WHO classification of hematopoietic and lymphoid neoplasms associated with NK cells [Swerdlow et al., 2008]
\\n\\n
Dr. Pletser’s experience includes 30 years of working with the European Space Agency as a Senior Physicist/Engineer and coordinating their parabolic flight campaigns, and he is the Guinness World Record holder for the most number of aircraft flown (12) in parabolas, personally logging more than 7,300 parabolas.
\\n\\nSeeing the 5,000th book published makes us at the same time proud, happy, humble, and grateful. This is a great opportunity to stop and celebrate what we have done so far, but is also an opportunity to engage even more, grow, and succeed. It wouldn't be possible to get here without the synergy of team members’ hard work and authors and editors who devote time and their expertise into Open Access book publishing with us.
\\n\\nOver these years, we have gone from pioneering the scientific Open Access book publishing field to being the world’s largest Open Access book publisher. Nonetheless, our vision has remained the same: to meet the challenges of making relevant knowledge available to the worldwide community under the Open Access model.
\\n\\nWe are excited about the present, and we look forward to sharing many more successes in the future.
\\n\\nThank you all for being part of the journey. 5,000 times thank you!
\\n\\nNow with 5,000 titles available Open Access, which one will you read next?
\\n\\nRead, share and download for free: https://www.intechopen.com/books
\\n\\n\\n\\n
\\n"}]',published:!0,mainMedia:null},components:[{type:"htmlEditorComponent",content:'
Preparation of Space Experiments edited by international leading expert Dr. Vladimir Pletser, Director of Space Training Operations at Blue Abyss is the 5,000th Open Access book published by IntechOpen and our milestone publication!
\n\n"This book presents some of the current trends in space microgravity research. The eleven chapters introduce various facets of space research in physical sciences, human physiology and technology developed using the microgravity environment not only to improve our fundamental understanding in these domains but also to adapt this new knowledge for application on earth." says the editor. Listen what else Dr. Pletser has to say...
\n\n\n\nDr. Pletser’s experience includes 30 years of working with the European Space Agency as a Senior Physicist/Engineer and coordinating their parabolic flight campaigns, and he is the Guinness World Record holder for the most number of aircraft flown (12) in parabolas, personally logging more than 7,300 parabolas.
\n\nSeeing the 5,000th book published makes us at the same time proud, happy, humble, and grateful. This is a great opportunity to stop and celebrate what we have done so far, but is also an opportunity to engage even more, grow, and succeed. It wouldn't be possible to get here without the synergy of team members’ hard work and authors and editors who devote time and their expertise into Open Access book publishing with us.
\n\nOver these years, we have gone from pioneering the scientific Open Access book publishing field to being the world’s largest Open Access book publisher. Nonetheless, our vision has remained the same: to meet the challenges of making relevant knowledge available to the worldwide community under the Open Access model.
\n\nWe are excited about the present, and we look forward to sharing many more successes in the future.
\n\nThank you all for being part of the journey. 5,000 times thank you!
\n\nNow with 5,000 titles available Open Access, which one will you read next?
\n\nRead, share and download for free: https://www.intechopen.com/books
\n\n\n\n
\n'}],latestNews:[{slug:"intechopen-signs-new-contract-with-cepiec-china-for-distribution-of-open-access-books-20210319",title:"IntechOpen Signs New Contract with CEPIEC, China for Distribution of Open Access Books"},{slug:"150-million-downloads-and-counting-20210316",title:"150 Million Downloads and Counting"},{slug:"intechopen-secures-indefinite-content-preservation-with-clockss-20210309",title:"IntechOpen Secures Indefinite Content Preservation with CLOCKSS"},{slug:"intechopen-expands-to-all-global-amazon-channels-with-full-catalog-of-books-20210308",title:"IntechOpen Expands to All Global Amazon Channels with Full Catalog of Books"},{slug:"stanford-university-identifies-top-2-scientists-over-1-000-are-intechopen-authors-and-editors-20210122",title:"Stanford University Identifies Top 2% Scientists, Over 1,000 are IntechOpen Authors and Editors"},{slug:"intechopen-authors-included-in-the-highly-cited-researchers-list-for-2020-20210121",title:"IntechOpen Authors Included in the Highly Cited Researchers List for 2020"},{slug:"intechopen-maintains-position-as-the-world-s-largest-oa-book-publisher-20201218",title:"IntechOpen Maintains Position as the World’s Largest OA Book Publisher"},{slug:"all-intechopen-books-available-on-perlego-20201215",title:"All IntechOpen Books Available on Perlego"}]},book:{item:{type:"book",id:"293",leadTitle:null,fullTitle:"Practical Applications and Solutions Using LabVIEW™ Software",title:"Practical Applications and Solutions Using LabVIEW™ Software",subtitle:null,reviewType:"peer-reviewed",abstract:"The book consists of 21 chapters which present interesting applications implemented using the LabVIEW environment, belonging to several distinct fields such as engineering, fault diagnosis, medicine, remote access laboratory, internet communications, chemistry, physics, etc. The virtual instruments designed and implemented in LabVIEW provide the advantages of being more intuitive, of reducing the implementation time and of being portable.\nThe audience for this book includes PhD students, researchers, engineers and professionals who are interested in finding out new tools developed using LabVIEW.\nSome chapters present interesting ideas and very detailed solutions which offer the immediate possibility of making fast innovations and of generating better products for the market. The effort made by all the scientists who contributed to editing this book was significant and as a result new and viable applications were presented.",isbn:null,printIsbn:"978-953-307-650-8",pdfIsbn:"978-953-51-5551-5",doi:"10.5772/819",price:139,priceEur:155,priceUsd:179,slug:"practical-applications-and-solutions-using-labview-software",numberOfPages:488,isOpenForSubmission:!1,isInWos:1,hash:"8709b37736bf2d4359e98e5542cae86c",bookSignature:"Folea Silviu",publishedDate:"August 1st 2011",coverURL:"https://cdn.intechopen.com/books/images_new/293.jpg",numberOfDownloads:134081,numberOfWosCitations:37,numberOfCrossrefCitations:28,numberOfDimensionsCitations:50,hasAltmetrics:0,numberOfTotalCitations:115,isAvailableForWebshopOrdering:!0,dateEndFirstStepPublish:"November 3rd 2010",dateEndSecondStepPublish:"December 1st 2010",dateEndThirdStepPublish:"April 7th 2011",dateEndFourthStepPublish:"May 7th 2011",dateEndFifthStepPublish:"July 6th 2011",currentStepOfPublishingProcess:5,indexedIn:"1,2,3,4,5,6,7",editedByType:"Edited by",kuFlag:!1,editors:[{id:"6084",title:"Prof.",name:"Silviu",middleName:null,surname:"Folea",slug:"silviu-folea",fullName:"Silviu Folea",profilePictureURL:"https://mts.intechopen.com/storage/users/6084/images/293_n.jpg",biography:"Folea, C., Silviu, PhD, is professor at the Technical University of Cluj-Napoca, Automation Department, Romania. 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\r\n\tPolyimide is nowadays fully acknowledged as one of the most efficient polymers in many industries for its excellent thermal, electrical and mechanical properties, as well as for its easy processability. Particularly, in the Electronic and Electrical Engineering industries, polyimide is widely used for decades thanks to its very good dielectric and insulating properties at high electric field and high temperature up to 250°C in long term-service.
\r\n\t
\r\n\tSince its discovery in the mid-50’s, a wide range of applications from low to high voltage appeared, putting polyimide as a key material to design more performing and reliable electrical devices and systems. On another hand, polyimide appears also essential for the development of new electronic devices where further considerations such as high power density, integration, higher temperature, thermal conduction management, energy storage, reliability or flexibility are required in order to sustain the growing electrical energy consumption needs of the global society.
\r\n\tConsequently, polyimide materials have and will have to face new exciting fundamental, technological and environmental challenges among which:
\r\n\t• a better understanding of its intrinsic electrical properties to identify current limitations and propose new advanced device designs,
\r\n\t• the development of innovative composites and nanocomposites structuration to tailor its physical properties by involving classical and original nanoparticles such as graphene layer, carbon nanotubes, metal, silicates, nitrides, etc.,
\r\n\t• the development of polyimide composites for energy storage, thermal management, reinforced nanodielectrics and corona-resistant nanocomposites,
\r\n\t• the development of new low and ultra-low dielectric constant polyimide for microelectronics (fluorinated polyimides, nanoporous, mesoporous),
\r\n\t• the development of new higher temperature reliable polyimide (high glass transition, high degradation temperature),
\r\n\t• the emergence of solvent-free processes to fit with environmental purposes
\r\n\tMoreover, many challenges regarding the aging mechanisms understanding under single or multiple constraints and the realistic lifetime prediction using robust physical modelling is a ubiquitous questioning in most of the electronic industries.
\r\n\tThis book will target to review both the state-of-the-art and new researches on Polyimide for Electronic and Electrical Engineering Applications. It will present interdisciplinary chapters on the state of knowledge of each topic under consideration through a combination of overviews and original unpublished research. Chapter proposals related to one of the following topics and their keywords (but not only restricted to them) are very welcome to be submitted for this book publication project:
\r\n\t• General Considerations and Technological Processes of Polyimide for Electronics and Electrical Systems
\r\n\tProcessability, Photosensitive and non-photosensitive polyimide, Curing temperature,
\r\n\tSpin-coating, Dip-coating, Extruded enameled wires, Other casting methods
\r\n\t• Polyimide in Microelectronic Applications
\r\n\tDielectric properties, Intermetal layer, Ultra Large-Scale Integration (ULSI), Low-k dielectrics, Fluorinated polyimide, Nanoporous polyimide, Flexible substrates, Thin film transistors, LCD devices, sensors and actuators (gas, humidity, pressure, tactile…)
\r\n\t• Polyimide in Medium and High Voltage Applications
\r\n\tElectrical insulation properties (conduction, breakdown), Digital isolators, Power electronics and devices, Power modules, Power integration, Passivation, Packaging, High voltage power systems, Enameled wires for fed-inverter rotating machine
Natural killer (NK) cell malignancy is a heterogeneous disorder and rare, representing <1% of non-Hodgkin lymphomas for most of the world, except in Asia and Latin America. In Asia,especially,the incidence of NK-cell lymphomas is approximately 7%–10% of lymphomas[Au et al., 2005].
