NT Health Research and Publications Online

Welcome to NT Health Research and Publications Online, an open access digital repository that showcases the research projects and output of researchers working for the Northern Territory Department of Health (NT Health), while also collecting and preserving publications and multimedia produced in an official capacity, that represent the department. This service is maintained by NT Health Library Services
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4194
Projects
61
People
216
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  • Publication
    Journal Article
    Childhood Cancer Incidence and Survival in South Australia and the Northern Territory, 1990-2017, with Emphasis on Indigenous Peoples.
    (2024-05-29)
    Mashtoub, Suzanne
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    Ullah, Shahid
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    Singh, Gurmeet R
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    Clark Adnyamathanha, Justine
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    Leemaqz, Shalem
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    Paltiel, Ora
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    Roder, David M
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    Saxon, Benjamin
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    McKinnon, Ross
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    Pandol, Stephen J
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    Roberts, Claire T
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    Barreto, Savio George
    Reports of a rise in childhood cancer incidence in Australia and globally prompted the investigation of cancer incidence and survival in South Australia (SA) and the Northern Territory (NT) over a 28-year period, with emphasis on Indigenous peoples.This cross-sectional analysis of two prospective longitudinal databases, the SA and NT Cancer Registries (1990-2017), included all reported cases of childhood cancers. Poisson regression provided estimates of incidence rate ratios and survival was modelled using Cox proportional hazard models for children aged <5 and ≥5 years.A total of 895 patients across SA ( = 753) and the NT ( = 142) were ascertained. Overall and in the NT, childhood cancer incidence was higher in males compared with females (IRR 1.19 [1.04-1.35] and 1.43 [1.02-2.01], respectively). Lymphocytic leukemia was the most reported cancer type across all locations. With reference to the 1990-1999 era (181.67/100,000), cancer incidence remained unchanged across subsequent eras in the combined cohort (SA and NT) (2000-2009: 190.55/100,000; 1.06 [0.91-1.25]; 2010-2017: 210.00/100,000; 1.15 [0.98-1.35]); similar outcomes were reflected in SA and NT cohorts. Cancer incidence amongst non-Indigenous children significantly decreased from the 1990-1999 era (278.32/100,000) to the 2000-2009 era (162.92/100,000; 0.58 [0.35-0.97]). Amongst 39 Indigenous children in the NT, incidence rates remained unchanged across eras ( > 0.05). With reference to the 1990-1999 era, overall survival improved in subsequent eras in SA (2000-2009: HR 0.53 [0.38-0.73]; 2010-2017: 0.44 [0.28-0.68]); however, remained unchanged in the NT (2000-2009: 0.78 [0.40-1.51]; 2010-2017: 0.50 [0.24-1.05]). In the NT, overall survival of Indigenous patients was significantly lower compared with the non-Indigenous cohort (3.42 [1.92-6.10]). While the survival of Indigenous children with cancer significantly improved in the last two eras ( < 0.05), compared to the 1990-1999 era, no change was noted amongst non-Indigenous children in the NT ( > 0.05).The incidence of childhood cancers has remained unchanged over 28-years in SA and the NT. Encouragingly, improved survival rates over time were observed in SA and amongst Indigenous children of the NT. Nevertheless, survival rates in Indigenous children remain lower than non-Indigenous children.
  • Person
  • Publication
    Journal Article
    Marginal zone lymphomas: a consensus practice statement from the Australasian Lymphoma Alliance.
    (2024-06-01)
    Lasica, Masa
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    Anderson, Mary A
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    Boussioutas, Alex
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    Gregory, Gareth P
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    Hamad, Nada
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    Manos, Kate
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    McKelvie, Penny
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    Ng, Michael
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    Campbell, Belinda
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    Salvaris, Ross
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    Weinkove, Robert
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    Wight, Joel
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    Opat, Stephen
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    Tam, Constantine
    Marginal zone lymphomas (MZLs) are a rare, indolent group of non-Hodgkin lymphomas with different diagnostic, genetic and clinical features and therapeutic implications. The most common is extranodal MZL of mucosa-associated lymphoid tissue, followed by splenic MZL and nodal MZL. Patients with MZL generally have good outcomes with long survival rates but frequently have a relapsing/remitting course requiring several lines of therapy. The heterogeneous presentation and relapsing course present the clinician with several diagnostic and therapeutic challenges. This position statement presents evidence-based recommendations in the setting of Australia and New Zealand.
  • Publication
    Journal Article
    Targeting Molecular Measurable Residual Disease and Low-Blast Relapse in AML With Venetoclax and Low-Dose Cytarabine: A Prospective Phase II Study (VALDAC).
