Imperial College London

DrKikkeriNaresh

Faculty of MedicineDepartment of Immunology and Inflammation

Visiting Professor
 
 
 
//

Contact

 

+44 (0)20 3313 3969k.naresh

 
 
//

Location

 

Office 6, Building 541, G-BlockHammersmith HospitalHammersmith Campus

//

Summary

 

Publications

Publication Type
Year
to

402 results found

Pai SA, Naresh KN, Borges AM, 2022, Report of a Case With Clinical and Pathologic Features of Castleman Disease That Predates Castleman's Report by More Than 50 Years., Arch Pathol Lab Med, Vol: 146, Pages: 1412-1415

CONTEXT.—: In 1954, Benjamin Castleman, MD, described what was then believed to be a new entity in lymph node pathology. Initially labeled "Hyperplasia of the mediastinal node" and then "Localized mediastinal lymph node hyperplasia resembling thymoma," we now recognize the condition with the eponym "Castleman disease." We document a paper that describes the same condition, a half century before Castleman did. OBJECTIVE.—: To report the striking resemblance between Castleman disease and the lymph node reported in the paper published by Edwin R. LeCount, MD, titled "Lymphoma, a benign tumor representing a lymph gland in structure," published in Journal of Experimental Medicine in 1899. We also provide an overview of the remarkable achievements of LeCount. DESIGN.—: We compared the elucidation in the original paper by LeCount with the morphologic details in the papers published by Castleman et al. Material on the life of LeCount was compiled from the scientific literature, the Internet, and the files of the University of Chicago. RESULTS.—: LeCount's description and illustrations of the lymph node are uncannily similar to the onion-skinning and vascularity that Castleman documented. CONCLUSIONS.—: LeCount deserves credit for his depiction of a hitherto-unreported entity.

Journal article

Fromm JR, Tang C, Naresh KN, 2022, Predictors of risk of relapse in classic Hodgkin lymphoma, JOURNAL OF CLINICAL PATHOLOGY, ISSN: 0021-9746

Journal article

Ju JY, Sorensen EP, Walsh JS, Shinohara MM, Naresh KNet al., 2022, CD5(+) Gamma Delta T-Cell Lymphoproliferative Disorder/Lymphoma Without Cytotoxic Granules in the Skin, AMERICAN JOURNAL OF DERMATOPATHOLOGY, Vol: 44, Pages: 680-682, ISSN: 0193-1091

Journal article

Naik A, Gooley T, Loeb K, Soma L, Smith SD, Gopal A, Naresh KNet al., 2022, The impact of histological grade on outcomes in follicular lymphoma: An analysis of patients in the SEER database in the context of evolving disease classification and treatment, BRITISH JOURNAL OF HAEMATOLOGY, ISSN: 0007-1048

Journal article

Bewicke-Copley F, Korfi K, Araf S, Hodkinson B, Kumar E, Cummin T, Ashton-Key M, Barrans SL, van Hoppe SJ, Burton C, Elshiekh M, Rule S, Crosbie N, Clear AJ, Calaminici M, Runge HFP, Hills RK, Scott DW, Rimsza LM, Menon G, Sha C, Davies J, Nagano A, Davies AJ, Painter D, Smith A, Gribben JG, Naresh KN, Westhead DR, Okosun J, Steele AJ, Hodson DJ, Balasubramanian S, Johnson PWM, Wang J, Fitzgibbon Jet al., 2022, Longitudinal expression profiling identifies a poor risk subset of patients with ABC-type Diffuse Large B Cell Lymphoma., Blood Adv

