Dr Anoop Enjeti

Dr Anoop Enjeti

Conjoint Associate Professor

School of Medicine and Public Health

Career Summary

Biography

Qualifications

MBBS   MD (Pondicherry Univ.)   FRCP (UK) FRCPA FASCP FACP MClin Epid (Molecular and Genetic Epidemiology, Univ. of Newcastle) Grad Cert Bioethics (Monash Univ.)    Master Cert in Healthcare Leadership (Cornell Univ., USA) Post Grad Cert in Nanotechnology (Oxford University, UK) Cert Competence Lymphoma (Ulm University, Germany) PhD (University of Newcastle)

Appointments

 

Clinical Appointment:

 

Senior Staff Specialist   Haematologist Calvary Mater Hospital Newcastle

 

Director of Haematology (NSW Health Pathology-John Hunter Hospital)

 

Research appointment:

 

Translational Clinical Research Fellow, NSW Health Pathology-Hunter/ Hunter New England Health/ HCRA/ Calvary Mater Newcastle

 

Conjoint Appointment: Conjoint Associate Professor, University of Newcastle

 

As a clinician researcher, I have the unique opportunity to work directly with patients and drive the translation of lab research developments into clinical practice. Our patients are a constant inspiration in our journey to research new treatments for blood disorders.

 

Working in collaboration with my clinical colleagues, researchers and students, we aim to revolutionise health systems, bringing world class research to the Hunter region as well as explore novel treatments and diagnostics to improve outcomes in terms of improved health, quality experience and system efficiencies.


Background

 

I am an early career clinician researcher and clinical haematologist with dual clinical fellowships (Physician & Pathology), a masters in epidemiology/biostatistics, a clinical doctorate (MD) and a PhD. I have also obtained postgraduate physician qualifications from the UK Royal College of Physicians and specialist haematology from the Royal College of Pathologists of Australasia. My physician and specialist haematology training has spanned across India, UK, Singapore and Australia including specialist training in genetics and molecular genetics where I contributed to a high impact publication outlining geographical variations in AML genetics.

 

Clinical trials and translational diagnostics

 

I am the clinical lead for the acute myeloid leukemia and myelodysplasia program at the Calvary Mater hospital.  I have collaborated with cancer researchers across the state as an active participant of the Hunter Cancer Research. I am the Myelodysplasia clinical lead for the Australasian Leukemia and Lymphoma Group (ALLG) – the national haematology cooperative clinical trial group. I have led over 35 clinical trials as an investigator at the Calvary Mater Hospital. As the molecular haematology lead, I recently established of the state-wide molecular haematology massive parallel sequencing platform. I also led the translation of DNA microarray into clinical practise for NSW Health Pathology.

 

Biology and Drug Development in Acute Leukemia/Myelodysplasia

 

Working closely with my colleagues Nikki Verrills, Matt Dun and Heather Lee we are understanding the molecular biology of leukemia at proteomic and single cell level. We believe that our work will lead to cutting edge understanding of biology and novel drug therapy startegies.

 

Publications and Grants

 

I have over 43 peer-reviewed publications, numerous conference presentations and five book chapters. I have received over 3 million dollars in competitive and   other research funding. I am the recipient of the prestigious ‘visiting fellowship’ in Molecular Oncologic Pathology Strategic Health Research Training Program in Cancer Research, Canada (funded by the Terry Fox Foundation) for the year 2016. I was the recipient of the HCRA fellowship in 2015 and more recently was awarded a Translational Research Fellowship from Pathology NSW - Hunter/HNE LHD /HCRA and Calvary Mater Hospital (2017-19) to pursue translational clinical research in Haematology. I am a co-lead of a successful NHMRC Ideas grant 2019 (Verrills and Enjeti, Targeting DNA-PK in acute myeloid leukaemia).

 

Leadership, Management and Advocacy

 

I am the Myelodysplasia lead for the Australasian Lymphoma and Leukemia group. I was the recent chair of the Future Leaders Group, an advocacy group for early career researchers as part of Hunter Cancer Research Alliance, a regional network of cancer researchers. I am the Director of Laboratory Haematology (NSW Health Pathology – John Hunter Hospital) and the molecular Haematology lead for NSW Health Pathology North Hunter. I am the president of the Thrombosis and Haemostasis society of Australia and New Zealand (THANZ). I am also on the Board of Education and Assessment (BEA) of the Royal College of Pathologists of Australasia (RCPA) as the chief examiner for haematology physician training. I am actively involved in community organizations such as Cancer Council and have edited the most recent version of the Council’s acute leukemia patient education booklets.

 

Student Supervision and Current Research Focus

 

I have trained and supervised numerous undergraduate, graduate and postgraduate students including physician haematology fellows. My research focus spans policy, health system interventions and translational molecular biology - this includes early phase clinical trials in haematological malignancies (AML/MDS), translational diagnostics for blood cancers, novel solutions to transfusion medicine challenges and investigation of   circulating microvesicles and miRNA in abnormal clonal haemopoiesis.

 

If you find these research areas exciting and wish to be a part, please do not hesitate to contact me.



Keywords

  • Acute Leukemia and Myelodysplasia
  • Blood wastage and transfusion related
  • Genomics for Haematological malignancies
  • Microvesicles
  • Thrombosis and Haemostasis

Fields of Research

Code Description Percentage
060408 Genomics 30
110202 Haematology 70

Professional Experience

Academic appointment

Dates Title Organisation / Department
3/4/2019 -  A/Professor Faculty of Health and Medicine, University of Newcastle
School of Medicine and Public Health
Australia
1/7/2017 - 2/2/2020 Translational Research Fellow NSW Health Pathology - Pathology North

Professional appointment

Dates Title Organisation / Department
3/2/2020 -  Director of Haematology NSW Health Pathology - Pathology North
1/1/2011 -  Senior Staff Specialist Calvary Mater Newcastle
Australia
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Publications

For publications that are currently unpublished or in-press, details are shown in italics.


Journal article (39 outputs)

Year Citation Altmetrics Link
2020 Berry NK, Scott RJ, Sutton R, Law T, Trahair TN, Dalla-Pozza L, et al., 'Enrichment of atypical hyperdiploidy and IKZF1 deletions detected by SNP-microarray in high-risk Australian AIEOP-BFM B-cell acute lymphoblastic leukaemia cohort', Cancer Genetics, 242 8-14 (2020)

© 2020 The Authors Acute lymphoblastic leukaemia (ALL) is the most common childhood malignancy with the majority of patients being classified as B-cell lineage (B-ALL). The sub-cl... [more]

© 2020 The Authors Acute lymphoblastic leukaemia (ALL) is the most common childhood malignancy with the majority of patients being classified as B-cell lineage (B-ALL). The sub-classification of B-ALL is based on genomic architecture. Recent studies have demonstrated the capability of SNP-microarrays to detect genomic changes in B-ALL which cannot be observed by conventional cytogenetic methods. In current clinical trials, B-ALL patients at high risk of relapse are mainly identified by adverse cancer genomics and/or poor response to early therapy. To test the hypothesis that inclusion of SNP-microarrays in frontline diagnostics could more efficiently and accurately identify adverse genomic factors than conventional techniques, we evaluated the Australian high-risk B-ALL cohort enrolled on AIEOP-BFM ALL 2009 study (n = 33). SNP-microarray analysis identified additional aberrations in 97% of patients (32/33) compared to conventional techniques. This changed the genomic risk category of 24% (8/33) of patients. Additionally, 27% (9/33) of patients exhibited a ¿hyperdiploid¿ genome, which is generally associated with a good genomic risk and favourable outcomes. An enrichment of IKZF1 deletions was observed with one third of the cohort affected. Our findings suggest the current classification system could be improved and highlights the need to use more sensitive techniques such as SNP-microarray for cytogenomic risk stratification in B-ALL.

