関: diffuse large B-cell lymphoma、diffuse large-cell lymphoma、DLCL

同: diffuse large B-cell lymphoblastic lymphoma

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2014/05/24 11:02:53」(JST)

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Diffuse large B-cell lymphoma (DLBCL or DLBL) is a cancer of B cells, a type of white blood cell responsible for producing antibodies. It is the most common type of non-Hodgkin lymphoma among adults,^[1] with an annual incidence of 7-8 cases per 100,000 people per year.^[2]^[3] This cancer occurs primarily in older individuals, with a median age of diagnosis at approximately 70 years of age,^[3] though it can also occur in children and young adults in rare cases.^[4] DLBCL is an aggressive tumour which can arise in virtually any part of the body,^[5] and the first sign of this illness is typically the observation of a rapidly growing mass, sometimes associated with fever, weight loss, and night sweats.^[6]

The causes of diffuse large B-cell lymphoma are not well understood. Usually DLBCL arises from normal B cells, but it can also represent a malignant transformation of other types of lymphoma or leukaemia. An underlying immunodeficiency, is a significant risk factor.^[7] Infection with Epstein-Barr virus has also been found to contribute to the development of some subgroups of DLBCL.^[8]

Diagnosis of DLBCL is made by removing a portion of the tumour through a biopsy, and then examining this tissue using a microscope. Usually an experienced hematopathologist makes this diagnosis.^[9] Several subtypes of DLBCL have been identified, each having a different clinical presentation and prognosis. However, the usual treatment for each of these is chemotherapy, often in combination with an antibody targeted at the tumour cells.^[10] Through these treatments, more than half of patients with DLBCL can be cured,^[11] and overall survival for older adults at five years is around 58%.^[12]

Classification

Diffuse large B-cell lymphoma encompasses a biologically and clinically diverse set of diseases,^[13] many of which cannot be separated from one another by well-defined and widely accepted criteria. The World Health Organization (WHO) classification system defines more than a dozen subtypes,^[14] each of which can be differentiated based on the location of the tumour, the presence of other cells within the tumour (such as T cells), and whether the patient has certain other illnesses related to DLBCL. One of these well-defined groupings of particular note is "primary mediastinal (thymic) large B-cell lymphoma", which arises within the thymus or mediastinal lymph nodes.^[15]

In some cases, a tumour may share many features with both DLBCL and Burkitt lymphoma. In these situations, the tumour is classified as simply “B-cell lymphoma, unclassifiable, with features intermediate between diffuse large B-cell lymphoma and Burkitt lymphoma”. A similar situation can arise between DLBCL and Hodgkin’s lymphoma; the tumour is then classified as “B-cell lymphoma, unclassifiable, with features intermediate between diffuse large B-cell lymphoma and Hodgkin’s lymphoma”.

When a case of DLBCL does not conform to any of the well-defined subtypes, and is also not considered unclassifiable, then it is classified as “diffuse large B-cell lymphoma, not otherwise specified” (DLBCL, NOS). The majority of DLBCL cases fall into this category. Much research has been devoted to separating this still-heterogeneous group; such distinctions are usually made along lines of cellular morphology, gene expression, and immunohistochemical properties.

Morphology

Within cellular morphology three variants are most commonly seen: centroblastic, immunoblastic, and anaplastic. Most cases of DLBCL are centroblastic, having the appearance of medium-to-large-sized lymphocytes with scanty cytoplasm. Oval or round nuclei containing fine chromatin are prominently visible, having two to four nucleoli within each nucleus. Sometimes the tumour may be monomorphic, composed almost entirely of centroblasts. However, most cases are polymorphic, with a mixture of centroblastic and immunoblastic cells.^[16]

Immunoblasts have significant basophilic cytoplasm and a central nucleolus. A tumour can be classified as immunoblastic if greater than 90% of its cells are immunoblasts.^[16] This distinction can be problematic, however, because hematopathologists reviewing the microscope slides may often disagree on whether a collection of cells is best characterized as centroblasts or immunoblasts.^[17] Such disagreement indicates poor inter-rater reliability.

The third morphologic variant, anaplastic, consists of tumour cells which appear very differently from their normal B cell counterparts. The cells are generally very large with a round, oval, or polygonal shape and pleomorphic nuclei, and may resemble Hodgkin cells or Reed-Sternberg cells.

