
Associate Professor Kelly Kiejda
CI NSW Fellow
School of Biomedical Sciences and Pharmacy (Medical Genetics)
- Email:kelly.kiejda@newcastle.edu.au
- Phone:4042 0309
Cancer crusader
Dr Kelly Avery-Kiejda hopes to improve diagnosis and treatment for breast cancer sufferers by identifying new biomarkers for the disease.
A protein known as 'the guardian of the genome' has been a source of scientific fascination to molecular biologist Dr Kelly Avery-Kiejda for the past seven years. The P53 protein is so named for its ability to prevent the propagation of mutations that can lead to cancer.
P53 is a tumour suppressor, which can put the brakes on cancer by inhibiting the division of cells with DNA damage. But the protein is deactivated in many types of cancers, neutralising this powerful protection against the disease. Avery-Kiejda's research is focused on gaining a better understanding of the function of the protein and the factors that influence its activation.
Avery-Kiejda's first postdoctoral project in 2005 involved the investigation of isoforms (variants) of P53 and their links to chemotherapy resistance in melanoma. She is now applying that expertise to breast cancer research, looking specifically at the role the protein plays in the progression of advanced cancer, with the aim of developing a better method of diagnosing a cancer's potential to develop metastases.
"P53 isoforms were only discovered in 2005 and there is very little known about their role in breast cancer. We are one of the few groups studying that and, to my knowledge, unique in our emphasis on their role in promoting metastatic disease," Avery-Kiejda points out. "Breast cancer, or any cancer, essentially becomes incurable once a secondary cancer develops, so if we can identify markers that will indicate at an early stage whether a patient is more likely to develop a metastasis, then we can treat that patient differently from the outset."
In a related line of research, Avery-Kiejda is pursuing a project that could expand treatment options for women diagnosed with triple-negative forms of breast cancer, which are resistant to most conventional forms of hormone therapy. Since 2009, she has been a key researcher on a multi-site project funded by the National Breast Cancer Foundation (NBCF) analysing the expression of microRNAs. These small molecules are known to play a role in some cancers and can be used as a prognostic tool. In a novel finding, her team has identified a subset of 27 microRNAs that appear to be irregular in breast cancer patients who have developed lymph node metastases.
"This is a critical and very exciting finding because it means we may be able to use this information either to develop a treatment target or to diagnose secondary cancers earlier," Avery-Kiejda explains. "We have been looking at this specifically in triple-negative breast cancers but it may be applicable to others as well."
Avery-Kiejda's research has attracted the support of key cancer organisations, including Cure Cancer Australia, Cancer Australia and the Melanoma Institute Australia. Her affiliation with the University of Newcastle and the Hunter Medical Research Institute (HMRI) has opened collaborations with influential researchers such as the Australia and New Zealand Breast Cancer Trials Group research director Professor John Forbes and internationally recognised cancer geneticist Professor Rodney Scott.
"Everyone, myself included, knows someone who has been affected by cancer," she notes. "It has always been my dream to do something that will make a difference to patients by contributing to more effective treatment strategies."
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Cancer crusader
Dr Kelly Avery-Kiejda hopes to improve diagnosis and treatment for breast cancer sufferers by identifying new biomarkers for the disease.
Career Summary
Biography
Research Expertise
Dr Avery-Kiejda is a Cancer Institute NSW Career Development Fellow and Associate Professor at the Faculty of Health and Medicine, School of Biomedical Sciences & Pharmacy, at the University of Newcastle and an affiliated researcher in the Cancer program of Hunter Medical Research Institute.
Kelly’s expertise is in the field of molecular biology where she explores the genetic mechanisms that occur within a cancer cell that allow it to resist treatment and move to distant sites in the body. Kelly’s research has made significant advancements in the knowledge of the genetic factors that promote progression of breast cancer and melanoma, which both have a particularly high incidence in Australia and are incurable when they migrate to distant organs.
Kelly is considered an international leader in the p53 tumour suppressor as demonstrated by numerous invitations to give plenaries at prestigious conferences (e.g. The 2nd and 3rd International p53 Isoforms Workshops, 22nd Annual Queenstown Molecular Biology Meeting: Cancer Biology Satellite) as well as academic institutions and to collaborate with her peers. As testament to her standing in the cancer biology field, she was selected a Board member of the Australasian Metastasis Research Society and the Hunter Cancer Research Alliance Steering Committee; groups dedicated to promotion of cancer research.
Kelly has numerous peer-reviewed research articles in highly regarded journals such as Nature Communications, Cancer Research and Clinical Cancer Research and that continue to be highly cited by her peers. She has presented findings at over 50 national/international conferences and was awarded the HMRI PULSE Education prize in 2010, in recognition of her achievements as a leading early career researcher in the Hunter. She has served on the National Health and Medical Research Council (NHMRC) Postdoctoral Reference Group, which aims to provide feedback on issues of relevance to early career researchers to better the NHMRC Research Committee. She has been a member of the Cancer Australia grant review committee, a reviewer for NHMRC project grants, Breast Cancer Now UK, Cancer Society NZ and several high-ranking journals, indicating her international reputation. Kelly has received continual peer-reviewed funding to support her research from several granting bodies as a chief investigator including Cancer Institute NSW, Tour de Cure, Cure Cancer and the NSW Cancer Council.
She has been actively involved in mentoring and training students throughout her career, with 4 PhD completions and she currently supervises 4 PhD candidates. Kelly is passionate about training the future generation of researchers and hopes that she can make a difference to breast cancer outcome through her research by determining genes associated with breast cancer progression, in turn identifying targets for its treatment and prevention.
Teaching Expertise
Dr Avery-Kiejda is a full-time research academic. In addition to HDR and Honours supervision, Dr Avery-Kiejda has supervised several undergraduate students for their 3rd year projects in the Biotechnology and Biomedical Science degree at UoN as well as international undergraduates. Dr Avery-Kiejda has developed and delivered lectures for the Medicine degree in MEDI1015 and MEDI1012.
Administrative Expertise
Journal Peer Review:
Editor for PloS One and Cancers. Reviewer for: Oncogene, Cancer Research, Neoplasia, Clinical Cancer Research, Molecular Cancer Therapeutics, International Journal of Cancer, Clinical & Experimental Metastasis, BMC Cancer, Breast Cancer Research, Cell & Tissue Research, British Journal of Cancer Grant.
Grant Peer review
Member of the Cancer Australia and National Breast Cancer Foundation Grant Review Committees, external assessor for NHMRC project grant funding rounds, Breast Cancer Now UK, Cancer Society NZ and Rutherford Discovery Fellowships NZ, assessor for the Hunter Cancer Research Alliance and Hunter Medical Research Institute grants.
Qualifications
- PhD (Medicine), University of Sydney
- Bachelor of Science (Biotechnology)(Honours), University of Newcastle
Keywords
- breast cancer
- gene expression
- miRNA
- p53
Languages
- English (Mother)
Awards
Recipient
Year | Award |
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2001 |
Australian Postgraduate Award University of Sydney |
2001 |
Millennium Foundation Stipend Enhancement Grant Unknown |
Recognition
Year | Award |
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2012 |
Emerging research leaders program University of Newcastle |
1999 |
Deans Commendation List University of Newcastle |
1998 |
Most Outstanding Performance in the subject Cell and Molecular Biology University of Newcastle |
Research Award
Year | Award |
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2010 |
HMRI PULSE Education Prize Unknown |
2006 |
HMRI Translational Cancer Research Conference Early Career Researcher Poster Award Hunter Medical Research Institute |
Publications
For publications that are currently unpublished or in-press, details are shown in italics.
Journal article (44 outputs)
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2020 |
Steffens Reinhardt L, Zhang X, Wawruszak A, Groen K, De Iuliis GN, Avery-Kiejda KA, 'Good Cop, Bad Cop: Defining the Roles of 40p53 in Cancer and Aging', Cancers, 12 (2020) [C1]
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2020 |
Bond DR, Kahl R, Brzozowski JS, Jankowski H, Naudin C, Pariyar M, et al., 'Tetraspanin CD9 is regulated by MiR-518f-5p and functions in breast cell migration and in vivo tumor growth', Cancers, 12 (2020) [C1]
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2020 |
Eiholzer RA, Mehta S, Kazantseva M, Drummond CJ, McKinney C, Young K, et al., 'Intronic TP53 Polymorphisms Are Associated with Increased 133TP53 Transcript, Immune Infiltration and Cancer Risk.', Cancers, 12 (2020) [C1]
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2020 |
Yusof KM, Rosli R, Abdullah M, Avery-Kiejda KA, 'The roles of non-coding RNAs in tumor-associated lymphangiogenesis', Cancers, 12 1-27 (2020) [C1] © 2020 by the authors. Licensee MDPI, Basel, Switzerland. Lymphatic vessels are regarded as the ¿forgotten¿ circulation. Despite this, growing evidence has shown significant roles... [more] © 2020 by the authors. Licensee MDPI, Basel, Switzerland. Lymphatic vessels are regarded as the ¿forgotten¿ circulation. Despite this, growing evidence has shown significant roles for the lymphatic circulation in normal and pathological conditions in humans, including cancers. The dissemination of tumor cells to other organs is often mediated by lymphatic vessels that serve as a conduit and is often referred to as tumor-associated lymphangiogenesis. Some of the most well-studied lymphangiogenic factors that govern tumor lymphangiogenesis are the vascular endothelial growth factor (VEGF-C/D and VEGFR-2/3), neuroplilin-2 (NRP2), fibroblast growth factor (FGF), and hepatocyte growth factor (HGF), to name a few. However, recent findings have illustrated that non-coding RNAs are significantly involved in regulating gene expression in most biological processes, including lymphangiogenesis. In this review, we focus on the regulation of growth factors and non-coding RNAs (ncRNAs) in the lymphatic development in normal and cancer physiology. Then, we discuss the lymphangiogenic factors that necessitate tumor-associated lymphangiogenesis, with regards to ncRNAs in various types of cancer. Understanding the different roles of ncRNAs in regulating lymphatic vasculature in normal and cancer conditions may pave the way towards the development of ncRNA-based anti-lymphangiogenic therapy.
