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Dr Vicki Maltby

Conjoint Lecturer

School of Medicine and Public Health

Career Summary

Biography

Research Expertise
Epigenetics and Medical Genetics

Teaching Expertise
Basic Genetics

Qualifications

  • PhD, University of British Columbia - Canada
  • Bachelor of Science, University of British Columbia - Canada

Keywords

  • Epigenetics
  • Genetics
  • Histone Modification
  • Immunology
  • Medical Genetics

Professional Experience

Academic appointment

Dates Title Organisation / Department
1/2/2012 -  Post Doctoral Fellow University of Newcastle
School of Biomedical Sciences and Pharmacy
Australia
1/5/2004 - 1/9/2004 Technician Pacific Agri-Food Research Centre
Australia
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Publications

For publications that are currently unpublished or in-press, details are shown in italics.


Journal article (26 outputs)

Year Citation Altmetrics Link
2020 Nguyen AL, Vodehnalova K, Kalincik T, Signori A, Havrdova EK, Lechner-Scott J, et al., 'Association of Pregnancy with the Onset of Clinically Isolated Syndrome', JAMA Neurology, 77 1496-1503 (2020) [C1]

Importance: Multiple sclerosis (MS) is usually diagnosed in women during their childbearing years. Currently, no consensus exists on whether pregnancy can delay the first episode ... [more]

Importance: Multiple sclerosis (MS) is usually diagnosed in women during their childbearing years. Currently, no consensus exists on whether pregnancy can delay the first episode of demyelination or clinically isolated syndrome (CIS). Objective: To investigate the association of pregnancy with time to CIS onset. Design, Setting, and Participants: This multicenter cohort study collected reproductive history (duration of each pregnancy, date of delivery, length of breastfeeding) on all participants between September 1, 2016, and June 25, 2019. Adult women being treated at the MS outpatient clinics of 4 tertiary hospitals in 2 countries (Charles University and General University Hospital in Prague, Czech Republic; Royal Melbourne Hospital in Melbourne, Australia; Alfred Hospital in Melbourne, Australia; and John Hunter Hospital in Newcastle, Australia) were recruited to participate in the study. Preexisting data (date of CIS onset, date of birth, sex, date of clinical onset, and Expanded Disability Status Scale result) were collected from MSBase, an international registry of long-term prospectively collected data on patients with MS. Data analyses were performed from June 1, 2019, to February 3, 2020. Exposures: Gravida (defined as any pregnancy, including pregnancy that ended in miscarriage and induced abortion) and parity (defined as childbirth after gestational age of more than 20 weeks, including livebirth and stillbirth) before CIS onset. Main Outcomes and Measures: Time to CIS onset. The following were assessed: (1) whether women with previous pregnancies and childbirths had a delayed onset of CIS compared with those who had never been pregnant and those who had never given birth, and (2) whether a dose response existed, whereby a higher number of gravidity and parity was associated with a later onset of CIS. Results: Of the 2557 women included in the study, the mean (SD) age at CIS onset was 31.5 (9.7) years. Of these women, before CIS onset, 1188 (46%) had at least 1 pregnancy and 1100 (43%) had at least 1 childbirth. The mean (SD) age at first pregnancy was 23.3 (4.5) years and at first childbirth was 23.8 (4.5) years. Women with previous pregnancies and childbirths had a later onset of CIS compared with those who had never been pregnant (HR, 0.68; 95% CI, 0.62-0.75; P <.001), with a median delay of 3.3 (95% CI, 2.5-4.1) years. Women who had given birth also had a later CIS onset compared with women who had never given birth (HR 0.68; 95% CI, 0.61-0.75; P <.001), with a similar median delay of 3.4 (95% CI, 1.6-5.2) years. A higher gravidity and parity number was not associated with delay in CIS onset. Conclusions and Relevance: This study suggests an association between previous pregnancies and childbirths and timing of CIS onset, but having more pregnancies or childbirths did not appear to be associated with a later CIS onset. Further studies are needed to help explain the mechanisms behind the associations between pregnancy and onset of multiple sclerosis 2020 American Medical Association. All rights reserved.

