Kelly A. Avery-Kiejda

Activation of Jun N-terminal kinase is a mediator of vincristine-induced apoptosis of melanoma cells.

Small molecular weight variants of p53 are expressed in human melanoma cells and are induced by the DNA-damaging agent cisplatin.

Up-regulation of Mcl-1 is critical for survival of human melanoma cells upon endoplasmic reticulum stress.

Glucose-regulated protein 78 antagonizes cisplatin and adriamycin in human melanoma cells.

Nucleotide excision repair gene expression after Cisplatin treatment in melanoma.

BRIP1, PALB2, and RAD51C mutation analysis reveals their relative importance as genetic susceptibility factors for breast cancer.

P53 in human melanoma fails to regulate target genes associated with apoptosis and the cell cycle and may contribute to proliferation.

Low prevalence of germline PALB2 mutations in Australian triple-negative breast cancer.

Regulators of global genome repair do not respond to DNA damaging therapy but correlate with survival in melanoma.

STaRRRT: a table of short tandem repeats in regulatory regions of the human genome.

The relative mRNA expression of p53 isoforms in breast cancer is associated with clinical features and outcome.

Decreased expression of key tumour suppressor microRNAs is associated with lymph node metastases in triple negative breast cancer.

The expression of Dicer and Drosha in matched normal tissues, tumours and lymph node metastases in triple negative breast cancer.

Methylome sequencing in triple-negative breast cancer reveals distinct methylation clusters with prognostic value.

Proteotranscriptomic Profiling of 231-BR Breast Cancer Cells: Identification of Potential Biomarkers and Therapeutic Targets for Brain Metastasis.

Novel genes associated with lymph node metastasis in triple negative breast cancer.

The presence of the intron 3 16 bp duplication polymorphism of p53 (rs17878362) in breast cancer is associated with a low Δ40p53:p53 ratio and better outcome.

MiRNAs and Other Epigenetic Changes as Biomarkers in Triple Negative Breast Cancer.

A polymorphic repeat in the IGF1 promoter influences the risk of endometrial cancer.

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.

The intron 3 16 bp duplication polymorphism of p53 (rs17878362) is not associated with increased risk of developing triple-negative breast cancer.