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2019 |
Morten BC, Chiu S, Oldmeadow C, Lubinski J, Scott RJ, Avery-Kiejda KA, 'The intron 3 16 bp duplication polymorphism of p53 (rs17878362) is not associated with increased risk of developing triple-negative breast cancer', Breast Cancer Research and Treatment, 173 727-733 (2019) [C1] © 2018, Springer Science+Business Media, LLC, part of Springer Nature. Purpose: Very little is known about the genetic risk factors associated with triple-negative breast cancer (... [more] © 2018, Springer Science+Business Media, LLC, part of Springer Nature. Purpose: Very little is known about the genetic risk factors associated with triple-negative breast cancer (TNBC), an aggressive clinical subtype characterised by the absence of ER, PR and HER2. p53, the tumour suppressor gene, is essential for maintaining genomic stability in response to cellular stress. In breast cancer, the mutation rates of TP53 vary depending on the subtype, such that ER-negative tumours have a high rate, and in ER-positive tumours they are less common. Previous studies have implicated the intronic polymorphism in TP53 (rs17878362; or PIN3) with an increased risk of developing breast cancer, although little has been discerned on its prevalence in different subtypes. In this study, we investigated the prevalence of the PIN3 genotype in the blood of cohorts with ER-positive and the ER-negative subtype TNBC, and assessed its association with outcome. Methods: We genotyped 656 TNBC and 648 ER-positive breast cancer patients, along with 436 controls, and compared the prevalence of polymorphism rs17878362 in these cohorts. Results: We found there to be no differences in the prevalence of the PIN3 genotype between the ER-positive and TNBC cohorts. Furthermore, no statistically significant difference was observed in the outcome of patients in either cohort with respect to their PIN3 genotype. Conclusions: Taken together, our results do not support an association of the PIN3 genotype with increased breast cancer risk, either in ER-positive or ER-negative patients.
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2019 |
Zhang X, Morten BC, Scott RJ, Avery-Kiejda KA, 'A Simple Migration/Invasion Workflow Using an Automated Live-cell Imager', JOVE-JOURNAL OF VISUALIZED EXPERIMENTS, (2019) [C1]
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2018 |
Wang Y, Lumbers ER, Arthurs AL, de Meaultsart CC, Mathe A, Avery-Kiejda KA, et al., 'Regulation of the human placental (pro)renin receptor-prorenin-angiotensin system by microRNAs.', Molecular human reproduction, 24 453-464 (2018) [C1]
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2018 |
Mehta SY, Morten BC, Antony J, Henderson L, Lasham A, Campbell H, et al., 'Regulation of the interferon-gamma (IFN- ) pathway by p63 and 133p53 isoform in different breast cancer subtypes', Oncotarget, 9 29146-29161 (2018) [C1] ©Mehta et al. The TP53 family consists of three sets of transcription factor genes, TP53, TP63 and TP73, each of which expresses multiple RNA variants and protein isoforms. Of the... [more] ©Mehta et al. The TP53 family consists of three sets of transcription factor genes, TP53, TP63 and TP73, each of which expresses multiple RNA variants and protein isoforms. Of these, TP53 is mutated in 25-30% of breast cancers. How TP53 mutations affect the interaction of TP53 family members and their isoforms in breast cancer is unknown. To investigate this, 3 independent breast cancer cohorts were stratified into 4 groups based on oestrogen receptor (ER) and TP53 mutation status. Using bioinformatic methodologies, principal signalling pathways associated with the expression of TP53 family members were identified. Results show an enrichment of IFN-¿ signalling associated with TP63 RNA in wild type TP53 (wtTP53), ER negative (ER-) tumours and with ¿133TP53 RNA in mutant TP53 (mTP53) ER positive (ER+) tumours. Moreover, tumours with low IFN-¿ signalling were associated with significantly poorer patient outcome. The predicted changes in expression of a subset of RNAs involved in IFN-¿ signalling were confirmed in vitro. Our data show that different members of the TP53 family can drive transcription of genes involved in IFN-¿ signalling in different breast cancer subgroups.
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2018 |
Chatterjee G, Pai T, Hardiman T, Avery-Kiejda K, Scott RJ, Spencer J, et al., 'Molecular patterns of cancer colonisation in lymph nodes of breast cancer patients', Breast cancer research : BCR, 20 (2018) [C1]
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2017 |
Avery-Kiejda KA, Mathe A, Scott RJ, 'Genome-wide miRNA, gene and methylation analysis of triple negative breast cancer to identify changes associated with lymph node metastases', Genomics Data, 14 1-4 (2017) [C1] © 2017 Triple negative breast cancer (TNBC) is a particularly important breast cancer subtype with an aggressive clinical phenotype that is associated with a higher likelihood of ... [more] © 2017 Triple negative breast cancer (TNBC) is a particularly important breast cancer subtype with an aggressive clinical phenotype that is associated with a higher likelihood of metastasis. This subtype is characterized by an absence of the estrogen (ER) and progesterone (PR) receptors, as well as the human epidermal growth factor receptor 2 (HER2/HER neu). The absence of the three receptors significantly reduces targeted treatment options for patients with TNBC and as such, there is an urgent need to identify novel treatment targets. Here, we provide detailed information regarding the design of a multi-platform dataset that describes genome-wide assessment of miRNA (assessed by microarray, GSE38167) and gene expression (assessed by microarray, GSE61723), as well as methylation (assessed by Illumina HM450K BeadChip, GSE78751) in TNBCs, matched normal adjacent tissues and matched lymph node metastases. The use of this multi-platform dataset is likely to uncover novel markers and key pathways involved in progression to lymph node metastasis in TNBC.
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2016 |
Morten BC, Scott RJ, Avery-Kiejda KA, 'Comparison of three different methods for determining cell proliferation in breast cancer cell lines', Journal of Visualized Experiments, 2016 (2016) [C1] © 2016 Journal of Visualized Experiments. Measuring cell proliferation can be performed by a number of different methods, each with varying levels of sensitivity, reproducibility ... [more] © 2016 Journal of Visualized Experiments. Measuring cell proliferation can be performed by a number of different methods, each with varying levels of sensitivity, reproducibility and compatibility with high-throughput formatting. This protocol describes the use of three different methods for measuring cell proliferation in vitro including conventional hemocytometer counting chamber, a luminescence-based assay that utilizes the change in the metabolic activity of viable cells as a measure of the relative number of cells, and a multi-mode cell imager that measures cell number using a counting algorithm. Each method presents its own advantages and disadvantages for the measurement of cell proliferation, including time, cost and high-throughput compatibility. This protocol demonstrates that each method could accurately measure cell proliferation over time, and was sensitive to detect growth at differing cellular densities. Additionally, measurement of cell proliferation using a cell imager was able to provide further information such as morphology, confluence and allowed for a continual monitoring of cell proliferation over time. In conclusion, each method is capable of measuring cell proliferation, but the chosen method is user-dependent.
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2016 |
Morten BC, Scott RJ, Avery-Kiejda KA, 'Comparison of the QuantiGene 2.0 assay and real-time RT-PCR in the detection of p53 isoform mRNA expression in formalin-fixed paraffin-embedded tissues- A preliminary study', PLoS ONE, 11 (2016) [C1] © 2016 Morten et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and repr... [more] © 2016 Morten et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. p53 is expressed as multiple smaller isoforms whose functions in cancer are not well understood. The p53 isoforms demonstrate abnormal expression in different cancers, suggesting they are important in modulating the function of full-length p53 (FLp53). The quantification of relative mRNA expression has routinely been performed using real-time PCR (qPCR). However, there are serious limitations when detecting p53 isoforms using this method, particularly for formalin-fixed paraffin-embedded (FFPE) tissues. The use of FFPE tumours would be advantageous to correlate expression of p53 isoforms with important clinical features of cancer. One alternative method of RNA detection is the hybridization-based QuantiGene 2.0 Assay, which has been shown to be advantageous for the detection of RNA from FFPE tissues. In this pilot study, we compared the QuantiGene 2.0 Assay to qPCR for the detection of FLp53 and its isoform ¿40p53 in matched fresh frozen (FF) and FFPE breast tumours. FLp53 mRNA expression was detected using qPCR in FF and FFPE tissues, but ¿40p53 mRNA was only detectable in FF tissues. Similar results were obtained for the QuantiGene 2.0 Assay. FLp53 relative mRNA expression was shown to be strongly correlated between the two methods (R2 = 0.9927, p = 0.0031) in FF tissues, however ¿40p53 was not (R2 = 0.4429, p = 0.3345). When comparing the different methods for the detection of FLp53 mRNA from FFPE and FF samples, no correlation (R2 = 0.0002, p = 0.9863) was shown using the QuantiGene 2.0 Assay, and in contrast, the level of expression was highly correlated between the two tissues using qPCR (R2 = 0.8753, p = 0.0644). These results suggest that both the QuantiGene 2.0 Assay and qPCR methods are inadequate for the quantification of ¿40p53 mRNA in FFPE tissues. Therefore, alternative methods of RNA detection and quantification are required to study the relative expression of ¿40p53 in FFPE samples.
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2016 |
Bolton KA, Avery-Kiejda KA, Holliday EG, Attia J, Bowden NA, Scott RJ, 'A polymorphic repeat in the IGF1 promoter influences the risk of endometrial cancer', ENDOCRINE CONNECTIONS, 5 115-122 (2016) [C1]
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2016 |
Morten BC, Wong-Brown MW, Scott RJ, Avery-Kiejda KA, 'The presence of the intron 3 16 bp duplication polymorphism of p53 (rs17878362) in breast cancer is associated with a low 40p53:p53 ratio and better outcome', Carcinogenesis, 37 81-86 (2016) [C1] © The Author 2015. Published by Oxford University Press. All rights reserved. Breast cancer is the most common female cancer, but it has relatively low rates of p53 mutations, sug... [more] © The Author 2015. Published by Oxford University Press. All rights reserved. Breast cancer is the most common female cancer, but it has relatively low rates of p53 mutations, suggesting other mechanisms are responsible for p53 inactivation. We have shown that the p53 isoform, ¿40p53, is highly expressed in breast cancer, where it may contribute to p53 inactivation. ¿40p53 can be produced by alternative splicing of p53 in intron 2 and this is regulated by the formation of G-quadruplex structures in p53 intron 3, from which the nucleotides forming these structures overlap with a common polymorphism, rs17878362. rs17878362 alters p53 splicing to decrease fully spliced p53 messenger RNA (mRNA) in vitro following ionizing radiation and this in turn alters ¿40p53:p53. Hence, the presence of rs17878362 may be important in regulating ¿40p53:p53 in breast cancer. This study aimed to determine if rs17878362 was associated with altered ¿40p53 and p53 expression and outcome in breast cancer. We sequenced p53 in breast tumours from 139 patients and compared this with ¿40p53 and p53 mRNA expression. We found that the ratio of ¿40p53:p53 was significantly lower in tumours homozygous for the polymorphic A2 allele compared with those who were wild-type (A1/A1). Furthermore, there was a lower proportion of breast cancers carrying the A2 allele from patients who subsequently developed metastasis compared with those that did not. Finally, we show that patients whose tumours carried the polymorphic A2 allele had significantly better disease-free survival. These results show that rs17878362 is associated with a low ¿40p53:p53 ratio in breast cancer and that this is associated with better outcome.