DOI 10.1001/jamaneurol.2020.3324
Citations Scopus - 7Web of Science - 9
Co-authors Jeannette Lechnerscott
2020 Lechner-Scott J, Hawkes CH, Giovannoni G, Levy M, Maltby V, 'Why should Neurologists get involved in family planning?', Multiple Sclerosis and Related Disorders, 46 (2020)
DOI 10.1016/j.msard.2020.102598
Co-authors Jeannette Lechnerscott
2020 Groen K, Maltby VE, Scott RJ, Tajouri L, Lechner-Scott J, 'Erythrocyte microRNAs show biomarker potential and implicate multiple sclerosis susceptibility genes.', Clinical and translational medicine, 10 74-90 (2020) [C1]
DOI 10.1002/ctm2.22
Citations Web of Science - 1
Co-authors Jeannette Lechnerscott, Kira Groen, Rodney Scott
2020 Maltby VE, Lea RA, Burnard S, Xavier A, Van Cao T, White N, et al., 'Epigenetic differences at the HTR2A locus in progressive multiple sclerosis patients', SCIENTIFIC REPORTS, 10 (2020) [C1]
DOI 10.1038/s41598-020-78809-x
Citations Scopus - 1Web of Science - 1
Co-authors Jeannette Lechnerscott, Kira Groen, Rodney Scott
2020 Groen K, Maltby VE, Scott RJ, Tajouri L, Lechner-Scott J, 'Concentrations of plasma-borne extracellular particles differ between multiple sclerosis disease courses and compared to healthy controls', Multiple Sclerosis and Related Disorders, 45 (2020) [C1]
DOI 10.1016/j.msard.2020.102446
Citations Scopus - 2Web of Science - 2
Co-authors Rodney Scott, Kira Groen, Jeannette Lechnerscott
2020 Maltby VE, Lea RA, Ribbons K, Lea MG, Schofield PW, Lechner-Scott J, 'Comparison of BICAMS and ARCS for assessment of cognition in multiple sclerosis and predictive value of employment status', Multiple Sclerosis and Related Disorders, 41 (2020) [C1]
DOI 10.1016/j.msard.2020.102037
Co-authors Peter Schofield, Jeannette Lechnerscott
2018 Groen K, Lea RA, Maltby VE, Scott RJ, Lechner-Scott J, 'Letter to the editor: blood processing and sample storage have negligible effects on methylation', CLINICAL EPIGENETICS, 10 (2018) [C1]
DOI 10.1186/s13148-018-0455-6
Citations Scopus - 8Web of Science - 8
Co-authors Rodney Scott, Kira Groen, Jeannette Lechnerscott
2018 Maltby VE, Lea RA, Graves MC, Sanders KA, Benton MC, Tajouri L, et al., 'Genome-wide DNA methylation changes in CD19+ B cells from relapsing-remitting multiple sclerosis patients.', Scientific reports, 8 (2018) [C1]
DOI 10.1038/s41598-018-35603-0
Citations Scopus - 17Web of Science - 18
Co-authors Moira Graves, Rodney Scott, Jeannette Lechnerscott
2018 Rhead B, Brorson IS, Berge T, Adams C, Quach H, Moen SM, et al., 'Increased DNA methylation of SLFN12 in CD4(+) and CD8(+) T cells from multiple sclerosis patients', PLOS ONE, 13 (2018) [C1]
DOI 10.1371/journal.pone.0206511
Citations Scopus - 16Web of Science - 16
Co-authors Rodney Scott, Jeannette Lechnerscott
2018 Groen K, Maltby VE, Lea RA, Sanders KA, Fink JL, Scott RJ, et al., 'Erythrocyte microRNA sequencing reveals differential expression in relapsing-remitting multiple sclerosis.', BMC medical genomics, 11 (2018) [C1]
DOI 10.1186/s12920-018-0365-7
Citations Scopus - 5Web of Science - 6
Co-authors Jeannette Lechnerscott, Kira Groen, Rodney Scott
2018 Maltby VE, Lea RA, Ribbons KA, Sanders KA, Kennedy D, Min M, et al., 'DNA methylation changes in CD4+ T cells isolated from multiple sclerosis patients on dimethyl fumarate.', Multiple Sclerosis Journal - Experimental, Translational and Clinical, 4 (2018) [C1]
DOI 10.1177/2055217318787826
Citations Scopus - 6
Co-authors Jeannette Lechnerscott, Rodney Scott
2017 Martin BJE, McBurney KL, Maltby VE, Jensen KN, Brind Amour J, Howe LAJ, 'Histone H3K4 and H3K36 methylation independently recruit the NuA3 histone acetyltransferase in Saccharomyces cerevisiae', Genetics, 205 1113-1123 (2017) [C1]

Histone post-translational modifications (PTMs) alter chromatin structure by promoting the interaction of chromatinmodifying complexes with nucleosomes. The majority of chromatin-... [more]

