Royal Melbourne Hospital

NSW extends virtual health service to adults Over a year since offering urgent virtual care service to children and youth statewide, the New South Wales government has come up with a similar service for adults. The new VirtualAdult service will provide urgent care via video conferencing for common illnesses or injuries, such as coughs and colds or flu, respiratory symptoms, vomiting and diarrhoea, and rashes. Following its launch this month, December, in Sydney, it is planned for statewide expansion by the end of 2025. The service is part of several initiatives introduced to relieve pressure on overwhelmed emergency departments across NSW. Digital pharmacy ordering now live in Victoria Compounding pharmacy Slade Health, part of cancer care provider Icon Group, has digitised its ordering system for public hospitals in Victoria. It recently integrated the digital medications management system, Charm Evolution by Magentus, with its in-house software, to automate information flow. In a media release, Slade Health says public health facilities and hospitals can now order through this digital system, doing away with manual entry. The system also provides the pharmacy with near real-time visibility into orders, updates, and cancellations. This integration makes Victoria the second state in Australia after Queensland to fully digitise ordering for hospital pharmacies. Royal Melbourne Hospital beefs up digital transformation Royal Melbourne Hospital has sought support from digital health accelerator ANDHealth for its digital transformation. It made the organisation its "innovation partner," helping keep updated and providing expert advice on new and emerging technologies. The hospital has also become ANDHealths' first core hospital system partner, providing insights into clinician and staff demand and needs from technology.

Researchers have shown that targeting a gene regulated by two cancer-fuelling proteins can kill cancerous cells and halt their growth in laboratory models of B-cell acute lymphoblastic leukemia (ALL). Researchers have found a new way to potentially treat one of the most common forms of acute lymphoblastic leukaemia. The study, led by WEHI and the Peter MacCallum Cancer Centre, was able to kill leukaemia cells in the lab and stop cancer cells from growing, after identifying two new proteins critical for the development of the aggressive disease. The findings could lead to enhanced treatment options in the future, with plans underway to develop a clinical trial based on the research. Around 5200 people are diagnosed with a form of leukaemia in Australia each year. An estimated 1500 of these cases are acute -- meaning the blood cancer appears suddenly and grows quickly. Blood cancers like leukaemia are notoriously difficult to treat in adults, with 50% of Australian patients relapsing after the first round of chemotherapy and subsequently becoming resistant to further treatments. Associate Professor Ashley Ng, a corresponding author on the paper, said this presented a unique treatment challenge for these blood cancers and highlighted the urgent need for new therapeutics. "About 135,000 people live with a blood cancer or blood disorder in Australia, with 16 people dying every day from the disease," Assoc Prof Ng, a WEHI researcher and clinical haematologist at the Peter MacCallum Cancer Centre and Royal Melbourne Hospital, said. "Despite the medical advancements made in the cancer field over the years, the incidence of blood cancer has grown by 47% in the past decade. "The best way to enhance treatment options for patients is to continually improve our understanding of how leukaemia cancers behave and what drives their growth. "Our new research has identified two proteins that are critical for the development of B-cell acute lymphoblastic leukaemia, expanding our knowledge into how these cancers can form. "By uncovering this new vulnerability in leukaemia formation, we hope to exploit the findings for therapeutic benefit and also apply them to other forms of the disease." The research is published in the journal Science Advances. Master regulators Assoc Prof Ng has spent over a decade researching a protein that regulates gene activity in the cell nucleus, known as ERG. Imbalances in this protein can lead to blood cancers, like acute lymphoblastic leukaemia. His previous research uncovered the protein's critical role in Down syndrome associated blood disease and normal blood cell function, including how B cells -- which are essential for producing antibodies to fight against infections -- develop. First author Dr Kira Behrens said the research team wanted to understand what other types of proteins ERG works with to fuel leukaemia development. "We looked at the proteins that control how specific genes switch 'on' or 'off' to analyse how normal B-cells -- and critically -- B-cell acute lymphoblastic leukaemia -- can develop," Dr Behrens said. "After analysing the genes regulated by ERG and another protein, c-MYC, we discovered that these proteins were actually the master regulators of several important pathways and processes within the leukaemia cell." Researchers then narrowed the list down to focus on one pathway essential for making proteins, known as ribosome biogenesis. This led the team to focus on targeting a key gene essential to this pathway, POL I, which is also controlled by these master regulator proteins. The gene helps direct an important cell growth and division process that can lead to the development of cancer if it goes awry. Dr Behrens said: "By targeting POL I with inhibitors, we were able to kill leukaemia cells and stop their growth in our pre-clinical and human tissue models." "This was a surprising, yet remarkable discovery, as we were able to unravel a new pathway and potential drug target that can hopefully be used in the fight against leukaemia in the future." The study also involved a collaboration with Associate Professor Elaine Sanij (St. Vincent's Institute of Medical Research) whose work focuses on targeting POL I and ribosome biogenesis in cancer therapy. "The findings show that a subset of aggressive acute lymphoblastic leukaemia exhibit a form of addiction to producing of ribosomes, the protein making molecular machinery," Assoc Prof Sanij said. "They render this aggressive leukaemia sensitive to POL I inhibitors which target ribosome production. "Altogether, our work highlights the importance of developing this new approach to cancer therapy to treat oncogene-driven cancers." Collaborative power One of the drugs used in the study to target POL I was an agent developed by the Peter MacCallum Cancer Centre. Professor Rick Pearson, former Associate Director of Laboratory Research at Peter Mac, said the team hopes to mimic the study in a future clinical trial to help patients with acute lymphoblastic leukaemia. "We worked with WEHI researchers to confirm our agent is effective in targeting POL I activity and demonstrated its potency in impeding the leukaemia cell growth and division. "These findings highlight the power of collaboration and the remarkable results that can be achieved when bringing together experts from across various areas. "We hope this research will translate into successful clinical trials and potentially offer doctors a new treatment option for patients with acute lymphoblastic leukaemia," Professor Pearson said. This research was supported by the German Research Foundation (Deutsche Forschungsgemeinschaft), the National Health and Medical Research Council (NHMRC), Cancer Council Victoria, National Stem Cell Foundation of Australia, the Leukaemia Foundation and Victorian Cancer Agency. The study, "ERG and c-MYC Regulate a Critical Gene Network in BCR::ABL1-Driven B-cell Acute Lymphoblastic Leukaemia," is published in Science Advances.