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2016 |
Bolton KA, Holliday EG, Attia J, Bowden NA, Avery-Kiejda KA, Scott RJ, 'A novel polymorphic repeat in the upstream regulatory region of the estrogen-induced gene EIG121 is not associated with the risk of developing breast or endometrial cancer', BMC Research Notes, 9 (2016) [C1] © 2016 The Author(s). Background: The estrogen-induced gene 121 (EIG121) has been associated with breast and endometrial cancers, but its mechanism of action remains unknown. In a... [more] © 2016 The Author(s). Background: The estrogen-induced gene 121 (EIG121) has been associated with breast and endometrial cancers, but its mechanism of action remains unknown. In a genome-wide search for tandem repeats, we found that EIG121 contains a short tandem repeat (STR) in its upstream regulatory region which has the potential to alter gene expression. The presence of this STR has not previously been analysed in relation to breast or endometrial cancer risk. Results: In this study, the lengths of this STR were determined by PCR, fragment analysis and sequencing using DNA from 223 breast cancer patients, 204 endometrial cancer patients and 220 healthy controls to determine if they were associated with the risk of developing breast or endometrial cancer. We found this repeat to be highly variable with the number of copies of the AG motif ranging from 27 to 72 and having a bimodal distribution. No statistically significant association was identified between the length of this STR and the risk of developing breast or endometrial cancer or age at diagnosis. Conclusions: The STR in the upstream regulatory region of EIG121 is highly polymorphic, but is not associated with the risk of developing breast or endometrial cancer in the cohorts analysed here. While this polymorphic STR in the regulatory region of EIG121 appears to have no impact on the risk of developing breast or endometrial cancer, its association with disease recurrence or overall survival remains to be determined.
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2016 |
Mathe A, Wong-Brown M, Locke WJ, Stirzaker C, Braye SG, Forbes JF, et al., 'DNA methylation profile of triple negative breast cancer-specific genes comparing lymph node positive patients to lymph node negative patients', SCIENTIFIC REPORTS, 6 (2016) [C1]
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2015 |
Dun MD, Chalkley RJ, Faulkner S, Keene S, Avery-Kiejda KA, Scott RJ, et al., 'Proteotranscriptomic profiling of 231-BR breast cancer cells: Identification of potential biomarkers and therapeutic targets for brain metastasis', Molecular and Cellular Proteomics, 14 2316-2330 (2015) [C1] © 2015 by The American Society for Biochemistry and Molecular Biology, Inc. Brain metastases are a devastating consequence of cancer and currently there are no specific biomarkers... [more] © 2015 by The American Society for Biochemistry and Molecular Biology, Inc. Brain metastases are a devastating consequence of cancer and currently there are no specific biomarkers or therapeutic targets for risk prediction, diagnosis, and treatment. Here the proteome of the brain metastatic breast cancer cell line 231-BR has been compared with that of the parental cell line MDA-MB-231, which is also metastatic but has no organ selectivity. Using SILAC and nanoLC-MS/MS, 1957 proteins were identified in reciprocal labeling experiments and 1584 were quantified in the two cell lines. A total of 152 proteins were confidently determined to be up- or down-regulated by more than twofold in 231-BR. Of note, 112/152 proteins were decreased as compared with only 40/152 that were increased, suggesting that down-regulation of specific proteins is an important part of the mechanism underlying the ability of breast cancer cells to metastasize to the brain. When matched against transcriptomic data, 43% of individual protein changes were associated with corresponding changes in mRNA, indicating that the transcript level is a limited predictor of protein level. In addition, differential miRNA analyses showed that most miRNA changes in 231-BR were up- (36/45) as compared with down-regulations (9/45). Pathway analysis revealed that proteome changes were mostly related to cell signaling and cell cycle, metabolism and extracellular matrix remodeling. The major protein changes in 231-BR were confirmed by parallel reaction monitoring mass spectrometry and consisted in increases (by more than fivefold) in the matrix metalloproteinase-1, ephrin-B1, stomatin, myc target-1, and decreases (by more than 10-fold) in transglutaminase-2, the S100 calcium-binding protein A4, and L-plastin. The clinicopathological significance of these major proteomic changes to predict the occurrence of brain metastases, and their potential value as therapeutic targets, warrants further investigation.
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2015 |
Stirzaker C, Zotenko E, Song JZ, Qu W, Nair SS, Locke WJ, et al., 'Methylome sequencing in triple-negative breast cancer reveals distinct methylation clusters with prognostic value', Nature Communications, 6 1-11 (2015) [C1]
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2015 |
Wong-Brown MW, Meldrum CJ, Carpenter JE, Clarke CL, Narod SA, Jakubowska A, et al., 'Prevalence of BRCA1 and BRCA2 germline mutations in patients with triple-negative breast cancer', Breast Cancer Research and Treatment, 150 71-80 (2015) [C1] © 2015, Springer Science+Business Media New York. Triple-negative breast cancers¿(TNBC) lack expression of oestrogen, progesterone and HER2 receptors. The gene expression profiles... [more] © 2015, Springer Science+Business Media New York. Triple-negative breast cancers¿(TNBC) lack expression of oestrogen, progesterone and HER2 receptors. The gene expression profiles of TNBCs are similar to those of breast tumours in women with BRCA1 mutations. Reports to date indicate that up to 20¿% of TNBC patients harbour germline BRCA mutations; however, the prevalence of BRCA mutations in TNBC patients varies widely between countries and from study to study. We studied 774 women with triple-negative breast cancer, diagnosed on average at age 58.0¿years. Samples of genomic DNA were provided by the Australian Breast Cancer Tissue Bank (ABCTB) (439 patients) and by the Department of Genetics and Pathology of the Pomeranian Medical University (335 patients). The entire coding regions and the exon¿intron boundaries of BRCA1 and BRCA2 were amplified and sequenced by next-generation sequencing. We identified a BRCA1 or BRCA2 mutation in 74 of 774 (9.6¿%) triple-negative patients. The mutation prevalence was 9.3¿% in Australia and was 9.9¿% in Poland. In both countries, the mean age of diagnoses of BRCA1 mutation carriers was significantly lower than that of non-carriers, while the age of onset of BRCA2 mutation carriers was similar to that of non-carriers. In the Australian cohort, 59¿% of the mutation-positive patients did not have a family history of breast or ovarian cancer, and would not have qualified for genetic testing. The triple-negative phenotype should be added as a criterion to genetic screening guidelines.
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2015 |
Mathe A, Scott RJ, Avery-Kiejda KA, 'MiRNAs and other epigenetic changes as biomarkers in triple negative breast cancer', International Journal of Molecular Sciences, 16 28347-28376 (2015) [C1] © 2015 by the authors; licensee MDPI, Basel, Switzerland. Triple negative breast cancer (TNBC) is characterised by the lack of receptors for estrogen (ER), progesterone (PR), and ... [more] © 2015 by the authors; licensee MDPI, Basel, Switzerland. Triple negative breast cancer (TNBC) is characterised by the lack of receptors for estrogen (ER), progesterone (PR), and human epidermal growth factor 2 (HER2). Since it cannot be treated by current endocrine therapies which target these receptors and due to its aggressive nature, it has one of the worst prognoses of all breast cancer subtypes. The only treatments remain chemo- and/or radio-therapy and surgery and because of this, novel biomarkers or treatment targets are urgently required to improve disease outcomes. MicroRNAs represent an attractive candidate for targeted therapies against TNBC, due to their natural ability to act as antisense interactors and regulators of entire gene sets involved in malignancy and their superiority over mRNA profiling to accurately classify disease. Here we review the current knowledge regarding miRNAs as biomarkers in TNBC and their potential use as therapeutic targets in this disease. Further, we review other epigenetic changes and interactions of these changes with microRNAs in this breast cancer subtype, which may lead to the discovery of new treatment targets for TNBC.
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2015 |
Mathe A, Wong-Brown M, Morten B, Forbes JF, Braye SG, Avery-Kiejda KA, Scott RJ, 'Novel genes associated with lymph node metastasis in triple negative breast cancer', Scientific Reports, 5 (2015) [C1] Triple negative breast cancer (TNBC) is the most aggressive breast cancer subtype with the worst prognosis and no targeted treatments. TNBC patients are more likely to develop met... [more] Triple negative breast cancer (TNBC) is the most aggressive breast cancer subtype with the worst prognosis and no targeted treatments. TNBC patients are more likely to develop metastases and relapse than patients with other breast cancer subtypes. We aimed to identify TNBC-specific genes and genes associated with lymph node metastasis, one of the first signs of metastatic spread. A total of 33 TNBCs were used; 17 of which had matched normal adjacent tissues available, and 15 with matched lymph node metastases. Gene expression microarray analysis was used to reveal genes that were differentially expressed between these groups. We identified and validated 66 genes that are significantly altered when comparing tumours to normal adjacent samples. Further, we identified 83 genes that are associated with lymph node metastasis and correlated these with miRNA-expression. Pathway analysis revealed their involvement in DNA repair, recombination and cell death, chromosomal instability and other known cancer-related pathways. Finally, four genes were identified that were specific for TNBC, of which one was associated with overall survival. This study has identified novel genes involved in LN metastases in TNBC and genes that are TNBC specific that may be used as treatment targets or prognostic indicators in the future.