Despite the effectiveness of immuno-chemotherapy, 40% of patients with diffuse large B-cell lymphoma (DLBCL) experience relapse or refractory disease. Longitudinal studies have previously focused on the mutational landscape of relapse but falling short of providing a consistent relapse-specific genetic signature. In our study, we have focussed attention on the changes in gene expression profile accompanying DLBCL relapse using archival paired diagnostic/relapse specimens from 38 de novo DLBCL patients. Cell of origin remained stable from diagnosis to relapse in 84% of patients, with only a single patient showing COO switching from ABC to GCB. Analysis of the transcriptomic changes that occur following relapse suggest ABC and GCB relapses are mediated via different mechanisms. We developed a 30-gene discriminator for ABC-DLBCLs derived from relapse-associated genes, that defined clinically distinct high and low risk subgroups in ABC-DLBCLs at diagnosis in datasets comprising both population-based and clinical trial cohorts. This signature also identified a population of <60-year-old patients with superior PFS and OS treated with Ibrutinib-R-CHOP as part of the PHOENIX trial. Altogether this new signature adds to the existing toolkit of putative genetic predictors now available in DLBCL that can be readily assessed as part of prospective clinical trials.

Journal article

Alaggio R, Amador C, Anagnostopoulos I, Attygalle AD, Araujo IBDO, Berti E, Bhagat G, Borges AM, Boyer D, Calaminici M, Chadburn A, Chan JKC, Cheuk W, Chng W-J, Choi JK, Chuang S-S, Coupland SE, Czader M, Dave SS, de Jong D, Du M-Q, Elenitoba-Johnson KS, Ferry J, Geyer J, Gratzinger D, Guitart J, Gujral S, Harris M, Harrison CJ, Hartmann S, Hochhaus A, Jansen PM, Karube K, Kempf W, Khoury J, Kimura H, Klapper W, Kovach AE, Kumar S, Lazar AJ, Lazzi S, Leoncini L, Leung N, Leventaki V, Li X-Q, Lim MS, Liu W-P, Louissaint A, Marcogliese A, Medeiros LJ, Michal M, Miranda RN, Mitteldorf C, Montes-Moreno S, Morice W, Nardi V, Naresh KN, Natkunam Y, Ng S-B, Oschlies I, Ott G, Parrens M, Pulitzer M, Rajkumar SV, Rawstron AC, Rech K, Rosenwald A, Said J, Sarkozy C, Sayed S, Saygin C, Schuh A, Sewell W, Siebert R, Sohani AR, Tooze R, Traverse-Glehen A, Vega F, Vergier B, Wechalekar AD, Wood B, Xerri L, Xiao Wet al., 2022, The 5th edition of the World Health Organization classification of haematolymphoid tumours: lymphoid neoplasms, Leukemia, Vol: 36, Pages: 1720-1748, ISSN: 0887-6924

We herein present an overview of the upcoming 5th edition of the World Health Organization Classification of Haematolymphoid Tumours focussing on lymphoid neoplasms. Myeloid and histiocytic neoplasms will be presented in a separate accompanying article. Besides listing the entities of the classification, we highlight and explain changes from the revised 4th edition. These include reorganization of entities by a hierarchical system as is adopted throughout the 5th edition of the WHO classification of tumours of all organ systems, modification of nomenclature for some entities, revision of diagnostic criteria or subtypes, deletion of certain entities, and introduction of new entities, as well as inclusion of tumour-like lesions, mesenchymal lesions specific to lymph node and spleen, and germline predisposition syndromes associated with the lymphoid neoplasms.

Journal article

Khoury JD, Solary E, Abla O, Akkari Y, Alaggio R, Apperley JF, Bejar R, Berti E, Busque L, Chan JKC, Chen W, Chen X, Chng W-J, Choi JK, Colmenero I, Coupland SE, Cross NCP, De Jong D, Elghetany MT, Takahashi E, Emile J-F, Ferry J, Fogelstrand L, Fontenay M, Germing U, Gujral S, Haferlach T, Harrison C, Hodge JC, Hu S, Jansen JH, Kanagal-Shamanna R, Kantarjian HM, Kratz CP, Li X-Q, Lim MS, Loeb K, Loghavi S, Marcogliese A, Meshinchi S, Michaels P, Naresh KN, Natkunam Y, Nejati R, Ott G, Padron E, Patel KP, Patkar N, Picarsic J, Platzbecker U, Roberts I, Schuh A, Sewell W, Siebert R, Tembhare P, Tyner J, Verstovsek S, Wang W, Wood B, Xiao W, Yeung C, Hochhaus Aet al., 2022, The 5th edition of the World Health Organization Classification of Haematolymphoid Tumours: Myeloid and Histiocytic/Dendritic Neoplasms, LEUKEMIA, Vol: 36, Pages: 1703-1719, ISSN: 0887-6924