\n\t\t\tThe pathogenesis of NK-cell malignancies has not yet been fully elucidated. In the 2008 World Health Organization (WHO) classification of tumors of hematopoietic and lymphoid tissues, there are two entities associated with NK cells: mature T-cell and NK-cell neoplasms (including chronic lymphoproliferative disorder of NK cells, aggressive NK-cell leukemia, and extranodal NK/T-cell lymphoma, nasal type) and NK-cell lymphoblastic leukemia/lymphoma, which is included provisionally in the category of acute leukemias of ambiguous lineage (Table 1) [Swedlow et al., 2008]. What was previously described as blastic NK-cell leukemia is defined as blasticplasmacytoid dendritic cell neoplasm in the WHO 2008 classification [Swedlow et al., 2008]. In pediatric patients, the four NK cell neoplasms are rare, with blastic NK-cell lymphoma being the most prevalent.
\n\t\t\tAcute leukemias of ambiguous lineage | \n\t\t\t\t\t
NK-cell lymphoblastic leukemia/lymphoma | \n\t\t\t\t\t
Mature T-cell and NK-cell neoplasms | \n\t\t\t\t\t
Chronic lymphoproliferative disorder of NK cells | \n\t\t\t\t\t
Aggressive NK-cell leukemia | \n\t\t\t\t\t
Extranodal NK/T-cell lymphoma, nasal type | \n\t\t\t\t\t
WHO classification of hematopoietic and lymphoid neoplasms associated with NK cells [Swerdlow et al., 2008]
A rigorous review of the literature to date is required to adequately understand and manage the various pediatric NK-cell malignant entities. The clinical characteristics of pediatric cases with these NK-cell malignant entities defined according to the 2008 WHO classification are discussed in this paperand compared to adult cases.
\n\t\tThe 2008 WHO classification of tumors of hematopoietic and lymphoid tissue recognizes four categories of NK-cell neoplasms: NK-cell lymphoblastic leukemia/lymphoma, chronic lymphoproliferative disorder of NK cells, aggressive NK-cell leukemia (ANKL), and extranodal NK/T-cell lymphoma, nasal type (ENKL) (Table 1).NK-cell lymphoblastic leukemia involves immature NK cells, while chronic lymphoblastic leukemia/lymphoma,chronic lymphoproliferative disorder of NK cells, and aggressive NK-cell leukemia are mainly neoplasms of mature NK cells. ENKL is the main neoplasm of mature NK cells. Among the four entities, ANKL and ENKL are associated with Epstein-Barr virus (EBV).
\n\t\t\tNK-cell lymphoblastic leukemia/lymphoma is a very rare disease in both adults and children. Because of limitations in NK-cell-specific markers, it is included as acute leukemia of ambiguous lineage according to the WHO 2008 classification[Swerdlow et al., 2008]. This neoplasm has been difficult to define. CD56 is the most important and sensitive NK-cell marker, but CD56 is not specific for NK cells. Previously, many cases were reported as NK-cell leukemia because of the expression of CD57 but are plasmacytoid dendritic cell leukemia in the WHO 2008 classification. This issue is discussed below.
\n\t\t\tChronic lymphoproliferative disorder of NK cells is rare, especially in pediatric patients. It occurs in adults at a median age of 60 years. This provisional entity in the WHO 2008 classification is characterized by a persistent (>6 months) increase in peripheral blood NK cells (usually 2 x 109/L) without a clearly identified cause. It is very difficult to distinguish between neoplastic and reactive NK cells. Cells have an NK-cell phenotype: CD16+, CD56+, CD2–, CD7–, surface CD3 (sCD3)–, and cytoplasmic CD3 (CD3ε)+. Cytotoxic markers including T-cell-restricted intracellular antigen-1 (TIA-1), granzyme B, and granzyme M are positive. EBV is negative. One pediatric case has been reportedfrom China [Kwong et al., 1995]. CD2 was positive and CD3 was weakly positive. EBV status was not described. The case was a 3-year-old female who presented hepatosplenomegaly. She died 11 days after diagnosis because of uncontrolled disease and did not receive chemotherapy. The clinical course of the majority of cases with chronic lymphoproliferative disorder of NK cells shows a good prognosis and transformation to aggressive disease has been rarely reported [Ohno et al., 1998].
\n\t\t\tANKL is a systemic proliferation of NK cells with primary involvement of peripheral blood and bone marrow, and shows a fulminant clinical course. The age distribution of ANKL patients has been reported to show two peaks, one at 20 years and the other at 40 years of age[Suzuki et al., 2004b]. The disease typically affects patients at a younger age compared to other NK-cell malignancies. The clinical features, and cytological and immunohistochemical findings of this rare pediatric NK-cell malignancy are summarized in Tables 2 and 3. EBV is closely associated with the pathogenesis of this disease. Latent EBV shows monoclonality and causes EBV-infected NK-cell lymphoproliferative disease.
\n\t\t\t\tPatients are diagnosed with ANKL when a proliferation of large granular lymphoblasts of an NK-cell phenotype is found in peripheral blood and/or bone marrow exceeding 30% of the total nucleated cells [Suzuki et al., 2004b].The immunophenotype of ANKL is typically defined by CD2+, sCD3–, CD3ε+, and CD56+. Loss of CD7 is occasionally observed. This immunophenotype is almost identical to that for extranodal NK/T-cell lymphoma, except for CD16+. T-cell receptor (TCR) genes are in germline configuration. Some cases are CD11b+ and CD57–. These neoplastic cells express FAS ligand and high levels of FAS ligand can found in the serum of affected patients [Kato et al., 1998].
\n\t\t\t\tTo date, 19 pediatric and adolescent cases (<19 years of age) have been reported in the literature from 1986 to 2010. Most patients have been reported from Japan and Korea. Table 2 summarizes the clinical findings of these 19 pediatric cases. Median age at diagnosis was 14 years (range, 2–19 years). Gender distribution was equal (9 females and 10 males), which is the same in adult patients. Acute lymphoblastic leukemia typically affects children at 2–6 years of age, while the median age of ANKL patients is generally higher.
\n\t\t\t\t\tPediatric ANKL patients presented acute and rapidly progressive symptomatology. The most common presenting symptom is fever (12/13, 92%). Hepatomegaly (10/13, 77%), splenomegaly (12/16, 75%), and lymphoadenopathy (6/16, 37%) are also frequently observed. The incidence of these symptoms is almost same as that of adult patients [Yoo et al., 2009]. Two patients (cases 3 and 5) presented a chronic course and spontaneous regression was seen and transformation to ANKL. In adult patients, transformation from chronic lymphoproliferative disorder of NK cells to ANKL has been rarely reported. Pediatric patients manifest features of chronic active EBV infection, leading to overlap with EBV-positive T-cell lymphoproliferative disorders [Suzuki et al., 2004a]. The clinical presentation of ANKL has aresemblance to EBV-associated hemophagocyticlymphohistiocytosis. Chronic active EBV infection occurs predominantly in children and young adults and the incidence of hemophagocytosis as a clinical feature is frequently observed in cases of pediatric ANKL. Hypersensitivity to mosquito bites is sometimes seen as a preceding feature of ANKL in pediatric and adolescent patients.
\n\t\t\t\t\tThis disease is typically resistant to chemotherapy and successful treatment has been infrequently reported. The complete response rate is below 20% and 2-year overall survival rate is 5% in adult patients [Suzuki, 2010; Suzuki et al., 2010]. There is insufficient data to interpret complete remission and overall survival rates in pediatric ANKL patients. Results have been unsatisfactory using combination chemotherapy regimens that are typically used for acute lymphoblastic leukemia or non-Hodgkin lymphoma. In adults, chemotherapy with L-asparaginase-containing regimens has been reported to be effective in some cases [Ichikawa et al., 2010]. Among pediatric ANKL cases, only two patients were reported as being alive and one patient died with complete remission, while 13 cases died and one (case 15) died of graft-versus-host disease (GVHD) and infection without relapse. The median survival time for patients who died is 4 months. Two cases received allogeneic stem cell transplantation: one died due to GVHD without diseaseand one was alive. Chemotherapy with L-asparaginase-containing regimens and subsequent allogeneic stem cell transplantation led to prolonged survival in a few young adult patients, even when the stem cell transplantation was performed in patients who did not have a complete response [Ito et al., 2008]. Better outcome is suggested among patients who received allogeneic stem cell transplantation.