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2014 |
Avery-Kiejda KA, Braye SG, Forbes JF, Scott RJ, 'The expression of Dicer and Drosha in matched normal tissues, tumours and lymph node metastases in triple negative breast cancer', BMC CANCER, 14 (2014) [C1]
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2014 |
Wong-Brown MW, Avery-Kiejda KA, Bowden NA, Scott RJ, 'Low prevalence of germline PALB2 mutations in Australian triple-negative breast cancer', International Journal of Cancer, 134 301-305 (2014) [C1] Triple-negative breast cancer (TNBC) is a tumour classification that is defined by oestrogen receptor, progesterone receptor and human epidermal growth factor receptor 2 receptor ... [more] Triple-negative breast cancer (TNBC) is a tumour classification that is defined by oestrogen receptor, progesterone receptor and human epidermal growth factor receptor 2 receptor negativity. TNBCs share a similar gene expression profile to BRCA-mutated tumours, have been shown to carry a high proportion of BRCA mutations and have a more adverse prognosis compared to other types of breast tumours. PALB2 has been shown to be a moderate-penetrance breast cancer susceptibility gene and is involved in the same DNA damage repair pathway as BRCA1 and BRCA2; this raises the possibility that germline PALB2 mutations may be involved in the pathogenesis of TNBCs. In our study, we sequenced the coding regions of PALB2 (including intron/exon boundaries) in genomic DNA from 347 patients diagnosed with TNBC to determine the prevalence of deleterious mutations in this population. Two novel truncating mutations (c.758dup and c.2390del) and one previously detected truncating mutation (c.3113+5G>C) were found. In addition, five variants predicted to be protein-affecting were also identified. Our study shows that the prevalence of PALB2 germline mutations in individuals with TNBC is ~1%, similar to the prevalence of PALB2 germline mutation of 1% in familial non-BRCA1/2 breast cancer cohorts. © 2013 UICC.
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2014 |
Avery-Kiejda KA, Braye SG, Mathe A, Forbes JF, Scott RJ, 'Decreased expression of key tumour suppressor microRNAs is associated with lymph node metastases in triple negative breast cancer', BMC Cancer, 14 (2014) [C1] Background: Breast cancer is the most common malignancy that develops in women, responsible for the highest cancer-associated death rates. Triple negative breast cancers represent... [more] Background: Breast cancer is the most common malignancy that develops in women, responsible for the highest cancer-associated death rates. Triple negative breast cancers represent an important subtype that have an aggressive clinical phenotype, are associated with a higher likelihood of metastasis and are not responsive to current targeted therapies. miRNAs have emerged as an attractive candidate for molecular biomarkers and treatment targets in breast cancer, but their role in the progression of triple negative breast cancer remains largely unexplored.Methods: This study has investigated miRNA expression profiles in 31 primary triple negative breast cancer cases and in 13 matched lymph node metastases compared with 23 matched normal breast tissues to determine miRNAs associated with the initiation of this disease subtype and those associated with its metastasis.Results: 71 miRNAs were differentially expressed in triple negative breast cancer, the majority of which have previously been associated with breast cancer, including members of the miR-200 family and the miR-17-92 oncogenic cluster, suggesting that the majority of miRNAs involved in the initiation of triple negative breast cancer are not subtype specific. However, the repertoire of miRNAs expressed in lymph node negative and lymph node positive triple negative breast cancers were largely distinct from one another. In particular, miRNA profiles associated with lymph node negative disease tended to be up-regulated, while those associated with lymph node positive disease were down-regulated and largely overlapped with the profiles of their matched lymph node metastases. From this, 27 miRNAs were identified that are associated with metastatic capability in the triple negative breast cancer subtype.Conclusions: These results provide novel insight into the repertoire of miRNAs that contribute to the initiation of and progression to lymph node metastasis in triple negative breast cancer and have important implications for the treatment of this breast cancer subtype. © 2014 Avery-Kiejda et al.; licensee BioMed Central Ltd.
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2014 |
Avery-Kiejda KA, Morten B, Wong-Brown MW, Mathe A, Scott RJ, 'The relative mRNA expression of p53 isoforms in breast cancer is associated with clinical features and outcome.', Carcinogenesis, 35 586-596 (2014) [C1]
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2013 |
Bolton KA, Ross JP, Grice DM, Bowden NA, Holliday EG, Avery-Kiejda KA, Scott RJ, 'STaRRRT: a table of short tandem repeats in regulatory regions of the human genome', BMC GENOMICS, 14 (2013) [C1]
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2013 |
Bowden NA, Ashton KA, Vilain RE, Avery-Kiejda KA, Davey RJ, Murray HC, et al., 'Regulators of Global Genome Repair Do Not Respond to DNA Damaging Therapy but Correlate with Survival in Melanoma', PLOS ONE, 8 (2013) [C1]
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2011 |
Kiejda KA, Bowden NA, Croft AJ, Scurr LL, Kairupan CF, Ashton KA, et al., 'P53 in human melanoma fails to regulate target genes associated with apoptosis and the cell cycle and may contribute to proliferation', BMC Cancer, 11 203-219 (2011) [C1]
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2011 |
Kiejda KA, Wong-Brown M, Scott R, 'Genetic markers in breast cancer - How far have we come from BRCA1?', Asia-Pacific Journal of Molecular Medicine, 1 1-15 (2011) [C1]
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2011 |
Wong-Brown M, Nordfors C, Mossman D, Pecenpetelovska G, Kiejda KA, Talseth-Palmer B, et al., 'BRIP1, PALB2, and RAD51C mutation analysis reveals their relative importance as genetic susceptibility factors for breast cancer', Breast Cancer Research and Treatment, 127 853-859 (2011) [C1]
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2010 |
Bowden NA, Ashton KA, Kiejda KA, Zhang XD, Hersey P, Scott R, 'Nucleotide excision repair gene expression after cisplatin treatment in melanoma', Cancer Research, 70 7918-7926 (2010) [C1]
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2009 |
Jiang CC, Mao ZG, Kiejda KA, Hersey P, Zhang XD, 'Glucose-regulated protein 78 antagonizes cisplatin and adriamycin in human melanoma cells', Carcinogenesis, 30 197-204 (2009) [C1]
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2008 |
Kiejda KA, Zhang XD, Adams LJ, Scott R, Vojtesek B, Lane DP, Hersey P, 'Small molecular weight variants of p53 are expressed in human melanoma cells and are induced by the DNA-damaging agent cisplatin', Clinical Cancer Research, 14 1659-1668 (2008) [C1]
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2008 |
Chen LH, Jiang CC, Watts R, Thorne RF, Kiejda KA, Zhang XD, Hersey P, 'Inhibition of endoplasmic reticulum stress-induced apoptosis of melanoma cells by the ARC protein', Cancer Research, 68 834-842 (2008) [C1]
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2008 |
Jiang CC, Lucas K, Kiejda KA, Wade M, Debock CE, Thorne RF, et al., 'Up-regulation of Mcl-1 is critical for survival of human melanoma cells upon endoplasmic reticulum stress', Cancer Research, 68 6708-6717 (2008) [C1]
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2008 |
Zhu B-K, Wang P, Zhang XD, Jiang CC, Chen LH, Kiejda KA, et al., 'Activation of Jun N-terminal kinase is a mediator of vincristine-induced apoptosis of melanoma cells', Anti-Cancer Drugs, 19 189-200 (2008) [C1]
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2007 |
Yu FW, Jiang CC, Kiejda KA, Gillespie S, Zhang XD, Hersey P, 'Apoptosis induction in human melanoma cells by inhibition of MEK is caspase-independent and mediated by the Bcl-2 family members PUMA, Bim, and Mcl-1', Clinical Cancer Research, 13 4934-4942 (2007) [C1]
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2007 |
Mhaidat NM, Wang Y, Kiejda KA, Zhang XD, Hersey P, 'Docetaxel-induced apoptosis in melanoma cells is dependent on activation of caspase-2', Molecular Cancer Therapeutics, 6 752-761 (2007) [C1]
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2007 |
Mhaidat NM, Zhang XD, Allen J, Kiejda KA, Scott R, Hersey P, 'Temozolomide induces senescence but not apoptosis in human melanoma cells', British Journal of Cancer, 97 1225-1233 (2007) [C1]
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2007 |
Jiang CC, Li HC, Gillespie S, Kiejda KA, Mhaidat N, Yu FW, et al., 'Tunicamycin sensitizes human melanoma cells to tumor necrosis factor-related apoptosis-inducing ligand-induced apoptosis by up-regulation of TRAIL-R2 via the unfolded protein response', Cancer Research, 67 5880-5888 (2007) [C1]
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2007 |
Jiang CC, Li HC, Gillespie S, Yu FW, Kiejda KA, Zhang XD, Hersey P, 'Inhibition of MEK sensitizes human melanoma cells to endoplasmic reticulum stress-induced apoptosis', Cancer Research, 67 9750-9761 (2007) [C1]
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2007 |
Chen LH, Jiang CC, Kiejda KA, Wang YF, Thorne RF, Zhang XD, Hersey P, 'Thapsigargin sensitizes human melanoma cells to TRAIL-induced apoptosis by up-regulation of TRAIL-R2 through the unfolded protein response', Carcinogenesis, 28 2328-2336 (2007) [C1]
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Show 41 more journal articles |
Conference (75 outputs)
Year | Citation | Altmetrics | Link | |||||
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2020 |
Yusof KM, Mahmud R, Abdullah M, Groen K, Avery-Kiejda KA, Rosli R, 'Identification of modifiable and molecular factors associated with breast cancer-related lymphedema in Malaysian breast cancer survivors', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2020)