Journal article

Trasanidis N, Katsarou A, Ponnusamy K, Shen Y-A, Kostopoulos I, Bergonia B, Keren K, Reema P, Xiao X, Szydlo RM, Sabbattini PMR, Roberts IAG, Auner HW, Naresh KN, Chaidos A, Wang T-L, Magnani L, Caputo VS, Karadimitris Aet al., 2022, Systems medicine dissection of chr1q-amp reveals a novel PBX1-FOXM1 axis for targeted therapy in multiple myeloma, BLOOD, Vol: 139, Pages: 1939-1953, ISSN: 0006-4971

Journal article

Attygalle AD, Dobson R, Chak PK, Vroobel KM, Wren D, Mugalaasi H, Morgan Y, Kaur M, Ahmad R, Chen Z, Naresh KN, Du M-Qet al., 2022, Parallel evolution of two distinct lymphoid proliferations in clonal haematopoiesis, HISTOPATHOLOGY, Vol: 80, Pages: 847-858, ISSN: 0309-0167

Journal article

Ponnusamy K, Tzioni MM, Begum M, Robinson ME, Caputo VS, Katsarou A, Trasanidis N, Xiao X, Kostopoulos I, Iskander D, Roberts I, Trivedi P, Auner HW, Naresh K, Chaidos A, Karadimitris Aet al., 2022, The innate sensor ZBP1-IRF3 axis regulates cell proliferation in multiple myeloma, HAEMATOLOGICA, Vol: 107, Pages: 721-732, ISSN: 0390-6078

Journal article

Ibanez K, Polke J, Hagelstrom RT, Dolzhenko E, Pasko D, Thomas ERA, Daugherty LC, Kasperaviciute D, Smith KR, Deans ZC, Hill S, Fowler T, Scott RH, Hardy J, Chinnery PF, Houlden H, Rendon A, Caulfield MJ, Eberle MA, Taft RJ, Tucci Aet al., 2022, Whole genome sequencing for the diagnosis of neurological repeat expansion disorders in the UK: a retrospective diagnostic accuracy and prospective clinical validation study, LANCET NEUROLOGY, Vol: 21, Pages: 234-245, ISSN: 1474-4422

Journal article

Chen X, Fromm JR, Naresh KN, 2022, "Blasts" in myeloid neoplasms - how do we define blasts and how do we incorporate them into diagnostic schema moving forward?, LEUKEMIA, Vol: 36, Pages: 327-332, ISSN: 0887-6924

Journal article

Naresh KN, Lazzi S, Santi R, Granai M, Onyango N, Leoncini Let al., 2021, A refined approach to the diagnosis of Burkitt lymphoma in a resource-poor setting, HISTOPATHOLOGY, Vol: 80, Pages: 743-745, ISSN: 0309-0167

Journal article

Trasanidis N, Katsarou A, Ponnusamy K, Shen Y-A, Kostopoulos IV, Bergonia B, Keren K, Reema P, Xiao X, Szydlo RM, Sabbattini PMR, Roberts IAG, Auner HW, Naresh KN, Chaidos A, Wang T-L, Magnani L, Caputo VS, Karadimitris Aet al., 2021, Systems medicine dissection of chromosome 1q amplification reveals oncogenic regulatory circuits and informs targeted therapy in cancer