\n\t\t\t\t\tCase | \n\t\t\t\t\t\t\t\tAge/gender | \n\t\t\t\t\t\t\t\tFever | \n\t\t\t\t\t\t\t\tHepato-megaly | \n\t\t\t\t\t\t\t\tSpleno-megaly | \n\t\t\t\t\t\t\t\tLymph-adenopathy | \n\t\t\t\t\t\t\t\tOthersites | \n\t\t\t\t\t\t\t\tTreatment | \n\t\t\t\t\t\t\t\tPrognosis | \n\t\t\t\t\t\t\t\tReference | \n\t\t\t\t\t\t\t
1 | \n\t\t\t\t\t\t\t\t6 y/M | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t\n\t\t\t\t\t\t\t\t | NHL-BFM 90/Allo-SCT | \n\t\t\t\t\t\t\t\tAlive | \n\t\t\t\t\t\t\t\tOhnuma et al., 1997 | \n\t\t\t\t\t\t\t
2 | \n\t\t\t\t\t\t\t\t14 y/F | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tSkin | \n\t\t\t\t\t\t\t\tVCR/Dox/Cy/CA | \n\t\t\t\t\t\t\t\tAggressive, died 4 mo | \n\t\t\t\t\t\t\t\tKoizumi et al., 1986 | \n\t\t\t\t\t\t\t
3 | \n\t\t\t\t\t\t\t\t13 y/M | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\t\n\t\t\t\t\t\t\t\t | ND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tKawa-Ha et al., 1989 | \n\t\t\t\t\t\t\t
4 | \n\t\t\t\t\t\t\t\t15 y/M | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\t\n\t\t\t\t\t\t\t\t | ND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tKawa-Ha et al., 1989 | \n\t\t\t\t\t\t\t
5 | \n\t\t\t\t\t\t\t\t16 y/F | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\t\n\t\t\t\t\t\t\t\t | ND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tKawa-Ha et al., 1989 | \n\t\t\t\t\t\t\t
6 | \n\t\t\t\t\t\t\t\t16 y/F | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t\n\t\t\t\t\t\t\t\t | ND | \n\t\t\t\t\t\t\t\tAggressive, died 32 mo | \n\t\t\t\t\t\t\t\tImamura et al., 1990 | \n\t\t\t\t\t\t\t
7 | \n\t\t\t\t\t\t\t\t13 y/F | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t\n\t\t\t\t\t\t\t\t | ND | \n\t\t\t\t\t\t\t\tAggressive, died 26 mo | \n\t\t\t\t\t\t\t\tImamura et al., 1990 | \n\t\t\t\t\t\t\t
8 | \n\t\t\t\t\t\t\t\t18 y/M | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tLung | \n\t\t\t\t\t\t\t\tVDS/THP-ADR/Cy/PSL | \n\t\t\t\t\t\t\t\tAggressive, died 4 mo | \n\t\t\t\t\t\t\t\tFuruno et al., 1994 | \n\t\t\t\t\t\t\t
9 | \n\t\t\t\t\t\t\t\t13 y/M | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t\n\t\t\t\t\t\t\t\t | PSL | \n\t\t\t\t\t\t\t\tAggressive, died 47 d | \n\t\t\t\t\t\t\t\tKaizu et al., 2004 | \n\t\t\t\t\t\t\t
10 | \n\t\t\t\t\t\t\t\t19 y/F | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\tHPS | \n\t\t\t\t\t\t\t\tDHAP | \n\t\t\t\t\t\t\t\tAggressive, died 14 d | \n\t\t\t\t\t\t\t\tKohrt & Advani, 2004 | \n\t\t\t\t\t\t\t
11 | \n\t\t\t\t\t\t\t\t17 y/F | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t\n\t\t\t\t\t\t\t\t | COP/BLM | \n\t\t\t\t\t\t\t\tAggressive, died 1 mo | \n\t\t\t\t\t\t\t\tSuzuki et al., 2004b | \n\t\t\t\t\t\t\t
12 | \n\t\t\t\t\t\t\t\t12 y/M | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t- | \n\t\t\t\t\t\t\t\t- | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tLung | \n\t\t\t\t\t\t\t\tDNR/Cy/VCR/L-Asp/PSL | \n\t\t\t\t\t\t\t\tAggressive, died 5 mo | \n\t\t\t\t\t\t\t\tSuzuki et al., 2004b | \n\t\t\t\t\t\t\t
13 | \n\t\t\t\t\t\t\t\t16 y/F | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\tKidney | \n\t\t\t\t\t\t\t\tPSL | \n\t\t\t\t\t\t\t\tAggressive, died 1 d | \n\t\t\t\t\t\t\t\tSuzuki et al., 2004b | \n\t\t\t\t\t\t\t
14 | \n\t\t\t\t\t\t\t\t18 y/F | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tTonsil | \n\t\t\t\t\t\t\t\tCHOP/Allo-SCT | \n\t\t\t\t\t\t\t\tDied due to GVHD 39 mo | \n\t\t\t\t\t\t\t\tSuzuki et al., 2004b | \n\t\t\t\t\t\t\t
15 | \n\t\t\t\t\t\t\t\t13 y/M | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t\n\t\t\t\t\t\t\t\t | AIEOP-95 | \n\t\t\t\t\t\t\t\tAlive, CCR 1447 d | \n\t\t\t\t\t\t\t\tPatel et al., 2010 | \n\t\t\t\t\t\t\t
16 | \n\t\t\t\t\t\t\t\t14 y/F | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\t\n\t\t\t\t\t\t\t\t | ND | \n\t\t\t\t\t\t\t\tAggressive, died 1 mo | \n\t\t\t\t\t\t\t\tYoo et al., 2009 | \n\t\t\t\t\t\t\t
17 | \n\t\t\t\t\t\t\t\t2 y/M | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\t\n\t\t\t\t\t\t\t\t | ND | \n\t\t\t\t\t\t\t\tAggressive, died 5 d | \n\t\t\t\t\t\t\t\tYoo et al., 2009 | \n\t\t\t\t\t\t\t
18 | \n\t\t\t\t\t\t\t\t16 y/M | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\t\n\t\t\t\t\t\t\t\t | ND | \n\t\t\t\t\t\t\t\tAggressive, died 11 mo | \n\t\t\t\t\t\t\t\tYoo et al., 2009 | \n\t\t\t\t\t\t\t
19 | \n\t\t\t\t\t\t\t\t5 y/M | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\tHPS | \n\t\t\t\t\t\t\t\tHLH2004 | \n\t\t\t\t\t\t\t\tAggressive, died 4 mo | \n\t\t\t\t\t\t\t\tPetterson et al., 2008 | \n\t\t\t\t\t\t\t
Clinical characteristics of pediatric patients with aggressive NK leukemia
Abbreviations: ADR, adriamycin; AIEOP-95, AssociazioneItalianaEmatologiaOncologiaPediatrica 95 protocol; Allo-SCT, allogeneic stem cell transplantation; BLM, bleomycin; CA, cytarabine; CCR, clinical complete response; CHOP, cyclophosphamide, doxorubicin, vincristine, prednisolone; COP, cyclophosphamide, vincristine, prednisolone; Cy, cyclophosphamide; d, days; DHAP, dexamethasone, high-dose cytarabine, cisplatin; Dox, doxorubicin; F, female; GVHD, graft-versus-host disease; HLH2004, hemophagocyticlymphohistiocytosis 2004 protocol; HPS, hemophagocytosis; L-Asp, L-asparaginase; M, male; mo, months; ND, not determined; NHL-BFM 90, non-Hodgkin lymphoma-Berlin-Frankfurt-Munster 90 protocol; mo, month; PSL, prednisolone; THP-ADR, pirarubicin; VCR, vincristine; VDS, vindesine; y, year.
Yoo et al. have reported that CD7 antigen loss is frequently observed among adult ANKL patients and the absence of CD7 may serve as a reliable marker for the diagnosis of ANKL in adults [Yoo et al., 2009]. However, CD7+ is shown in 13 of 16 pediatric ANKL patients (Table 3). Immunophenotypic analysis of CD7 expression is therefore not useful in the diagnosis of ANKL in pediatric patients. EBV DNA is detected in almost all pediatric patients.
\n\t\t\t\t\tCase | \n\t\t\t\t\t\t\t\tCD2 | \n\t\t\t\t\t\t\t\tCD3ε | \n\t\t\t\t\t\t\t\tsCD3 | \n\t\t\t\t\t\t\t\tCD4 | \n\t\t\t\t\t\t\t\tCD7 | \n\t\t\t\t\t\t\t\tCD8 | \n\t\t\t\t\t\t\t\tCD16 | \n\t\t\t\t\t\t\t\tCD56 | \n\t\t\t\t\t\t\t\tCD57 | \n\t\t\t\t\t\t\t\tEBV DNA | \n\t\t\t\t\t\t\t\tReference | \n\t\t\t\t\t\t\t
1 | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tOhnuma et al., 1997 | \n\t\t\t\t\t\t\t
2 | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tKoizumi et al.,1986 | \n\t\t\t\t\t\t\t
3 | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tKawa-Ha et al., 1989 | \n\t\t\t\t\t\t\t
4 | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tKawa-Ha et al., 1989 | \n\t\t\t\t\t\t\t
5 | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tKawa-Ha et al., 1989 | \n\t\t\t\t\t\t\t
6 | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\t- | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tImamura et al., 1990 | \n\t\t\t\t\t\t\t
7 | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tImamura et al., 1990 | \n\t\t\t\t\t\t\t
8 | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tFuruno et al., 1994 | \n\t\t\t\t\t\t\t
9 | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tKaizu et al., 2004 | \n\t\t\t\t\t\t\t
10 | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tKohrt & Advani, 2004 | \n\t\t\t\t\t\t\t
11 | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tSuzuki et al., 2004b | \n\t\t\t\t\t\t\t
12 | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tSuzuki et al., 2004b | \n\t\t\t\t\t\t\t
13 | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tSuzuki et al., 2004b | \n\t\t\t\t\t\t\t
14 | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t- | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tSuzuki et al., 2004b | \n\t\t\t\t\t\t\t
15 | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tPatel et al., 2010 | \n\t\t\t\t\t\t\t
16 | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tYoo et al., 2009 | \n\t\t\t\t\t\t\t
17 | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tYoo et al., 2009 | \n\t\t\t\t\t\t\t
18 | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\tYoo et al., 2009 | \n\t\t\t\t\t\t\t
19 | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tPetterson et al., 2008 | \n\t\t\t\t\t\t\t
Phenotypic characteristics of pediatric patients with aggressive NK leukemia. Case numbers correspond with those in Table 2\n\t\t\t\t\t\t\t
Abbreviations: EBV, Epstein-Barr virus; ND, not determined.
ENKL is characterized by vascular damage and destruction, prominent necrosis, a cytotoxic phenotype, and an association with EBV. ENKL typically presents in the nasal cavity or nasopharynx, with most cases having tumors localized in the upper aerodigestive tract (UAT) including nasal cavity, nasopharynx, oral cavity, oropharynx, and hypopharynx. Primary tumors that present outside the UAT, but share identical histologic features with the UAT disease, have also been categorized as non-nasal-type NK/T-cell lymphoma (NUAT-ENKL). There is clinical heterogeneity between nasal and extranasalUAT-ENKL or between UAT-ENKL and NUAT-ENKL [Kohrt et al., 2009; Kim et al., 2008]. Kim et al. reported that NUAT-ENKL had significantly higher proportions of disseminated disease, aggressive biologic features, and worse prognosis than UAT-ENKL[Kim et al., 2008]. In the UAT-ENKL group, there are differences in clinical prognostic factors between nasal UAT and extranasal UAT. Patients with extranasal UAT showed a higher proportion of advanced disease (stages III and IV on the Ann Arbor system) and regional lympohadenopathy. However, there did not seem to be any difference between extranasal UAT-ENKL and nasal UAT-ENKL with respect to survival rate. Compared to patients with UAT-ENKL (including both nasal and extranasal UAT ENKL), patients with NUAT-ENKL showed significantly higher proportions of advanced-stage disease, two or more extranodal sites, positive regional lymphadenopathy, presence of B symptoms, and poor Eastern Cooperative Oncology Group performance status. As a result of the aggressive features of NUAT-ENKL, survival rates were lower than those of UAT-ENKL (5-year overall survival rate: 22% versus 41%, P <0.001) [Kim et al., 2008].