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2018 |
Mathe A, Wong-Brown M, Morten BC, Braye SG, Locke WJ, Stirzaker C, et al., 'Defining the Key Mediators of Breast Cancer Progression and Treatment Resistance in the triple Negative Subtype', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2018)
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2017 |
Pariyar M, Scott R, Avery-Kiejda K, 'Validation of Four Triple Negative Breast Cancer-Specific Genes and their Association with Prognosis', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2017)
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2015 |
Morten B, Wong-Brown M, Scott R, Avery-Kiejda K, 'ASSOCIATION OF THE POLYMORPHIC INTRON 3 16 BP DUPLICATION IN TP53 (RS17878362) WITH A LOW Delta 40P53:P53 RATIO AND BETTER OUTCOME IN BREAST CANCER', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2015) [E3]
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2014 |
Morten B, Campbell HG, Brown MW, Mathe A, Braithwaite AW, Scott RJ, Kiejda KA, ' 40p53 regulation of estrogen responsiveness in breast cancer.', 16th International p53 Workshop Proceedings, Stockholm, Sweden (2014) [E3]
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2014 | Morten B, Scott RJ, Avery-Kiejda KA, 'Comparison of the Quantigene 2.0 Assay for the detection of p53 isoform mRNA expression in FFPE tissues.', 16th International p53 Workshop Proceedings, Stockholm, Sweden (2014) [E3] | |||||||
2014 |
Morten B, Scott RJ, Kiejda KA, 'The role of 40p53 and p53 in Estrogen-Receptor-a signaling pathways in breast cancer.', 23rd Biennial Congress of the European Association for Cancer Research Proceedings Book, Munich, Germany (2014) [E3]
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2014 |
Morten B, Campbell HG, Wong-Brown MW, Mathe A, Braithwaite AW, Scott RJ, Avery-Kiejda KA, 'Delta-40P53 regulation of ERa-mediated signalling in breast cancer.', The 29th International Association for Breast Cancer Research Conference Proceedings, Manly, NSW, Australia (2014) [E3]
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2014 |
Mathe A, Avery-Kiejda KA, Wong-Brown M, Forbes JF, Braye SG, Scott RJ, 'Can microRNAs impact cell migration in triple negative breast cancer?', The Australian Society for Medical Research (ASMR) Satellite Scientific Meeting Programme, Newcastle, NSW, Australia (2014) [E3]
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2014 |
Morten B, Scott RJ, Avery-Kiejda KA, ' 40p53 and p53 mediate ER-a expression in breast cancer cells.', The Australian Society for Medical Research (ASMR) Satellite Scientific Meeting Programme, Newcastle, NSW, Australia (2014) [E3]
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2014 |
Avery-Kiejda KA, Morten B, Wong-Brown MW, Mathe A, Scott RJ, 'The relationship between p53 isoforms and prognosis in breast cancer.', The Australian Society for Medical Research (ASMR) Satellite Scientific Meeting Programme, Newcastle, NSW, Australia (2014) [E3]
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2014 |
Bolton KA, Ross JP, Grice DM, Bowden NA, Holliday EG, Kiejda KA, Scott RJ, 'Short tandem repeats are variable genetic elements that may have major consequences for multiple diseases.', The Australian Society for Medical Research (ASMR) Satellite Scientific Meeting Programme, Newcastle, NSW, Australia (2014) [E3]
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2014 |
Mathe A, Avery-Kiejda KA, Wong-Brown M, Morten B, Forbes JF, Braye SG, Scott RJ, 'IDENTIFICATION OF NOVEL TRANSCRIPTS SPECIFIC TO TRIPLE NEGATIVE BREAST CANCER THAT ARE ASSOCIATED WITH LYMPH NODE METASTASIS', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2014) [E3]
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2014 |
Morten B, Scott RJ, Avery-Kiejda KA, 'Delta 40P53 CAN ALTER BREAST CANCER CELL GROWTH BY MEDIATING THE ESTROGEN RESPONSE', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2014) [E3]
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2014 |
Mathe A, Avery-Kiejda KA, Wong-Brown M, Forbes JF, Braye SG, Scott RJ, 'Eight microRNAs as biomarkers for metastatic spread in triple negative breast cancer', EUROPEAN JOURNAL OF CANCER (2014) [E3]
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2014 |
Morten B, Scott RJ, Avery-Kiejda KA, 'The role of Delta-40p53 and p53 in Estrogen Receptor-alpha signalling pathways in breast cancer', EUROPEAN JOURNAL OF CANCER (2014) [E3]
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2014 |
Bolton KA, Holliday EG, Bowden NA, Avery-Kiejda KA, Scott RJ, 'A highly polymorphic AG repeat in the upstream regulatory region of the estrogen-induced gene EIG121 is a modifier of disease risk in endometrial cancer', EUROPEAN JOURNAL OF CANCER (2014) [E3]
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2014 |
Bolton KA, Holliday EG, McEvoy M, Attia J, Proietto A, Otton G, et al., 'A highly polymorphic AG repeat in the upstream regulatory region of the estrogen gene EIG121 is a potential modifier of endometrial cancer risk.', Asia-Pacific Journal of Clinical Oncology, Newcastle, NSW, Australia (2014) [E3]
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2013 |
Zotenko E, Stirzaker C, Song JZ, Qu W, Nair S, Avery-Kiejda KA, et al., 'Genome-wide DNA methylation analysis of archival formalin-fixed paraffin-embedded tissue (FFPET) using MDBCAP-Seq identifies novel epigenetic diagnostic biomarker loci in breast cancer.', 25th Lorne Cancer Conference Proceedings, Lorne, VIC, Australia (2013) [E3]
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2013 |
Morten B, Mathe A, Scott RJ, Avery-Kiejda KA, 'mRNA expression analysis of p53 isoforms in breast cancer.', 25th Lorne Cancer Conference Proceedings, Lorne, VIC, Australia (2013) [E3]
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2013 |
Avery-Kiejda KA, Mathe A, Braye SG, Forbes JF, Scott RJ, 'The expression of Dicer and Drosha in lymph node metastases of triple negative breast cancer.', 25th Lorne Cancer Conference Proceedings, Lorne, VIC, Australia (2013) [E3]
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2013 |
Mathe A, Avery-Kiejda KA, Wong-Brown MW, Forbes JF, Braye SG, Scott RJ, 'Target gene identification of microRNAs associated with lymph node metastases in triple negative breast cancer.', 25th Lorne Cancer Conference Proceedings, Lorne, VIC, Australia (2013) [E3]
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2013 |
Bolton KA, Ross J, Grice DM, Avery-Kiejda KA, Bowden NA, Holliday EG, Scott RJ, 'Role of Short Tandem Repeats in Disease and Evolutionary Mechanisms.', 34th Lorne Genome Conference Proceedings, Lorne, VIC, Australia (2013) [E3]
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2013 |
Mathe A, Avery-Kiejda KA, Wong-Brown M, Forbes JF, Braye SG, Scott RJ, 'Integration of microRNA and gene expression profiling in triple negative breast cancer to identify possible biomarkers for metastases.', Breakthrough Breast Cancer TNBC Conference Proceedings, London, UK (2013) [E3]
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2013 |
Wong-Brown M, Li S, Wilkins M, Avery-Kiejda KA, Bowden N, Scott R, 'Targeted resequencing of BRCA1 and BRCA2 in familial breast cancer.', Kathleen Cunningham Foundation Consortium for Research into Familial Aspects of Cancer 2013 Research and Practice Proceedings, Cairns, QLD, Australia. (2013) [E3]
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2013 |
Wong-Brown M, Avery-Kiejda K, Bowden N, Scott R, 'Prevalence of BRCA1 and BRCA2 germline mutations in triple-negative breast cancer', Programme, Newcastle (2013) [E3]
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2013 |
Morten B, Scott RJ, Avery-Kiejda KA, 'Microarray analysis of differentially expressed genes in patients with high 40p53 expression.', Translational Cancer Research Conference Abstract booklet, Newcastle, Australia (2013) [E3]
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2013 |
Bolton KA, Avery-Kiejda KA, Grice DM, Holliday EG, Bowden NA, Ross J, Scott RJ, 'STaRRRT: Our new resource for identifying candidates of genetic risk in breast and endometrial cancer.', Translational Cancer Research Conference Abstract booklet, Newcastle, Australia (2013) [E3]
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2013 |
Mathe A, Wong-Brown M, Forbes JF, Braye SG, Scott RJ, Avery-Kiejda KA, 'Identification of biomarkers for metastatic spread in triple negative breast cancer.', Translational Cancer Research Conference Abstract booklet, Newcastle, Australia (2013) [E3]
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2012 |
Bolton KA, Ross J, Grice DM, Kiejda KA, Bowden NA, Holliday EG, Scott R, 'Potential role of short tandem repeats in disease processes', Abstracts. 6th Australian Health & Medical Research Congress, Adelaide, SA (2012) [E3]
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2012 |
Kiejda KA, Forbes JF, Braye SG, Scott R, 'Identification of miRNAs associated with lymph node metastasis in triple-negative breast cancer', Human Genome Meeting 2012: Genetics and Genomics in Personalised Medicine. Abstract Book, Sydney, NSW (2012) [E3]
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2012 |
Wong-Brown M, Li S, Wilkins M, Kiejda KA, Bowden NA, Scott R, 'Exploratory targeted resequencing of BRCA1 and BRCA2 in inherited breast cancer', Programme. kConFab Familial Aspects of Cancer: Research & Practice 2012, Kingscliff, NSW (2012) [E3]
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2012 |
Wong-Brown M, Li S, Wilkins M, Kiejda KA, Bowden NA, Scott R, 'Targeted resequencing of BRCA1 and BRCA2 in inherited breast cancer', Cancer Research, San Antonio, Texas (2012) [E3]
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2011 |
Bowden NA, Ashton KA, Kiejda KA, Zhang XD, Hersey P, Scott R, 'Downstream effects of reduction in nucleotide excision repair in response to cisplatin treatment in melanoma', Pigment Cell & Melanoma Research, Tampa, FL (2011) [E3]