Histone post-translational modifications (PTMs) alter chromatin structure by promoting the interaction of chromatinmodifying complexes with nucleosomes. The majority of chromatin-modifying complexes contain multiple domains that preferentially interact with modified histones, leading to speculation that these domains function in concert to target nucleosomes with distinct combinations of histone PTMs. In Saccharomyces cerevisiae, the NuA3 histone acetyltransferase complex contains three domains, the PHD finger in Yng1, the PWWP domain in Pdp3, and the YEATS domain in Taf14; which in vitro bind to H3K4 methylation, H3K36 methylation, and acetylated and crotonylated H3K9, respectively. While the in vitro binding has been well characterized, the relative in vivo contributions of these histone PTMs in targeting NuA3 is unknown. Here, through genome-wide colocalization and by mutational interrogation, we demonstrate that the PHD finger of Yng1, and the PWWP domain of Pdp3 independently target NuA3 to H3K4 and H3K36 methylated chromatin, respectively. In contrast, we find no evidence to support the YEATS domain of Taf14 functioning in NuA3 recruitment. Collectively our results suggest that the presence of multiple histone PTM binding domains within NuA3, rather than restricting it to nucleosomes containing distinct combinations of histone PTMs, can serve to increase the range of nucleosomes bound by the complex. Interestingly, however, the simple presence of NuA3 is insufficient to ensure acetylation of the associated nucleosomes, suggesting a secondary level of acetylation regulation that does not involve control of HAT-nucleosome interactions.

DOI 10.1534/genetics.116.199422
Citations Scopus - 13Web of Science - 13
2017 Maltby VE, Lea RA, Sanders KA, White N, Benton MC, Scott RJ, Lechner-Scott J, 'Differential methylation at MHC in CD4

Background: Although many genetic variants have been associated with multiple sclerosis (MS) risk, they do not explain all the disease risk and there remains uncertainty as to how... [more]

Background: Although many genetic variants have been associated with multiple sclerosis (MS) risk, they do not explain all the disease risk and there remains uncertainty as to how these variants contribute to disease. DNA methylation is an epigenetic mechanism that can influence gene expression and has the potential to mediate the effects of environmental factors on MS. In a previous study, we found a differentially methylation region (DMR) at MHC HLA-DRB1 that was associated within relapsing-remitting MS (RRMS) patients in CD4+ T cells. This study aimed to confirm this earlier finding in an independent RRMS cohort of treatment-naive female patients. Methods: Total genomic DNA was extracted from CD4+ T cells of 28 female RRMS and 22 age-matched healthy controls subjects. DNA was bisulfite-converted and hybridised to Illumina 450K arrays. Beta values for all CpGs were analysed using the DMPFinder function in the MINFI program, and a follow-up prioritisation process was applied to identify the most robust MS-associated DMRs. Results: This study confirmed our previous findings of a hypomethylated DMR at HLA-DRB1 and a hypermethylated DMR at HLA-DRB5 in this RRMS patient cohort. In addition, we identified a large independent DMR at MHC, whereby 11 CpGs in RNF39 were hypermethylated in MS cases compared to controls (max. ¿beta = 0.19, P = 2.1 × 10-4). We did not find evidence that SNP genotype was influencing the DMR in this cohort. A smaller MHC DMR was also identified at HCG4B, and two non-MHC DMRs at PM20D1 on chr1 and ERICH1 on chr8 were also identified. Conclusions: The findings from this study confirm our previous results of a DMR at HLA-DRB1 and also suggest hypermethylation in an independent MHC locus, RNF39, is associated with MS. Taken together, our results highlight the importance of epigenetic factors at the MHC locus in MS independent of treatment, age and sex. Prospective studies are now required to discern whether methylation at MHC is involved in influencing risk of disease onset or whether the disease itself has altered the methylation profile.

DOI 10.1186/s13148-017-0371-1
Citations Scopus - 25Web of Science - 25
Co-authors Rodney Scott, Jeannette Lechnerscott
2016 Sanders KA, Benton MC, Lea RA, Maltby VE, Agland S, Griffin N, et al., 'Next-generation sequencing reveals broad down-regulation of microRNAs in secondary progressive multiple sclerosis CD4+T cells', CLINICAL EPIGENETICS, 8 (2016) [C1]
DOI 10.1186/s13148-016-0253-y
Citations Scopus - 25Web of Science - 28
Co-authors Jeannette Lechnerscott, Rodney Scott
2016 Groen K, Maltby VE, Sanders KA, Scott RJ, Tajouri L, Lechner-Scott J, 'Erythrocytes in multiple sclerosis - forgotten contributors to the pathophysiology?', Multiple Sclerosis Journal Experimental, Translational and Clinical, 2 2055217316649981-2055217316649981 (2016) [C1]
DOI 10.1177/2055217316649981
Citations Scopus - 4
Co-authors Jeannette Lechnerscott, Rodney Scott, Kira Groen
2016 Murray HC, Maltby VE, Smith DW, Bowden NA, 'Nucleotide excision repair deficiency in melanoma in response to UVA', Experimental Hematology and Oncology, 5 (2016) [C1]

Background: The causative link between UV exposure and melanoma development is well known, however the mechanistic relationship remains incompletely characterised. UVA and UVB com... [more]

