M. T. , Ingram, A. and Ball, K. (2002) PDK1-dependent activation of atypical PKC leads to degradation of the p21 tumour modifier protein. EMBO Journal, 21(24), pp. 6771-6780. (doi: 10.1093/emboj/cdf684) (PMID:12485998) (PMCID:PMC139104)

2000

Scott, M. T. , Morrice, N. and Ball, K. L. (2000) Reversible phosphorylation at the C-terminal regulatory domain of p21Waf1/Cip1 modulates proliferating cell nuclear antigen binding. Journal of Biological Chemistry, 275(15), pp. 11529-11537. (doi: 10.1074/jbc.275.15.11529) (PMID:10753973)

1996

Taverne, J., Sheikh, N., Elased, K., Playfair, J., Scott, M. and Saggerson, D. (1996) Malaria toxins: TNF-mediated phenomena. Parasitology Today, 12(7), p. 290. (doi: 10.1016/0169-4758(96)80817-9) (PMID:15275196)

This list was generated on Thu Nov 21 03:11:23 2024 GMT.
Number of items: 28.

Articles

Khalaf, A. et al. (2024) Nutrient-sensitizing drug repurposing screen identifies lomerizine as a mitochondrial metabolism inhibitor of chronic myeloid leukemia. Science Translational Medicine, 16(751), eadi5336. (doi: 10.1126/scitranslmed.adi5336) (PMID:38865484)

Dawson, A. et al. (2024) Leukaemia exposure alters the transcriptional profile and function of BCR::ABL1 negative macrophages in the bone marrow niche. Nature Communications, 15, 1090. (doi: 10.1038/s41467-024-45471-0) (PMID:38316788) (PMCID:PMC10844594)

Scott, M. T. et al. (2024) Activating p53 abolishes self-renewal of quiescent leukaemic stem cells in residual CML disease. Nature Communications, 15, 651. (doi: 10.1038/s41467-024-44771-9) (PMID:38246924) (PMCID:PMC10800356)

Rattigan, K. M. et al. (2023) Arginine dependency is a therapeutically exploitable vulnerability in chronic myeloid leukaemic stem cells. EMBO Reports, 24, e56279. (doi: 10.15252/embr.202256279) (PMID:37489735) (PMCID:PMC10561355)

Rattigan, K. M. et al. (2023) Pyruvate anaplerosis is a targetable vulnerability in persistent leukaemic stem cells. Nature Communications, 14, 4634. (doi: 10.1038/s41467-023-40222-z) (PMID:37591854) (PMCID:PMC10435520)

Ianniciello, A. et al. (2021) ULK1 inhibition promotes oxidative stress–induced differentiation and sensitizes leukemic stem cells to targeted therapy. Science Translational Medicine, 13(613), eabd5016. (doi: 10.1126/scitranslmed.abd5016) (PMID:34586834)

Kinstrie, R. et al. (2020) CD93 is expressed on chronic myeloid leukemia stem cells and identifies a quiescent population which persists after tyrosine kinase inhibitor therapy. Leukemia, 34(6), pp. 1613-1625. (doi: 10.1038/s41375-019-0684-5) (PMID:31896780) (PMCID:PMC7272220)

Bugler, J., Kinstrie, R., Scott, M. T. and Vetrie, D. (2019) Epigenetic reprogramming and emerging epigenetic therapies in CML. Frontiers in Cell and Developmental Biology, 7, 136. (doi: 10.3389/fcell.2019.00136) (PMID:31380371) (PMCID:PMC6652210)

Baquero, P. et al. (2019) Targeting quiescent leukemic stem cells using second generation autophagy inhibitors. Leukemia, 33(4), pp. 981-994. (doi: 10.1038/s41375-018-0252-4) (PMID:30185934) (PMCID:PMC6292500)

Pellicano, F. et al. (2018) Hsa-mir183/EGR1-mediated regulation of E2F1 is required for CML stem/progenitor cell survival. Blood, 131(14), pp. 1532-1544. (doi: 10.1182/blood-2017-05-783845) (PMID:29437554) (PMCID:PMC6027092)

Scott, M. T. et al. (2016) Epigenetic reprogramming sensitizes CML stem cells to combined EZH2 and tyrosine kinase inhibition. Cancer Discovery, 6(11), pp. 1248-1257. (doi: 10.1158/2159-8290.CD-16-0263) (PMID:27630125) (PMCID:PMC6538532)

Abraham, S. A. et al. (2016) Dual targeting of P53 and C-MYC induces selective elimination of leukemic stem cells. Nature, 534(7607), pp. 341-346. (doi: 10.1038/nature18288) (PMID:27281222) (PMCID:PMC4913876)

Aspinall-O'Dea, M., Pierce, A., Pellicano, F., Williamson, A. J., Scott, M. T. , Walker, M. J., Holyoake, T. L. and Whetton, A. D. (2015) Antibody-based detection of protein phosphorylation status to track the efficacy of novel therapies using nanogram protein quantities from stem cells and cell lines. Nature Protocols, 10(1), pp. 149-168. (doi: 10.1038/nprot.2015.007) (PMID:25521791)

Pellicano, F. et al. (2014) The antiproliferative activity of kinase inhibitors in chronic myeloid leukemia cells is mediated by FOXO transcription factors. Stem Cells, 32(9), pp. 2324-2337. (doi: 10.1002/stem.1748) (PMID:24806995) (PMCID:PMC4282530)