<jats:title>Abstract</jats:title><jats:p>Understanding the biological and clinical impact of copy number aberrations (CNA) in cancer remains an unmet challenge. Genetic amplification of chromosome 1q (chr1q-amp) is a major CNA conferring adverse prognosis in several cancers, including the blood cancer, multiple myeloma (MM). Although several chr1q genes portend high-risk MM disease, the underpinning molecular aetiology remains elusive. Here we integrate patient multi-omics datasets with genetic variables to identify 103 adverse prognosis genes in chr1q-amp MM. Amongst these, the transcription factor PBX1 is ectopically expressed by genetic amplification and epigenetic activation of its own preserved 3D regulatory domain. By binding to reprogrammed super-enhancers, PBX1 directly regulates critical oncogenic pathways, whilst in co-operation with FOXM1, activates a proliferative gene signature which predicts adverse prognosis across multiple cancers. Notably, pharmacological disruption of the PBX1-FOXM1 axis, including with a novel PBX1 inhibitor is selectively toxic against chr1q-amp cancer cells. Overall, our systems medicine approach successfully identifies CNA-driven oncogenic circuitries, links them to clinical phenotypes and proposes novel CNA-targeted therapy strategies in cancer.</jats:p><jats:sec><jats:title>Significance</jats:title><jats:p>We provide a comprehensive systems medicine strategy to unveil oncogenic circuitries and inform novel precision therapy decisions against CNA in cancer. This first clinical multi-omic analysis of chr1q-amp in MM identifies a central PBX1-FOXM1 regulatory axis driving high-risk prognosis, as a novel therapeutic target against chr1q-amp in cancer.</jats:p></jats:sec>

Journal article

Smedley D, Smith KR, Martin A, Thomas EA, McDonagh EM, Cipriani V, Ellingford JM, Arno G, Tucci A, Vandrovcova J, Chan G, Williams HJ, Ratnaike T, Wei W, Stirrups K, Ibanez K, Moutsianas L, Wielscher M, Need A, Barnes MR, Vestito L, Buchanan J, Wordsworth S, Ashford S, Rehmstrom K, Li E, Fuller G, Twiss P, Spasic-Boskovic O, Halsall S, Floto RA, Poole K, Wagner A, Mehta SG, Gurnell M, Burrows N, James R, Penkett C, Dewhurst E, Graf S, Mapeta R, Kasanicki M, Haworth A, Savage H, Babcock M, Reese MG, Bale M, Baple E, Boustred C, Brittain H, de Burca A, Bleda M, Devereau A, Halai D, Haraldsdottir E, Hyder Z, Kasperaviciute D, Patch C, Polychronopoulos D, Matchan A, Sultana R, Ryten M, Tavares ALT, Tregidgo C, Turnbull C, Welland M, Wood S, Snow C, Williams E, Leigh S, Foulger RE, Daugherty LC, Niblock O, Leong IUS, Wright CF, Davies J, Crichton C, Welch J, Woods K, Abulhoul L, Aurora P, Bockenhauer D, Broomfield A, Cleary MA, Lam T, Dattani M, Footitt E, Ganesan V, Grunewald S, Compeyrot-Lacassagne S, Muntoni F, Pilkington C, Quinlivan R, Thapar N, Wallis C, Wedderburn LR, Worth A, Bueser T, Compton C, Deshpande C, Fassihi H, Haque E, Izatt L, Josifova D, Mohammed S, Robert L, Rose S, Ruddy D, Sarkany R, Say G, Shaw AC, Wolejko A, Habib B, Burns G, Hunter S, Grocock RJ, Humphray SJ, Robinson PN, Haendel M, Simpson MA, Banka S, Clayton-Smith J, Douzgou S, Hall G, Thomas HB, O'Keefe RT, Michaelides M, Moore AT, Malka S, Pontikos N, Browning AC, Straub V, Gorman GS, Horvath R, Quinton R, Schaefer AM, Yu-Wai-Man P, Turnbull DM, McFarland R, Taylor RW, O'Connor E, Yip J, Newland K, Morris HR, Polke J, Wood NW, Campbell C, Camps C, Gibson K, Koelling N, Lester T, Nemeth AH, Palles C, Roy NBA, Sen A, Taylor J, Cacheiro P, Jacobsen JO, Seaby EG, Davison V, Chitty L, Douglas A, Naresh K, McMullan D, Ellard S, Temple IK, Mumford AD, Wilson G, Beales P, Bitner-Glindzicz M, Black G, Bradley JR, Brennan P, Burn J, Chinnery PF, Elliott P, Flinter F, Houlden H, Irving M, Newman W, Raet al., 2021, 100,000 Genomes Pilot on Rare-Disease Diagnosis in Health Care - Preliminary Report, NEW ENGLAND JOURNAL OF MEDICINE, Vol: 385, Pages: 1868-1880, ISSN: 0028-4793