\n\t\t\t\tENKL is rare in Western countries, but is more frequent in East Asia, and Central and South America [Oshimi, 1996]. It represents 3.3% of all non-Hodgkin lymphoma in Japan, 6% in Hong Kong, 8% in Korea, and 5% in Taiwan [Lymphoma Study Group of Japanese Pathologists, 2000]. ENKL is the most common lymphoma type among primary nasal-type lymphomas in Asian patients. The male:female ratio in approximately 3:1 and the median age of presentation is middle age [Ishida & Kwong, 2010]. ENKL shows onset at an older age than ANKL.
\n\t\t\t\tThe immunophenotype of ENKL is typically CD2+, CD56+, CD3ε+, sCD3–, CD4–, CD20–, and CD30–. CD56, a highly useful marker for NK cells, is not specific for ENKL and can be expressed in peripheral T-cell lymphomas. Occasional cases are CD7+ or CD30+. ENKL shares many feature with ANKL, such as the presence of azurophilic granules in the cytoplasm of the neoplastic cells and identical immunophenotype except for CD16 expression. CD16 is negative in ENKL cases, but is positive in most ANKL cases [Nava & Jaffe, 2005]. As with ANKL, ENKL tumor cells are usually EBV positive. Cytotoxic molecules are positive (granzyme B, TIA-1, and perforin). Lymphomas that demonstrate a CD3ε+ and CD56–immunophenotype are also classified ENKL if both cytotoxic molecules and EBV are positive. TCR rearrangement is in the germline configuration. CD56 is a highly useful marker of NK cells but is not specific for ENKL. CD56 is expressed in peripheral T-cell lymphomas, particularly those that show the gamma delta TCR configuration.
\n\t\t\t\tIn this literature review, all journals were searched from 1996 to date for ENKL cases (Tables 4 and 5). Twenty-one pediatric cases with ENKL were reported: seven from Asia, 11 from
\n\t\t\t\t\tCase | \n\t\t\t\t\t\t\t\tAge/gender | \n\t\t\t\t\t\t\t\tStage (Ann Arbor) | \n\t\t\t\t\t\t\t\tFever | \n\t\t\t\t\t\t\t\tSubtype(primary site) | \n\t\t\t\t\t\t\t\tSitesinvolved | \n\t\t\t\t\t\t\t\tOther signs | \n\t\t\t\t\t\t\t\tTreatment | \n\t\t\t\t\t\t\t\tPrognosis | \n\t\t\t\t\t\t\t\tReference | \n\t\t\t\t\t\t\t
1 | \n\t\t\t\t\t\t\t\t17 y/M | \n\t\t\t\t\t\t\t\tIV | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tNUAT | \n\t\t\t\t\t\t\t\tL/S/LN | \n\t\t\t\t\t\t\t\tHPS | \n\t\t\t\t\t\t\t\tmBACOD, 2-CdA | \n\t\t\t\t\t\t\t\tAggressive, died 2 mo | \n\t\t\t\t\t\t\t\tKwong et al., 1997 | \n\t\t\t\t\t\t\t
2 | \n\t\t\t\t\t\t\t\t17 y/F | \n\t\t\t\t\t\t\t\tI | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\tUAT (nasal) | \n\t\t\t\t\t\t\t\t\n\t\t\t\t\t\t\t\t | \n\t\t\t\t\t\t\t\t | CHOP | \n\t\t\t\t\t\t\t\tAlive 27 mo | \n\t\t\t\t\t\t\t\tKwong et al., 1997 | \n\t\t\t\t\t\t\t
3 | \n\t\t\t\t\t\t\t\t18 y/F | \n\t\t\t\t\t\t\t\tI | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\tUAT (nasal) | \n\t\t\t\t\t\t\t\t\n\t\t\t\t\t\t\t\t | \n\t\t\t\t\t\t\t\t | CHOP | \n\t\t\t\t\t\t\t\tAlive 107 mo | \n\t\t\t\t\t\t\t\tKwong et al., 1997 | \n\t\t\t\t\t\t\t
4 | \n\t\t\t\t\t\t\t\t16 y/F | \n\t\t\t\t\t\t\t\tII | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tNUAT | \n\t\t\t\t\t\t\t\tCecum | \n\t\t\t\t\t\t\t\t\n\t\t\t\t\t\t\t\t | CHOP | \n\t\t\t\t\t\t\t\tAggressive, died 7 mo | \n\t\t\t\t\t\t\t\tLei et al., 1997 | \n\t\t\t\t\t\t\t
5 | \n\t\t\t\t\t\t\t\t15 y/F | \n\t\t\t\t\t\t\t\tIV | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tNUAT | \n\t\t\t\t\t\t\t\tL/S/Meso/BM | \n\t\t\t\t\t\t\t\t\n\t\t\t\t\t\t\t\t | – | \n\t\t\t\t\t\t\t\tAggressive, died 59 d | \n\t\t\t\t\t\t\t\tCatlin et al., 1999 | \n\t\t\t\t\t\t\t
6 | \n\t\t\t\t\t\t\t\t1 mo/M | \n\t\t\t\t\t\t\t\tIV | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tNUAT | \n\t\t\t\t\t\t\t\tL/S/BM | \n\t\t\t\t\t\t\t\t\n\t\t\t\t\t\t\t\t | IFN-( | \n\t\t\t\t\t\t\t\tAggressive, died 6 d | \n\t\t\t\t\t\t\t\tCatlin et al., 1999 | \n\t\t\t\t\t\t\t
7 | \n\t\t\t\t\t\t\t\t9 y/M | \n\t\t\t\t\t\t\t\tII | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\tNUAT | \n\t\t\t\t\t\t\t\tSk/LN | \n\t\t\t\t\t\t\t\t\n\t\t\t\t\t\t\t\t | POG9219/CCG1883/HDC | \n\t\t\t\t\t\t\t\tAlive, 41 mo | \n\t\t\t\t\t\t\t\tShaw et al., 2001 | \n\t\t\t\t\t\t\t
8 | \n\t\t\t\t\t\t\t\t12 y/M | \n\t\t\t\t\t\t\t\tII | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\tNUAT | \n\t\t\t\t\t\t\t\tM/LN | \n\t\t\t\t\t\t\t\t\n\t\t\t\t\t\t\t\t | POG9219/ICE/HDC | \n\t\t\t\t\t\t\t\tAlive, 15 mo | \n\t\t\t\t\t\t\t\tShaw et al., 2001 | \n\t\t\t\t\t\t\t
9 | \n\t\t\t\t\t\t\t\t17 y/M | \n\t\t\t\t\t\t\t\tIV | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tNUAT | \n\t\t\t\t\t\t\t\tSk | \n\t\t\t\t\t\t\t\tHPS | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tDied 33 mo | \n\t\t\t\t\t\t\t\tKo et al., 2004 | \n\t\t\t\t\t\t\t
10 | \n\t\t\t\t\t\t\t\t17 y/M | \n\t\t\t\t\t\t\t\tIV | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\tNUAT | \n\t\t\t\t\t\t\t\tL/Sk/LN | \n\t\t\t\t\t\t\t\t\n\t\t\t\t\t\t\t\t | GEM/IRI | \n\t\t\t\t\t\t\t\tAggressive, died 67 d | \n\t\t\t\t\t\t\t\tPol-Rodriguez et al., 2006 | \n\t\t\t\t\t\t\t
11 | \n\t\t\t\t\t\t\t\t17 y/F | \n\t\t\t\t\t\t\t\tIV | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tNUAT | \n\t\t\t\t\t\t\t\tLN/Sk/S/K/P/O | \n\t\t\t\t\t\t\t\tHPS/HMB | \n\t\t\t\t\t\t\t\tCHOP | \n\t\t\t\t\t\t\t\tAggressive, died 3 mo | \n\t\t\t\t\t\t\t\tAydin et al., 2007 | \n\t\t\t\t\t\t\t
12 | \n\t\t\t\t\t\t\t\t0.7 y/F | \n\t\t\t\t\t\t\t\tI | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tUAT (mastoid) | \n\t\t\t\t\t\t\t\t\n\t\t\t\t\t\t\t\t | \n\t\t\t\t\t\t\t\t | POG9219 | \n\t\t\t\t\t\t\t\tAlive | \n\t\t\t\t\t\t\t\tHutchinson et al., 2008 | \n\t\t\t\t\t\t\t
13 | \n\t\t\t\t\t\t\t\t16.3 y/M | \n\t\t\t\t\t\t\t\tI | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tUAT (nasal) | \n\t\t\t\t\t\t\t\t\n\t\t\t\t\t\t\t\t | \n\t\t\t\t\t\t\t\t | POG9219 | \n\t\t\t\t\t\t\t\tDied | \n\t\t\t\t\t\t\t\tHutchinson et al., 2008 | \n\t\t\t\t\t\t\t
14 | \n\t\t\t\t\t\t\t\t16.3 y/F | \n\t\t\t\t\t\t\t\tII | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tUAT (nasal) | \n\t\t\t\t\t\t\t\tSk | \n\t\t\t\t\t\t\t\t\n\t\t\t\t\t\t\t\t | POG9219 | \n\t\t\t\t\t\t\t\tAlive | \n\t\t\t\t\t\t\t\tHutchinson et al., 2008 | \n\t\t\t\t\t\t\t
15 | \n\t\t\t\t\t\t\t\t16.6 y/M | \n\t\t\t\t\t\t\t\tII | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tUAT (nasal) | \n\t\t\t\t\t\t\t\t\n\t\t\t\t\t\t\t\t | \n\t\t\t\t\t\t\t\t | POG9219 | \n\t\t\t\t\t\t\t\tDied | \n\t\t\t\t\t\t\t\tHutchinson et al., 2008 | \n\t\t\t\t\t\t\t
16 | \n\t\t\t\t\t\t\t\t16 y/M | \n\t\t\t\t\t\t\t\tI | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\tUAT (nasal) | \n\t\t\t\t\t\t\t\t\n\t\t\t\t\t\t\t\t | \n\t\t\t\t\t\t\t\t | CHOP | \n\t\t\t\t\t\t\t\tAlive, CCR "/24 mo | \n\t\t\t\t\t\t\t\tChang et al., 2008 | \n\t\t\t\t\t\t\t
17 | \n\t\t\t\t\t\t\t\t12 y/F | \n\t\t\t\t\t\t\t\tI | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\tUAT (nasal) | \n\t\t\t\t\t\t\t\t\n\t\t\t\t\t\t\t\t | \n\t\t\t\t\t\t\t\t | CHOP/IR | \n\t\t\t\t\t\t\t\tAlive, CCR 8 mo | \n\t\t\t\t\t\t\t\tLee et al., 2008 | \n\t\t\t\t\t\t\t
18 | \n\t\t\t\t\t\t\t\t11 y/M | \n\t\t\t\t\t\t\t\tIV | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tUAT (nasal) | \n\t\t\t\t\t\t\t\tBM | \n\t\t\t\t\t\t\t\tHPS | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\tAggressive, died 5 mo | \n\t\t\t\t\t\t\t\tBrodkin et al., 2008 | \n\t\t\t\t\t\t\t
19 | \n\t\t\t\t\t\t\t\t9 y/F | \n\t\t\t\t\t\t\t\tI | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tUAT (nasopharynx) | \n\t\t\t\t\t\t\t\t\n\t\t\t\t\t\t\t\t | HMB | \n\t\t\t\t\t\t\t\tCHOP | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tZhang et al., 2009 | \n\t\t\t\t\t\t\t
20 | \n\t\t\t\t\t\t\t\t15 y/F | \n\t\t\t\t\t\t\t\tIV | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tUAT (tonsil) | \n\t\t\t\t\t\t\t\t\n\t\t\t\t\t\t\t\t | HPS/Li/S | \n\t\t\t\t\t\t\t\tCHOP | \n\t\t\t\t\t\t\t\tDied 1 mo | \n\t\t\t\t\t\t\t\tPellier et al., 2009 | \n\t\t\t\t\t\t\t
