224 research outputs found
Cancer Institute
This record was harvested from a previous catalogue system and will be withdrawn in 2025. Information in this record may be superseded or incomplete. Visit this record in UMA's new catalogue at: https://archives.library.unimelb.edu.au/nodes/view/446197Dates are approximate.
YFA Job No 3100.
Inscription: PETER MacCALLUM HOSPITAL Exterior and Interior308565
Sub-item: [2018.0115.02007] "Cancer Institute
High-dose therapy and autologous transplantation for lymphoma: The Peter MacCallum Cancer Institute experience
Abstract Background: High‐dose therapy (HDT) with autologous bone marrow or blood cell transplantation for the treatment of lymphoma commenced at Peter MacCallum Cancer Institute in 1986. Aim: To examine the patient characteristics and outcomes of patients with non‐Hodgkin’s lymphoma (NHL) and Hodgkin’s disease (HD) treated with HDT and autologous transplantation at our Institute in the first 10 years of the service (1986–95). Methods: A retrospective analysis was performed examining patient characteristics, prior chemotherapy regimens, pretransplant disease status, HDT regimen, source of stem cells, time for haematopoietic recovery, complications of transplantation, response rates, overall survival (OS) and progression‐free survival (PFS). Results: Sixty‐seven patients with NHL were treated with an estimated 5‐year OS rate of 44% (95% confidence interval (CI) 32–56%) and PFS rate of 34% (95% CI 21–44%). Factors independently predictive of an unfavourable PFS on multivariate analyses were presence of constitutional symptoms at transplant (P < 0.002) and chemotherapy‐resistant disease at transplant (P = 0.02). Twenty‐three patients with HD were treated with a 5‐year predicted OS rate of 74% (95% CI 56–92%) and PFS rate of 57% (95% CI 36–77%). There was no difference in PFS for HD patients who relapsed either within 12 months of completion of front‐line therapy or after this time (P = 0.5). The transplant‐related mortality for the entire cohort was 17%, with a progressive decrease over time. Conclusion: HDT with autologous transplanta‐ tion achieves durable PFS and OS in patients with lymphoma. Improved patient selection, therapy modifications according to prognostic factors and ongoing improvements in supportive care should improve outcomes further. (Intern Med J 2001; 31: 279–289
High-dose therapy and autologous transplantation for lymphoma: The Peter MacCallum Cancer Institute experience
Abstract Background: High‐dose therapy (HDT) with autologous bone marrow or blood cell transplantation for the treatment of lymphoma commenced at Peter MacCallum Cancer Institute in 1986. Aim: To examine the patient characteristics and outcomes of patients with non‐Hodgkin’s lymphoma (NHL) and Hodgkin’s disease (HD) treated with HDT and autologous transplantation at our Institute in the first 10 years of the service (1986–95). Methods: A retrospective analysis was performed examining patient characteristics, prior chemotherapy regimens, pretransplant disease status, HDT regimen, source of stem cells, time for haematopoietic recovery, complications of transplantation, response rates, overall survival (OS) and progression‐free survival (PFS). Results: Sixty‐seven patients with NHL were treated with an estimated 5‐year OS rate of 44% (95% confidence interval (CI) 32–56%) and PFS rate of 34% (95% CI 21–44%). Factors independently predictive of an unfavourable PFS on multivariate analyses were presence of constitutional symptoms at transplant (P < 0.002) and chemotherapy‐resistant disease at transplant (P = 0.02). Twenty‐three patients with HD were treated with a 5‐year predicted OS rate of 74% (95% CI 56–92%) and PFS rate of 57% (95% CI 36–77%). There was no difference in PFS for HD patients who relapsed either within 12 months of completion of front‐line therapy or after this time (P = 0.5). The transplant‐related mortality for the entire cohort was 17%, with a progressive decrease over time. Conclusion: HDT with autologous transplanta‐ tion achieves durable PFS and OS in patients with lymphoma. Improved patient selection, therapy modifications according to prognostic factors and ongoing improvements in supportive care should improve outcomes further. (Intern Med J 2001; 31: 279–289
Person
This record was harvested from a previous catalogue system and will be withdrawn in 2025. Information in this record may be superseded or incomplete. Visit this record in UMA's new catalogue at: https://archives.library.unimelb.edu.au/nodes/view/57869Peter MacCallum was born in 1885 and was educated at Canterbury University College in New Zealand and Edinburgh University. In 1915 he enlisted with the Royal Army Medical Corp where he served in Belgium and France as Captain. MacCallum returned to Edinburgh in 1919 where he researched and lectured in Pathology. He was appointed Professor of Pathology at the University of Melbourne in 1925, retiring in 1950. He helped to design the Royal Melbourne Hospital and was instrumental in the establishment of the Cancer Institute. MacCallum was also Executive Chairman of the Anti-Cancer Council of Victoria from from 1945 and National Chairman of the Red Cross 1951-1958
Therapeutic Cancer Vaccines