Griaud, F., Pierce, A., Gonzalez Sanchez, M.B., Scott, M. , Abraham, S.A., Holyoake, T.L., Tran, D.D.H., Tamura, T. and Whetton, A.D. (2013) A pathway from leukemogenic oncogenes and stem cell chemokines to RNA processing via THOC5. Leukemia, 27(4), pp. 932-940. (doi: 10.1038/leu.2012.283)

Pang, L. Y., Scott, M. , Hayward, R. L., Mohammed, H., Whitelaw, C. B. A., Smith, G. C.M. and Hupp, T. R. (2011) p21WAF1 is component of a positive feedback loop that maintains the p53 transcriptional program. Cell Cycle, 10(6), pp. 932-950. (doi: 10.4161/cc.10.6.15012) (PMID:21368573)

Xu, N., Hegarat, N., Black, E. J., Scott, M. , Hochegger, H. and Gillespie, D.A. (2010) Akt/PKB suppresses DNA damage processing and checkpoint activation in late G2. Journal of Cell Biology, 190(3), pp. 297-305. (doi: 10.1083/jcb.201003004)

Walker, M., Black, E.J., Oehler, V., Gillespie, D.A. and Scott, M.T. (2009) Chk1 C-terminal regulatory phosphorylation mediates checkpoint activation by de-repression of Chk1 catalytic activity. Oncogene, 28(24), pp. 2314-2323. (doi: 10.1038/onc.2009.102) (PMID:19421147) (PMCID:PMC2857325)

Scorah, J., Dong, M.-Q., Yates, J.R., Scott, M. , Gillespie, D. and McGowan, C.H. (2008) A conserved proliferating cell nuclear antigen-interacting protein sequence in Chk1 is required for checkpoint function. Journal of Biological Chemistry, 283(25), pp. 17250-17259. (doi: 10.1074/jbc.M800369200)

Craig, A. L., Chrystal, J. A., Fraser, J. A., Sphyris, N., Lin, Y., Harrison, B. J., Scott, M. T. , Dornreiter, I. and Hupp, T. R. (2007) The MDM2 ubiquitination signal in the DNA-binding domain of p53 forms a docking site for calcium calmodulin kinase superfamily members. Molecular and Cellular Biology, 27(9), pp. 3542-3555. (doi: 10.1128/MCB.01595-06) (PMID:17339337) (PMCID:PMC1899961)

Zachos, G., Black, E. J., Walker, M., Scott, M. T. , Vagnarelli, P., Earnshaw, W. C. and Gillespie, D. A.F. (2007) Chk1 is required for spindle checkpoint function. Developmental Cell, 12(2), pp. 247-260. (doi: 10.1016/j.devcel.2007.01.003) (PMID:17276342)

Burch, L. R., Scott, M. , Pohler, E., Meek, D. and Hupp, T. (2004) Phage-peptide display identifies the Interferon-responsive, death-activated protein kinase family as a novel modifier of MDM2 and p21WAF1. Journal of Molecular Biology, 337(1), pp. 115-128. (doi: 10.1016/j.jmb.2003.10.081) (PMID:15001356)

Craig, A., Scott, M. , Burch, L., Smith, G., Ball, K. and Hupp, T. (2003) Allosteric effects mediate CHK2 phosphorylation of the p53 transactivation domain. EMBO Reports, 4(8), pp. 787-792. (doi: 10.1038/sj.embor.embor901) (PMID:12897801) (PMCID:PMC1326341)

Scott, M. T. , Ingram, A. and Ball, K. (2002) PDK1-dependent activation of atypical PKC leads to degradation of the p21 tumour modifier protein. EMBO Journal, 21(24), pp. 6771-6780. (doi: 10.1093/emboj/cdf684) (PMID:12485998) (PMCID:PMC139104)

Scott, M. T. , Morrice, N. and Ball, K. L. (2000) Reversible phosphorylation at the C-terminal regulatory domain of p21Waf1/Cip1 modulates proliferating cell nuclear antigen binding. Journal of Biological Chemistry, 275(15), pp. 11529-11537. (doi: 10.1074/jbc.275.15.11529) (PMID:10753973)

Taverne, J., Sheikh, N., Elased, K., Playfair, J., Scott, M. and Saggerson, D. (1996) Malaria toxins: TNF-mediated phenomena. Parasitology Today, 12(7), p. 290. (doi: 10.1016/0169-4758(96)80817-9) (PMID:15275196)

Conference or Workshop Item

Zarou, M. M. et al. (2023) Leukaemia Exposure Alters the Transcriptional Profile and Function of Macrophages in the Bone Marrow Niche. 65th ASH Annual Meeting and Exposition, San Diego, California, USA, 09-12 Dec 2023. (doi: 10.1182/blood-2023-181630)

Scott, M. T. et al. (2013) Misregulation of the PRC2 Complex in CML Stem Cells Confers Sensitivity to an EZH2 Inhibitor. American Society of Hematology 55th Annual Meeting, New Orleans, LA, USA, 7-10 Dec 2013.

This list was generated on Thu Nov 21 03:11:23 2024 GMT.

Grants

Grants and Awards listed are those received whilst working with the University of Glasgow.

  • Identification of biomarkers predictive of TKI response in diagnostic chronic phase CML patient samples
    Tenovus Scotland
    2024 - 2025
     
  • Functional and molecular analysis of leukaemia stem cell sub-types in chronic myeloid leukaemia
    Leukaemia UK
    2023 - 2026
     
  • Modulation of H3K27 methylation to eradicate TKI-persistant CML stem cells
    Blood Cancer UK
    2014 - 2017