Background: The causative link between UV exposure and melanoma development is well known, however the mechanistic relationship remains incompletely characterised. UVA and UVB components of sunlight are implicated in melanomagenesis; however the majority of studies have focused on the effects of UVB and UVC light. Interestingly, melanoma tumour sequencing has revealed an overrepresentation of mutations signature of unrepaired UV-induced DNA damage. Repair of UVA-induced DNA damage is thought to occur primarily through the Nucleotide Excision Repair (NER) pathway, which recognises and repairs damage either coupled to transcription (Transcription Coupled Repair; TCR), or through global genome scanning (Global Genome Repair; GGR). Current literature suggests NER is deficient in melanoma, however the cause of this remains unknown; and whether reduced NER activity in response to UVA may be involved in melanoma development remains uncharacterised. In this study we aimed to determine if melanoma cells exhibit reduced levels of NER activity in response to UVA. Methods: Melanocyte and melanoma cell lines were UVA-irradiated, and DNA damage levels assessed by immunodetection of Cyclobutane Pyrimidine Dimer (CPD) and (6-4) Photoproduct [(6-4)PP] lesions. Expression of NER pathway components and p53 following UVA treatment was quantified by qPCR and western blot. Results: UVA did not induce detectable induction of (6-4)PP lesions, consistent with previous studies. Repair of CPDs induced by UVA was initiated at 4 h and complete within 48 h in normal melanocytes, whereas repair initiation was delayed to 24 h and >40 % of lesions remained in melanoma cell lines at 48 h. This was coupled with a delayed and reduced induction of GGR component XPC in melanoma cells, independent of p53. Conclusion: These findings support that NER activity is reduced in melanoma cells due to deficient GGR. Further investigation into the role of NER in UVA-induced melanomagenesis is warranted and may have implications for melanoma treatment.

DOI 10.1186/s40164-016-0035-4
Citations Scopus - 14Web of Science - 12
Co-authors Heather Murray, Nikola Bowden, Douglas Smith
2015 Maltby VE, Graves MC, Lea RA, Benton MC, Sanders KA, Tajouri L, et al., 'Genome-wide DNA methylation profiling of CD8+T cells shows a distinct epigenetic signature to CD4+T cells in multiple sclerosis patients', CLINICAL EPIGENETICS, 7 (2015) [C1]
DOI 10.1186/s13148-015-0152-7
Citations Scopus - 50Web of Science - 47
Co-authors Jeannette Lechnerscott, Moira Graves, Rodney Scott
2014 Maltby VE, Crock PA, Luedecke DK, 'A rare case of pituitary infarction leading to spontaneous tumour resolution and CSF-sella syndrome in an 11-year-old girl and a review of the paediatric literature', JOURNAL OF PEDIATRIC ENDOCRINOLOGY & METABOLISM, 27 939-946 (2014) [C3]
DOI 10.1515/jpem-2014-0143
Citations Scopus - 5Web of Science - 5
2014 Smith CJA, Bensing S, Maltby VE, Zhang M, Scott RJ, Smith R, et al., 'Intermediate lobe immunoreactivity in a patient with suspected lymphocytic hypophysitis', Pituitary, 17 22-29 (2014) [C1]

Lymphocytic hypophysitis is an organ-specific autoimmune disease characterised by destruction of pituitary hormone-secreting cells due to attack by self-reactive T lymphocytes. Th... [more]

Lymphocytic hypophysitis is an organ-specific autoimmune disease characterised by destruction of pituitary hormone-secreting cells due to attack by self-reactive T lymphocytes. The spectrum of pituitary autoantibodies characterised by indirect immunofluorescence (IF) in these patients has not been substantially defined. The purpose of this study was to determine the spectrum of pituitary autoantibodies in 16 lymphocytic hypophysitis patients. Pituitary sections were prepared from guinea pigs and sera from 16 lymphocytic hypophysitis patients (13 biopsy proven and 3 suspected cases) and 13 healthy controls were evaluated for immunoreactivity to the pituitary tissue by immunofluorescence. A single patient was found to have high titre pituitary autoantibodies against guinea pig pituitary tissue. Immunoreactivity was directed against cells of the intermediate lobe. We present the case report of the patient who is a 24 year old woman that presented with headaches, polyuria and polydipsia. A uniformly enlarged pituitary mass was visible on MRI and a diagnosis of suspected lymphocytic hypophysitis was made. Based on our IF study, we postulate this patient has an autoimmune process directed towards the major cell type in the intermediate lobe, the melanotroph. Pre-adsorption with peptides representing adrenocorticotropic hormone, a-melanocyte stimulating hormone or ß-endorphin did not affect the IF signal suggesting our patient's pituitary autoantibodies may target some other product of Proopiomelanocortin (POMC) processing, such as corticotrophin-like intermediate peptide or ¿-lipoprotein. Alternatively, the autoantibodies may target a peptide completely unrelated to POMC processing. © 2013 Springer Science+Business Media New York.