Journal article

Medani H, Elshiekh M, Naresh KN, 2021, Improving precise counting of mitotic cells in mantle cell lymphoma using phosphohistone H3 (PHH3) antibody, JOURNAL OF CLINICAL PATHOLOGY, Vol: 74, Pages: 646-649, ISSN: 0021-9746

Journal article

Claudiani S, Mason CC, Milojkovic D, Bianchi A, Pellegrini C, Di Marco A, Fiol CR, Robinson M, Ponnusamy K, Mokretar K, Chowdhury A, Albert M, Reid AG, Deininger MW, Naresh K, Apperley JF, Khorashad JSet al., 2021, Carfilzomib Enhances the Suppressive Effect of Ruxolitinib in Myelofibrosis, CANCERS, Vol: 13

Journal article

Xu D, Naresh KN, 2021, Leukemic presentation of a highly aggressive ALK-negative anaplastic large cell lymphoma, BLOOD, Vol: 138, Pages: 1198-1198, ISSN: 0006-4971

Journal article

Iskander D, Wang G, Heuston EF, Christodoulidou C, Psaila B, Ponnusamy K, Ren H, Mokhtari Z, Robinson M, Chaidos A, Trivedi P, Trasanidis N, Katsarou A, Szydlo R, Palii CG, Zaidi MH, Al-Oqaily Q, Caputo VS, Roy A, Harrington Y, Karnik L, Naresh K, Mead AJ, Thongjuea S, Brand M, de la Fuente J, Bodine DM, Roberts I, Karadimitris Aet al., 2021, Single-cell profiling of human bone marrow progenitors reveals mechanisms of failing erythropoiesis in Diamond-Blackfan anemia, SCIENCE TRANSLATIONAL MEDICINE, Vol: 13, ISSN: 1946-6234

Journal article

Ibanez K, Polke J, Hagelstrom T, Dolzhenko E, Pasko D, Thomas E, Daugherty L, Kasperaviciute D, McDonagh EM, Smith KR, Martin AR, Polychronopoulos D, Angus-Leppan H, Bhatia KP, Davison JE, Festenstein R, Fratta P, Giunti P, Howard R, Prasad Korlipara LV, Laurá M, McEntagart M, Menzies L, Morris H, Reilly MM, Robinson R, Rosser E, Faravelli F, Schrag A, Schott JM, Warner TT, Wood NW, Bourn D, Eggleton K, Labrum R, Twiss P, Abbs S, Santos L, Almheiri G, Sheikh I, Vandrovcova J, Patch C, Taylor Tavares AL, Hyder Z, Need A, Brittain H, Baple E, Moutsianas L, Deshpande V, Perry DL, Ajay S, Chawla A, Rajan V, Oprych K, Chinnery PF, Douglas A, Wilson G, Ellard S, Temple K, Mumford A, McMullan D, Naresh K, Flinter F, Taylor JC, Greenhalgh L, Newman W, Brennan P, Sayer JA, Raymond FL, Chitty LS, Deans ZC, Hill S, Fowler T, Scott R, Houlden H, Rendon A, Caulfield MJ, Eberle MA, Taft RJ, Tucci Aet al., 2020, Whole genome sequencing for diagnosis of neurological repeat expansion disorders