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2011 |
Kiejda KA, Forbes JF, Hope TL, Braye SG, Scott R, 'Differential expression of miRNAs in triple-negative breast cancer', AMATA Conference Canberra 2011 Handbook, Canberra, ACT (2011) [E3]
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2011 |
Kiejda KA, Forbes JF, Braye SG, Scott R, 'MicroRNA expression profiling in triple-negative breast cancer', Keystone Symposia on Mollecular and Cellular Biology: MicroRNAs and Non-coding RNAs and Cancer, Banff, AL (2011) [E3]
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2010 |
Croft AJ, Kiejda KA, Bowden NA, Zhang X, Scott R, Hersey P, 'Expression profiling on apoptosis-related genes in cisplatin-treated human melanoma cell lines', 22nd Lorne Cancer Conference: Abstracts and Delegate Information, Lorne, Vic. (2010) [E3]
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2010 |
Wong-Brown M, Bowden NA, Kiejda KA, Scott R, 'BRIP1 and PALB2 mutation detection in Hunter-New England familial breast cancer cohort', 27th HUGO-IABCR Congress 2010. Genomics, Biology and Breast Cancer Treatment. Programme & Abstract Book, Biopolis, Singapore (2010) [E3]
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2010 |
Bowden NA, Ashton KA, Kiejda KA, Zhang XD, Hersey P, Scott R, 'Altered nucleotide excision repair gene expression after cisplatin treatment in melanoma', AACR 101st Annual Meeting 2010. Abstracts, Washington, DC (2010) [E3]
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2010 |
Ashton KA, Bowden NA, Kairupan CF, Kiejda KA, Zhang XD, Hersey P, Scott R, 'Base excision repair and gene expression profiling in malignant melanoma', Sydney Cancer Conference 2010. Profiling Risk, Personalising Treatment and Predicting Outcomes. Conference Program and Abstract Book, Sydney, NSW (2010) [E3]
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2010 |
Kiejda KA, Forbes JF, Braye SG, Scott R, 'The relationship between p53 isofor and estrogen receptor-alpha expression in breast cancer', Sydney Cancer Conference 2010. Profiling Risk, Personalising Treatment and Predicting Outcomes. Conference Program and Abstract Book, Sydney, NSW (2010) [E3]
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2010 |
Ashton KA, Bowden NA, Vilain RE, Kairupan CF, Kiejda KA, Zhang XD, et al., 'Genetic variation of the base excision repair gene, MUTYH, and melanoma development', Melanoma 2010 Congress. Oral and Poster Abstracts, Sydney, NSW (2010) [E3]
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2010 |
Bowden NA, Ashton KA, Kiejda KA, Vilain RE, Braye SG, Kairupan CF, et al., 'Nucleotide excision repair gene expression in melanoma', Melanoma 2010 Congress. Oral and Poster Abstracts, Sydney, NSW (2010) [E3]
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2009 |
Kiejda KA, Scurr LL, Wade MA, Jiang CC, Weir AJW, Bowden NA, et al., 'Cisplatin induces apoptosis independently of Noxa or PUMA in human melanoma cells', 21st Lorne Cancer Conference, Lorne, VIC (2009) [E3]
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2009 |
Zhang XD, Jiang CC, Kiejda KA, Hersey P, 'Up-regulation of Mcl-1 by the unfolded protein response is critical for survival of melanoma cells upon ER stress', 7th World Congress on Melanoma, 5th Congress of the European Association of Dermato-Oncology (EADO): Final Program, Vienna, Austria (2009) [E3]
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2008 |
Bowden NA, Ashton KA, Kiejda KA, Zhang XD, Hersey P, Scott R, 'Altered nucleotide excision repair gene expression after cisplatin treatment in melanoma', Proceedings of the Australian Health and Medical Research Congress 2008, Brisbane, QLD (2008) [E3]
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2008 |
Kiejda KA, Zhang XD, Adams LJ, Scott R, Vojtesek B, Lane DP, Hersey P, 'The P53 splice variants, P53B and 40P53, are expressed in human melanoma cells and can differnetially regulate the transcription of P53 target genes in response to cisplatin', 20th Lorne Cancer Conference, Lorne, VIC (2008) [E3]
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2008 |
Jiang CC, Wade MA, Kiejda KA, Wang Y, Zhang XD, Hersey P, 'Up-regulation of MCL-1 is critical for survival of human melanoma cells upon ER stress', 20th Lorne Cancer Conference, Lorne, VIC (2008) [E3]
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2008 |
Zhang XD, Jiang CC, Wang YF, Kiejda KA, Hersey P, 'The MEK/ERK pathway potentiates adaptation of human melanoma to endoplasmic reticulum stress', 20th Lorne Cancer Conference, Lorne, VIC (2008) [E3]
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2007 |
Jiang CC, Chen IH, Kiejda KA, Gillespie SK, Hersey P, Zhang XD, 'The unfolded protein response induced by tunicamycin or thapsigargin sensitizes human melanoma cells to trail-induced apoptosis by selective up-regulaton of trail-R2 on te cell surface', 19th Lorne Cancer Conference, Lorne, VIC (2007) [E3]
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2007 |
Kiejda KA, Zhang XD, Hersey P, 'The P53 splice variant, P53B, is widely expressed in human melanoma', 19th Lorne Cancer Conference, Lorne, VIC (2007) [E3]
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2007 |
Zhang XD, Jiang CC, Wang YF, Kiejda KA, Gillespie SK, Hersey P, 'Regulation of the BCL-2 family members BIM, PUMA and MCL-1 by MEK/ERK signaling plays a critical role in survival of melanoma cells', 19th Lorne Cancer Conference, Lorne, VIC (2007) [E3]
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2007 |
Kiejda KA, Zhang XD, Adams LJ, Scott R, Vojtesek B, Lane DP, Hersey P, 'MEK/ERK-mediated regulation of the Bcl-2 family members Mcl-1, PUMA, and Bim contributes to survival of human melanoma cells', 4th Garvan Signalling Symposium. Conference Proceedings, Sydney, NSW (2007) [E3]
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2007 |
Kiejda KA, Zhang XD, Adams LJ, Scott R, Vojtesek B, Lane DP, Hersey P, 'Small molecular weight variants of p53 are expressed in human melanoma cells and are induced by cisplatin', 4th Garvan Signalling Symposium. Conference Proceedings, Sydney, NSW (2007) [E3]
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2007 |
Zhang XD, Jiang CC, Wang YF, Kiejda KA, Hersey P, 'The MEK-ERK pathway potentiates adaptation of melanoma to endoplasmic reticulum stress', 4th Garvan Signalling Symposium. Conference Proceedings, Sydney, NSW (2007) [E3]
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2007 |
Jiang CC, Wang YF, Kiejda KA, Gillespie SK, Zhang XD, Hersey P, 'Regulation of the Bcl-2 family members Bim, PUMA and Mcl-1 by MEK/ERK signaling plays a critical role in survival of melanoma cells', AACR Meeting Abstracts Online (Abstracts of the 98th AACR Annual Meeting), Los Angeles (2007) [E3]
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2006 |
Kiejda KA, Zhang XD, Hersey P, 'p53 variants in human melanoma', 13th Annual p53 Workshop. Program & Abstracts, New York (2006) [E3]
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2006 |
Jiang CC, Wang YF, Kiejda KA, Zhang XD, Hersey P, 'CD133, A potential marker for cancer stem cells in melanoma', HMRI Conference on Translational Cancer Research. Molecular Mechanisms and Implications for Treatment, Newcastle, NSW (2006) [E3]
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2006 |
Kiejda KA, Zhang XD, Hersey P, 'Expression of P53 variants in human melanoma', HMRI Conference on Translational Cancer Research. Molecular Mechanisms and Implications for Treatment, Newcastle, NSW (2006) [E3]
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2006 |
Wang YF, Jiang CC, Kiejda KA, Zhang XD, Hersey P, 'Suppression of the BH3-only proteins BUM and PUMA by MEK/ERK signaling plays a crucial role in maintaining survival of melanoma cells', HMRI Conference on Translational Cancer Research. Molecular Mechanisms and Implications for Treatment, Newcastle, NSW (2006) [E3]
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Show 72 more conferences |
Grants and Funding
Summary
Number of grants | 36 |
---|---|
Total funding | $4,725,779 |
Click on a grant title below to expand the full details for that specific grant.
20211 grants / $286,439
2021 HMRI MRSP - Cancer Program$286,439
Funding body: Hunter Medical Research Institute
Funding body | Hunter Medical Research Institute |
---|---|
Project Team | Laureate Professor Rodney Scott, Laureate Professor Rodney Scott, Associate Professor Kelly Kiejda, Professor Amanda Baker, Doctor Michelle Bovill, Associate Professor Matt Dun, Doctor Anoop Enjeti, Doctor Liz Fradgley, Associate Professor Gillian Gould, Conjoint Professor Peter Greer, Professor Hubert Hondermarck, Associate Professor Lei Jin, Doctor Heather Lee, Conjoint Associate Professor Joerg Lehmann, Professor Christine Paul, Doctor Steve Smith, Professor Pradeep Tanwar, Associate Professor Nikki Verrills, Professor Xu Dong Zhang, Doctor Peter Pockney, Professor Adam McCluskey |
Scheme | NSW MRSP Infrastructure Grant |
Role | Investigator |
Funding Start | 2021 |
Funding Finish | 2021 |
GNo | G2001330 |
Type Of Funding | C2220 - Aust StateTerritoryLocal - Other |
Category | 2220 |
UON | Y |
20191 grants / $200,000
Development of a diagnostic test for p53 and its isoforms to aid treatment decisions in melanoma$200,000
Funding body: Tour De Cure
Funding body | Tour De Cure |
---|---|
Project Team | Associate Professor Kelly Kiejda, Laureate Professor Rodney Scott, Dr Jean-Christophe Bourdon |
Scheme | Research Project |
Role | Lead |
Funding Start | 2019 |
Funding Finish | 2019 |
GNo | G1701206 |
Type Of Funding | C3112 - Aust Not for profit |
Category | 3112 |
UON | Y |
20184 grants / $1,541,881
Development of a predictive test for p53 and its isoforms to aid the clinical treatment of breast cancer$552,460
Funding body: Cancer Institute NSW
Funding body | Cancer Institute NSW |
---|---|
Project Team | Associate Professor Kelly Kiejda, Miss Luiza Steffens Reinhardt |
Scheme | Career Development Fellowship |
Role | Lead |
Funding Start | 2018 |
Funding Finish | 2022 |
GNo | G1800605 |