DOI 10.1016/j.cancergen.2020.01.051
Co-authors Rodney Scott
2019 Arthur C, Jeffrey A, Yip E, Katsioulas V, Nalpantidis A, Kerridge I, et al., 'Prolonged administration of low-dose cytarabine and thioguanine in elderly patients with acute myeloid leukaemia (AML) achieves high complete remission rates and prolonged survival', LEUKEMIA & LYMPHOMA, 61 831-839 (2019)
DOI 10.1080/10428194.2019.1697876
2019 Enjeti AK, Lincz LF, Seldon M, Isbister GK, 'Circulating microvesicles in snakebite patients with microangiopathy', RESEARCH AND PRACTICE IN THROMBOSIS AND HAEMOSTASIS, 3 121-125 (2019) [C1]
DOI 10.1002/rth2.12164
Citations Web of Science - 2
Co-authors Lisa Lincz, Geoffrey Isbister
2019 Joseph J, Rabbolini D, Enjeti AK, Favaloro E, Kopp M-C, McRae S, et al., 'Diagnosis and management of heparin-induced thrombocytopenia: a consensus statement from the Thrombosis and Haemostasis Society of Australia and New Zealand HIT Writing Group', MEDICAL JOURNAL OF AUSTRALIA, 210 509-515 (2019)
DOI 10.5694/mja2.50213
Citations Scopus - 1Web of Science - 2
2019 Chapman K, Scorgie FE, Ariyarajah A, Stephens E, Enjeti AK, Lincz LF, 'The effects of tetrahydrocurcumin compared to curcuminoids on human platelet aggregation and blood coagulation in vitro', Thrombosis Research, 179 28-30 (2019) [C1]
DOI 10.1016/j.thromres.2019.04.029
Co-authors Lisa Lincz
2019 Sillar JR, Enjeti AK, 'Targeting apoptotic pathways in acute myeloid leukaemia', Cancers, 11 1-18 (2019) [C1]
DOI 10.3390/cancers11111660
2019 Enjeti AK, Lincz LF, Seldon M, Isbister GK, 'Microangiopathy in snake bitesbubble trouble: Response to commentary', RESEARCH AND PRACTICE IN THROMBOSIS AND HAEMOSTASIS, 3 298-299 (2019)
DOI 10.1002/rth2.12187
Co-authors Geoffrey Isbister, Lisa Lincz
2019 Berry NK, Scott RJ, Rowlings P, Enjeti AK, 'Clinical use of SNP-microarrays for the detection of genome-wide changes in haematological malignancies', Critical Reviews in Oncology/Hematology, 142 58-67 (2019) [C1]

© 2019 The Author(s) Single nucleotide polymorphism (SNP) microarrays are commonly used for the clinical investigation of constitutional genomic disorders; however, their adoption... [more]

© 2019 The Author(s) Single nucleotide polymorphism (SNP) microarrays are commonly used for the clinical investigation of constitutional genomic disorders; however, their adoption for investigating somatic changes is being recognised. With increasing importance being placed on defining the cancer genome, a shift in technology is imperative at a clinical level. Microarray platforms have the potential to become frontline testing, replacing or complementing standard investigations such as FISH or karyotype. This ¿molecular karyotype approach¿ exemplified by SNP-microarrays has distinct advantages in the investigation of several haematological malignancies. A growing body of literature, including guidelines, has shown support for the use of SNP-microarrays in the clinical laboratory to aid in a more accurate definition of the cancer genome. Understanding the benefits of this technology along with discussing the barriers to its implementation is necessary for the development and incorporation of SNP-microarrays in a clinical laboratory for the investigation of haematological malignancies.

DOI 10.1016/j.critrevonc.2019.07.016
Co-authors Rodney Scott
2019 Wei AH, Strickland SA, Hou J-Z, Fiedler W, Lin TL, Walter RB, et al., 'Venetoclax Combined With Low-Dose Cytarabine for Previously Untreated Patients With Acute Myeloid Leukemia: Results From a Phase Ib/II Study', JOURNAL OF CLINICAL ONCOLOGY, 37 1277-+ (2019)
DOI 10.1200/JCO.18.01600
Citations Scopus - 76Web of Science - 62
2019 Stevenson W, Bryant J, Watson R, Sanson-Fisher R, Oldmeadow C, Henskens F, et al., 'A multi-center randomized controlled trial to reduce unmet needs, depression, and anxiety among hematological cancer patients and their support persons', JOURNAL OF PSYCHOSOCIAL ONCOLOGY, (2019)
DOI 10.1080/07347332.2019.1692991
Co-authors Christopher Oldmeadow, Rob Sanson-Fisher, Jamie Bryant, Frans Henskens, Flora Tzelepis, Chris Paul
2019 Simpson JD, Hopkins A, Amil A, Ross B, Enjeti AK, 'Transfusion-associated circulatory overload in ambulatory patients', Vox Sanguinis, 114 216-222 (2019) [C1]

© 2019 International Society of Blood Transfusion Background and Objectives: Transfusion-associated circulatory overload is a leading cause of transfusion-related adverse events. ... [more]

© 2019 International Society of Blood Transfusion Background and Objectives: Transfusion-associated circulatory overload is a leading cause of transfusion-related adverse events. The frequency and risks for transfusion-associated circulatory overload in ambulatory haematology patients are not known. Materials and Methods: A retrospective cohort analysis of ambulatory patients transfused in a tertiary haematology centre, using medical records and an electronic transfusion database, was undertaken between January and December 2014. Variables studied included age, gender, diagnosis, heart failure, kidney disease and details of transfusions. Transfusion-associated circulatory overload was defined according to proposed International Society of Blood Transfusion criteria. Patients with clinical evidence of hypervolaemia, not meeting the TACO definition and/or who were prescribed otherwise unscheduled diuretic agent, were collectively deemed to be at ¿risk of clinically significant hypervolaemia¿ (ROCSH). Results: In the study period, 93 ambulatory patients (male¿=¿49, female¿=¿44, mean age¿=¿75·89¿±¿11·37¿years) attended 715 transfusion encounters, totalling 1536 packed red cell units. No cases of TACO occurred whilst ¿ROCSH¿ events occurred in 57/715 (8%) of transfusion encounters. In a univariate model, age was significantly associated with ¿ROCSH¿, odds ratio¿=¿1·05 (P¿=¿0·017 95%, CI 1·01¿1·09) and no factors were significant on multivariate analysis. Conclusions: Transfusion-associated circulatory overload occurs infrequently haematology patients receiving ambulatory blood transfusions. To our knowledge, this is the first study to report on occurrence and risk factors for circulatory overload in ambulatory transfusions. This study provides vital baseline data for future prospective studies on this important aspect of haemovigilance.

DOI 10.1111/vox.12753
2018 Alkhatatbeh MJ, Enjeti AK, Baqar S, Ekinci EI, Liu D, Thorne RF, Lincz LF, 'Strategies for enumeration of circulating microvesicles on a conventional flow cytometer: Counting beads and scatter parameters.', Journal of Circulating Biomarkers, 7 1-10 (2018) [C1]
DOI 10.1177/1849454418766966
Citations Scopus - 4
Co-authors Lisa Lincz, Rick Thorne
2018 Staudt D, Murray HC, McLachlan T, Alvaro F, Enjeti AK, Verrills NM, Dun MD, 'Targeting Oncogenic Signaling in Mutant FLT3 Acute Myeloid Leukemia: The Path to Least Resistance', INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, 19 (2018) [C1]
DOI 10.3390/ijms19103198
Citations Scopus - 12Web of Science - 8
Co-authors Matt Dun, Nikki Verrills
2018 van der Pol E, Sturk A, van Leeuwen T, Nieuwland R, Coumans F, Mobarrez F, et al., 'Standardization of extracellular vesicle measurements by flow cytometry through vesicle diameter approximation', Journal of Thrombosis and Haemostasis, 16 1236-1245 (2018) [C1]

© 2018 The Authors. Journal of Thrombosis and Haemostasis published by Wiley Periodicals, Inc. on behalf of International Society on Thrombosis and Haemostasis. Essentials Platele... [more]

© 2018 The Authors. Journal of Thrombosis and Haemostasis published by Wiley Periodicals, Inc. on behalf of International Society on Thrombosis and Haemostasis. Essentials Platelet extracellular vesicles (EVs) concentrations measured by flow cytometers are incomparable. A model is applied to convert ambiguous scatter units to EV diameter in nanometer. Most included flow cytometers lack the sensitivity to detect EVs of 600 nm and smaller. The model outperforms polystyrene beads for comparability of platelet EV concentrations. Summary: Background Detection of extracellular vesicles (EVs) by flow cytometry has poor interlaboratory comparability, owing to differences in flow cytometer (FCM) sensitivity. Previous workshops distributed polystyrene beads to set a scatter-based diameter gate in order to improve the comparability of EV concentration measurements. However, polystyrene beads provide limited insights into the diameter of detected EVs. Objectives To evaluate gates based on the estimated diameter of EVs instead of beads. Methods A calibration bead mixture and platelet EV samples were distributed to 33 participants. Beads and a light scattering model were used to set EV diameter gates in order to measure the concentration of CD61¿phycoerythrin-positive platelet EVs. Results Of the 46 evaluated FCMs, 21 FCMs detected the 600¿1200-nm EV diameter gate. The 1200¿3000-nm EV diameter gate was detected by 31 FCMs, with a measured EV concentration interlaboratory variability of 81% as compared with 139% with the bead diameter gate. Part of the variation in both approaches is caused by precipitation in some of the provided platelet EV samples. Flow rate calibration proved essential because systems configured to 60 µL min-1 differed six-fold in measured flow rates between instruments. Conclusions EV diameter gates improve the interlaboratory variability as compared with previous approaches. Of the evaluated FCMs, 24% could not detect 400-nm polystyrene beads, and such instruments have limited utility for EV research. Finally, considerable differences were observed in sensitivity between optically similar instruments, indicating that maintenance and training affect the sensitivity.

