A5014846710- Ubiquitin and proteasome pathways
- Protein Kinase Regulation and GTPase Signaling
- Cancer, Lipids, and Metabolism
- PI3K/AKT/mTOR signaling in cancer
- Prostate Cancer Treatment and Research
- Cancer-related Molecular Pathways
- Neuroendocrine Tumor Research Advances
- Inflammatory mediators and NSAID effects
- Growth Hormone and Insulin-like Growth Factors
- Hormonal and reproductive studies
- DNA Repair Mechanisms
- Eicosanoids and Hypertension Pharmacology
- Molecular Biology Techniques and Applications
- Hypothalamic control of reproductive hormones
- Estrogen and related hormone effects
- Advanced Breast Cancer Therapies
- Pituitary Gland Disorders and Treatments
- Hedgehog Signaling Pathway Studies
- Thyroid Cancer Diagnosis and Treatment
- Flavonoids in Medical Research
- Phytochemicals and Antioxidant Activities
- Glycosylation and Glycoproteins Research
- Mechanisms of cancer metastasis
- Microtubule and mitosis dynamics
- DNA and Nucleic Acid Chemistry
Cancer Australia
2025
The University of Sydney
2014-2024
Royal Prince Alfred Hospital
2011-2022
Western Sydney University
2011-2020
Harry Perkins Institute of Medical Research
2018
Robert Bosch (Australia)
2008-2016
Camden and Campbelltown Hospitals
2012
St George Hospital
2012
UNSW Sydney
2012
Endocrinology Research Center
2008
Multiple endocrine neoplasia–type 1 (MEN1) is an autosomal dominant familial cancer syndrome characterized by tumors in parathyroids, enteropancreatic tissues, and the anterior pituitary. DNA sequencing from a previously identified minimal interval on chromosome 11q13 several candidate genes, one of which contained 12 different frameshift, nonsense, missense, in-frame deletion mutations 14 probands 15 families. The MEN1 gene contains 10 exons encodes ubiquitously expressed 2.8-kilobase...
Effective treatment of prostate cancer should be based on targeting interactions between tumour cell signalling pathways and key converging downstream effectors. Here, we determined how the tumourigenic phosphoinositide 3-kinase/protein kinase B (PI3K/AKT), tumour-suppressive phosphatase tensin homologue deleted chromosome 10 (PTEN) transforming growth factor-β (TGF-β) are integrated via metastasis suppressor, N-myc downstream-regulated gene-1 (NDRG1). Moreover, assessed novel anti-tumour...
Abstract Chromosome 17q21-ter is commonly gained in neuroblastoma, but it unclear which gene the region important for tumorigenesis. The JMJD6 at activates transcription. Here we show that forms protein complexes with N-Myc and BRD4, E2F2, c-Myc Knocking down reduces neuroblastoma cell proliferation survival vitro tumor progression mice, high levels of expression human tissues independently predict poor patient prognosis. In addition, associated transcriptional super-enhancers. Combination...
Abstract Purpose: Cytosolic phospholipase A2-α (cPLA2-α) provides intracellular arachidonic acid to supply both cyclooxygenase and lipoxygenase pathways. We aim determine the expression activation of cPLA2-α in prostate cancer cell lines tissue effect targeting vitro vivo. Experimental Design: The was determined cells by reverse transcription-PCR, Western blot, immunocytochemistry. Growth inhibition, apoptosis, activity were after inhibition with small interfering RNA or inhibitor (Wyeth-1)....
Familial multiple endocrine neoplasia type 1 (MEN1) is an autosomal dominant disorder with affected individuals developing parathyroid, gastrointestinal (GI) endocrine, and anterior pituitary tumors. Four large kindreds from the Burin peninsula/Fortune Bay area of Newfoundland prominent features prolactinomas, carcinoids, parathyroid tumors (referred to as MEN1Burin) have been described, they show linkage 11q13, same locus that MEN1. Haplotype analysis 16 polymorphic markers now reveals...
Loss of heterozygosity (LOH) for polymorphic markers flanking the multiple endocrine neoplasia type 1 (MEN-1) gene in parathyroid and pancreatic islet tumors from subjects with familial MEN-1 (FMEN-1) has been well documented led to hypothesis that functions as a tumor suppressor. To assess role pathogenesis less commonly associated MEN-1, we employed large number highly informative closely linked study series 13 such FMEN-1 LOH at 11q13. We were able identify or more 11q13 2 3 pituitary...
Abstract Mortality from prostate cancer is associated with progression of tumors to androgen-independent growth and metastasis. Eicosanoid products both the cyclooxygenase (COX) lipoxygenase (LOX) pathways are important mediators proliferation cells in culture regulate tumor vascularization metastasis animal models. Pharmacologic agents that block either COX or LOX effectively reduce size xenografts. Phospholipase A2 (PLA2) enzymes provision arachidonic acid COX- LOX-derived eicosanoids, a...
Quiescent cancer cells (QCCs), also known as dormant cells, resist and survive chemo- radiotherapy, resulting in treatment failure later recurrence when QCCs resume cell cycle progression. However, drugs selectively targeting are lacking. Saikosaponin A (SSA) derived from Bupleurum DC., is highly potent eradicating multidrug-resistant prostate compared with proliferative cells. By further exacerbating the already increased autophagy through inactivation of Akt-mTOR signaling, SSA triggered...
ABSTRACT This study aimed to determine the effect of streptozotocin (STZ)-induced diabetes on pulsatile LH secretion in mature male rat. pulse frequency was reduced by 56% and amplitude 54%, with a consequential decrease 72% mean levels 8 days after i.v. administration STZ (55 mg/kg) castrated Wistar rats compared non-diabetic controls. Twice daily insulin treatment completely reversed all parameters control values. Food-restricted controls, studied distinguish metabolic from that concurrent...
Abstract Cell cycle re-entry by quiescent cancer cells is an important mechanism for progression. While high levels of c-MYC expression are sufficient cell re-entry, the modality to block expression, and subsequent limited. Using reversible quiescence rendered serum withdrawal or contact inhibition in PTEN null /p53 WT (LNCaP) mut (PC-3) prostate cells, we have identified a compound that able impede through c-MYC. Guttiferone K (GUTK) blocked resumption DNA synthesis preserved phase...
Quiescent cancer cells (QCCs) reversibly reside in G 0 phase, thus allowing them to survive chemotherapy and radiotherapy, which generally target proliferating cells. Surviving QCCs may re-proliferate, consequently result progression, recurrence, metastasis. Therefore, understanding the key players governing QCC survival activation is crucial for developing QCC-targeting agents. This review presents an overview of (1) mechanisms underlying regulation status (2) recent advances development...
Abstract BACKGROUND To understand the molecular mechanisms underlying prostate cancer, we have utilized gene expression array to search for genes whose is altered in this disease. METHODS RNA quality from manual microdissected tissue was compared with that microselected by electrophoresis. For analysis, malignant and normal epithelium enriched using microselection technique cancer peripheral zone of a prostate. Identical membrane hybridized labeled cDNA, respectively. The differentially...
Activating mutations encoding substitutions at positions Arg201 and Gln227 of the alpha-subunit stimulatory G protein. G10 have been found in about 40% pituitary somatotroph tumors. Although etiology thyrotroph adenomas is unknown, their autonomous behavior blunted response to hypothalamic hormone superficially resemble those We hypothesized that a subset tumors might be caused by dominant somatic lead inappropriate activation Gq/phospholipase C beta/Ca2+/protein kinase C. pathway normally...