    (2024-06-20)
    Tiong, Ing Soo
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    Hiwase, Devendra K
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    Abro, Emad
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    Bajel, Ashish
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    Beligaswatte, Ashanka
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    Reynolds, John
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    Anstee, Natasha
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    Nguyen, Tamia
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    Loo, Sun
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    Chua, Chong Chyn
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    Ashby, Michael
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    Wiltshire, Kaitlyn M
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    Fleming, Shaun
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    Fong, Chun Y
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    Teh, Tse-Chieh
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    Blombery, Piers
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    Dillon, Richard
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    Ivey, Adam
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    Wei, Andrew H
    A prospective phase II study examined the safety and efficacy of venetoclax combined with low-dose cytarabine (LDAC) in AML at first measurable residual disease (MRD) or oligoblastic relapse.Patients with either MRD (≥1 log rise) or oligoblastic relapse (blasts 5%-15%) received venetoclax 600 mg once daily D1-28 plus LDAC once daily D1-10 in 28-day cycles. The primary objective was MRD response in the MRD relapse cohort or complete remission (CR/CRh/CRi) in the oligoblastic relapse cohort.Forty-eight adults with either MRD (n = 26) or oligoblastic (n = 22) relapse were enrolled. Median age was 67 years (range, 18-80) and 94% had received previous intensive chemotherapy. Patients received a median of four cycles of therapy; 17% completed ≥12 cycles. Patients with oligoblastic relapse had more grade ≥3 anemia (32% 4%; = .02) and infections (36% 8%; = .03), whereas grade 4 neutropenia (32 23%) or thrombocytopenia (27 15%) were comparable with the MRD relapse cohort. Markers of molecular MRD relapse included mutant (77%), (4%), (4%), or (4%). Three patients with a log rise in / (12%) were included. By cycle 2 in the MRD relapse cohort, a log reduction in MRD was observed in 69%; 46% achieved MRD negative remission. In the oligoblastic relapse cohort, 73% achieved CR/CRh/CRi. Overall, 21 (44%) underwent hematopoietic cell transplantation. Median overall survival (OS) was not reached in either cohort. Estimated 2-year OS rate was 67% (95% CI, 50 to 89) in the MRD and 53% (95% CI, 34 to 84) in the oligoblastic relapse cohorts.For AML in first remission and either MRD or oligoblastic relapse, venetoclax plus LDAC is well tolerated and highly effective.
  • Publication
    Journal Article
    Genomic Testing in Patients with Kidney Failure of an Unknown Cause: a National Australian Study.
    (2024-05-03)
    Mallawaarachchi, Amali C
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    Fowles, Lindsay
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    Wardrop, Louise
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    Wood, Alasdair
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    O'Shea, Rosie
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    Biros, Erik
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    Harris, Trudie
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    Alexander, Stephen I
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    Bodek, Simon
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    Boudville, Neil
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    Burke, Jo
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    Burnett, Leslie
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    Casauria, Sarah
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    Chadban, Steve
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    Chakera, Aron
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    Crafter, Sam
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    Dai, Pei
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    De Fazio, Paul
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    Faull, Randall
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    Honda, Andrew
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    Huntley, Vanessa
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    Jahan, Sadia
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    Jayasinghe, Kushani
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    Jose, Matthew
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    Leaver, Anna
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    MacShane, Mandi
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    Madelli, Evanthia Olympia
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    Nicholls, Kathy
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    Pawlowski, Rhonda
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    Rangan, Gopi
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    Snelling, Paul
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    Soraru, Jacqueline
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    Tchan, Michel
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    Valente, Giulia
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    Wallis, Mathew
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    Wedd, Laura
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    Welland, Matthew
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    Whitlam, John
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    Wilkins, Ella J
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    McCarthy, Hugh
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    Simons, Cas
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    Quinlan, Catherine
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    Patel, Chirag
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    Stark, Zornitza
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    Mallett, Andrew
    The cause of kidney failure is unknown in approximately 10% of patients with stage 5 chronic kidney disease (CKD). For those who first present to nephrology care with kidney failure, standard investigations of serology, imaging, urinalysis and kidney biopsy are limited differentiators of etiology. We aimed to determine the diagnostic utility of whole-genome sequencing (WGS) with analysis of a broad kidney gene panel in patients with kidney failure of unknown cause.We prospectively recruited 100 participants who reached CKD stage 5 at 50 years of age and had an unknown cause of kidney failure after standard investigation. Clinically-accredited WGS was performed in this national cohort after genetic counselling. The primary analysis was targeted to 388 kidney-related genes with second-tier genome-wide and mitochondrial analysis.The cohort was 61% male and the average age of participants at stage 5 CKD was 32 years (9 months to 50 years). A genetic diagnosis was made in 25% of participants. Disease-causing variants were identified across autosomal dominant tubulointerstitial kidney disease (6), glomerular disorders (4), ciliopathies (3), tubular disorders (2), Alport syndrome (4) and mitochondrial disease (1). Most diagnoses (80%) were in autosomal dominant, X-linked or mitochondrial conditions (UMOD; COL4A5; INF2; CLCN5; TRPC6; COL4A4; EYA1; HNF1B; WT1; NBEA; m.3243A>G). Patients with a family history of CKD were more likely to have a positive result (OR 3.29, 95% CI 1.10-11.29). Thirteen percent of participants without a CKD family history had a positive result. In those who first presented in stage 5 CKD, WGS with broad analysis of a curated kidney-disease gene panel was diagnostically more informative than kidney biopsy, with biopsy being inconclusive in 24 of 25 participants.In this prospectively ascertained Australian cohort, we identified a genetic diagnosis in 25% of patients with kidney failure of unknown cause.
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