Type Of Funding | C2210 - Aust StateTerritoryLocal - Own Purpose |
Category | 2210 |
UON | Y |
Hunter Cancer Biobank$538,523
Funding body: NSW Health Pathology - Pathology North
Funding body | NSW Health Pathology - Pathology North |
---|---|
Project Team | Professor Marjorie Walker, Laureate Professor Rodney Scott, Conjoint Professor Stephen Ackland, Mrs Susan Goode, Professor Pradeep Tanwar, Associate Professor Nikki Verrills, Professor Hubert Hondermarck, Doctor Simon King, Mr Ricardo Vilain, Associate Professor Nikola Bowden, Associate Professor Kelly Kiejda, Professor Simon Keely, Doctor Christopher Rowe |
Scheme | Research Grant |
Role | Investigator |
Funding Start | 2018 |
Funding Finish | 2020 |
GNo | G1800704 |
Type Of Funding | C2220 - Aust StateTerritoryLocal - Other |
Category | 2220 |
UON | Y |
MHF Brain Cancer GARD: Mark Hughes Foundation Brain Cancer Collaborative Genomics pipeline for Advancing Research into biomarker Discovery$425,898
Funding body: Hunter Medical Research Institute
Funding body | Hunter Medical Research Institute |
---|---|
Project Team | Laureate Professor Rodney Scott, Associate Professor Kelly Kiejda |
Scheme | Project Grant |
Role | Investigator |
Funding Start | 2018 |
Funding Finish | 2020 |
GNo | G1801388 |
Type Of Funding | C3120 - Aust Philanthropy |
Category | 3120 |
UON | Y |
The functional role of ¿40p53 in breast cancer stem cells$25,000
Funding body: Hunter Medical Research Institute
Funding body | Hunter Medical Research Institute |
---|---|
Project Team | Doctor Brianna Morten, Associate Professor Kelly Kiejda, Laureate Professor Rodney Scott |
Scheme | Project Grant |
Role | Investigator |
Funding Start | 2018 |
Funding Finish | 2018 |
GNo | G1801369 |
Type Of Funding | C3120 - Aust Philanthropy |
Category | 3120 |
UON | Y |
20171 grants / $570,000
Beyond the Next Generation of DNA Sequencing: Long Read Sequencing using Sequel$570,000
Funding body: Cancer Institute NSW
Funding body | Cancer Institute NSW |
---|---|
Project Team | Laureate Professor Rodney Scott, Professor Hubert Hondermarck, Associate Professor Kevin Spring, Doctor Anoop Enjeti, Mr Ricardo Vilain, Professor Christopher Scarlett, Associate Professor Kelly Kiejda, Doctor Heather Lee, Professor Simon Keely, Associate Professor Lei Jin |
Scheme | Research Equipment Grant |
Role | Investigator |
Funding Start | 2017 |
Funding Finish | 2017 |
GNo | G1700427 |
Type Of Funding | C2210 - Aust StateTerritoryLocal - Own Purpose |
Category | 2210 |
UON | Y |
20161 grants / $23,750
Circulating exosomes in pancreatic cancer as a source of novel diagnostic biomarkers$23,750
Funding body: Hunter Medical Research Institute
Funding body | Hunter Medical Research Institute |
---|---|
Project Team | Professor Christopher Scarlett, Doctor Jude Weidenhofer, Associate Professor Kelly Kiejda |
Scheme | Project Grant |
Role | Investigator |
Funding Start | 2016 |
Funding Finish | 2016 |
GNo | G1601070 |
Type Of Funding | Grant - Aust Non Government |
Category | 3AFG |
UON | Y |
20154 grants / $450,805
The Hunter Cancer Biobank (HCB): Maximising community value through validation, annotation and distribution throughout NSW$300,000
Funding body: Cancer Institute NSW
Funding body | Cancer Institute NSW |
---|---|
Project Team | Professor Marjorie Walker, Conjoint Professor Stephen Ackland, Laureate Professor Rodney Scott, Emeritus Professor John Forbes, Professor Xu Dong Zhang, Professor Pradeep Tanwar, Associate Professor Nikola Bowden, Doctor Craig Gedye, Doctor James Lynam, Associate Professor Kelly Kiejda, Doctor Jennette Sakoff, Mr Loui Rassam, Dr Tara Roberts, Professor Soon Lee, Dr Betty Kan |
Scheme | Research Infrastructure Grants |
Role | Investigator |
Funding Start | 2015 |
Funding Finish | 2018 |
GNo | G1500825 |
Type Of Funding | C2210 - Aust StateTerritoryLocal - Own Purpose |
Category | 2210 |
UON | Y |
Live cell imager for enhancement of pre-clinical cancer studies in the Hunter Translational Cancer Research Centre$124,938
Funding body: Cancer Institute NSW
Funding body | Cancer Institute NSW |
---|---|
Project Team | Conjoint Professor Stephen Ackland, Associate Professor Kelly Kiejda, Associate Professor Kevin Spring, Professor Xu Dong Zhang, Associate Professor Deborah Marsh, Professor Christopher Scarlett, Professor Pradeep Tanwar, Associate Professor Kathryn Skelding, Doctor Rick Thorne, Associate Professor Nikola Bowden |
Scheme | Research Equipment Grant |
Role | Investigator |
Funding Start | 2015 |
Funding Finish | 2016 |
GNo | G1500598 |
Type Of Funding | Other Public Sector - State |
Category | 2OPS |
UON | Y |
Live cell imager for enhancement of pre-clinical cancer studies in the Hunter Translational Cancer Research Centre$25,000
Funding body: University of Newcastle
Funding body | University of Newcastle |
---|---|
Project Team | Conjoint Professor Stephen Ackland, Associate Professor Kelly Kiejda, Associate Professor Kevin Spring, Professor Xu Dong Zhang, Associate Professor Deborah Marsh, Professor Christopher Scarlett, Professor Pradeep Tanwar, Associate Professor Kathryn Skelding, Doctor Rick Thorne, Associate Professor Nikola Bowden |
Scheme | Equipment Grant |
Role | Investigator |
Funding Start | 2015 |
Funding Finish | 2015 |
GNo | G1500953 |
Type Of Funding | Internal |
Category | INTE |
UON | Y |
Familial Aspects of Cancer 2015 Research and Practice, Mantra on Salt Beach, Kingscliff, 26 - 28 August 2015$867
Funding body: University of Newcastle - Faculty of Health and Medicine
Funding body | University of Newcastle - Faculty of Health and Medicine |
---|---|
Project Team | Associate Professor Kelly Kiejda |
Scheme | Travel Grant |
Role | Lead |
Funding Start | 2015 |
Funding Finish | 2015 |
GNo | G1501069 |
Type Of Funding | Internal |
Category | INTE |
UON | Y |
20142 grants / $145,199
Visualisation of microparticles for development of biomarkers and targeted drug delivery mechanisms$125,199
Funding body: Cancer Institute NSW
Funding body | Cancer Institute NSW |
---|---|
Project Team | Professor Christopher Scarlett, Associate Professor Kathryn Skelding, Doctor Jude Weidenhofer, Associate Professor Matt Dun, Associate Professor Kelly Kiejda, Professor Adam McCluskey, Doctor Elham Sadeqzadeh, Professor Hubert Hondermarck, Doctor Rick Thorne, Laureate Professor Rodney Scott |
Scheme | Research Equipment Grant |
Role | Investigator |
Funding Start | 2014 |
Funding Finish | 2014 |
GNo | G1400627 |
Type Of Funding | Other Public Sector - State |
Category | 2OPS |
UON | Y |
A new frontier in breast cancer: Can small molecules in the blood predict outcome?$20,000
Funding body: Hunter Medical Research Institute
Funding body | Hunter Medical Research Institute |
---|---|
Project Team | Associate Professor Kelly Kiejda, Doctor Jude Weidenhofer, Laureate Professor Rodney Scott |
Scheme | Project Grant |
Role | Lead |
Funding Start | 2014 |
Funding Finish | 2014 |
GNo | G1401454 |
Type Of Funding | Grant - Aust Non Government |
Category | 3AFG |
UON | Y |
20132 grants / $40,000
The function of the delta-40p53 isoform in breast cancer.$30,000
Funding body: Hunter Medical Research Institute
Funding body | Hunter Medical Research Institute |
---|---|
Project Team | Associate Professor Kelly Kiejda, Doctor Brianna Morten, Laureate Professor Rodney Scott |
Scheme | Project Grant |
Role | Lead |
Funding Start | 2013 |
Funding Finish | 2013 |
GNo | G1300583 |
Type Of Funding | Contract - Aust Non Government |
Category | 3AFC |
UON | Y |
miRNA regulation of growth, invasion and treatment response in triple negative breast cancer$10,000
Funding body: Hunter Medical Research Institute
Funding body | Hunter Medical Research Institute |
---|---|
Project Team | Associate Professor Kelly Kiejda, Doctor Andrea Johns |
Scheme | Project Grant |
Role | Lead |
Funding Start | 2013 |
Funding Finish | 2013 |
GNo | G1300728 |
Type Of Funding | Grant - Aust Non Government |
Category | 3AFG |
UON | Y |
20125 grants / $484,300
The Hunter Cancer Biobank (HCB): Maximising community value through validation, annotation and distribution throughout NSW$292,300
Funding body: Cancer Institute NSW
Funding body | Cancer Institute NSW |
---|---|
Project Team | Emeritus Professor John Forbes, Conjoint Professor Stephen Ackland, Laureate Professor Rodney Scott, Conjoint Associate Professor Barbara Young, Professor Hubert Hondermarck, Emeritus Professor Leonie Ashman, Professor Xu Dong Zhang, Associate Professor Kelly Kiejda, Associate Professor Nikki Verrills, Doctor Jennette Sakoff, Ms Janine Lombard, Doctor Jude Weidenhofer, Professor Pradeep Tanwar |
Scheme | Research Infrastructure Grants |
Role | Investigator |
Funding Start | 2012 |
Funding Finish | 2015 |
GNo | G1200798 |
Type Of Funding | Other Public Sector - State |
Category | 2OPS |
UON | Y |
Small p53 isoforms, BIG implications for treatment response in breast cancer$90,000
Funding body: Hunter Medical Research Institute
Funding body | Hunter Medical Research Institute |
---|---|
Project Team | Associate Professor Kelly Kiejda, Laureate Professor Rodney Scott |
Scheme | Project Grant |
Role | Lead |
Funding Start | 2012 |
Funding Finish | 2015 |
GNo | G1200322 |
Type Of Funding | C3120 - Aust Philanthropy |
Category | 3120 |
UON | Y |
p53 isoforms in breast cancer - MM Sawyer Estate Scholarship$85,000
Funding body: Hunter Medical Research Institute
Funding body | Hunter Medical Research Institute |
---|---|
Project Team | Associate Professor Kelly Kiejda, Laureate Professor Rodney Scott |
Scheme | Mary Minto Sawyer Grant |
Role | Lead |
Funding Start | 2012 |
Funding Finish | 2014 |
GNo | G1200615 |
Type Of Funding | C3120 - Aust Philanthropy |
Category | 3120 |
UON | Y |
2011 Emerging Research Leaders Program$15,000
Funding body: University of Newcastle
Funding body | University of Newcastle |
---|---|
Project Team | Associate Professor Kelly Kiejda |
Scheme | Emerging Research Leaders Program |
Role | Lead |
Funding Start | 2012 |
Funding Finish | 2012 |
GNo | G1200817 |
Type Of Funding | Internal |
Category | INTE |
UON | Y |