DOI 10.1007/s11102-013-0461-9
Citations Scopus - 3Web of Science - 2
Co-authors Rodney Scott, Roger Smith
2012 Maltby VE, Martin BJ, Brind'Amour J, Chruscicki AT, McBurney KL, Schulze JM, et al., 'Histone H3K4 demethylation is negatively regulated by histone H3 acetylation in Saccharomyces cerevisiae', Proceedings of the National Academy of Sciences of USA, 109 8505-8510 (2012) [C1]
Citations Scopus - 37Web of Science - 36
2012 Maltby VE, Martin BJ, Schulze JM, Johnson IJ, Hentrich T, Sharma A, et al., 'Histone H3 lysine 36 methylation targets the Isw1b remodeling complex to chromatin', Molecular and Cellular Biology, 32 3479-3485 (2012) [C1]
Citations Scopus - 50Web of Science - 49
2010 Chruscicki AT, MacDonald VE, Young BP, Loewen CJ, Howe LJ, 'Critical Determinants for Chromatin Binding by Saccharomyces cerevisiae Yng1 Exist Outside of the Plant Homeodomain Finger', Genetics, 185 469-477 (2010) [C1]
Citations Scopus - 9Web of Science - 10
2009 MacDonald VE, Howe LJ, 'Histone acetylation: where to go and how to get there.', Epigenetics, 4 139-143 (2009) [C2]
Citations Scopus - 76Web of Science - 72
2006 Martin DG, Baetz K, Shi X, Walter K, MacDonald VE, Wlodarski MJ, et al., 'The Yng1p plant homeodomain finger is a methyl-histone binding module that recognizes lysine 4-methylated histone H3.', Molecular and Cellular Biology, 26 7871-7879 (2006) [C1]
Citations Scopus - 129Web of Science - 128
Maltby VE, Lea RA, Monif M, Fabris-Pedrini MJ, Buzzard K, Kalincik T, et al., 'Cladribine: a multicentre, LOng-term efficacy Biomarker Australian Study (CLOBAS). A six- Otherwise we list them as CLOBAS investigators year, real-world study of multiple sclerosis patients (Preprint)
DOI 10.2196/preprints.24969
Maltby VE, Lea RA, Monif M, Fabris-Pedrini MJ, Buzzard K, Kalincik T, et al., 'Cladribine: a multicentre, LOng-term efficacy and Biomarker Australian Study (CLOBAS). Protocol for a six- year, real-world, phase IV study of people with multiple sclerosis taking cladribine tablets. (Preprint)', JMIR Research Protocols,
DOI 10.2196/24969
Show 23 more journal articles

Conference (19 outputs)