DOI 10.1111/jth.14009
Citations Scopus - 40
2018 Lapuz C, Enjeti AK, O'Brien PC, Capp AL, Holliday EG, Gupta SA, 'Outcomes and relapse patterns following chemotherapy in advanced Hodgkin lymphoma in the positron emission tomography era', BLOOD AND LYMPHATIC CANCER-TARGETS AND THERAPY, 8 13-20 (2018) [C1]
DOI 10.2147/BLCTT.S160404
Co-authors Liz Holliday
2017 Ayyalil F, Irwin G, Ross B, Manolis M, Enjeti AK, 'Zeroing in on red blood cell unit expiry.', Transfusion, 57 2870-2877 (2017) [C1]
DOI 10.1111/trf.14321
2017 Lim MS, Ariyarajah A, Oldmeadow C, Hall A, Enjeti AK, 'A Systematic Review and Meta-analysis Comparing Anticoagulation versus No Anticoagulation and Shorter versus Longer duration of Anticoagulation for Treatment of Isolated Distal Deep Vein Thrombosis', Seminars in Thrombosis and Hemostasis, 43 836-848 (2017) [C1]

Isolated distal deep vein thrombosis (DVT) represents an important clinical problem but there is no consensus regarding its management. The aim of this review was to evaluate the ... [more]

Isolated distal deep vein thrombosis (DVT) represents an important clinical problem but there is no consensus regarding its management. The aim of this review was to evaluate the safety, efficacy, and shorter versus longer duration of anticoagulation in patients with isolated distal DVT. A systematic search was conducted using MEDLINE, EMBASE, Cochrane Central Register of Controlled Trials, and Cochrane Database of Systemic Reviews. Studies reporting rates of symptomatic pulmonary embolism (PE), recurrent DVT, proximal extension, and/or major bleeding were included. Fourteen studies (six randomized controlled trials, eight cohorts) involving 2,918 patients met the eligibility criteria (with a total of 13 meeting criteria for the meta-analysis). Compared with no anticoagulation, anticoagulation was associated with a significant reduction in proximal extension (odds ratio [OR]: 0.29; 95% confidence interval [CI]: 0.13-0.67; p < 0.004), recurrent DVT (OR: 0.16; 95% CI: 0.04-0.65; p = 0.01), and the composite end-point of proximal extension/PE (OR: 0.34; 95% CI: 0.16-0.72; p = 0.005); however, no significant differences in PE (OR: 0.47; 95% CI: 0.17-1.34; p = 0.16) or major bleeding (OR: 1.49; 95% CI: 0.33-6.86; p = 0.60) were observed. Anticoagulation for a longer duration (=8 vs. =6 weeks) was associated with a significant reduction in proximal extension (OR: 0.23; 95% CI: 0.11-0.48; p < 0.001) but not for other outcomes.

DOI 10.1055/s-0037-1604085
Citations Scopus - 3Web of Science - 2
Co-authors Christopher Oldmeadow
2017 Enjeti AK, Ariyarajah A, D'Crus A, Seldon M, Lincz LF, 'Circulating microvesicle number, function and small RNA content vary with age, gender, smoking status, lipid and hormone profiles', Thrombosis Research, 156 65-72 (2017) [C1]

© 2017 Background Characterization of circulating microvesicles (MV) in healthy subjects in relation to various biological factors is not well studied. Objectives We evaluated the... [more]

© 2017 Background Characterization of circulating microvesicles (MV) in healthy subjects in relation to various biological factors is not well studied. Objectives We evaluated the influence of age, gender, smoking status, lipid and hormone profiles on circulating MV in healthy subjects. Methods Platelet free plasma from 143 volunteer blood donors (males¿=¿80, females¿=¿63) was evaluated by standardized flow cytometry for MV expressing CD41 (platelet-derived), CD105 (endothelial-derived), CD235 (red cell-derived), TF (tissue factor) and phosphatidylserine (PS) MV. Procoagulant function was measured by the Xa based assay (XaCT) and endogenous thrombin potential (ETP) using thrombin generation assay. Results Those =¿29¿years and =¿60¿years had higher levels of MV subsets (CD41, CD235, TF and PS) compared to those aged 30¿59¿years. The median CD41, CD105, CD235, TF and PS expressing MV by flow cytometry were similar or lower in females, whilst procoagulant activity by the XaCT assay was higher (p¿=¿0.002). In smokers (n¿=¿21), certain MV subsets (CD41, TF and PS) and functional activity (ETP) was lower (p¿<¿0.05). Regression analysis showed that MV parameters of CD41, CD105, TF and ETP could be predicted independently by age, whilst smoking predicted for CD105, CD235, TF, PS and ETP. Certain MV parameters also correlated with BMI, lipid and hormone levels. The small RNA and miRNA levels did not differ by age group, smoking status or gender. Conclusions It is important to recognize that differences may arise depending on age, gender, BMI, lipid, hormone levels and smoking status in apparently healthy subjects when evaluating MV for pathogenic potential.

DOI 10.1016/j.thromres.2017.04.019
Citations Scopus - 14Web of Science - 12
Co-authors Lisa Lincz
2017 Berry NK, Dixon-McIver A, Scott RJ, Rowlings P, Enjeti AK, 'Detection of complex genomic signatures associated with risk in plasma cell disorders.', Cancer genetics, 218-219 1-9 (2017) [C1]
DOI 10.1016/j.cancergen.2017.08.004
Citations Scopus - 2Web of Science - 2
Co-authors Rodney Scott
2016 Lim MS, Lemmert K, Enjeti A, 'Blastic plasmacytoid dendritic cell neoplasm (BPDCN): A rare entity', BMJ Case Reports, 2016 (2016)

Copyright 2016 BMJ Publishing Group. All rights reserved. Blastic plasmacytoid dendritic cell neoplasm (BPDCN) is a rare and aggressive haematological malignancy in the elderly, w... [more]

Copyright 2016 BMJ Publishing Group. All rights reserved. Blastic plasmacytoid dendritic cell neoplasm (BPDCN) is a rare and aggressive haematological malignancy in the elderly, with a high frequency of cutaneous and bone marrow involvement and poor prognosis. We report a case of BPDCN with classic presentation and discuss its treatment and the value of different investigation tools used in diagnosis and response assessment.