21 | \n\t\t\t\t\t\t\t\t4 y/M | \n\t\t\t\t\t\t\t\tI | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tUAT (nasal) | \n\t\t\t\t\t\t\t\t\n\t\t\t\t\t\t\t\t | \n\t\t\t\t\t\t\t\t | CHOP | \n\t\t\t\t\t\t\t\tAggressive, died 18 d | \n\t\t\t\t\t\t\t\tMiles et al., 2010 | \n\t\t\t\t\t\t\t
Clinical characteristics of pediatric patients with extranodal NK leukemia
Abbreviations: BM, bone marrow; CCG1883, Childhood Cancer Group 1883 protocol; CCR, clinical complete response; CHOP, cyclophosphamide, doxorubicin, vincristine, prednisolone; d, days; F, female; GEM, gemcitabine; HDC, high-dose chemotherapy; HMB, hypersensitivity to mosquito bites; HPS, hemophagocytosis; ICE, ifosfamide, carboplatin, etoposide; IFN-(, interferon alpha; IR, irinotecan; K, kidney; L, lung; Li, liver; LN, lymph node; M, mastoid; mo, months; P, pancreas; POG9219, Pediatric Onocology Group 9219 protocol; M, male; mBACOD; bleomycin, adriamycin, cyclophosphamide, vincristine, dexamethasone, methotrexate; meso, mesosalpinx; ND, not determined; NUAT; non-upper aerodigestive tract; O, oral; S, spleen; Sk, skin; UAT; upper aerodigestive tract; y, years; 2-CdA, 2-chlorodeoxyadenosine.
Case | \n\t\t\t\t\t\t\t\tCD2 | \n\t\t\t\t\t\t\t\tCD3ε | \n\t\t\t\t\t\t\t\tsCD3 | \n\t\t\t\t\t\t\t\tCD4 | \n\t\t\t\t\t\t\t\tCD7 | \n\t\t\t\t\t\t\t\tCD8 | \n\t\t\t\t\t\t\t\tCD16 | \n\t\t\t\t\t\t\t\tCD56 | \n\t\t\t\t\t\t\t\tCytotoxic markers | \n\t\t\t\t\t\t\t\tTCR re-arrangement | \n\t\t\t\t\t\t\t\tEBV DNA | \n\t\t\t\t\t\t\t\tReference | \n\t\t\t\t\t\t\t
1 | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tKwong et al., 1997 | \n\t\t\t\t\t\t\t
2 | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tKwong et al., 1997 | \n\t\t\t\t\t\t\t
3 | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tKwong et al., 1997 | \n\t\t\t\t\t\t\t
4 | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t\n\t\t\t\t\t\t\t\t | + | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tLei et al., 1997 | \n\t\t\t\t\t\t\t
5 | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\tNT | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tNT | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tCatlin et al., 1999 | \n\t\t\t\t\t\t\t
6 | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tNT | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tCatlin et al., 1999 | \n\t\t\t\t\t\t\t
7 | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\tShaw et al., 2001 | \n\t\t\t\t\t\t\t
8 | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tShaw et al., 2001 | \n\t\t\t\t\t\t\t
9 | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tKo et al., 2004 | \n\t\t\t\t\t\t\t
10 | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tTIA-1+ | \n\t\t\t\t\t\t\t\tNT | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tPol-Rodriguez et al., 2006 | \n\t\t\t\t\t\t\t
11 | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\tGranzyme B+ | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\tAydin et al., 2007 | \n\t\t\t\t\t\t\t
12 | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tHutchinson et al., 2008 | \n\t\t\t\t\t\t\t
13 | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tHutchinson et al., 2008 | \n\t\t\t\t\t\t\t
14 | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tHutchinson et al., 2008 | \n\t\t\t\t\t\t\t
15 | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\tHutchinson et al., 2008 | \n\t\t\t\t\t\t\t
16 | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tNT | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\tNT | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\tTIA-1, granzyme B+ | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tChang et al., 2008 | \n\t\t\t\t\t\t\t
17 | \n\t\t\t\t\t\t\t\tNT | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tNT | \n\t\t\t\t\t\t\t\tNT | \n\t\t\t\t\t\t\t\tNT | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tNT | \n\t\t\t\t\t\t\t\tNT | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\tLee et al., 2008 | \n\t\t\t\t\t\t\t
18 | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tNT | \n\t\t\t\t\t\t\t\tNT | \n\t\t\t\t\t\t\t\t- | \n\t\t\t\t\t\t\t\tNT | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tNT | \n\t\t\t\t\t\t\t\tNT | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tBrodkin et al., 2008 | \n\t\t\t\t\t\t\t
19 | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tNT | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tNT | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tNT | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\tTIA-1 + | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tZhang et al., 2009 | \n\t\t\t\t\t\t\t
20 | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tND | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tPellier et al., 2009 | \n\t\t\t\t\t\t\t
21 | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tNT | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tNT | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\tTIA-1+ | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\tMiles et al., 2010 | \n\t\t\t\t\t\t\t
Phenotypic characteristics of pediatric patients with extranodal NK leukemia. Case numbers correspond with those in Table 4\n\t\t\t\t\t\t\t
Abbreviations: EBV, Epstein Barr virus; ND, not determined; NT, not tested; TCR, T-cell antigen receptor; TIA-1, T-cell-restricted intracellular antigen-1.
US (including one with acquired disease), and one each from Turkey, South America, and France. In adult patients, the International Peripheral T-cell Lymphoma Project reported a four-fold higher relative frequency of ENKL among lymphoma in Asian countries compared to Western countries [Au et al., 2009]. For peripheral T-cell lymphoma, ENKL was the most common histology in Asian countries (range 34%–56%) except for Japan (11%) [Au et al., 2009]. In children and adolescents, the frequency of Asian cases is the same as in adults. Median age is 16 years (range, 0.7–18 years excluding the infant with acquired disease) and the mean age is 13 years. ENKL presents at a higher age than other forms of pediatric leukemia/lymphoma in a similar manner to other NK-lineage leukemias/lymphomas. There were 11 males and 9 females (male to female ratio, 1.22:1) and male predominance has been reported in adults.
\n\t\t\t\t\tOf the 21 pediatric patients, 14 patients had local disease (stage I and II) and seven had disseminated disease (stage III and IV) on the Ann Arbor staging system. The ratio of patients with UAT-ENKL as compared to those with NUAT-ENKL is 7:2 in adults and 2:1 in pediatric patients (Table 4). In pediatric patients, the frequency of NUAT-ENKL patients is higher than in adults [Oshimi et al., 2005]. In pediatric ENKL patients, about half of them presented UAT-ENKL: nine patients had a nasal site and three patients had an extranasal site, including mastoid, tonsil, and skin. UAT patients have been regarded as having no dissemination to other sites [Kim & Heo, 2009]. Cases 18 and 21 are therefore exceptional cases. They had significant hepatomegaly and lymphadenopathy. Their condition deteriorated progressively and lymph node biopsy and bone marrow aspiration presented the invasion of ENKL cells. Case 18 died after 4 days and case 20 died after 30 days from onset [Brodkin et al., 2008]. In adult patients, only 16% of UAT-ENKL patients are reported to have involvement of an extranodal site [Kim et al., 2008].
\n\t\t\t\t\tThe proportion of pediatric NUAT-ENKL with a primary tumor outside the UAT is higher than that in adults. In adults, Kim et al. reported three patients with local disease (stage II) and six with disseminated disease (stage IV) [Kim et al., 2008]. Patients with NUAT-ENKL showed higher proportions of advanced-stage disease than adult patients with NUAT- ENKL. In pediatric patients tumor tended to disseminate. The sites involved were lymph node (5 cases), spleen (5 cases), lung (4 cases), bone marrow (2 cases), and skin (2 cases). The predominant site of adult NUAT-ENKL group is skin (37%), liver or spleen (31%), and the GI tract (24%).
