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Dr Vicki Maltby

Research Fellow

School of Biomedical Sciences and Pharmacy

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

Fields of Research

Code Description Percentage
060404 Epigenetics (incl. Genome Methylation and Epigenomics) 80
110311 Medical Genetics (excl. Cancer Genetics) 10
110706 Immunogenetics (incl. Genetic Immunology) 10

Professional Experience

UON Appointment

Title Organisation / Department
Research Fellow University of Newcastle
School of Biomedical Sciences and Pharmacy
Australia

Academic appointment

Dates Title Organisation / Department
1/02/2012 -  Post Doctoral Fellow University of Newcastle
School of Biomedical Sciences and Pharmacy
Australia
1/05/2004 - 1/09/2004 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For publications that are currently unpublished or in-press, details are shown in italics.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 (10 outputs)

Year Citation Altmetrics Link
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.', Clin Epigenetics, 8 87 (2016)
DOI 10.1186/s13148-016-0253-y
Co-authors Rodney Scott
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]

© 2016 Murray et al.Background: The causative link between UV exposure and melanoma development is well known, however the mechanistic relationship remains incompletely character... [more]

© 2016 Murray et al.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
Co-authors Douglas Smith, Nikola Bowden
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 - 3Web of Science - 2
Co-authors 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 - 1Web of Science - 1
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 - 1Web of Science - 1
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 - 14Web of Science - 15
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 - 28Web of Science - 25
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 - 6Web of Science - 5
2009 MacDonald VE, Howe LJ, 'Histone acetylation: where to go and how to get there.', Epigenetics, 4 139-143 (2009) [C2]
Citations Scopus - 59Web of Science - 54
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 - 109Web of Science - 108
Show 7 more journal articles

Conference (6 outputs)

Year Citation Altmetrics Link
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 (2016)
Co-authors 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 (2016)
Co-authors 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]
Co-authors Rodney Scott
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 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 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 (2014) [E3]
DOI 10.1111/pcmr.12292
Co-authors Nikola Bowden
Show 3 more conferences
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Grants and Funding

Summary

Number of grants 9
Total funding $466,425

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


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 Associate Professor Jeannette Lechner-Scott, Dr 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

Funding body Multiple Sclerosis Research Australia Limited
Project Team Doctor Vicki Maltby
Scheme Postdoctoral Fellowship
Role Lead
Funding Start 2014
Funding Finish 2016
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, 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, 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 2012
GNo G1201000
Type Of Funding Internal
Category INTE
UON Y
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Dr Vicki Maltby

Position

Research Fellow
School of Biomedical Sciences and Pharmacy
Faculty of Health and Medicine

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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