DOI 10.1136/bcr-2015-214093
2016 Enjeti AK, D'Crus A, Melville K, Verrills NM, Rowlings P, 'A systematic evaluation of the safety and toxicity of fingolimod for its potential use in the treatment of acute myeloid leukaemia', Anti-Cancer Drugs, 27 560-568 (2016) [C1]

© 2016 Wolters Kluwer Health, Inc. All rights reserved. Treatment of acute myeloid leukaemia (AML) is challenging and emerging treatment options include protein phosphatase 2A (PP... [more]

© 2016 Wolters Kluwer Health, Inc. All rights reserved. Treatment of acute myeloid leukaemia (AML) is challenging and emerging treatment options include protein phosphatase 2A (PP2A) activators. Fingolimod is a known PP2A activator that inhibits multiple signalling pathways and has been used extensively in patients with multiple sclerosis and other indications. The initial positive results of PP2A activators in vitro and mouse models of AML are promising; however, its safety for use in AML has not been assessed. From human studies of fingolimod in other indications, it is possible to evaluate whether the safety and toxicity profile of the PP2A activators will allow their use in treating AML. A literature review was carried out to assess safety before the commencement of Phase I trials of the PP2A activator Fingolimod in AML. From human studies of fingolimod in other indications, it is possible to evaluate whether the safety and toxicity profile of the PP2A activators will allow their use in treating AML. A systematic review of published literature in Medline, EMBASE and the Cochrane Library of critical reviews was carried out. International standards for the design and reporting of search strategies were followed. Search terms and medical subject headings used in trials involving PP2A activators as well as a specific search were performed for 'adverse events','serious adverse events', 'delays in treatment', ' side effects' and 'toxicity' for primary objectives. Database searches were limited to papers published in the last 12 years and available in English. The search yielded 677 articles. A total of 69 journal articles were identified as relevant and included 30 clinical trials, 24 review articles and 15 case reports. The most frequently reported adverse events were nausea, diarrhoea, fatigue, back pain, influenza viral infections, nasopharyngitis and bronchitis. Specific safety concerns include monitoring of the heart rate and conduction at commencement of treatment as cardiotoxicity has been reported. There is little evidence to suggest specific bone marrow toxicity. Lymophopenia is a desired effect in the management of multiple sclerosis, but may have implications in patients with acute leukaemia as it may potentially increase susceptibility to viral infections such as influenza. Fingolimod is a potential treatment option for AML with an acceptable risk to benefit ratio, given its lack of bone marrow toxicity and the relatively low rate of serious side effects. As most patients with AML are elderly, specific monitoring for cardiac toxicity as well as infection would be required.

DOI 10.1097/CAD.0000000000000358
Citations Scopus - 10Web of Science - 9
Co-authors Nikki Verrills
2016 Enjeti AK, Ariyarajah A, D'Crus A, Seldon M, Lincz LF, 'Correlative analysis of nanoparticle tracking, flow cytometric and functional measurements for circulating microvesicles in normal subjects', Thrombosis Research, 145 18-23 (2016) [C1]

© 2016 Introduction Circulating microvesicles (MV) can be analysed using a number of different techniques. The aim of this study was to evaluate the correlation between functional... [more]

© 2016 Introduction Circulating microvesicles (MV) can be analysed using a number of different techniques. The aim of this study was to evaluate the correlation between functional procoagulant based assays including thrombin generation, factor Xa activation test (XaCT), and phosphatidylserine factor Xa-activity by ELISA with optical MV enumeration by flow cytometry and nanoparticle tracking analysis. Methods Citrated blood samples were collected from 60 healthy volunteer blood donors after informed consent. Platelet free plasma was prepared using a standardized published protocol. MV subsets were enumerated by flow cytometry (BDFACS Canto) after staining with specific antibodies for platelets (CD41), endothelial cells (CD105), red cells (CD235) monocytes (CD14), tissue factor (CD142) and for phosphatidylserine expression by binding to annexin V. A standardized protocol using counting beads was employed. Nanotracking analysis was performed on both scatter and fluorescent settings after MV staining with quantum dot stain, Qdot 655. Procoagulant function was assessed by the XaCT assay on an automated coagulation analyser and by thrombin generation assay measuring endogenous thrombin potential (ETP), lagtime, peak (PEAK) and time to peak (ttPEAK) using a Calibrated Automated Thrombogram (CAT). The statistical analysis was carried out with Statistica 12 software using non-parametric tests (Spearman rank order correlations, with significance set at p¿<¿0.05). Results In normal healthy subjects, thrombin generation parameters correlated with levels of MV measured by flow cytometry. ETP, lagtime, ttPEAK and PEAK correlated with MV expressing phosphatidylserine (rs, Spearman rank order correlation was 0.29, 0.40, 0.31 and 0.34 respectively, p¿<¿0.05), and MV expressing tissue factor (rs was 0.29, 0.40, 0.31 and 0.34 respectively, p¿<¿0.05), whilst red cell derived MV correlated with lagtime, ttPEAK and PEAK (rs, was 0.35,0.30 and 0.3, respectively, p¿<¿0.05). Lagtime and ttPEAK negatively correlated with the clot based XaCT test (rs, was -¿0.34 and -¿0.30 respectively, p¿<¿0.05) and positively correlated with the ELISA MP-activity assay (rs¿=¿0.42 for both, p¿<¿0.05). In addition, endothelial MV levels weakly correlated with white cell counts (rs = 0.27, p¿<¿0.05). Conclusions Thrombin generation and flow cytometry for phosphatidylserine or tissue factor expressing MV correlate well as markers for procoagulant activity. A combination of optical or non-optical enumeration as well as functional methods may be required for a complete profiling of circulating MV.

DOI 10.1016/j.thromres.2016.06.029
Citations Scopus - 9Web of Science - 8
Co-authors Lisa Lincz
2016 Lim MS, Chapman K, Swanepoel P, Enjeti AK, 'Sensitivity of routine coagulation assays to direct oral anticoagulants: patient samples versus commercial drug-specific calibrators', Pathology, 48 712-719 (2016) [C1]

© 2016 Royal College of Pathologists of Australasia Most studies on the sensitivities of coagulation assays to direct oral anticoagulants (DOACs) are based on normal plasma spiked... [more]

© 2016 Royal College of Pathologists of Australasia Most studies on the sensitivities of coagulation assays to direct oral anticoagulants (DOACs) are based on normal plasma spiked with anticoagulant in the laboratory. Recent studies have shown that reagent sensitivity varies significantly depending on whether spiked or patient samples are used. The aim of this study was to compare the sensitivities of routine coagulation assays in patient samples and commercial drug specific calibrators using commonly used activated partial thromboplastin time (APTT) and prothrombin time (PT) reagents (i.e., Actin FS and Neoplastine CI Plus for APTT and PT, respectively) in Australian laboratories. Samples collected at Pathology North Hunter (PN-H) for dabigatran (n¿=¿39), rivaroxaban, (n¿=¿56) or apixaban levels (n¿=¿22) between February 2013 and November 2015 were analysed and compared to two different commercial drug specific calibrators from different manufacturers for each DOAC. Our results show that dabigatran (Hyphen and Technoclone) and rivaroxaban (Stago) calibrators tend to overestimate the APTT but are similar to patient samples for PT. A cut-off DOAC level of 50¿ng/mL based on results from patient samples within the laboratory can be used as the lower limit which will result in prolongation of APTT for dabigatran (sensitivity 96%, n¿=¿25) and PT for rivaroxaban (sensitivity 97%, n¿=¿29), respectively. Individual laboratories should be familiar with the sensitivity of their coagulation reagents to different DOACs including differences between patient samples versus different commercial drug specific calibrators.

DOI 10.1016/j.pathol.2016.07.008
Citations Scopus - 11Web of Science - 9
2016 Lim MS, Enjeti AK, 'Safety of anticoagulation in the treatment of venous thromboembolism in patients with haematological malignancies and thrombocytopenia: Report of 5 cases and literature review', CRITICAL REVIEWS IN ONCOLOGY HEMATOLOGY, 105 92-99 (2016) [C1]
DOI 10.1016/j.critrevonc.2016.06.011
Citations Scopus - 9Web of Science - 10
2016 Smith AM, Dun MD, Lee EM, Harrison C, Kahl R, Flanagan H, et al., 'Activation of protein phosphatase 2A in FLT3+ acute myeloid leukemia cells enhances the cytotoxicity of FLT3 tyrosine kinase inhibitors', Oncotarget, 7 47465-47478 (2016) [C1]

Constitutive activation of the receptor tyrosine kinase Fms-like tyrosine kinase 3 (FLT3), via co-expression of its ligand or by genetic mutation, is common in acute myeloid leuke... [more]

Constitutive activation of the receptor tyrosine kinase Fms-like tyrosine kinase 3 (FLT3), via co-expression of its ligand or by genetic mutation, is common in acute myeloid leukemia (AML). In this study we show that FLT3 activation inhibits the activity of the tumor suppressor, protein phosphatase 2A (PP2A). Using BaF3 cells transduced with wildtype or mutant FLT3, we show that FLT3-induced PP2A inhibition sensitizes cells to the pharmacological PP2A activators, FTY720 and AAL(S). FTY720 and AAL(S) induced cell death and inhibited colony formation of FLT3 activated cells. Furthermore, PP2A activators reduced the phosphorylation of ERK and AKT, downstream targets shared by both FLT3 and PP2A, in FLT3/ITD+ BaF3 and MV4-11 cell lines. PP2A activity was lower in primary human bone marrow derived AML blasts compared to normal bone marrow, with blasts from FLT3-ITD patients displaying lower PP2A activity than WT-FLT3 blasts. Reduced PP2A activity was associated with hyperphosphorylation of the PP2A catalytic subunit, and reduced expression of PP2A structural and regulatory subunits. AML patient blasts were also sensitive to cell death induced by FTY720 and AAL(S), but these compounds had minimal effect on normal CD34+ bone marrow derived monocytes. Finally, PP2A activating compounds displayed synergistic effects when used in combination with tyrosine kinase inhibitors in FLT3-ITD+ cells. A combination of Sorafenib and FTY720 was also synergistic in the presence of a protective stromal microenvironment. Thus combining a PP2A activating compound and a FLT3 inhibitor may be a novel therapeutic approach for treating AML.