This project will develop and test a new cell-based anticancer vaccine for patients with Prostate cancer. The collaboration will involve French, Italian, Austrian and German researchers. Blood will be taken from patients in the clinical trial, the patient's cells will be converted into a cell vaccine, and these cells will be labelled with a radioactive tracer and re-injected into the host. Australian researchers at the Centre for Blood Cell Therapies at the Peter MacCallum Cancer Centre will then track the performance of the vaccine using advanced diagnostic imaging to determine how effective the vaccine is in stimulating the body's own defence mechanisms to fight the cancer. Multiple versions of the treatment are being developed by the international collaboration and the Institute will help determine which approach is most effective in combating cancer. The Peter MacCallum Cancer Centre is the foremost centre worldwide for this type of cell tracking study.$AUD 180,923.00NHMRC Strategic AwardsAust/EU Collaborative Research Gran
Clinical Application of Poly(ADP-ribose) Polymerase (PARP) Inhibitors in Prostate Cancer
Approximately a quarter of men with metastatic castrate resistant prostate cancer (mCRPC) have alterations in homologous recombination repair (HRR). These patients exhibit enhanced sensitivity to poly(ADP-ribose) polymerase (PARP) inhibitors. Leveraging the synthetic lethality between PARP inhibition and HRR deficiency, studies have established marked clinical benefit and a survival advantage from PARP inhibitors (PARPi) in mCRPC, most notably in cancers with BRCA1/2 alterations. The role of PARPi is evolving beyond patients with HRR alterations, with studies increasingly focused on exploiting synergistic effects from combination therapeutics. Strategies combining PARP inhibitors with androgen receptor pathway inhibitors, radiation, radioligand therapy, chemotherapy and immunotherapy demonstrate potential additional benefits in mCRPC and these approaches are rapidly moving into the metastatic hormone sensitive treatment paradigm. In this review we summarise the development and expanding role of PARPi in prostate cancer including biomarkers of response, the relationship between the androgen receptor and PARP, evidence for combination therapeutics and the future directions of PARPi in precision medicine for prostate cancer
Immunological and molecular features of the tumor microenvironment of long-term survivors of ovarian cancer
BACKGROUNDDespite an overall poor prognosis, about 15% of patients with advanced-stage tubo-ovarian high-grade serous carcinoma (HGSC) survive 10 or more years after standard treatment.METHODSWe evaluated the tumor microenvironment of this exceptional, understudied group using a large international cohort enriched for long-term survivors (LTS; 10+ years; n = 374) compared with mid-term (MTS; 5-7.99 years; n = 433) and short-term survivors (STS; 2-4.99 years; n = 416). Primary tumor samples were immunostained and scored for intraepithelial and intrastromal densities of 10 immune-cell subsets (including T cells, B cells, plasma cells, myeloid cells, PD-1+ cells, and PD-L1+ cells) and epithelial content.RESULTSPositive associations with LTS compared with STS were seen for 9 of 10 immune-cell subsets. In particular, the combination of intraepithelial CD8+ T cells and intrastromal B cells showed near 5-fold increased odds of LTS compared with STS. All of these associations were stronger in tumors with high epithelial content and/or the C4/Differentiated molecular subtype, despite immune-cell densities generally being higher in tumors with low epithelial content and/or the C2/Immunoreactive molecular subtype.CONCLUSIONThe tumor microenvironment of HGSC LTS is distinguished by the intersection of T and B cell coinfiltration, high epithelial content, and C4/differentiated molecular subtype, features which may inspire new approaches to immunotherapy.FUNDINGOvarian Cancer Research Program (OCRP) of the Congressionally Directed Medical Research Program (CDMRP), U.S. Department of Defense (DOD); American Cancer Society; BC Cancer Foundation; Canada's Networks of Centres of Excellence; Canadian Cancer Society; Canadian Institutes of Health Research; Cancer Councils of New South Wales, Victoria, Queensland, South Australia, and Tasmania, Cancer Foundation of Western Australia; Cancer Institute NSW; Cancer Research UK; Deutsche Forschungsgesellschaft; ELAN Funds of the University of Erlangen-Nuremberg; Fred C. and Katherine B. Andersen Foundation; Genome BC; German Cancer Research Center; German Federal Ministry of Education and Research, Programme of Clinical Biomedical Research; Instituto de Salud Carlos III; Mayo Foundation; Minnesota Ovarian Cancer Alliance; Ministerio de Economía y Competitividad; Medical Research Council (MRC); National Center for Advancing Translational Sciences; National Health and Medical Research Council of Australia (NHMRC); Ovarian Cancer Australia; Peter MacCallum Foundation; Sydney West Translational Cancer Research Centre; Terry Fox Research Institute; The Eve Appeal (The Oak Foundation); UK National Institute for Health Research Biomedical Research Centres at the University of Cambridge; University of Pittsburgh School of Medicine; U.S. National Cancer Institute of the National Institutes of Health; VGH & UBC Hospital Foundation; Victorian Cancer Agency
Evaluation of variation in the phosphoinositide-3-kinase catalytic subunit alpha oncogene and breast cancer risk.