Year Citation Altmetrics Link
2020 Maltby VE, Lea R, Burnard S, Theodoropoulou E, Marabita F, Bos S, et al., 'Epigenetic Age Acceleration in Multiple Sclerosis Patients', MULTIPLE SCLEROSIS JOURNAL, Melbourne, AUSTRALIA (2020)
Co-authors Rodney Scott, Jeannette Lechnerscott
2020 Groen K, Maltby VE, Scott RJ, Tajouri L, Lechner-Scott J, 'Increased erythrocyte microRNA-183 cluster expression during relapse - A potential new MS-specific marker for disease activity?', MULTIPLE SCLEROSIS JOURNAL, Melbourne, AUSTRALIA (2020)
Co-authors Jeannette Lechnerscott, Kira Groen, Rodney Scott
2020 Maltby V, Lydon A, Monif M, Kilpatrick T, Butzkueven H, Taylor B, et al., 'Cladribine: a multicentre LOng-term efficacy Biomarker Australian Study (CLOBAS)', NEUROLOGY, Toronto, CANADA (2020)
Co-authors Jeannette Lechnerscott
2019 Monif M, Abdollahi S, Stankovich J, Maltby V, Lechner-Scott J, Kalincik T, et al., 'CLADIN: CLADRIBINE AND INNATE IMMUNE RESPONSES', JOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY, Sydney, AUSTRALIA (2019)
DOI 10.1136/jnnp-2019-anzan.116
Co-authors Jeannette Lechnerscott
2019 Lechner-Scott J, Maltby V, Lyndon A, Monif M, Kilpatrick T, Butzkueven H, et al., 'CLADRIBINE: A MULTICENTRE LONG-TERM EFFICACY BIOMARKER AUSTRALIAN STUDY (CLOBAS)', JOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY, Sydney, AUSTRALIA (2019)
DOI 10.1136/jnnp-2019-anzan.119
Co-authors Jeannette Lechnerscott
2019 Maltby VE, Lea RA, Groen K, Burnard S, Sanders K, Seeto R, et al., 'Genome-wide DNA Methylation in Secondary Progressive Multiple Sclerosis Patients Reveals Unique Epigenetic Signature.', MULTIPLE SCLEROSIS JOURNAL, Sydney, AUSTRALIA (2019)
Co-authors Kira Groen, Rodney Scott, Jeannette Lechnerscott
2019 Groen K, Burnard S, Maltby VE, Scott RJ, Tajouri L, Lechner-Scott J, 'Increased plasma-borne extracellular vesicles in Multiple Sclerosis - Where did they come from?', MULTIPLE SCLEROSIS JOURNAL, Sydney, AUSTRALIA (2019)
Co-authors Rodney Scott, Jeannette Lechnerscott, Kira Groen
2019 Groen K, Maltby VE, Scott RJ, Tajouri L, Lechner-Scott J, 'Increased erythrocyte microRNA-183 cluster expression during relapse - A potential new MS-specific marker for disease activity?', MULTIPLE SCLEROSIS JOURNAL, Stockholm, SWEDEN (2019)
Co-authors Kira Groen, Rodney Scott, Jeannette Lechnerscott, Egbert Groen
2018 Groen K, Burnard S, Maltby V, Scott R, Tajouri L, Lechner-Scott J, 'Plasma-borne exctracellular vesicles in multiple sclerosis where did they come from?', MULTIPLE SCLEROSIS JOURNAL, Berlin, GERMANY (2018)
Co-authors Jeannette Lechnerscott, Rodney Scott, Kira Groen
2018 Brorson IS, Rhead B, Berge T, Adams C, Quach H, Moen SM, et al., 'SLFN12 is differentially methylated in multiple sclerosis CD4+and CD8+T cells', MULTIPLE SCLEROSIS JOURNAL, Berlin, GERMANY (2018)
Co-authors Jeannette Lechnerscott, Rodney Scott
2017 Lechner-Scott J, Maltby VE, Ribbons KA, Min M, Lea R, 'Dimethyl fumarate changes the methylation pattern in CD4+cells of MS patients', MULTIPLE SCLEROSIS JOURNAL, Paris, FRANCE (2017)
Co-authors Jeannette Lechnerscott
2017 Sanders KA, Maltby VE, Lea RA, Benton MC, Scott RJ, Tajouri L, Lechner-Scott J, 'miR-29b: microRNA biogenesis and dysregulation meets DNA hypermethylation in SPMS', MULTIPLE SCLEROSIS JOURNAL, Paris, FRANCE (2017)
Co-authors Jeannette Lechnerscott, Rodney Scott
2017 Groen K, Maltby VE, Tajouri L, Lea RA, Fink L, Sanders KA, et al., 'Altered erythrocyte MicroRNA profiles in relapsing-remitting multiple sclerosis', MULTIPLE SCLEROSIS JOURNAL, Paris, FRANCE (2017)
Co-authors Rodney Scott, Jeannette Lechnerscott, Kira Groen
2016 Maltby VE, Graves M, Lea R, Benton MC, Sanders KA, Tajouri L, et al., 'Genome-wide DNA methylation profiling of CD8+T cells reveals distinct epigenetic signatures', MULTIPLE SCLEROSIS JOURNAL, New Orleans, LA (2016)
Co-authors Jeannette Lechnerscott, Rodney Scott
2016 Sanders KA, Benton MC, Maltby VE, Lea R, Agland S, Griffin N, et al., 'A negative regulator of T-cell activation, SOCS6, is up-regulated in response to decreased microRNA expression in SPMS CD4+T-cells', MULTIPLE SCLEROSIS JOURNAL, New Orleans, LA (2016)
Co-authors Jeannette Lechnerscott, Rodney Scott
2015 Sanders K, Benton MC, Lea RA, Maltby VE, Agland S, Scott RJ, et al., 'MicroRNA sequencing identifies four down-regulated microRNAs in CD4+T-cells of secondary progressive multiple sclerosis patients', MULTIPLE SCLEROSIS JOURNAL (2015) [E3]
Citations Web of Science - 1
Co-authors Rodney Scott, Jeannette Lechnerscott
2015 Maltby V, Graves M, Lea R, Benton M, Sanders K, Lechner-Scott J, et al., 'Minor methylation differences at various loci in CD8+T-Cells are associated with multiple sclerosis', MULTIPLE SCLEROSIS JOURNAL (2015) [E3]
Co-authors Moira Graves, Jeannette Lechnerscott, Rodney Scott
2015 Sanders KA, Benton MC, Lea RA, Maltby VE, Agland S, Scott RJ, et al., 'MicroRNA sequencing identifies down-regulated microRNA in CD4+T-cells of secondary progressive multiple sclerosis patients', MULTIPLE SCLEROSIS JOURNAL (2015) [E3]
Co-authors Jeannette Lechnerscott, Rodney Scott
2014 Murray HC, Maltby VE, Bowden NA, 'Nucleotide excision repair in response to UVA is deficient in melanoma.', Pigment Cell and Melanoma Research, Singapore (2014) [E3]
DOI 10.1111/pcmr.12292
Co-authors Nikola Bowden
Show 16 more conferences
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Grants and Funding

Summary

Number of grants 19
Total funding $1,028,789

Click on a grant title below to expand the full details for that specific grant.


