Dr Anoop Enjeti

Dr Anoop Enjeti

Conjoint Senior Lecturer

School of Medicine and Public Health

Career Summary

Biography

MBBS   MD (Pondicherry Univ.)   FRCP (UK)  FRCPA  FASCP FACP  M Clin 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)

Clinical Appointment: Senior Staff Specialist   Haematologist Calvary Mater Hospital Newcastle

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

Conjoint Appointment:Conjoint Senior Lecturer, University of Newcastle

Dr Enjeti obtained his postgraduate physician qualifications from the UK Royal College of Physicians and specialist haematology from the Royal College of Pathologists of Australasia (2006). His physician and specialist haematology training has spanned across India, UK, Singapore and Australia including specialist training in genetics and molecular genetics where he has contributed to a high impact publication outlining geographical variations in AML genetics. Other training includes a MD in Pathology (Pondicherry University 2001), GradCert in Bioethics (Monash, 2012) as well as Masters in Clinical Epidemiology (Molecular Genetics, University of Newcastle 2010). Dr Enjeti is currently employed as a clinical haematologist at the Calvary Mater Hospital, with a special interest in acute myeloid leukaemia and myeloidysplasia. He is an active member of the Hunter Cancer Research Alliance (HCRA) where he has established active collaborations with cancer researchers locally and across the state.  He has over 25 peer-reviewed publications, numerous conference  presentations and three book chapters. He is 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. Dr Enjeti 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. His research focus includes  early phase clinical trials in haematological malignancies( AML/MDS) and translational diagnostics as well as in  circulating microvesicles and their impact on thrombosis/cancer/abnormal clonal haemopoiesis. 



Keywords

  • Acute Leukemia and Myelodysplasia
  • Genomics for Haematological malignancies
  • Thrombosis and Haemostasis

Fields of Research

Code Description Percentage
060408 Genomics 30
110202 Haematology 70

Professional Experience

Academic appointment

Dates Title Organisation / Department
1/07/2017 -  Translational Research Fellow NSW Health Pathology - Pathology North
1/01/2014 -  Conjoint Senior Lecturer Faculty of Health and Medicine, University of Newcastle
School of Medicine and Public Health
Australia

Professional appointment

Dates Title Organisation / Department
6/01/2017 -  Staff Specialist NSW Health Pathology - Pathology North
6/01/2017 -  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 (25 outputs)

Year Citation Altmetrics Link
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.', Semin Thromb Hemost, 43 836-848 (2017)
DOI 10.1055/s-0037-1604085
Citations Scopus - 1Web of Science - 1
Co-authors Christopher Oldmeadow, Alix Hall
2017 Ayyalil F, Irwin G, Ross B, Manolis M, Enjeti AK, 'Zeroing in on red blood cell unit expiry', Transfusion, (2017)

© 2017 AABB. BACKGROUND: Expiry of red blood cell (RBC) units is a significant contributor to wastage of precious voluntary donations. Effective strategies aimed at optimal resou... [more]

© 2017 AABB. BACKGROUND: Expiry of red blood cell (RBC) units is a significant contributor to wastage of precious voluntary donations. Effective strategies aimed at optimal resource utilization are required to minimize wastage. STUDY DESIGN AND METHODS: This retrospective study analyzed the strategic measures implemented to reduce expiry of RBC units in an Australian tertiary regional hospital. The measures, which included inventory rearrangement, effective stock rotation, and the number of emergency courier services required during a 24-month period, were evaluated. RESULTS: There was no wastage of RBC units due to expiry over the 12 months after policy changes. Before these changes, approximately half of RBC wastage (261/511) was due to expiry. The total number of transfusions remained constant in this period and there was no increase in the use of emergency couriers. Policy changes implemented were decreasing the RBC inventory level by one-third and effective stock rotation and using a computerized system to link the transfusion services across the area. Effective stock rotation resulted in a reduction in older blood ( > 28 days) received in the main laboratory rotated from peripheral hospitals, down from 6%-41% to 0%-2.5%. CONCLUSION: Age-related expiry of blood products is preventable and can be significantly reduced by improving practices in the pathology service. This study provides proof of principle for "zero tolerance for RBC unit expiry" across a large networked blood banking service.