Gene expression

Gene expression profiling studies have also attempted to distinguish heterogeneous groups of DLBCL from each other. These studies examine thousands of genes simultaneously using a DNA microarray, looking for patterns which may help in grouping cases of DLBCL. Many studies now suggest that cases of DLBCL, NOS can be separated into two groups on the basis of their gene expression profiles; these groups are known as germinal centre B-cell-like (GCB) and activated B-cell-like (ABC).^[13]^[18]^[19]^[20] Tumour cells in the germinal centre B-cell-like subgroup resemble normal B cells in the germinal centre closely, and are generally associated with a favourable prognosis.^[21]^[22] Activated B-cell-like tumour cells are associated with a poorer prognosis,^[22] and derive their name from studies which show the continuous activation of certain pathways normally activated when B cells interact with an antigen. The NF-κB pathway, which is normally involved in transforming B cells into plasma cells, is an important example of one such pathway.^[23]

Another notable finding of recent gene expression studies is the importance of the cells and microscopic structures interspersed between the malignant B cells within the DLBCL tumour, an area commonly known as the tumour microenvironment. The presence of gene expression signatures commonly associated with macrophages, T cells, and remodelling of the extracellular matrix seems to be associated with an improved prognosis and better overall survival.^[22]^[24] Alternatively, expression of genes coding for pro-angiogenic factors is correlated with poorer survival.^[22]

Immunohistochemistry

With the apparent success of gene expression profiling in separating biologically distinct cases of DLBCL, NOS, some researchers examined whether a similar distinction could be made using immunohistochemical staining (IHC), a widely used method for characterizing tissue samples. This technique uses highly specific antibody-based stains to detect proteins on a microscope slide, and since microarrays are not widely available for routine clinical use, IHC is a desirable alternative.^[25]^[26] Many of these studies focused on stains against the products of prognostically significant genes which had been implicated in DLBCL gene expression studies. Examples of such genes include BCL2, BCL6, MUM1, LMO2, MYC, and p21. Several algorithms for separating DLBCL cases by IHC arose out of this research, categorizing tissue samples into groups most commonly known as GCB and non-GCB.^[26]^[27]^[28]^[29] The correlation between these GCB/non-GCB immunohistochemical groupings and the GCB/ABC groupings used in gene expression profiling studies is uncertain,^[21]^[28] as is their prognostic value.^[21] This uncertainty may arise in part due to poor inter-rater reliability in performing common immunohistochemical stains.^[25]

Symptoms

The most typical symptom at the time of diagnosis is a mass that is rapidly enlarging and located in a part of the body with multiple lymph nodes.^[30]

Treatment

Standard treatment is CHOP-R,^[31] also referred to as R-CHOP, an improved form of CHOP with the addition of rituximab (Rituxan),^[32] which has increased the rates of complete responses for DLBCL patients, particularly elderly patients.^[33] R-CHOP is a combination of one monoclonal antibody, 3 chemotherapy drugs, and one steroid: rituximab (Rituxan), cyclophosphamide (Cytoxan) doxorubicin (Hydroxydaunorubicin), vincristine (Oncovin), and prednisone.^[34] Chemotherapy is administered intravenously and is most effective when it is administered multiple times over a period of months (e.g. every 3 weeks, over 6 to 8 cycles). People receiving chemotherapy commonly have a PICC line (Peripherally inserted central catheter) in their arm near the elbow or a surgically implanted port.

Radiation is another common treatment and is most effective if done prior to the chemotherapy, or as the last treatment after chemotherapy has been completed.

Prognosis

The germinal-center subtype has the best prognosis,^[33] with 66.6% of treated patients surviving more than five years.^[35]

For children with diffuse large B-cell lymphomas, most studies have found 5-year survival rates ranging from about 70% to more than 90%.^[36]

Research

A second regimen under evaluation is R-EPOCH (rituximab with etoposide-prednisone-vincristine-doxorubicin-cyclophosphamide), which demonstrated a 5-year progression-free survival (PFS) of 79% in a phase II trial. A phase III trial, CALGB 50303, is now comparing R-EPOCH with R-CHOP in patients with newly diagnosed DLBCL.^[37]