\n\t\t\t\t\tHemophagocytosis (HPS) can be a complication in ENKL (2%–8% of patients) [Kim et al., 2008]. In pediatric patients, four (1 UAT and 3 NUAT) of 20 cases were reported with HPS (Table 4). The frequency of HPS in pediatric patients may be higher than that of adults.
\n\t\t\t\tHypersensitivity to mosquito bite (HMB) syndrome is characterized by an intense skin reaction and systemic symptomatology such as high fever, lymphadenopathy, and hepatosplenomegaly. This condition has been mostly reported in Japanese children. HMB syndrome occurs in association with NK-cell lymphocytosis-related chronic EBV infection. CD4+ T cells from patients respond markedly to mosquito salivary gland extracts, and CD4+ T cells stimulated by mosquito bites may play a key role in the development of HMB syndrome and NK-cell oncogenesis. It is unclear how stimulated CD4+ T cells are involved in viral reactivation of viral oncogene expression in NK cells (Fig. 1)[Asada, 2007]. In the 20 pediatric ENKL cases in this review, two cases may have exhibited HMB syndrome before ENKL; one from China and the other from Turkey.
\n\t\t\t\tCD4+ T cells stimulated by mosquito bites may play a key role in the development of hypersensitivity to mosquito bites (HMB) and NK-cell oncogenesis via the induction of Epstein-Barr virus (EBV) reactivation and EBV-oncogene latent membrane protein 1 (LMP1) expression, respectively [
There remains a lack of consensus on the treatment of ENKL and there is no standard therapy in adults or pediatric patients. ENKL shows an aggressive clinical course with various clinicopathologic characteristics. Due to this clinical heterogeneity of ENKL, optimal treatment and prognostic factors have been difficult to determine with the conventional Ann Arbor staging system.NUAT-ENKL has a pathologic similarity to UAT–ENKL but is a clinically distinct subtype.
\n\t\t\t\t\tFor early-stage ENKL, both UAT and NUAT, experience with radiation therapy, chemotherapy, and combined therapy has been reported. The largest study with radiotherapy or radiotherapy plus chemotherapy was reported by Kim et al. [2001]. In this report of 143 patients, 104 received upfront radiotherapy alone with a median dose of 50.4 Gy (range, 20–70 Gy). Of those who received radiotherapy alone, 69% of patients achieved a complete response (CR), while only 8% of those who received chemotherapy prior to radiotherapy achieved CR [Kim et al., 2001; Korht & Advani 2009]. Huang et al. reported CR and 5-year overall survival (OS) rates of 100% in patients who received radiotherapy alone, while those who received chemotherapy (CHOP) alone had rates of 25% and 90%, respectively [Huang et al., 2008]. Li et al. reported overall response in 85 of 87 (97.7%) patients with stage I UAT-ENKL who received radiotherapy with 50–56 Gy (standard is 50 Gy). The 5-year OS, 5-year progression-free survival (PFS), and local control rates for all patients were 80%, 69%, and 93%, respectively [Li et al., 2011b].
\n\t\t\t\t\t\tThe dose and field of radiation in stage I or II ENKL is an important factor with respect to outcome. A radiation dose of at least 54 Gy is seen as being associated with better outcome. Comparing those who received ≥54 Gy versus <54 Gy, 5-year OS and disease-free survival (DFS) rates were higher with the former: 75% vs 46% and 60% vs 46%, respectively [Huang et al., 2008]. Systemic failure is shown in 25% to 30% of patients with stage II and II disease treated with radiotherapy alone. This shows the role of chemotherapy in control of clinically occult disease.
\n\t\t\t\t\tThere are few studies that included patients treated with chemotherapy alone. Studies of chemotherapy regimens including cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) are disappointing because of high rates of refractory disease or early relapse: the CR rate with chemotherapy alone was <33% and 2-year DFS and OS were 23% and 44%, respectively [Kim et al., 2003]. This poor prognosis with chemotherapy alone appears related to high P-glycoprotein (P-gp) expression in this NK-cell neoplasm. P-gp is associated drug efflux and treatment resistance.
\n\t\t\t\t\tFor the control of clinically occult early-stage disease, a combined modality therapy is anticipated to reduce distant failure and overall risk of relapse. In a series of 108 patients with early-stage ENKL receiving radiotherapy followed by chemotherapy consisting with cyclophosphamide, epirubicin, vincristine, prednisolone, and bleomycin[Avilés et al., 2003], combined therapy demonstrated high efficacy with a 92% overall response rate and 8-year OS of 86%. In early-stage ENKL, Guo et al. reported that patients who received CHOP followed by radiotherapy (45 Gy) had a CR rate of only 49% as compared to 100% for those who received radiotherapy prior to CHOP [Guo et al., 2008]. Li et al. reported that patients with early-stage UAT-ENKL (stages I and II) treated with radiotherapy or radiotherapy plus chemotherapy had 5-year OS and PFS rates of 72% and 65%, respectively, overall. The cumulative rates of 5-year systemic failure and OS, respectively, were 24% and 74% for combined modality therapy as compared to 28% and 70%for radiotherapy alone. There was no significant difference between radiotherapy alone and combined modality therapy. A very low incidence of cervical lymph node or CNS relapse was observed. As a result, the addition of chemotherapy did not significantly decrease the systemic failure rate or improve survival [Li et al., 2011a]. In the Japanese JCOG 0211 study [Yamaguchi et al. 2008], 27 patients received radiotherapy (50 Gy) and reduced-dose chemotherapy (carboplatin etoposide, ifosfamide, and dexamethasone). The CR rate was 77% and overall response rate was 81%. Of the ten patients with disease recurrence, nine failed at a distant site. These studies demonstrate that local control using radiotherapy should precede systemic chemotherapy. Prospective studies are needed to clarify the role of chemotherapy.
\n\t\t\t\t\tCombined chemotherapy and radiotherapy is the most commonly used approach for advanced-stage disease. Due to the limited number and size of series, the efficacy of intensive therapy has not been demonstrated. For CHOP or m-BACOD (bleomycin, vincristine, dexamethasone, and methotrexate) followed by radiotherapy, the CR rate in patients with advanced-stage disease was 25% and median OS was 2 months as compared to 75% and 12 months, respectively, in those with early-stage disease [Kwong et al., 1997].
\n\t\t\t\t\t\tL-asparaginase has been reported as a novel approach for the treatment of advanced-stage ENKL. NK-cell tumors appear highly sensitive to L-asparaginasein vitro, as NK cells express low levels of asparaginase synthase. In a series of 15 patients with relapsed or refractory ENKL treated with L-asparaginasemonotherapy, seven achieved a CR with an overall response rate of 87% [Jaccard et al., 2009]. Yamaguchi et al. have reported the efficacy of the SMILE regimen consisting with steroids, methotrexate, ifosfamide, L-asparaginase, and etoposide. These agents are independent of the multidrug resistant mechanism (mediated by P-gp) in tumor cells. This phase I study included six patients with advanced-stage disease. The overall response rate after 2 cycles of SMILE therapy was 67%, with 50% achieving CR [Yamaguchi et al., 2008].
\n\t\t\t\t\tAutologous and allogeneic stem cell transplantation (SCT) have been evaluated for consolidation and for relapsed or refractory disease. Suzuki et al. reported 25 CR patients who received SCT and 4-year OS was 68% [Suzuki et al., 2006]. This demonstrated a significant benefit compared to 188 historical controls who had 4-year OS of 21%. As there have been few reports of SCT, the ability to define its role as therapy for relapsed or refractory disease remains limited. For refractory and relapsed ENKL patients, Yokoyama et al. reported a retrospective analysis of five cases treated with allogeneic SCT [Yokoyama et al., 2010]. All five patients received a myeloablative conditioning regimen (total body irradiation/cyclophosphamide with or without cytarabine) and survived without disease (median follow-up period of 1,911 days). This small case series suggests that allogeneic SCT might improve the outcome of advanced-stage ENKL.
\n\t\t\t\t\tIn the pediatric ENKL patients (excluding case 19 whose prognosis was not reported), eight of 12 patients with early-stage (stage I and II) disease including UAT and NUAT were alive (Table 4). Two cases were not described in detail and another two cases died within 1 year. The CR rate is 61%. Case 21 had nasal and right cervical lymphadenopathy and his tumor was not controlled; he died despite CHOP and more intensive chemotherapy. The outcome of pediatric early-stage patients was worse than in adults. The reason is that most cases did not receive radiotherapy and received chemotherapy alone, generally CHOP.
\n\t\t\t\t\t\tIn advanced-stage disease (stage IV), all cases died and average survival was 181 days (6 days to 33 months). Both UAT and NUAT cases show very progressive disease and poor prognosis. Two cases with NUAT received high-dose chemotherapy, had complete remission, and were alive. Case 9 received cord blood SCT after a conditioning regimen consisting of total body irradiation (12 Gy), thiotepa, and cyclophosphamide, while case 10 received autologous SCT after thiotepa and cyclophosphamide.
\n\t\t\t\t\t\tThere have been no large studies in pediatric patients. The largest is a report from China. Wang et al. reported the outcome of 37 pediatric and adolescent UAT-ENKL patients. Among the patients with stage I and II disease, 19 patients received primary radiotherapy with or without chemotherapy, and 14 patients received chemotherapy followed by radiotherapy. The CR rate after initial radiotherapy was 74%, which was significantly higher than the response rate after initial chemotherapy (17%). The median radiation dose for the primary tumor was 50 Gy (range, 15–60 Gy), with dose fractions of 1.8–2 Gy. They reported no late side effects, e.g. secondary malignancy [Wang et al., 2009].
\n\t\t\t\t\tBlasticplasmacytoid dendritic cell neoplasm (pDCL) defines leukemia/lymphoma with expression of CD4 and CD56 without any other lineage-specific markers. pDCL is rare and presents a <1% of acute leukemias and 0.7% of cutaneous lymphomas[Garnache-Ottou et al., 2007]. It primarily affects the elderly (median age 69 years) [Feuillard et al., 2002]. The clinical course is very aggressive and rapidly fatal [Reimer et al., 2003]. Histologically, this malignancy is classified as blastic NK-cell lymphoma/leukemia. The 2000 WHO classification considers this malignancy as blastic NK-cell lymphoma[Harris et al., 2000].