DOI 10.1111/trf.14321
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 th... [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 phosphatidyls erine (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
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
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 (P... [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 - 3Web of Science - 3
Co-authors Nikki Verrills
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, 97 247-262 (2016) [C1]
DOI 10.1016/j.critrevonc.2015.08.025
Citations Web of Science - 5
Co-authors Alix Hall, Marita Lynagh, Chris Paul
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 functiona... [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 (r s, Spearman rank order correlation was 0.29, 0.40, 0.31 and 0.34 respectively, p¿ < ¿0.05), and MV expressing tissue factor (r s 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 (r s, was 0.35,0.30 and 0.3, respectively, p¿ < ¿0.05). Lagtime and ttPEAK negatively correlated with the clot based XaCT test (r s, was -¿0.34 and -¿0.30 respectively, p¿ < ¿0.05) and positively correlated with the ELISA MP-activity assay (r s ¿=¿0.42 for both, p¿ < ¿0.05). In addition, endothelial MV levels weakly correlated with white cell counts (r s = 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 - 2Web of Science - 2
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 spike... [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 - 3Web of Science - 2
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 - 1Web of Science - 3
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 - 5Web of Science - 4
Co-authors Leonie Ashman, Kathryn Skelding, Matt Dun, Nikki Verrills
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 ... [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 Pat hology, 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 - 4Web of Science - 6
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 - 6Web of Science - 5
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 - 22Web of Science - 22
Co-authors Lisa Lincz, Rick Thorne
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 - 4Web of Science - 4
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 - 28Web of Science - 30
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 - 9Web 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 - 17Web of Science - 17
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 - 58Web of Science - 58
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 - 90Web of Science - 84
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 - 15Web 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 - 17
Show 22 more journal articles

Conference (12 outputs)

Year Citation Altmetrics Link
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]
Co-authors Milton Hasnat
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]
Co-authors Milton Hasnat
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 Kathryn Skelding, Nikki Verrills
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 Murray Cairns, Matt Dun, Nikki Verrills
2014 Hall AE, Paul C, Bryant J, Lynagh M, Rowlings P, Enjeti AK, et al., 'TO ADHERE OR NOT TO ADHERE: RATES AND FACTORS IMPACTING ON MEDICATION ADHERENCE IN HAEMATOLOGICAL CANCER PATIENTS', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2014) [E3]
Citations Scopus - 7
Co-authors Chris Paul, Marita Lynagh, Alix Hall
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]
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Grants and Funding

Summary

Number of grants 29
Total funding $2,293,750

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


20179 grants / $1,201,850

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, Associate Professor Christopher Scarlett, Doctor Kelly Kiejda, Doctor Heather Lee, Associate Professor Simon Keely, Doctor Lei Jin
Scheme Research Equipment Grant
Role Investigator
Funding Start 2017
Funding Finish 2017
GNo G1700427
Type Of Funding Other Public Sector - State
Category 2OPS
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 Grant - Aust Non Government
Category 3AFG
UON Y

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

Funding body: Hunter Medical Research Institute (HMRI)

Funding body Hunter Medical Research Institute (HMRI)
Scheme Project Grant
Role Lead
Funding Start 2017
Funding Finish 2018
GNo
Type Of Funding Other Public Sector - Local
Category 2OPL
UON N

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 Doctor Kathryn Skelding, Doctor 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 Grant - Aust Non Government
Category 3AFG
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, Doctor 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 Grant - Aust Non Government
Category 3AFG
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

Total current UON EFTSL

Masters0.1
PhD0.43

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 M Philosophy (Medicine), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor
2014 PhD Use of Molecular Approaches for the Genomic Risk Stratification of B-Cell Neoplasms where Conventional Karyotyping is Limiting 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

1/02/2018 - 1/06/2020

Contact

Doctor Anoop Enjeti


anoop.enjeti@newcastle.edu.au

Research -PhD program

Leukemia, myelodysplasia and translational genomics

PHD

Faculty Of Health

1/02/2018 - 1/02/2020

Contact

Doctor Anoop Enjeti


anoop.enjeti@newcastle.edu.au

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Dr Anoop Enjeti

Position

Conjoint Senior Lecturer
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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