<jats:title>ABSTRACT</jats:title><jats:sec><jats:title>Background</jats:title><jats:p>Repeat expansion (RE) disorders affect ~1 in 3000 individuals and are clinically heterogeneous diseases caused by expansions of short tandem DNA repeats. Genetic testing is often locus-specific, resulting in under diagnosis of atypical clinical presentations, especially in paediatric patients without a prior positive family history. Whole genome sequencing (WGS) is emerging as a first-line test for rare genetic disorders, but until recently REs were thought to be undetectable by this approach.</jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p>WGS pipelines for RE disorder detection were deployed by the 100,000 Genomes Project and Illumina Clinical Services Laboratory. Performance was retrospectively assessed across the 13 most common neurological RE loci using 793 samples with prior orthogonal testing (182 with expanded alleles and 611 with alleles within normal size) and prospectively interrogated in 13,331 patients with suspected genetic neurological disorders.</jats:p></jats:sec><jats:sec><jats:title>Findings</jats:title><jats:p>WGS RE detection showed minimum 97·3% sensitivity and 99·6% specificity across all 13 disease-associated loci. Applying the pipeline to patients from the 100,000 Genomes Project identified pathogenic repeat expansions which were confirmed in 69 patients, including seven paediatric patients with no reported family history of RE disorders, with a 0.09% false positive rate.</jats:p></jats:sec><jats:sec><jats:title>Interpretation</jats:title><jats:p>We show here for the first time that WGS enables the detection of causative repeat expansions with high sensitivity and specificity, and that it can be used to resolve previously undiagnosed neurological disorders. This includes children w

Journal article

Iskander D, Wang G, Heuston EF, Christodoulidou C, Psaila B, Robinson ME, Chaidos A, Trivedi P, Trasanidis N, Katsarou A, Szydlo R, Al-Oqaily Q, Caputo VS, Ponnusamy K, Roy A, Karnik L, Naresh K, Mead AJ, Thongjuea S, Brand M, De la Fuente J, Bodine DM, Roberts Iet al., 2020, Single-Cell Transcriptional Landscapes of Human Bone Marrow Reveal Distinct Erythroid Phenotypes Underpinned By Genotype in Diamond-Blackfan Anemia, Publisher: AMER SOC HEMATOLOGY, ISSN: 0006-4971

Conference paper

Ziepert M, Lazzi S, Santi R, Vergoni F, Granai M, Mancini V, Staiger AM, Horn H, Loffler M, Poschel V, Held G, Wulf G, Trumper LH, Schmitz N, Rosenwald A, Sabattini E, Naresh KN, Stein H, Ott G, Leoncini Let al., 2020, A 70% cut-off for MYC protein expression in diffuse large B-cell lymphoma identifies a high-risk group of patients, HAEMATOLOGICA, Vol: 105, Pages: 2667-2670, ISSN: 0390-6078

Journal article

Ziepert M, Lazzi S, Santi R, Vergoni F, Granai M, Mancini V, Staiger A, Horn H, Löffler M, Pöschel V, Held G, Wulf G, Trümper LH, Schmitz N, Rosenwald A, Sabattini E, Naresh KN, Stein H, Ott G, Leoncini Let al., 2020, A 70% cut-off for MYC protein expression in diffuse large B cell lymphoma identifies a high-risk group of patients., Haematologica, Vol: 105, Pages: 2667-2670

Journal article

Hanley B, Naresh KN, Roufosse C, Nicholson AG, Weir J, Cooke GS, Thursz M, Manousou P, Corbett R, Goldin R, Al-Sarraj S, Abdolrasouli A, Swann OC, Baillon L, Penn R, Barclay WS, Viola P, Osborn Met al., 2020, Histopathological findings and viral tropism in UK patients with severe fatal COVID-19: a post-mortem study, The Lancet Microbe, Vol: 1, Pages: e245-e253, ISSN: 2666-5247