20212 grants / $46,492

Circulating extracellular vesicles in multiple sclerosis and their potential to serve as windows to the brain$24,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Vicki Maltby, Doctor Kira Groen
Scheme Research Grant
Role Lead
Funding Start 2021
Funding Finish 2021
GNo G2101115
Type Of Funding C3300 – Aust Philanthropy
Category 3300
UON Y

Develop a cell free DNA assay that can accurately and rapidly differentiate between relapsing and remitting MS patients to improve their outcomes$22,492

Funding body: Multiple Sclerosis Research Australia Limited (MSRA)

Funding body Multiple Sclerosis Research Australia Limited (MSRA)
Project Team Laureate Professor Rodney Scott, Conjoint Professor Jeannette Lechner-Scott, Associate Professor Rodney Lea, Doctor Vicki Maltby, Mr Rodney Lea, David Leppert, Associate Professor David Leppert, Dr Joel Petit
Scheme Incubator Grant
Role Investigator
Funding Start 2021
Funding Finish 2021
GNo G2000852
Type Of Funding C1700 - Aust Competitive - Other
Category 1700
UON Y

20201 grants / $235,000

Effect of dimethyl fumarate (Tecfidera) on microstructure and biochemistry in the brain of MS patients (TECSPEC) $235,000

Funding body: Hunter New England Local Health District

Funding body Hunter New England Local Health District
Project Team Conjoint Professor Jeannette Lechner-Scott, Associate Professor Saadallah Ramadan, Doctor Vicki Maltby, Rodney Lea
Scheme Research Funds
Role Investigator
Funding Start 2020
Funding Finish 2021
GNo G2000076
Type Of Funding C2300 – Aust StateTerritoryLocal – Own Purpose
Category 2300
UON Y

20191 grants / $50,000

Can mindfulness or exercise based approaches reduce fatigue in multiple sclerosis patients?$50,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Vicki Maltby, Mr Oun Issa Salman Al-Iedani
Scheme Research Grant
Role Lead
Funding Start 2019
Funding Finish 2020
GNo G1901452
Type Of Funding C3200 – Aust Not-for Profit
Category 3200
UON Y

20182 grants / $50,000

Red blood cell-derived extracellular vesicle microRNAs in Multiple Sclerosis - A form of intercellular communication$25,000

Funding body: Multiple Sclerosis Research Australia Limited (MSRA)

Funding body Multiple Sclerosis Research Australia Limited (MSRA)
Project Team Conjoint Professor Jeannette Lechner-Scott, Doctor Vicki Maltby, Doctor Kira Groen, Miss Kira Groen, Dr Lotti Tajouri, Dr Lotti Tajouri
Scheme Incubator Grant
Role Investigator
Funding Start 2018
Funding Finish 2019
GNo G1800511
Type Of Funding C3200 – Aust Not-for Profit
Category 3200
UON Y

Epigenetic Age Acceleration in Multiple Sclerosis Patients$25,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Vicki Maltby, Conjoint Professor Jeannette Lechner-Scott, Associate Professor Rodney Lea
Scheme Project Grant
Role Lead
Funding Start 2018
Funding Finish 2018
GNo G1801339
Type Of Funding C3300 – Aust Philanthropy
Category 3300
UON Y

20173 grants / $63,000

Prader-Willi Syndrome: assessment of central hypothyroidism using novel biomarkers (serum micro-RNA)$25,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Dr Komal Vora, Conjoint Associate Professor Patricia Crock, Doctor Vicki Maltby, Professor Geoffrey Ambler, Associate Professor Charles Verge, Professor Mark Harris
Scheme Project Grant
Role Investigator
Funding Start 2017
Funding Finish 2017
GNo G1701033
Type Of Funding C3300 – Aust Philanthropy
Category 3300
UON Y

The effect of common multiple sclerosis treatment on epigenetic markers in patients$20,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Vicki Maltby, Conjoint Professor Jeannette Lechner-Scott, Associate Professor Rodney Lea
Scheme Project Grant
Role Lead
Funding Start 2017
Funding Finish 2017
GNo G1701562
Type Of Funding C3300 – Aust Philanthropy
Category 3300
UON Y

Investigation of erythrocyte microRNA content in Multiple Sclerosis$18,000

Funding body: Multiple Sclerosis Research Australia Limited (MSRA)

Funding body Multiple Sclerosis Research Australia Limited (MSRA)
Project Team Conjoint Professor Jeannette Lechner-Scott, Laureate Professor Rodney Scott, Doctor Vicki Maltby
Scheme Incubator Grant
Role Investigator
Funding Start 2017
Funding Finish 2017
GNo G1600995
Type Of Funding Aust Competitive - Non Commonwealth
Category 1NS
UON Y