\n\t\t\t\tThe ontogenic origin of this malignancy has not been clearly identified. Chaperot et al. have demonstrated the origin of these tumor cells as dendritic cells [Chaperot et al., 2001]. These malignant cells express interleukin-3 (IL-3) receptor maturation with IL-3 and produce interferon alpha (IFN-α) in response to influenza virus. These cells become a powerful inducer of naïve CD4+ T-cell proliferation and promote T-helper 2 polarization. Finally, these authors concluded the origin of this neoplasm is a plasmacytoid dendritic cell subset. Feuilliard et al. reported 23 cases with CD4+, CD56+leukemia. The majority of patients were elderly adults, but three children were included in their report. At diagnosis, most patients had cutaneous involvement, with disseminated purple lesions on the dermis. Lymphadenopathy and/or splenomegaly were frequent [Chaperot et al., 2001]. Morphologic and cytochemical analysis revealed a high frequency of vacuolization with pseudopodia-like cytoplasmic expansions. Myeloperoxidase and monocytic esterase activity were never detected.
\n\t\t\t\tHowever, all cases of pDCL do not produce IFN-α and secretion levels of IFN-α have been lower than their normal counterparts. pDCL cells proved incapable of differentiating into NK cells, B cells, myeloid cells, or monocytes, and differentiation into mature pDC was only possible. Furthermore, a subset of pDCL demonstrated the expression of blood dendritic cell antigen 2 (BDCA-2), a specific dendritic cell marker. This fact supports that the origin of pDCL as dendritic cells[Jaye et al., 2006]. However, some other reports remain undetermined concerning the possible origin of pDCL. More investigation is required to establish the definitive nature of these CD4+/CD56+ tumor cells.
\n\t\t\t\t\n\t\t\t\t\t\tTable 6 shows the differential diagnosis. ENKL is associated with EBV infection, while this has not been reported for pDCL. Although expression of CD56+, CD2+, CD7+, and intraplasmicgranzyme B can be in common between ENKL and pDCL, ENKL never expresses CD4+[Harris et al., 1997]. In about 10% to 20% of acute myelogenous leukemia patients, tumor cells express CD33+, CD4+, and CD56+. Very undifferentiated acute myelogenous leukemia weakly shows myelocytic or monoblastic markers. In these cases, identification of pDC-specific markers (e.g. BDCA-2) is useful[Garnache-Outtu et al., 2007]
\n\t\t\t\t\tMixed myeloblastic/NK-cell leukemia are defined as types of myeloid leukemia in the WHO 2008 classification [Swerdlow et al., 2008]. These leukemias express CD7+, CD33+, and CD56+. They correspond to proliferation of animmature precursor with myeloid and NK potential [Suzuki et al., 1997]. The leukemia phenotype is different from pDCL as they do not express CD4 and CD36 in reported cases [Suzuki et al., 1997]. Furthermore, in pDCL, there is no expression of CD34, while its expression has always shown in mixed myeloblastic/NK-cell leukemia cells.
\n\t\t\t\t\tMarker | \n\t\t\t\t\t\t\t\tpDCL | \n\t\t\t\t\t\t\t\tENKL | \n\t\t\t\t\t\t\t\tAML | \n\t\t\t\t\t\t\t\tMixed myeloblastic/NK-cell leukemia | \n\t\t\t\t\t\t\t
CD2 | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t\n\t\t\t\t\t\t\t |
CD7 | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t± | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t
CD56 | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t
CD4 | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t
Granzyme B | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t\n\t\t\t\t\t\t\t\t | \n\t\t\t\t\t\t\t |
CD33 | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t
CD117 | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t\n\t\t\t\t\t\t\t |
CD34 | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t± | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t
CD36 | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t
BDCA-2 | \n\t\t\t\t\t\t\t\t+ | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t\t– | \n\t\t\t\t\t\t\t
Differential diagnosis of blasticplasmacytoid dendritic cell neoplasms
Abbreviations: AML, acute myelogenous leukemia; BDCA-2, blood dendritic cell antigen 2; ENKL, extranodal NK-cell leukemia; pDCL, blasticplasmacytoid dendritic cell neoplasm.
Pediatric pDCL is very rare and limited to a few case reports and small case series. Jegalian et al. reported 25 pediatric cases (20 in the literature, 9 at their institution) with pDCL[Jegalian et al., 2010]. They demonstrated the clinical features and prognosis of pediatric patients. In pediatric patients, 24% of patients lacked cutaneous involvement, which is slightly higher rate than adults. In adult patients, pDCL clinical presentation at the time of diagnosis usually consists of a cutaneous involvement and the patients without cutaneous involvement are very rare. In adult patients, especially the elderly, prognosis is very poor. Median OS was only 13 months for all patients. Allogeneic SCT is a useful treatment in younger adult patients. They reported a regimen suited to acute lymphoblastic leukemia followed by SCT is more effective than using an acute myelogenous leukemia or non-Hodgkin lymphoma regimen. While the OS of pediatric patients receiving SCT was 67% (4 of 6 patients), that for patients without SCT was 74%. In pediatric patients, treatment with a high-risk regimen appears effective without SCT. SCT was useful for only relapsed or secondary remission disease. Outcome of pediatric patients was more favorable than that of adults [Jegalian et al., 2010].
\n\t\t\tNK-cell malignancy is difficult to define and there is confusion in diagnosis. One of the reasons for the confusion is that CD56 is not only expressed in NK-cell malignancy but in various other hematopoietic malignancies, e.g. acute myelogenous leukemia non-Hodgkin lymphoma, pDCL. It is hoped that more specific markers for NK-cell malignancy will assist in defining these malignancies. NK-cell precursor tumors with lymphomatous presentation that expressed NK-specific CD94A1 transcripts have been described[Lin et al., 2005]. I used this method and clarified the origin of one case[Hashii et al., 2010]. Antibodies against killer immunoglobulin-like receptors (KIRs) will hopefully provide a useful tool for clarification of the diagnosis of the NK-cell malignancies. Currently, these antibodies are not commonly used. Although, BDCA-2 is useful for clarifying the difference between NK-cell malignancy and pDCL, it is not commonly used. The diagnosis of precursor NK-cell lymphoblastic leukemia/lymphoma may be considered in cases that express CD56+ along with immature T-cell markers (CD2+, CD7+, and CD3ε+) without B-cell or myeloid markers.
\n\t\tBiomedical signals are electrical activities recorded by sensors from a part of the body, such as the brain, heart, muscles, etc. They can be recorded as images e.g. functional Magnetic resonance Image (fMRI) from brain or a temporal signal e.g. Electrocardiogram (ECG), Electroencephalogram (EEG), Electromyogram (EMG), Galvanic Skin Response (GSR), etc. These signals contain useful information to analyse and understand the underlying physiological response of the body, thus they are also referred to as physiological signals. Biomedical signals are extensively used in healthcare to diagnose deceases and monitor health. With recent advancements and ease of using the devices to record the biomedical signals have open a window to use it to analyse and understand the day-to-day activities, emotions, and, experiences [1, 2, 3]. While recording the physiological activities through sensors, the signals are usually contaminated by noise and various artefacts [4]. Corrupted signals mislead the analysis and understanding of the underlying physiology [5]. The characteristics of wavelet to identify the time-localised events makes it suitable for the biomedical signals to clean, process, feature extraction, and analyse for various applications. Recent studies have shown the promising results of using wavelet in biomedical signals [6].
In this chapter, first, we introduce one kind of biomedical signal - EEG. We will explain the conventional features used in EEG studies. We will introduce the artefacts that commonly contaminate EEG signals, which makes it harder to use. The chapter then will move towards a short description of Wavelet analysis techniques, namely Continues Wavelet Transform (CWT), Discrete Wavelet Transform (DWT), and Wavelet Packet Decomposition (WPD). We would, then, compare CWT and STFT for EEG signal. Then, we will discuss artefact removal algorithms, with more details on Wavelet-based algorithms. The chapter will show the comparative analysis of artefact removal algorithm. The approach and analysis shown in this chapter for EEG signals can easily be applied to other biological signals.
The brain processes any information by means of neurons that use electrical and chemical signals to communicate by releasing and receiving neurotransmitters. The neural activity in the human brain is an electrical change. The brain generates electrical signals throughout the day for various activities. Studying these electrical signals is vital to understanding the neurophysiological behaviour of the brain [4]. A number of techniques are used to study brain activities. Functional magnetic resonance imaging (fMRI), Functional Near-Infrared Spectroscopy (firs), and Electroencephalography (EEG) recordings widely used techniques. The fMRI measures brain activity by scanning the blood flow. The fNIRS measures brain activity by measuring hemodynamic response in the brain through detecting the temporal changes in infrared light source. The EEG measures the electrical activity of the brain by electrodes placed on the scalp. Comparing to the other two, EEG measures brain activity directly, with high temporal resolution and most accessible and portable for the research. The fMRI has a high spatial resolution but very expensive, therefore it is mostly limited to medical diagnosis and treatments.
The EEG signal is measured by placing multiple electrodes on the scalp that measure the current flow from neurons. A setup for EEG recording is shown in Figure 1. Each neuron (brain cell), when activated, it produced an electrical and magnetic field around the scalp. Since there are 100 billion neurons in the brain, when an electrode is placed on the scalp, it measures the accumulative activity of many neurons together. The complex structure of the brain attenuates the electrical signals, therefore an electrode can record the brain activity, only when a large number of neurons generate enough potential. The EEG devices amplify the recorded signal to store and process it [4].