DOI 10.18632/oncotarget.10167
Citations Scopus - 24Web of Science - 22
Co-authors Kathryn Skelding, Nikki Verrills, Matt Dun, Leonie Ashman
2015 Enjeti AK, Chapman K, Taylor PJ, Meldrum C, 'Congenital late onset thrombotic thrombocytopenic purpura: A diagnostic challenge', Pathology, 47 585-586 (2015) [C3]
DOI 10.1097/PAT.0000000000000303
2015 Enjeti A, Granter N, Ashraf A, Fletcher L, Branford S, Rowlings P, Dooley S, 'A longitudinal evaluation of performance of automated BCR-ABL1 quantitation using cartridge-based detection system', Pathology, 47 570-574 (2015)

Copyright © 2015 Royal College of Pathologists of Australasia. All rights reserved. An automated cartridge-based detection system (GeneXpert; Cepheid) is being widely adopted in l... [more]

Copyright © 2015 Royal College of Pathologists of Australasia. All rights reserved. An automated cartridge-based detection system (GeneXpert; Cepheid) is being widely adopted in low throughput laboratories for monitoring BCR-ABL1 transcript in chronic myelogenous leukaemia. This Australian study evaluated the longitudinal performance specific characteristics of the automated system.The automated cartridge-based system was compared prospectively with the manual qRT-PCR-based reference method at SA Pathology, Adelaide, over a period of 2.5 years. A conversion factor determination was followed by four re-validations. Peripheral blood samples (n = 129) with international scale (IS) values within detectable range were selected for assessment. The mean bias, proportion of results within specified fold difference (2-, 3- and 5-fold), the concordance rate of major molecular remission (MMR) and concordance across a range of IS values on paired samples were evaluated.The initial conversion factor for the automated system was determined as 0.43. Except for the second re-validation, where a negative bias of 1.9-fold was detected, all other biases fell within desirable limits. A cartridge-specific conversion factor and efficiency value was introduced and the conversion factor was confirmed to be stable in subsequent re-validation cycles. Concordance with the reference method/laboratory at >0.1-=10 IS was 78.2% and at =0.001 was 80%, compared to 86.8% in the >0.01-=0.1 IS range. The overall and MMR concordance were 85.7% and 94% respectively, for samples that fell within ± 5-fold of the reference laboratory value over the entire period of study.Conversion factor and performance specific characteristics for the automated system were longitudinally stable in the clinically relevant range, following introduction by the manufacturer of lot specific efficiency values.

DOI 10.1097/PAT.0000000000000293
Citations Scopus - 6Web of Science - 7
2014 Berry NK, Bain NL, Enjeti AK, Rowlings P, 'Genomic profiling of plasma cell disorders in a clinical setting: integration of microarray and FISH, after CD138 selection of bone marrow', JOURNAL OF CLINICAL PATHOLOGY, 67 66-69 (2014) [C1]
DOI 10.1136/jclinpath-2013-201691
Citations Scopus - 10Web of Science - 9
2013 Alkhatatbeh MJ, Enjeti AK, Acharya S, Thorne RF, Lincz LF, 'The origin of circulating CD36 in type 2 diabetes', NUTRITION & DIABETES, 3 (2013) [C1]
DOI 10.1038/nutd.2013.1
Citations Scopus - 36Web of Science - 34
Co-authors Rick Thorne, Lisa Lincz
2012 Lincz L, Scorgie FE, Enjeti A, Seldon M, 'Variable plasma levels of Factor V Leiden correlate with circulating platelet microparticles in carriers of Factor V Leiden', Thrombosis Research, 129 192-196 (2012) [C1]
Citations Scopus - 6Web of Science - 6
Co-authors Lisa Lincz
2011 Alkhatatbeh MJ, Mhaidat NM, Enjeti AK, Lincz L, Thorne RF, 'The putative diabetic plasma marker, soluble CD36, is non-cleaved, non-soluble and entirely associated with microparticles', Journal of Thrombosis and Haemostasis, 9 844-851 (2011) [C1]
DOI 10.1111/j.1538-7836.2011.04220.x
Citations Scopus - 38Web of Science - 36
Co-authors Rick Thorne, Lisa Lincz
2011 Upanal NN, Enjeti A, 'Primary lymphoma of the uterus and cervix: Two case reports and review of the literature', Australian and New Zealand Journal of Obstetrics and Gynaecology, 51 559-562 (2011) [C3]
DOI 10.1111/j.1479-828x.2011.01365.x
Citations Scopus - 17
2010 Enjeti A, Lincz L, Scorgie FE, Seldon MR, 'Circulating microparticles are elevated in carriers of Factor V Leiden', Thrombosis Research, 126 250-253 (2010) [C1]
DOI 10.1016/j.thromres.2009.11.019
Citations Scopus - 10Web of Science - 9
Co-authors Lisa Lincz
2008 Enjeti AK, Lincz L, Seldon MR, 'Bio-maleimide as a generic stain for detection and quantitation of microparticles', International Journal of Laboratory Hematology, 30 196-199 (2008) [C1]
DOI 10.1111/j.1751-553x.2007.00937.x
Citations Scopus - 23Web of Science - 21
Co-authors Lisa Lincz
2008 Enjeti AK, Lincz L, Seldon MR, 'Microparticles in health and disease', Seminars in Thrombosis and Haemostasis, 34 683-692 (2008) [C1]
DOI 10.1055/s-0028-1104547
Citations Scopus - 61Web of Science - 62
Co-authors Lisa Lincz
2007 Enjeti AK, Lincz L, Seldon M, 'Detection and measurement of microparticles: An evolving research tool for vascular biology', Seminars in Thrombosis and Hemostasis, 33 771-779 (2007) [C1]
DOI 10.1055/s-2007-1000369
Citations Scopus - 92Web of Science - 88
Co-authors Lisa Lincz
2005 Enjeti AK, Walsh M, Seldon M, 'Spontaneous major bleeding in acquired factor X deficiency secondary to AL-amyloidosis', HAEMOPHILIA, 11 535-538 (2005)
DOI 10.1111/j.1365-2516.2005.01125.x
Citations Scopus - 16Web of Science - 16
2005 Enjeti AK, Seldon M, Braye S, 'Bilateral breast lumps in a patient after sex mismatched allogeneic transplantation for aplastic anaemia', JOURNAL OF CLINICAL PATHOLOGY, 58 670-671 (2005)
Citations Scopus - 2Web of Science - 2
2004 Enjeti AK, Tien SL, Sivaswaren CR, 'Cytogenetic abnormalities in de novo acute myeloid leukemia in adults: Relation to morphology, age, sex and ethnicity - A single center study from Singapore', Hematology Journal, 5 419-425 (2004)

Background: Cytogenetic analysis performed at diagnosis is considered to be the most valuable prognostic factor in acute myeloid leukemia (AML). Large systematic studies of cytoge... [more]

Background: Cytogenetic analysis performed at diagnosis is considered to be the most valuable prognostic factor in acute myeloid leukemia (AML). Large systematic studies of cytogenetic abnormalities in AML patients from Southeast Asia are not available. The karyotypic patterns in AML patients from a single center in Singapore were studied and compared with reports from other regions of the world to identify possible geographic heterogeneity. Methods: Analysis was performed on 501 consecutive de novo AML patients diagnosed according to the FAB criteria in the Singapore General Hospital. The cytogenetic findings were analyzed for possible associations between karyotypic pattern and the age, gender, ethnicity as well as morphological (FAB) subtypes. Results: A total of 454 patients were studied of which 275(61%) had abnormal cytogenetics (median age 48 years). The t(15;17) and trisomy 8 were the most frequent karyotypic abnormalities - seen in 52(11%) and 33(7.3%) cases, respectively. Inv(16) and t(16;16) were uncommon, seen only in five (1.1%) cases. The abnormalities del 5/5q and del 7/7q were seen in 30(6.6%) and 32(7%) of the cases. Complex karyotypes were seen in 78(17%) of the cases. Recurrent cytogenetic abnormalities correlated with the FAB subtypes. In all, 21 novel cytogenetic abnormalities were observed. Conclusions: Certain differences such as the age at presentation and frequency of recurrent balanced translocations were noted in comparison to previous reports. These point to the need for extensive epidemiological studies to clarify the role of genetic as well as geographic heterogeneity in the pathogenesis of AML. © 2004 The European Hematology Association All rights reserved.