One area of active research is on separating patients into groups based on their prognosis and how likely they are to benefit from different drugs. Methods like gene expression profiling and next-generation sequencing may result in more effective and more personalized treatment.^[38]^[39]

References

^ "A clinical evaluation of the International Lymphoma Study Group classification of non-Hodgkin's lymphoma. The Non-Hodgkin's Lymphoma Classification Project". Blood 89 (11): 3909–3918. 1997. PMID 9166827. edit
^ Morton, L. M.; Wang, S. S.; Devesa, S. S.; Hartge, P.; Weisenburger, D. D.; Linet, M. S. (2006). "Lymphoma incidence patterns by WHO subtype in the United States, 1992-2001". Blood 107 (1): 265–276. doi:10.1182/blood-2005-06-2508. PMC 1895348. PMID 16150940. edit
^ ^a ^b Smith, A.; Howell, D.; Patmore, R.; Jack, A.; Roman, E. (2011). "Incidence of haematological malignancy by sub-type: A report from the Haematological Malignancy Research Network". British Journal of Cancer 105 (11): 1684–1692. doi:10.1038/bjc.2011.450. PMC 3242607. PMID 22045184. edit
^ Smith, A.; Roman, E.; Howell, D.; Jones, R.; Patmore, R.; Jack, A.; Haematological Malignancy Research Network (2010). "The Haematological Malignancy Research Network (HMRN): A new information strategy for population based epidemiology and health service research". British Journal of Haematology 148 (5): 739–753. doi:10.1111/j.1365-2141.2009.08010.x. PMC 3066245. PMID 19958356. edit
^ Vinay Kumar; Abul K. Abbas; Nelson Fausto; Jon C. Aster (28 May 2009). Robbins & Cotran Pathologic Basis of Disease. Elsevier Health Sciences. p. 607. ISBN 978-1-4377-2015-0. Cite uses deprecated parameters (help)
^ Arnold S. Freeman; Jon C. Aster (2012). "Epidemiology, clinical manifestations, pathologic features, and diagnosis of diffuse large B cell lymphoma". In Denise S. Basow. UpToDate. Waltham, MA: UpToDate. Retrieved 15 August 2012.
^ Swerdlow, S.H.; Campo, E.; Jaffe, E.S. et al., eds. (2008). WHO Classification of Tumours of Haematopoietic and Lymphoid Tissues. Lyon: IARC. p. 233. ISBN 978-92-832-2431-0. |displayeditors= suggested (help)
^ Swerdlow et al. 2008, p. 243.
^ Goldman, Lee; Schafer, Andrew I. (2012). Goldman's Cecil Medicine (24 ed.). p. 1222. ISBN 978-1-4377-1604-7.
^ Goldman & Schafer 2012, p. 1225.
^ Akyurek, N.; Uner, A.; Benekli, M.; Barista, I. (2011). "Prognostic significance of MYC, BCL2, and BCL6 rearrangements in patients with diffuse large B-cell lymphoma treated with cyclophosphamide, doxorubicin, vincristine, and prednisone plus rituximab". Cancer: n/a. doi:10.1002/cncr.27396. PMID 22213394. edit
^ Feugier, P.; Van Hoof, A.; Sebban, C.; Solal-Celigny, P.; Bouabdallah, R.; Fermé, C.; Christian, B.; Lepage, E.; Tilly, H.; Morschhauser, F.; Gaulard, P.; Salles, G.; Bosly, A.; Gisselbrecht, C.; Reyes, F.; Coiffier, B. (2005). "Long-Term Results of the R-CHOP Study in the Treatment of Elderly Patients with Diffuse Large B-Cell Lymphoma: A Study by the Groupe d'Etude des Lymphomes de l'Adulte". Journal of Clinical Oncology 23 (18): 4117–4126. doi:10.1200/JCO.2005.09.131. PMID 15867204. edit