Australian scientists have pinpointed likely 'cells of origin', the source cells that can grow into breast cancer, in women carrying a faulty BRCA2 gene who are at high risk of developing the disease. The study also showed these cells have potential to be targeted with an existing cancer drug to delay tumour growth, in findings that may lead to future preventive treatments for the disease. Australian scientists have pinpointed likely 'cells-of-origin', the source cells that can grow into breast cancer, in women carrying a faulty BRCA2 gene who are at high risk of developing the disease. The WEHI-led study also showed these cells have potential to be targeted with an existing cancer drug to delay tumour growth, in findings that may lead to future preventive treatments for the disease. Abnormal cells Women who inherit and carry a faulty BRCA2 gene have a substantially increased risk of developing breast cancer -- approximately 70% of carriers will develop the disease over their lifetime. These cancers often occur at a young age and can be clinically aggressive. Early screening is encouraged and some women undertake preventive breast surgery (mastectomy) to reduce their breast cancer risk. In a milestone finding published in Nature Cell Biology, researchers have discovered the likely 'cells-of-origin' of cancer in BRCA2 carriers. By comparing cancer-free tissue samples from both carriers and non-carriers, they identified an aberrant population of cells that divide more quickly. Study joint first author Dr Rachel Joyce said this perturbed cell population was found in the majority of tissue samples from women with a faulty BRCA2 gene. "Given they were found in most of the BRCA2 tissue samples from healthy females, we believe these may be the cells-of-origin that lead to future breast cancers in women that carry the BRCA2 mutation," Dr Joyce said. Treatment targets The aberrant cells in BRCA2 tissue, a subset of breast ductal cells called luminal progenitor cells, stood out to the scientific team because they displayed altered protein production, which is critical for the correct growth and functioning of tissues in our bodies. "These changes may also make the cells more vulnerable to certain therapies aimed at preventing or delaying breast cancer development," said study joint first author Dr Rosa Pascual. Lead author Professor Jane Visvader said the team developed a pre-clinical BRCA2 model that showed similar alterations in the ductal cells, and targeted them with the existing cancer drug everolimus, which is approved to treat patients with relapsed breast cancer. "Through pinpointing this vulnerability in protein production, we were able to show that pre-treatment with this drug delayed the formation of tumours in the pre-clinical model," said Prof Visvader, joint head of the ACRF Cancer Biology and Stem Cells Division and the Breast Cancer Laboratory at WEHI. "This raises the possibility that targeting specific aspects of protein production in this way could represent a new breast cancer prevention strategy for women with a faulty BRCA2 gene." Towards prevention The findings are an important first step towards the goal of preventative treatments for breast cancer in BRCA2-mutation carriers. Study author and cancer clinician, Professor Geoff Lindeman said that while the findings were exciting, more work was needed before they could be applied in the clinic. "While everolimus did delay tumour development in the lab, this drug can have side-effects, which might limit its capacity to be used as a preventative treatment," said Prof Lindeman, joint head of the ACRF Cancer Biology and Stem Cells Division at WEHI, and a medical oncologist at the Royal Melbourne Hospital and Peter MacCallum Cancer Centre. "Our team want to further explore which specific parts of protein processing are dysregulated, and use this information to develop more selective and tolerable preventative treatments. "There's still a way to go, but we're a big step closer. "A few years ago, we identified the likely cells-of-origin for breast cancer in females carrying a fault in the BRCA1 gene, which is also associated with a high risk of developing breast cancer. That research has since led to an international breast cancer prevention study (BRCA-P). "We hope that our new findings will now inform future treatment and prevention for women with a faulty BRCA2 gene." The study, 'Identification of aberrant luminal progenitors and mTORC1 as a potential breast cancer prevention target in BRCA2 mutation carriers', is published in Nature Cell Biology (DOI: 10.1038/s41556-023-01315-5). The research was carried out on breast tissue samples kindly donated by women undergoing breast surgery, with assistance from the Victorian Cancer Biobank (funded by the Victorian Government) and the Kathleen Cuningham Foundation Consortium for research into Familial Breast cancer. The research was supported by the National Health and Medical Research Council, Breast Cancer Research Foundation, the National Breast Cancer Foundation, The Medical Research Future Fund, the Two Sisters Foundation and the Heine Family.