DOI 10.1038/sj.thj.6200544
Citations Scopus - 20
Show 36 more journal articles

Conference (29 outputs)

Year Citation Altmetrics Link
2019 Enjeti AK, Ariyarajah A, D'Crus A, Riveros C, Seldon M, Lincz LF, 'Circulating microvesicles are less procoagulant and carry different miRNA cargo in myelodysplasia', BLOOD CELLS MOLECULES AND DISEASES (2019)
DOI 10.1016/j.bcmd.2018.11.001
Co-authors Lisa Lincz, Carlos Riveros
2019 Murray HC, Enjeti AK, Kahl RGS, Flanagan HM, Dun MD, Verrills NM, 'Phosphoproteomic Characterisation of Acute Myeloid Leukaemia (AML)', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2019)
Co-authors Matt Dun
2019 Fodeades AA, Berry NK, Chamberlain J, Maley P, Enjeti AK, Scott RJ, 'Detection of an IKZF1(Plus) Paediatric B-ALL and the Impact on Clinical Management: A Case Study', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2019)
Co-authors Rodney Scott
2018 Enjeti AK, 'Tears, Sweat and Blood', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2018)
2018 Berry N, Scott R, Sutton R, Trahair TN, Rowlings P, Enjeti AK, 'Australian AIEOP-BFM 2009 Acute Lymphoblastic Leukemia High-Risk Findings Enrichment of IKZF1 Deletions and Other Curious Findings', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2018)
Co-authors Rodney Scott
2018 Wei A, Strickland SA, Hou J-Z, Fiedler W, Lin TL, Walter RB, et al., 'Venetoclax with Low-Dose Cytarabine Induces Rapid, Deep, and Durable Responses in Previously Untreated Older Adults with AML Ineligible for Intensive Chemotherapy', BLOOD, San Diego, CA (2018)
DOI 10.1182/blood-2018-99-118729
Citations Web of Science - 13
2018 Murray H, Enjeti AK, Kahl R, Flanagan H, Verrills N, Dun M, 'Combinatorial Targeting of the c-KIT Receptor Tyrosine Kinase in Acute Myeloid Leukemia', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2018)
Co-authors Matt Dun, Nikki Verrills
2017 Rigby C, Toop H, Al Mazi J, Morris J, Enjeti A, Verrills N, Dun M, 'Novel PP2A Inhibitory Protein in C-KIT Mutant Myeloid Progenitor Cells', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2017)
Co-authors Matt Dun
2017 Murray H, Kahl R, Smith N, Enjeti A, Larsen M, Verrills N, Dun M, 'Targeting Error-Prone DNA Double-Strand Break Repair in Acute Myeloid Leukaemia (AML)', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2017)
Co-authors Matt Dun
2017 Berry N, Scott R, Sutton R, Trahair T, Rowlings P, Enjeti A, 'HD-SNP Microarray Analysis of the Study 9 High-Risk all Patients - Increased Yield of Important Prognostic Information', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2017)
Co-authors Rodney Scott
2017 Berry N, Dixon-McIver A, Scott R, Ziolkowski A, Enjeti A, 'Evaluation of Integrating HD-SNP Microarray into the Workflow for CLL and MM: Challenges and Culture Changes', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2017)
Co-authors Rodney Scott
2016 Sillar J, Murray H, Al Mazi J, Skerrett-Byrne D, Kahl R, Flanagan H, et al., 'QUANTITATIVE, HIGH-RESOLUTION PROTEOMICS FOR A SYSTEMS BIOLOGICAL ANALYSIS OF ACUTE MYELOID LEUKEMIA', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2016)
Co-authors Hubert Hondermarck, David Skerrett-Byrne, Matt Dun
2016 Berry N, Scott R, Enjeti A, 'HD-SNP MICROARRAY ANALYSIS OF THE STUDY NINE HIGH-RISK ALL PATIENTS - PROVIDING KEY PROGNOSTIC INFORMATION USING ARRAYS', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2016)
Co-authors Rodney Scott
2016 Enjeti A, Ariyarajah A, D'Crus A, Seldon M, Lincz L, 'Circulating Microvesicle Number, Function and Small RNA Content Vary with Age, Gender, Lipid, Hormone Profile and Smoking Status', BLOOD, San Diego, CA (2016)
DOI 10.1182/blood.V128.22.4951.4951
Co-authors Lisa Lincz
2016 Hall AE, Paul C, Bryant J, Lynagh MC, Rowlings P, Enjeti A, Small H, 'To adhere or not to adhere: Rates and reasons of medication adherence in hematological cancer patients', CRITICAL REVIEWS IN ONCOLOGY HEMATOLOGY (2016) [C1]
DOI 10.1016/j.critrevonc.2015.08.025
Citations Scopus - 24Web of Science - 20
Co-authors Chris Paul, Jamie Bryant, Marita Lynagh
2016 Murray H, Al Mazi J, Kahl R, Flanagan H, Smith N, Enjeti A, et al., 'DNA-PK INHIBITION SENSITIZES FLT3-ITD AML CELLS TO CYTARABINE AND SORAFENIB', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2016)
Co-authors Matt Dun
2016 Lim MS, Enjeti AK, Lemmert K, 'Case report of blastic plasmacytoid dendritic cell neoplasm (BPDCN) a rare entity.', Pathology, England (2016)
DOI 10.1016/j.pathol.2015.12.284
2015 Dun M, Murray H, Al-mazi J, Kahl R, Flanagan H, Smith N, et al., 'IDENTIFICATION AND SYNERGISTIC TARGETING OF FLT3-ACTIVATED PATHWAYS IN ACUTE MYELOID LEUKAEMIA', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2015) [E3]
Co-authors Matt Dun, Nikki Verrills
2015 Ashraf A, Enjeti A, Hasnat M, Rowlings P, 'ASSESSMENT OF BLOOD TRANSFUSION PRACTICES IN PATIENTS WITH MYELODYSPLASTIC SYNDROMES IN THE ERA OF HYPOM-ETHYLATING AGENTS', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2015) [E3]
2015 Ashraf A, Enjeti A, Hasnat M, Rowlings P, 'ASSESSMENT OF EPIDEMIOLOGIC PROFILE OF PATIENTS WITH MYELODYSPLASTIC SYNDROMES IN HUNTER REGION', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2015) [E3]
2015 Rigby C, Kahl R, Flanagan H, Li X, Enjeti A, Verrills N, Dun M, 'CHARACTERISATION OF A NOVEL PP2A INHIBITORY ONCOPROTEIN IN ACUTE MYELOID LEUKAEMIA (AML)', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2015) [E3]
Co-authors Matt Dun, Nikki Verrills
2014 Yoon E-J, Chi MN, Enjeti AK, Verrills NM, Skelding KA, 'CHARACTERISING A NEW TARGET FOR THE TREATMENT OF ACUTE LEUKAEMIAS', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2014) [E3]
Co-authors Nikki Verrills, Kathryn Skelding
2014 Dun MD, Kahl RGS, Flanagan H, Cairns MMJ, Smith ND, Enjeti AK, et al., 'IDENTIFICATION OF ONCOGENIC SIGNALLING PATHWAYS IN ACUTE MYELOID LEUKAEMIA (AML) PATIENTS BY PHOSPHOPROTEOMICS', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2014) [E3]
Co-authors Matt Dun, Nikki Verrills, Murray Cairns
2013 Enjeti A, D'Cruz A, Seldon M, Lincz L, 'Circulating microparticle number and function vary with age: a study of 120 healthy blood donors', JOURNAL OF THROMBOSIS AND HAEMOSTASIS (2013) [E3]
Co-authors Lisa Lincz
2012 Kaithal Shahir A, Asharaf A, Yachmenikova V, Campbell T, Nanra RS, Gillies AH, et al., 'Very late onset, EBV driven, primary, intracranial hodgin-like post-transplant lymphoproliferative disorder (HL-PTLD) in a kidney transplant recipient', Immunology and Cell Biology: Abstracts of the 30th Annual Scientific Meeting of the Transplantation Society of Australia and New Zealand, Canberra, ACT (2012) [E3]
2011 Alkhatatbeh MJ, Mhaidat NM, Enjeti AK, Lincz LF, Thorne RF, 'Circulating plasma CD36+microparticles as a marker of type 2 diabetes and its complications', Clinical Biochemistry, Mashhad, Iran (2011) [E3]
Co-authors Rick Thorne, Lisa Lincz
2009 Enjeti A, 'Microparticles: Measuring up the miniature markers', Journal of Vascular Research, Queenstown, NZ (2009) [E3]
2008 Enjeti A, Lincz L, Scorgie F, Seldon M, 'Miniature microparticles measuring less than 0.1 um exist in human plasma and contribute to procoagulant activity', International Journal of Laboratory Hematology, Sydney, NSW (2008) [E3]
Co-authors Lisa Lincz
2008 Enjeti A, Scorgie FE, Lincz L, Brown S, Isbister GK, Seldon MR, 'Circulating microparticles in snake bite patients with microangiopathy', 50th ASH Annual Meeting and Exposition. Online Program and Abstracts, San Francisco, CA (2008) [E3]
Co-authors Lisa Lincz, Geoffrey Isbister
Show 26 more conferences
Edit