Ninth International NRAi, MicroRNAs & Single Cell Biology - 2012, Hilton Garden Inn, Waltham, Massachusetts, USA, 1 - 2 May 2012$2,000
Funding body: University of Newcastle - Faculty of Health and Medicine
Funding body | University of Newcastle - Faculty of Health and Medicine |
---|---|
Project Team | Associate Professor Kelly Kiejda |
Scheme | Travel Grant |
Role | Lead |
Funding Start | 2012 |
Funding Finish | 2013 |
GNo | G1200588 |
Type Of Funding | Internal |
Category | INTE |
UON | Y |
20113 grants / $50,375
p53 isoforms, a prognostic indicator in breast cancer?$45,000
Funding body: Hunter Medical Research Institute
Funding body | Hunter Medical Research Institute |
---|---|
Project Team | Associate Professor Kelly Kiejda, Laureate Professor Rodney Scott, Emeritus Professor John Forbes |
Scheme | Breast Cancer Project Grant |
Role | Lead |
Funding Start | 2011 |
Funding Finish | 2011 |
GNo | G1001006 |
Type Of Funding | Contract - Aust Non Government |
Category | 3AFC |
UON | Y |
PULSE Education Prize$4,000
Funding body: Hunter Medical Research Institute
Funding body | Hunter Medical Research Institute |
---|---|
Project Team | Associate Professor Kelly Kiejda |
Scheme | PULSE Education Prize |
Role | Lead |
Funding Start | 2011 |
Funding Finish | 2011 |
GNo | G1001021 |
Type Of Funding | Contract - Aust Non Government |
Category | 3AFC |
UON | Y |
Annual meeting fo the Australasian Microarray & Associated Technologies Association (AMATA), Shine Dome in Canberra, 9 - 12 October 2011$1,375
Funding body: University of Newcastle - Faculty of Health and Medicine
Funding body | University of Newcastle - Faculty of Health and Medicine |
---|---|
Project Team | Associate Professor Kelly Kiejda |
Scheme | Travel Grant |
Role | Lead |
Funding Start | 2011 |
Funding Finish | 2011 |
GNo | G1100938 |
Type Of Funding | Internal |
Category | INTE |
UON | Y |
20101 grants / $21,600
The identification of microRNA's as therapeutic targets for the treatment of advanced breast cancer$21,600
Funding body: Hunter Medical Research Institute
Funding body | Hunter Medical Research Institute |
---|---|
Project Team | Associate Professor Kelly Kiejda, Laureate Professor Rodney Scott, Emeritus Professor John Forbes |
Scheme | Research Grant |
Role | Lead |
Funding Start | 2010 |
Funding Finish | 2010 |
GNo | G0900144 |
Type Of Funding | Contract - Aust Non Government |
Category | 3AFC |
UON | Y |
20094 grants / $387,000
Targeting p53 isoforms, delta-40p53 and p53-beta, to promote chemo-sensitivity in human melanoma$272,000
Funding body: Cancer Council NSW
Funding body | Cancer Council NSW |
---|---|
Project Team | Professor Xu Dong Zhang, Conjoint Professor Peter Hersey, Associate Professor Kelly Kiejda |
Scheme | Research Grant |
Role | Investigator |
Funding Start | 2009 |
Funding Finish | 2011 |
GNo | G0188913 |
Type Of Funding | Grant - Aust Non Government |
Category | 3AFG |
UON | Y |
Targeting p53 isoforms, delta-40p53 and p53-beta, to promote chemo-sensitivity in human melanoma$75,000
Funding body: Cancer Australia
Funding body | Cancer Australia |
---|---|
Project Team | Associate Professor Kelly Kiejda, Professor Xu Dong Zhang, Conjoint Professor Peter Hersey |
Scheme | Priority-driven Collaborative Cancer Research Scheme |
Role | Lead |
Funding Start | 2009 |
Funding Finish | 2009 |
GNo | G0188914 |
Type Of Funding | Aust Competitive - Commonwealth |
Category | 1CS |
UON | Y |
Targeting p53 isoforms in human melanoma$30,000
Funding body: Calvary Mater Newcastle
Funding body | Calvary Mater Newcastle |
---|---|
Project Team | Kelly Avery-Kiejda |
Scheme | Project Grant |
Role | Lead |
Funding Start | 2009 |
Funding Finish | 2009 |
GNo | |
Type Of Funding | Internal |
Category | INTE |
UON | N |
The microRNA signature of endoplasmic reticulum stress in melanoma$10,000
Funding body: Calvary Mater Newcastle
Funding body | Calvary Mater Newcastle |
---|---|
Project Team | XD Zhang |
Scheme | Project Grant |
Role | Investigator |
Funding Start | 2009 |
Funding Finish | 2009 |
GNo | |
Type Of Funding | Internal |
Category | INTE |
UON | N |
20073 grants / $105,000
Characterization of p53 isoforms in human melanoma: do they play a role in chemoresistance?$75,000
Funding body: Cure Cancer Australia Foundation
Funding body | Cure Cancer Australia Foundation |
---|---|
Project Team | XD Zhang |
Scheme | Research Grant |
Role | Investigator |
Funding Start | 2007 |
Funding Finish | 2007 |
GNo | |
Type Of Funding | Grant - Aust Non Government |
Category | 3AFG |
UON | N |
The role of p53 Isoforms in chemoresistances of human melanoma$20,000
Funding body: Hunter Medical Research Institute
Funding body | Hunter Medical Research Institute |
---|---|
Project Team | Professor Xu Dong Zhang, Associate Professor Kelly Kiejda |
Scheme | Project Grant |
Role | Investigator |
Funding Start | 2007 |
Funding Finish | 2007 |
GNo | G0187239 |
Type Of Funding | Contract - Aust Non Government |
Category | 3AFC |
UON | Y |
The role of p53 isoforms in chemoresistance of human melanoma$10,000
Funding body: Calvary Mater Newcastle
Funding body | Calvary Mater Newcastle |
---|---|
Project Team | XD Zhang |
Scheme | Project Grant |
Role | Investigator |
Funding Start | 2007 |
Funding Finish | 2007 |
GNo | |
Type Of Funding | Internal |
Category | INTE |
UON | N |
20061 grants / $332,000
Cameron Fellowship in Melanoma Research$332,000
Funding body: Melanoma and Skin Cancer Research Institute
Funding body | Melanoma and Skin Cancer Research Institute |
---|---|
Project Team | Kelly Avery-Kiejda |
Scheme | fellowship |
Role | Lead |
Funding Start | 2006 |
Funding Finish | 2009 |
GNo | |
Type Of Funding | Internal |
Category | INTE |
UON | N |
20012 grants / $82,750
Australian Postgraduate Award$64,750
Funding body: Department of Education, Training & Youth Affairs
Funding body | Department of Education, Training & Youth Affairs |
---|---|
Project Team | Kelly Avery |
Scheme | Scholarship support for PhD |
Role | Lead |
Funding Start | 2001 |
Funding Finish | 2004 |
GNo | |
Type Of Funding | Aust Competitive - Commonwealth |
Category | 1CS |
UON | N |
Millennium Foundation Stipend Enhancement Grant$18,000
Funding body: Millennium Foundation
Funding body | Millennium Foundation |
---|---|
Project Team | Kelly Avery |
Scheme | Stipend enhancement grant |
Role | Lead |
Funding Start | 2001 |
Funding Finish | 2004 |
GNo | |
Type Of Funding | Not Known |
Category | UNKN |
UON | N |
1 grants / $4,680
Service contract for IncuCyte ZOOM live-cell imaging system$4,680
Funding body: Hunter Medical Research Institute
Funding body | Hunter Medical Research Institute |
---|---|
Project Team | Associate Professor Kelly Kiejda, Doctor Brianna Morten, Doctor Gerard Kaiko |
Scheme | Early and Mid-Career Equipment Grant |
Role | Lead |
Funding Start | |
Funding Finish | |
GNo | G1900064 |
Type Of Funding | C3120 - Aust Philanthropy |
Category | 3120 |
UON | Y |
Research Supervision
Number of supervisions
Current Supervision
Commenced | Level of Study | Research Title | Program | Supervisor Type |
---|---|---|---|---|
2019 | PhD | The Link Between Aberrations in the P53 Pathway and Outcome from DNA-Damaging Therapies in Breast Cancer | PhD (Medical Genetics), College of Health, Medicine and Wellbeing, The University of Newcastle | Principal Supervisor |
2018 | PhD | Evaluation of Lymphedema Status and Deciphering the Molecular Mechanisms of Breast Cancer-Related Lymphedema in Malaysian Breast Cancer Survivors | PhD (Medical Genetics), College of Health, Medicine and Wellbeing, The University of Newcastle | Principal Supervisor |
2017 | PhD | Validation of novel genes differentially expressed in triple negative breast cancer and their association with prognosis. | PhD (Medical Genetics), College of Health, Medicine and Wellbeing, The University of Newcastle | Principal Supervisor |
2015 | PhD | Circulating Exosomes in Pancreatic Cancer as a Source of Novel Diagnostic Biomarkers | PhD (Biological Sciences), College of Engineering, Science and Environment, The University of Newcastle | Co-Supervisor |
Past Supervision
Year | Level of Study | Research Title | Program | Supervisor Type |
---|---|---|---|---|
2020 | PhD | The Function of ¿40p53 in Breast Cancer | PhD (Medical Genetics), College of Health, Medicine and Wellbeing, The University of Newcastle | Principal Supervisor |
2019 | Honours | Genetic Differences Between Two Breast Cancer Subtypes, and their Effect on Survival | Genetics, Faculty of Health and Medicine, University of Newcastle | Principal Supervisor |
2017 | PhD | The Regulation, Function and Expression of delta40p53 in Breast Cancer | PhD (Medical Genetics), College of Health, Medicine and Wellbeing, The University of Newcastle | Principal Supervisor |
2016 | PhD | The Role of Short Tandem Repeats in Genetic Susceptibility to Breast and Endometrial Cancers | PhD (Medical Genetics), College of Health, Medicine and Wellbeing, The University of Newcastle | Co-Supervisor |
2016 | PhD | Genetic and Epigenetic Changes Associated with the Development of Lymph Node Metastasis in Triple Negative Breast Cancer | PhD (Medical Genetics), College of Health, Medicine and Wellbeing, The University of Newcastle | Co-Supervisor |
2014 | PhD | The Contribution of Genetic Susceptibility to Breast Cancer | PhD (Medical Genetics), College of Health, Medicine and Wellbeing, The University of Newcastle | Co-Supervisor |
2011 | Honours | p53 isoforms in breast cancer | Medical Science, University of Newcastle | Principal Supervisor |
News
Funding awarded for innovative cancer research
February 14, 2019
Associate Professor Kelly Kiejda
Position
CI NSW Fellow
Information Based Medicine
School of Biomedical Sciences and Pharmacy
College of Health, Medicine and Wellbeing
Focus area
Medical Genetics
Contact Details
kelly.kiejda@newcastle.edu.au | |
Phone | 4042 0309 |
Fax | 4042 0031 |
Office
Room | Rm 3104, Lvl 3, West. |
---|---|
Building | Hunter Medical Research Institute |
Location | Lot 1 Kookaburra Circuit, New Lambton Heights, NSW 2305 , |