20152 grants / $20,750

The effect of treatment on patients with Multiple Sclerosis$20,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Vicki Maltby, Conjoint Professor Jeannette Lechner-Scott, Associate Professor Rodney Lea
Scheme Project Grant
Role Lead
Funding Start 2015
Funding Finish 2015
GNo G1501393
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

Epigenetics 2015, Hotel Grand Chancellor, Hobart, 12 - 14 November 2015$750

Funding body: University of Newcastle - Faculty of Health and Medicine

Funding body University of Newcastle - Faculty of Health and Medicine
Project Team Doctor Vicki Maltby
Scheme Travel Grant
Role Lead
Funding Start 2015
Funding Finish 2015
GNo G1501097
Type Of Funding Internal
Category INTE
UON Y

20144 grants / $435,000

Characterization of epigenetic profiles in patients with Multiple Sclerosis $225,000

Funding body: Multiple Sclerosis Research Australia Limited (MSRA)

Funding body Multiple Sclerosis Research Australia Limited (MSRA)
Project Team Doctor Vicki Maltby
Scheme Postdoctoral Fellowship
Role Lead
Funding Start 2014
Funding Finish 2018
GNo G1300732
Type Of Funding Aust Competitive - Non Commonwealth
Category 1NS
UON Y

Characterization of Epigenetic Profiles in Patients with Multiple Sclerosis$150,000

Funding body: Canadian Institutes of Health Research

Funding body Canadian Institutes of Health Research
Project Team Doctor Vicki Maltby, Laureate Professor Rodney Scott
Scheme Fellowship Award
Role Lead
Funding Start 2014
Funding Finish 2016
GNo G1301250
Type Of Funding International - Competitive
Category 3IFA
UON Y

Characterization of non-genetic factors causing Multiple Sclerosis$35,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Vicki Maltby
Scheme Project Grant
Role Lead
Funding Start 2014
Funding Finish 2014
GNo G1401414
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

Antipituitary Autoantibodies and Pituitary Target Autoantigen Characterization$25,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Vicki Maltby, Conjoint Associate Professor Patricia Crock, Laureate Professor Rodney Scott
Scheme Project Grant
Role Lead
Funding Start 2014
Funding Finish 2014
GNo G1301324
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

20132 grants / $9,655

Hunter Children’s Research Foundation Travel Award$6,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Vicki Maltby
Scheme Research Grant
Role Lead
Funding Start 2013
Funding Finish 2013
GNo G1300523
Type Of Funding Contract - Aust Non Government
Category 3AFC
UON Y

43rd Annual Scientific Meeting of the Australasian Society for immunology, New Zealand 2-5 December 2013$3,655

Funding body: University of Newcastle - Faculty of Health and Medicine

Funding body University of Newcastle - Faculty of Health and Medicine
Project Team Doctor Vicki Maltby
Scheme Travel Grant
Role Lead
Funding Start 2013
Funding Finish 2013
GNo G1300971
Type Of Funding Internal
Category INTE
UON Y

20121 grants / $1,020

42nd Annual Scientific meeting of the Australasian Society for Immunology, Melbourne Convention and Exhibition Centre, 2 - 6 December 2012$1,020

Funding body: University of Newcastle - Faculty of Health and Medicine

Funding body University of Newcastle - Faculty of Health and Medicine
Project Team Doctor Vicki Maltby
Scheme Travel Grant
Role Lead
Funding Start 2012
Funding Finish 2013
GNo G1201000
Type Of Funding Internal
Category INTE
UON Y

1 grants / $117,872

Epigenetics of MS progression$117,872

Funding body: National Multiple Sclerosis Society

Funding body National Multiple Sclerosis Society
Project Team Conjoint Professor Jeannette Lechner-Scott, Doctor Vicki Maltby, Associate Professor Rodney Lea, Dr Vilija Jokubaitis
Scheme International Progressive MS Alliance
Role Investigator
Funding Start
Funding Finish
GNo G2001051
Type Of Funding C3500 – International Not-for profit
Category 3500
UON Y
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Research Supervision

Number of supervisions

Completed1
Current0

Past Supervision

Year Level of Study Research Title Program Supervisor Type
2020 PhD Investigation of Erythrocyte and Erythrocyte-derived Extracellular Vesicle Content and Function in Multiple Sclerosis PhD (Medicine), College of Health, Medicine and Wellbeing, The University of Newcastle Co-Supervisor
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Dr Vicki Maltby

Position

Conjoint Lecturer
School of Medicine and Public Health
College of Health, Medicine and Wellbeing

Contact Details

Email vicki.e.maltby@newcastle.edu.au
Phone (02) 4042 0286
Fax (02) 4042 0031

Office

Room HMRI 3 West
Building HMRI
Location HMRI

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