Grants and Funding

Summary

Number of grants 36
Total funding $3,345,830

Click on a grant title below to expand the full details for that specific grant.


20202 grants / $796,610

Targeting DNA-PK in acute myeloid leukaemia$741,610

Funding body: NHMRC (National Health & Medical Research Council)

Funding body NHMRC (National Health & Medical Research Council)
Project Team

Nikki Verrills and Anoop Enjeti

Scheme Ideas Grant
Role Investigator
Funding Start 2020
Funding Finish 2023
GNo
Type Of Funding C1100 - Aust Competitive - NHMRC
Category 1100
UON N

Multiple Myeloma Equipment Grant$55,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Anoop Enjeti
Scheme Equipment Grant
Role Lead
Funding Start 2020
Funding Finish 2020
GNo G2000004
Type Of Funding C3120 - Aust Philanthropy
Category 3120
UON Y

20192 grants / $203,800

Funding Support from NSW Health Pathology, North – Hunter PPTF for post doc position$183,800

Funding body: NSW Health Pathology - Pathology North

Funding body NSW Health Pathology - Pathology North
Project Team Doctor Anoop Enjeti
Scheme Research Grant
Role Lead
Funding Start 2019
Funding Finish 2020
GNo G1900921
Type Of Funding C2210 - Aust StateTerritoryLocal - Own Purpose
Category 2210
UON Y

An A(r)Ray of hope for paediatric ALL$20,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Dr Andrew Ziolkowski, Doctor Anoop Enjeti, Doctor Frank Alvaro, Doctor Janis Chamberlain, Doctor Liz Hesketh, Miss Nadine Berry
Scheme Project Grant
Role Lead
Funding Start 2019
Funding Finish 2019
GNo G1900572
Type Of Funding C3120 - Aust Philanthropy
Category 3120
UON Y

20184 grants / $101,670

Predicting tOxicity for Myeloma Therapy (PrOMT)$50,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Anoop Enjeti, Doctor Wojt Janowski, Doctor Chen Chen Jiang, Associate Professor Aaron Sverdlov
Scheme Project Grant
Role Lead
Funding Start 2018
Funding Finish 2018
GNo G1900030
Type Of Funding C3120 - Aust Philanthropy
Category 3120
UON Y

Targeting Reactive Oxygen Species Generation as a Novel Treatment Target in Acute Myeloid Leukaemia - RA support$25,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Matt Dun, Doctor Jonathan Sillar, Doctor Anoop Enjeti, Associate Professor Nikki Verrills
Scheme Project Grant
Role Investigator
Funding Start 2018
Funding Finish 2018
GNo G1800399
Type Of Funding C3112 - Aust Not for profit
Category 3112
UON Y

Investigating the role of stromal heterogeneity in Myelodysplastic Syndrome following Azacitadine therapy $20,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Danielle Bond, Doctor Heather Lee, Doctor Anoop Enjeti
Scheme Project Grant
Role Investigator
Funding Start 2018
Funding Finish 2018
GNo G1801353
Type Of Funding C3120 - Aust Philanthropy
Category 3120
UON Y

Haematology Research$6,670

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Anoop Enjeti, Miss Nadine Berry
Scheme Project Grant
Role Lead
Funding Start 2018
Funding Finish 2018
GNo G1800485
Type Of Funding C3120 - Aust Philanthropy
Category 3120
UON Y

20178 grants / $1,151,850

Beyond the Next Generation of DNA Sequencing: Long Read Sequencing using Sequel$570,000

Funding body: Cancer Institute NSW

Funding body Cancer Institute NSW
Project Team Laureate Professor Rodney Scott, Professor Hubert Hondermarck, Associate Professor Kevin Spring, Doctor Anoop Enjeti, Mr Ricardo Vilain, Professor Christopher Scarlett, Doctor Kelly Kiejda, Doctor Heather Lee, Professor Simon Keely, Doctor Lei Jin
Scheme Research Equipment Grant
Role Investigator
Funding Start 2017
Funding Finish 2017
GNo G1700427
Type Of Funding C2210 - Aust StateTerritoryLocal - Own Purpose
Category 2210
UON Y

Translational Research Fellowship grant$360,000

Funding body: NSW Health Pathology - Pathology North

Funding body NSW Health Pathology - Pathology North
Scheme HNE LHD/ CMN/ HCRA/ Pathology NSW- Hunter translational research fellowship
Role Lead
Funding Start 2017
Funding Finish 2020
GNo
Type Of Funding Other Public Sector - Local
Category 2OPL
UON N

Genome wide approach to risk assess Multiple Myeloma and precursor plasma cell disorders$50,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Anoop Enjeti, Miss Nadine Berry, Laureate Professor Rodney Scott, Doctor Wojt Janowski, Conjoint Professor Philip Rowlings
Scheme Project Grant
Role Lead
Funding Start 2017
Funding Finish 2017
GNo G1701577
Type Of Funding C3120 - Aust Philanthropy
Category 3120
UON Y

Research Equipment grant (Tape station)$50,000

Funding body: Faculty of Health, University of Newcastle

Funding body Faculty of Health, University of Newcastle
Scheme Faculty of Health, Equipment Grant
Role Investigator
Funding Start 2017
Funding Finish 2018
GNo
Type Of Funding Other Public Sector - Local
Category 2OPL
UON N

Rural Supplementation grant$49,850

Funding body: RCPA

Funding body RCPA
Scheme Education and training grant
Role Lead
Funding Start 2017
Funding Finish 2018
GNo
Type Of Funding Other Public Sector - Commonwealth
Category 2OPC
UON N

Re-purposing PARP inhibitors to treat childhood leukaemias$25,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Associate Professor Kathryn Skelding, Associate Professor Nikola Bowden, Doctor Lisa Lincz, Doctor Anoop Enjeti, Doctor Frank Alvaro
Scheme Project Grant
Role Investigator
Funding Start 2017
Funding Finish 2017
GNo G1701561
Type Of Funding C3120 - Aust Philanthropy
Category 3120
UON Y

Determining the mechanisms underpinning leukaemic transformation for children suffering from Shwachman-Diamond Syndrome (SDS)$25,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Matt Dun, Associate Professor Nikki Verrills, Doctor Bryony Ross, Doctor Anoop Enjeti, Dr Jeremy Robertson
Scheme Project Grant
Role Investigator
Funding Start 2017
Funding Finish 2017
GNo G1701574
Type Of Funding C3120 - Aust Philanthropy
Category 3120
UON Y

Research Fellowship Grant$22,000

Funding body: Hunter Cancer Research Alliance (HCRA)