EEG recording setup: (a) a wireless device Emotiv Epoch mounted on a subject, transmitting EEG signal to a computer. (b) Electrode positions as 10–20 system, source:
The placement of electrodes has been standardised with the specific anatomical landmarks with a distance between electrodes as 10% or 20% of total length. This placement is called the 10–20 system, as shown in Figure 1b. The number of electrodes used for EEG recording varies, depending on the device. One of the low spatial resolutions can be of a 14-channel EEG device and high spatial resolution with 128 or 256 channels. The name of the electrode position is labelled as character followed by a number to identify the part of the brain. The characters are
The raw recording of EEG signal in the time-domain is complex to interpret. Similar to many other signals, frequency domain analysis has been widely used. The decades of work on EEG studies have identified five major frequency bands for EEG signals and established the correlation between behaviour and neural activity of a certain part of the brain. The frequency bands widely used are; Delta (
The signal channel raw EEG signal and corresponding frequency bands: Delta (
Due to multichannel signals, it is usually viewed as topographical brain activity (heatmap over an image of head) under different frequency bands. An example of 5 seconds EEG recording with a 14-channel device is shown in Figure 3. The first second of all the channels are used to compute the energy distribution over brain regions. In Figure 3, the top left shows the raw EEG signal and corresponding brain activity, which shows a high activity in the frontal lobe of the brain. However, under different frequency bands, the different part of the brain shows higher activity.
Topographical view of brain activity: Energy distribution of EEG recording over different brain regions under five frequency bands and raw signal.
The frequency bands; Delta, Theta, Alpha, Beta, and Gamma, are also called brain rhythms. Brain rhythms have been investigated over decades and a few characteristic behaviour of these brain rhythms have been established [4].
While recording, EEG signals are frequently contaminated with various artefacts. The most common types of artefacts are motion, muscular, ocular, and cardiac artefacts [4], which are shown in Figure 4. The motion artefacts are caused by the physical movement of the person’s body. As shown in Figure 4a, motion artefacts produce a sudden high valued spike in all the channels of EEG recording. The muscular artefacts, shown in Figure 4b are caused by any muscular contraction such as grinding the teeth. It produces high-frequency bursts in EEG recording as circled in the Figure 4b. The cardiac artefacts, shown in Figure 4c, are caused by the electrical activities of the heart. They appear as a weak form of QRS wave of heart and most likely to be appeared in the channels near to ears (temporal lobe), though it can be sometimes present in channels from the frontal lobe [7]. The ocular artefacts are slow oscillating waves appear on the frontal lobe, caused by the eye movements or closed eyes, as circled in the Figure 4d. The higher magnitude of the artefacts corrupts the EEG recording and leads to misinterpretations of the results and analysis [5]. Even though there are many algorithms to remove the artefacts, but there is always a possibility of losing the cerebral information while removing the artefacts.
Common type of artefacts in EEG. Corresponding artefacts are circled in the figure.
Most of the real-life signals are non-stationary in behaviour, which means their properties change over time. To localise the events of interest, time-frequency analysis is widely used. The conventional way of time-frequency analysis is the Short-Time Fourier Transform (STFT), where Fourier transform of the signal is taken over short-windows, resulting spectrogram plot. STFT has limitations on resolutions, due to Heisenberg’s uncertainty principle, e.g. improvement in time resolution results in poorer frequency resolution and vice-versa. The alternative to STFT is wavelet transform, which exploits the property of low-frequency signals being widespread over time and high-frequency bursts occurring on short intervals. Wavelet transform uses the variable size of windows with a wavelet function.
Wavelet analysis is usually applied in two ways, Continuous Wavelet Transform (CWT) and Discrete Wavelet Transform (DWT). CWT uses a wavelet function
4-level decomposition tree for (a) discrete wavelet transform (DWT), (b) wavelet packet decomposition (WPD).
As shown in Figure 5, block LP is a lowpass filter
As discussed, a conventional way to time-frequency analysis is STFT, however, using CWT with different wavelet functions can enrich the analysis with more details. In this section, we will show, how a continuous wavelet function (
A spectrogram is obtained using STFT, which is Fourier Transform computed for a short windows. STFT
CWT operation from Eq. (2) can be seen as convolution of input signal
where
Continues wavelet functions.
where
where
where
where
where
where
An example of using the above six wavelet functions for a small single-channel EEG segment is shown in Figure 7, along with spectrogram. It can be observed, spectrogram highlights a few events in signal (sharp peaks and lowpass wave), however, using CWT with different Wavelet functions, much richer information can be observed. Since, we observed that in the formulation of wavelet functions that they are similar to the underlying principle, we could also observe the similarities across different scalograms. Specifically, spectrogram using Complex Shannon and Complex Mexican hat wavelet are much similar. Interestingly, Morlate and Poisson wavelet functions are able to produce a better resolution towards lower frequencies.
Scalogram and spectrogram of a segment of signal channel EEG signal with six wavelet functions and STFT. Figure obtained using spkit python library -
Artefacts in EEG recording is a primary obstacle that all researchers have to deal with. There are decades of research work in literature to remove these artefacts [15, 16]. A range of methods have been proposed to remove the artefacts, starts with a statistical with interpolation method [17] and regression method [18]. The most commonly used approaches are based on Blind Source Separation (BSS) using Independent Component Analysis (ICA) [19, 20]. ICA based approach have been widely explored with statistical measures [21, 22, 23, 24], and variant of ICA as FastICA, InfoMax, and Extended InfoMax [25, 26, 27]. Wavelet-based approaches are well suited for time-localised short events, as opposed to ICA. This property has been exploited to remove artefacts from single-channel EEG. In contrast to a single channel, wavelet has also been used for multi-channel EEG [28] and in combination with ICA [29, 30, 31, 32, 33, 34], in which identified artifactual component is cleaned with wavelet rather than removed. The ICA-based approaches can only be applied to multi-channel EEG and need an expert to select artifactual component, which has been automated with heuristics [21, 35, 36]. In contrast, most wavelet-based algorithms remove artefacts from each channel individually.
The key idea of wavelet-based artefact removal algorithms is to apply DWT on single-channel EEG signal
where
A block diagram of ATAR algorithm [
where
Wavelet filtering modes for ATAR algorithm. For
where
Figure 10 shows a visual comparative analysis of wavelet-based approaches (i.e. Global threshold, STD threshold, and ATAR algorithm) and ICA based approaches (FastICA, InfoMax, and Extended-InfoMax) to remove the artefacts. It is visually apparent that wavelet-based approaches are better than ICA-based approaches. Among wavelet-based approaches, using ATAR gives much control over Global and STD based threshold selection. Other quantitative analyses of the above-mentioned approaches are discussed in the article [41], which also demonstrate the effect of tuning parameter and filtering modes on different predictive tasks of EEG signal. The formulation of relationship, algorithmic implementation details, and comparative results are given in article [41].
Comparison of artefact removal approaches from [
This chapter presents the overview of Wavelet for EEG analysis. The first chapter introduces EEG signal, commonly used features for predictive analysis, and artefacts that often contaminate EEG signal. Then chapter discusses the Wavelet analysis approaches, namely CWT, DWT, and WPD. The richness of CWT over STFT for time-frequency analysis using various wavelet functions is demonstrated. Finally, the artefact removal algorithms based on wavelet and ICA are discussed. The comparative analysis present in the chapter shows that the wavelet-based approach outperforms ICA based approach. Specifically, a recent algorithm (ATAR) allows controlling the removal or suppression of assumed artifactual components in the signal, which can be tuned to improve the performance of any predictive tasks. The techniques presented in this chapter show how wavelet can be used for EEG studies to extract rich information and removing the artefacts. The comparative analysis shows wavelet based approaches are well suited for EEG signal processing. Further, similar approaches can be used with other biomedical signals such as electrocardiogram (ECG or EKG), Electromyography (EMG) etc.
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After obtaining a Master's degree in Mechanical Engineering, he continued his PhD studies in Robotics at the Vienna University of Technology. Here he worked as a robotic researcher with the university's Intelligent Manufacturing Systems Group as well as a guest researcher at various European universities, including the Swiss Federal Institute of Technology Lausanne (EPFL). During this time he published more than 20 scientific papers, gave presentations, served as a reviewer for major robotic journals and conferences and most importantly he co-founded and built the International Journal of Advanced Robotic Systems- world's first Open Access journal in the field of robotics. Starting this journal was a pivotal point in his career, since it was a pathway to founding IntechOpen - Open Access publisher focused on addressing academic researchers needs. Alex is a personification of IntechOpen key values being trusted, open and entrepreneurial. Today his focus is on defining the growth and development strategy for the company.",institutionString:null,institution:{name:"TU Wien",country:{name:"Austria"}}},{id:"19816",title:"Prof.",name:"Alexander",middleName:null,surname:"Kokorin",slug:"alexander-kokorin",fullName:"Alexander Kokorin",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/19816/images/1607_n.jpg",biography:"Alexander I. Kokorin: born: 1947, Moscow; DSc., PhD; Principal Research Fellow (Research Professor) of Department of Kinetics and Catalysis, N. Semenov Institute of Chemical Physics, Russian Academy of Sciences, Moscow.\r\nArea of research interests: physical chemistry of complex-organized molecular and nanosized systems, including polymer-metal complexes; the surface of doped oxide semiconductors. 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I received a B.Eng. degree in Computer Engineering with First Class Honors in 2008 from Prince of Songkla University, Songkhla, Thailand, where I received a Ph.D. degree in Electrical Engineering. My research interests are primarily in the area of biomedical signal processing and classification notably EMG (electromyography signal), EOG (electrooculography signal), and EEG (electroencephalography signal), image analysis notably breast cancer analysis and optical coherence tomography, and rehabilitation engineering. I became a student member of IEEE in 2008. During October 2011-March 2012, I had worked at School of Computer Science and Electronic Engineering, University of Essex, Colchester, Essex, United Kingdom. In addition, during a B.Eng. I had been a visiting research student at Faculty of Computer Science, University of Murcia, Murcia, Spain for three months.\n\nI have published over 40 papers during 5 years in refereed journals, books, and conference proceedings in the areas of electro-physiological signals processing and classification, notably EMG and EOG signals, fractal analysis, wavelet analysis, texture analysis, feature extraction and machine learning algorithms, and assistive and rehabilitative devices. I have several computer programming language certificates, i.e. Sun Certified Programmer for the Java 2 Platform 1.4 (SCJP), Microsoft Certified Professional Developer, Web Developer (MCPD), Microsoft Certified Technology Specialist, .NET Framework 2.0 Web (MCTS). 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