BACKGROUND: Somatic mutations in phosphoinositide-3-kinase catalytic subunit alpha (PIK3CA) are frequent in breast tumours and have been associated with oestrogen receptor (ER) expression, human epidermal growth factor receptor-2 overexpression, lymph node metastasis and poor survival. The goal of this study was to evaluate the association between inherited variation in this oncogene and risk of breast cancer. METHODS: A single-nucleotide polymorphism from the PIK3CA locus that was associated with breast cancer in a study of Caucasian breast cancer cases and controls from the Mayo Clinic (MCBCS) was genotyped in 5436 cases and 5280 controls from the Cancer Genetic Markers of Susceptibility (CGEMS) study and in 30 949 cases and 29 788 controls from the Breast Cancer Association Consortium (BCAC). RESULTS: Rs1607237 was significantly associated with a decreased risk of breast cancer in MCBCS, CGEMS and all studies of white Europeans combined (odds ratio (OR)=0.97, 95% confidence interval (CI) 0.95-0.99, P=4.6 × 10(-3)), but did not reach significance in the BCAC replication study alone (OR=0.98, 95% CI 0.96-1.01, P=0.139). CONCLUSION: Common germline variation in PIK3CA does not have a strong influence on the risk of breast cancer
Common breast cancer susceptibility alleles are associated with tumour subtypes in BRCA1 and BRCA2 mutation carriers: results from the Consortium of Investigators of Modifiers of BRCA1/2
The associations of the 12 SNPs with risk for BRCA1 and BRCA2 carriers differ by ER-positive or ER-negative breast cancer status. The apparent differences in SNP associations between BRCA1 and BRCA2 carriers, and non-carriers, may be explicable by differences in the prevalence of tumour subtypes. As more risk modifying variants are identified, incorporating these associations into breast cancer subtype-specific risk models may improve clinical management for mutation carriers
source file related the manuscript "<b>Single-base tiled screen reveals new design principles of </b><b><i>Psp</i></b><b>Cas13b for potent and off-target-free RNA silencing</b>" by Hu et al, 2024
This file contains raw data related to the manuscript "Single-base tiled screen reveals new design principles of PspCas13b for potent and off-target-free RNA silencing" by Hu et al, 2024.Authors:Wenxin Hu1,2, Amit Kumar1,2,8, Syed Faraz Ahmed6,7, Shijiao Qi1,2, David K.G. Ma2,3, Honglin Chen1,2, Gurjeet J. Singh1,2, Joshua M.L. Casan1,2, Michelle Haber4,5, Ilia Voskoboinik1,2, Matthew McKay6,7, Joseph A. Trapani1,2, Paul G. Ekert1,2,3,4,5 and Mohamed Fareh1,2,*Affiliations1Peter MacCallum Cancer Centre, Melbourne, 3000, Australia2Sir Peter MacCallum Department of Oncology, The University of Melbourne, Parkville, 3052, Australia3Murdoch Children’s Research Institute, Royal Children's Hospital, 50 Flemington Rd, Parkville, Melbourne, 3052, Australia4Children’s Cancer Institute, Lowy Cancer Research Centre, UNSW Sydney, NSW Australia 20525School of Women’s and Children’s Health, UNSW Sydney, Sydney, NSW, Australia6Department of Electrical and Electronic Engineering, The University of Melbourne, Parkville, VIC 3010, Australia7Department of Microbiology and Immunology, The Peter Doherty Institute for Infection and Immunity, The University of Melbourne, Melbourne, VIC 3000, Australia8 Present address: Diagnostic Genomics, Monash Health Pathology, Monash Medical Centre, 246 Clayton Rd, Clayton VIC 3168</p
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