Funding body Hunter Cancer Research Alliance (HCRA)
Scheme Fellowship grant
Role Lead
Funding Start 2017
Funding Finish 2018
GNo
Type Of Funding Other Public Sector - Local
Category 2OPL
UON N

20152 grants / $73,400

Rural supplementation grant$49,000

Funding body: RCPA

Funding body RCPA
Scheme Education and training grant
Role Lead
Funding Start 2015
Funding Finish 2016
GNo
Type Of Funding Aust Competitive - Non Commonwealth
Category 1NS
UON N

Clinical Research fellowship$24,400

Funding body: Hunter Cancer Research Alliance (HCRA)

Funding body Hunter Cancer Research Alliance (HCRA)
Scheme Fellowship grant
Role Lead
Funding Start 2015
Funding Finish 2015
GNo
Type Of Funding Other Public Sector - Local
Category 2OPL
UON N

20143 grants / $357,000

Novel Agents in AML$200,000

Funding body: Cure Cancer Australia Foundation

Funding body Cure Cancer Australia Foundation
Scheme Project Grant
Role Investigator
Funding Start 2014
Funding Finish 2015
GNo
Type Of Funding Aust Competitive - Non Commonwealth
Category 1NS
UON N

Post Graduate Fellowship funding$100,000

Funding body: Hunter Area Pathology Service

Funding body Hunter Area Pathology Service
Scheme PTTF research grants
Role Lead
Funding Start 2014
Funding Finish 2015
GNo
Type Of Funding Other Public Sector - Local
Category 2OPL
UON N

Rural supplementation grants$57,000

Funding body: RCPA

Funding body RCPA
Scheme Education and training grant
Role Lead
Funding Start 2014
Funding Finish 2015
GNo
Type Of Funding Aust Competitive - Non Commonwealth
Category 1NS
UON N

20134 grants / $158,250

Postgraduate registrar/fellow funding$50,000

Funding body: Hunter Area Pathology Service

Funding body Hunter Area Pathology Service
Scheme PTTF research grants
Role Lead
Funding Start 2013
Funding Finish 2014
GNo
Type Of Funding Other Public Sector - Local
Category 2OPL
UON N

Microparticles research equipment grant$50,000

Funding body: Hunter Area Pathology Service

Funding body Hunter Area Pathology Service
Scheme PTTF research grants
Role Lead
Funding Start 2013
Funding Finish 2014
GNo
Type Of Funding Other Public Sector - Local
Category 2OPL
UON N

Myeloma genomic profiling research grant$48,250

Funding body: Hunter Area Pathology Service

Funding body Hunter Area Pathology Service
Scheme PTTF research grants
Role Lead
Funding Start 2013
Funding Finish 2014
GNo
Type Of Funding Other Public Sector - Local
Category 2OPL
UON N

Mater research equipment grant$10,000

Funding body: Calvary Mater Newcastle

Funding body Calvary Mater Newcastle
Scheme 2013 equipment funds
Role Lead
Funding Start 2013
Funding Finish 2014
GNo
Type Of Funding Other Public Sector - Local
Category 2OPL
UON N

20123 grants / $71,750

Microparticles in Thrombosis and Haemostasis$51,750

Funding body: Hunter Area Pathology Service

Funding body Hunter Area Pathology Service
Scheme PTTF research grants
Role Lead
Funding Start 2012
Funding Finish 2013
GNo
Type Of Funding Other Public Sector - Local
Category 2OPL
UON N

Review grant for FTY720 in acute myeloid leukemia$10,000

Funding body: HTCRU

Funding body HTCRU
Scheme HTCRU research grant
Role Lead
Funding Start 2012
Funding Finish 2013
GNo
Type Of Funding Aust Competitive - Non Commonwealth
Category 1NS
UON N

Review grant for medication adherence in CML$10,000

Funding body: HTCRU

Funding body HTCRU
Scheme HTCRU research grants
Role Investigator
Funding Start 2012
Funding Finish 2013
GNo
Type Of Funding Aust Competitive - Non Commonwealth
Category 1NS
UON N

20112 grants / $325,000

Targeting PP2A as a Novel Therapeutic Strategy for mutant FLT3+ Acute Myeloid Leukaemia$300,000

Funding body: Cancer Council NSW

Funding body Cancer Council NSW
Scheme Project Grant
Role Investigator
Funding Start 2011
Funding Finish 2012
GNo
Type Of Funding Aust Competitive - Non Commonwealth
Category 1NS
UON N

Genomics in Myeloma$25,000

Funding body: Hunter Area Pathology Service

Funding body Hunter Area Pathology Service
Scheme PTTF research grants
Role Lead
Funding Start 2011
Funding Finish 2012
GNo
Type Of Funding Other Public Sector - Local
Category 2OPL
UON N

20101 grants / $25,000

Targeting PP2A as a Novel Therapeutic Strategy for mutant FLT3+ Acute Myeloid Leukaemia$25,000

Funding body: Hunter Medical Research Institute (HMRI)

Funding body Hunter Medical Research Institute (HMRI)
Scheme Project Grant
Role Investigator
Funding Start 2010
Funding Finish 2011
GNo
Type Of Funding Other Public Sector - Local
Category 2OPL
UON N

20082 grants / $41,500

ANZSBT research grants$31,500

Funding body: ANZSBT

Funding body ANZSBT
Scheme Research Grants
Role Lead
Funding Start 2008
Funding Finish 2009
GNo
Type Of Funding Aust Competitive - Non Commonwealth
Category 1NS
UON N

RCPA research grant for Investigation into Microparticles$10,000

Funding body: RCPA

Funding body RCPA
Scheme Research Grant
Role Lead
Funding Start 2008
Funding Finish 2009
GNo
Type Of Funding Aust Competitive - Non Commonwealth
Category 1NS
UON N

20072 grants / $30,000

Hunter Area Pathology Service PTTF grants$20,000

Funding body: Hunter Area Pathology Service

Funding body Hunter Area Pathology Service
Scheme PTTF research grants
Role Lead
Funding Start 2007
Funding Finish 2008
GNo
Type Of Funding Other Public Sector - Local
Category 2OPL
UON N

ANZSBT Research Grant for Microparticles research$10,000

Funding body: ANZSBT

Funding body ANZSBT
Scheme Research Grants
Role Lead
Funding Start 2007
Funding Finish 2008
GNo
Type Of Funding Aust Competitive - Non Commonwealth
Category 1NS
UON N

20061 grants / $10,000

Jane Reid Harle$10,000

Funding body: Calvary Mater Newcastle

Funding body Calvary Mater Newcastle
Scheme Research Grants
Role Lead
Funding Start 2006
Funding Finish 2007
GNo
Type Of Funding Aust Competitive - Non Commonwealth
Category 1NS
UON N
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Research Supervision

Number of supervisions

Completed0
Current4

Current Supervision

Commenced Level of Study Research Title Program Supervisor Type
2017 PhD Targeting Cancer-Initiating Cells with DNA Methyltransferase Inhibitors: Single-cell Analysis to Decipher Molecular Mechanisms and Improve Efficacy PhD (Medical Genetics), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor
2016 PhD Reactive Oxygen Species Promoted Leukaemogenesis; Altered Signalling Pathways as New Drug Targets for the Improved Treatment of Acute Myeloid Leukaemia PhD (Medical Biochemistry), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor
2016 Masters Myelodysplastic Syndromes and Utilisation of Blood Products in the Era of Hypomethylating Agents M Philosophy (Medicine), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor
2014 PhD Clinical Use of SNP-microarrays for the Detection of Genome-wide Changes in Haematological Malignancies PhD (Medical Genetics), Faculty of Health and Medicine, The University of Newcastle Principal Supervisor
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Research Opportunities

Research studentships - honours, masters

Leukemia, myelodysplasia and translational genomics ; Haemostasis and Thrombosis

Research Masters

Faculty Of Health

1/2/2018 - 1/6/2020

Contact

Doctor Anoop Enjeti


anoop.enjeti@newcastle.edu.au

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Dr Anoop Enjeti

Position

Conjoint Associate Professor
Calvary Mater Newcastle, NSW Health Pathology , HCRA Translational research Fellow
School of Medicine and Public Health
Faculty of Health and Medicine

Contact Details

Email anoop.enjeti@newcastle.edu.au
Phone (02) 40143021
Fax (02) 49602136

Office

Room Level 4 New Med Building Calvary Mater Newcastle
Location Level 4 Calvary Mater Newcastle and Level 3 HMRI

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