BackgroundSevere COVID-19 has a high mortality rate. Comprehensive pathological descriptions of COVID-19 are scarce and limited in scope. We aimed to describe the histopathological findings and viral tropism in patients who died of severe COVID-19.MethodsIn this case series, patients were considered eligible if they were older than 18 years, with premortem diagnosis of severe acute respiratory syndrome coronavirus 2 infection and COVID-19 listed clinically as the direct cause of death. Between March 1 and April 30, 2020, full post-mortem examinations were done on nine patients with confirmed COVID-19, including sampling of all major organs. A limited autopsy was done on one additional patient. Histochemical and immunohistochemical analyses were done, and histopathological findings were reported by subspecialist pathologists. Viral quantitative RT-PCR analysis was done on tissue samples from a subset of patients.FindingsThe median age at death of our cohort of ten patients was 73 years (IQR 52–79). Thrombotic features were observed in at least one major organ in all full autopsies, predominantly in the lung (eight [89%] of nine patients), heart (five [56%]), and kidney (four [44%]). Diffuse alveolar damage was the most consistent lung finding (all ten patients); however, organisation was noted in patients with a longer clinical course. We documented lymphocyte depletion (particularly CD8-positive T cells) in haematological organs and haemophagocytosis. Evidence of acute tubular injury was noted in all nine patients examined. Major unexpected findings were acute pancreatitis (two [22%] of nine patients), adrenal micro-infarction (three [33%]), pericarditis (two [22%]), disseminated mucormycosis (one [10%] of ten patients), aortic dissection (one [11%] of nine patients), and marantic endocarditis (one [11%]). Viral genomes were detected outside of the respiratory tract in four of five patients. The presence of subgenomic viral RNA transcripts provided evidence of

Journal article

Thomas SJ, Morley N, Lashen H, Naresh KN, Fernando Met al., 2020, Indolent T-Cell Lymphoproliferative Disorder of the Uterine Corpus: A Case Report, INTERNATIONAL JOURNAL OF GYNECOLOGICAL PATHOLOGY, Vol: 39, Pages: 503-506, ISSN: 0277-1691

Journal article

Ponnusamy K, Tzioni MM, Begum M, Robinson ME, Caputo VS, Katsarou A, Trasanidis N, Xiao X, Kostopoulos IV, Iskander D, Roberts I, Trivedi P, Auner HW, Naresh K, Chaidos A, Karadimitris Aet al., 2020, The innate sensor ZBP1-IRF3 axis regulates cell proliferation in multiple myeloma

<jats:title>Abstract</jats:title><jats:p>ZBP1 is an inducible, non-constitutively expressed cellular nucleic acid sensor that triggers type I interferon (IFN) responses via phosphorylation and activation of the transcription factor (TF) IRF3 by TBK1. However, the role of the ZBP1-IRF3 axis in cancer is not known. Here we show that ZBP1 is selectively and constitutively expressed in late B cell development and it is required for optimal T cell-dependent humoral immune responses. In the plasma cell (PC) cancer multiple myeloma, interaction of constitutively expressed ZBP1 with TBK1 and IRF3 results in IRF3 phosphorylation. Notably, rather than IFN type I response genes, IRF3 directly activates, in part through co-operation with the PC lineage-defining TF IRF4, cell cycle genes thus promoting myeloma cell proliferation. This generates a novel, potentially therapeutically targetable and relatively selective myeloma cell addiction to the ZBP1-IRF3 axis. These data expand our knowledge of the role of cellular immune sensors in cancer biology.</jats:p>

Journal article

Shah V, Sherborne AL, Johnson DC, Ellis S, Price A, Chowdhury F, Kendall J, Jenner MW, Drayson MT, Owen RG, Gregory WM, Morgan GJ, Davies FE, Cook G, Cairns DA, Houlston RS, Jackson G, Kaiser MFet al., 2020, Predicting ultrahigh risk multiple myeloma by molecular profiling: an analysis of newly diagnosed transplant eligible myeloma XI trial patients, LEUKEMIA, Vol: 34, Pages: 3091-3096, ISSN: 0887-6924

Journal article

Medani H, Elshiekh M, Naresh K, 2020, Accurate Mitotic Counts in Mantle Cell Lymphoma Using Phosphohistone H3 (PHH3) Immunohistochemistry, 109th Annual Meeting of the United-States-and-Canadian-Academy-of-Pathology (USCAP), Publisher: SPRINGERNATURE, Pages: 1346-1347, ISSN: 0893-3952

Conference paper

This data is extracted from the Web of Science and reproduced under a licence from Thomson Reuters. You may not copy or re-distribute this data in whole or in part without the written consent of the Science business of Thomson Reuters.

Request URL: http://wlsprd.imperial.ac.uk:80/respub/WEB-INF/jsp/search-html.jsp Request URI: /respub/WEB-INF/jsp/search-html.jsp Query String: respub-action=search.html&id=00395490&limit=30&person=true