^ ^a ^b Alizadeh, A. A.; Eisen, M. B.; Davis, R. E.; Ma, C.; Lossos, I. S.; Rosenwald, A.; Boldrick, J. C.; Sabet, H.; Tran, T.; Yu, X.; Powell, J. I.; Yang, L.; Marti, G. E.; Moore, T.; Hudson Jr, J.; Lu, L.; Lewis, D. B.; Tibshirani, R.; Sherlock, G.; Chan, W. C.; Greiner, T. C.; Weisenburger, D. D.; Armitage, J. O.; Warnke, R.; Levy, R.; Wilson, W.; Grever, M. R.; Byrd, J. C.; Botstein, D.; Brown, P. O. (2000). "Distinct types of diffuse large B-cell lymphoma identified by gene expression profiling". Nature 403 (6769): 503–511. doi:10.1038/35000501. PMID 10676951. edit
^ Swerdlow et al. 2008, pp. 233–237.
^ Swerdlow et al. 2008, pp. 250–251.
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^ Harris, N. L.; Jaffe, E. S.; Stein, H.; Banks, P. M.; Chan, J. K.; Cleary, M. L.; Delsol, G.; De Wolf-Peeters, C.; Falini, B.; Gatter, K. C. (1994). "A revised European-American classification of lymphoid neoplasms: A proposal from the International Lymphoma Study Group". Blood 84 (5): 1361–1392. PMID 8068936. edit
^ Shipp, M. A.; Ross, K. N.; Tamayo, P.; Weng, A. P.; Kutok, J. L.; Aguiar, R. C. T.; Gaasenbeek, M.; Angelo, M.; Reich, M.; Pinkus, G. S.; Ray, T. S.; Koval, M. A.; Last, K. W.; Norton, A.; Lister, T. A.; Mesirov, J.; Neuberg, D. S.; Lander, E. S.; Aster, J. C.; Golub, T. R. (2002). "Diffuse large B-cell lymphoma outcome prediction by gene-expression profiling and supervised machine learning". Nature Medicine 8 (1): 68–74. doi:10.1038/nm0102-68. PMID 11786909. edit
^ Rosenwald, A.; Wright, G.; Chan, W. C.; Connors, J. M.; Campo, E.; Fisher, R. I.; Gascoyne, R. D.; Muller-Hermelink, H. K.; Smeland, E. B.; Giltnane, J. M.; Hurt, E. M.; Zhao, H.; Averett, L.; Yang, L.; Wilson, W. H.; Jaffe, E. S.; Simon, R.; Klausner, R. D.; Powell, J.; Duffey, P. L.; Longo, D. L.; Greiner, T. C.; Weisenburger, D. D.; Sanger, W. G.; Dave, B. J.; Lynch, J. C.; Vose, J.; Armitage, J. O.; Montserrat, E.; López-Guillermo, A. (2002). "The Use of Molecular Profiling to Predict Survival after Chemotherapy for Diffuse Large-B-Cell Lymphoma". New England Journal of Medicine 346 (25): 1937–1947. doi:10.1056/NEJMoa012914. PMID 12075054. edit
^ ^a ^b Wright, G.; Tan, B.; Rosenwald, A.; Hurt, E. H.; Wiestner, A.; Staudt, L. M. (2003). "A gene expression-based method to diagnose clinically distinct subgroups of diffuse large B cell lymphoma". Proceedings of the National Academy of Sciences 100 (17): 9991–9996. doi:10.1073/pnas.1732008100. PMC 187912. PMID 12900505. edit
^ ^a ^b ^c Gutierrez-Garcia, G.; Cardesa-Salzmann, T.; Climent, F.; González-Barca, E.; Mercadal, S.; Mate, J. L.; Sancho, J. M.; Arenillas, L.; Serrano, S.; Escoda, L.; Martínez, S.; Valera, A.; Martínez, A.; Jares, P.; Pinyol, M.; García-Herrera, A.; Martínez-Trillos, A.; Giné, E.; Villamor, N.; Campo, E.; Colomo, L.; López-Guillermo, A.; Grup per l'Estudi dels Limfomes de Catalunya I Balears (GELCAB) (2011). "Gene-expression profiling and not immunophenotypic algorithms predicts prognosis in patients with diffuse large B-cell lymphoma treated with immunochemotherapy". Blood 117 (18): 4836–4843. doi:10.1182/blood-2010-12-322362. PMID 21441466. edit
^ ^a ^b ^c ^d Lenz, G.; Wright, G.; Dave, S. S.; Xiao, W.; Powell, J.; Zhao, H.; Xu, W.; Tan, B.; Goldschmidt, N.; Iqbal, J.; Vose, J.; Bast, M.; Fu, K.; Weisenburger, D. D.; Greiner, T. C.; Armitage, J. O.; Kyle, A.; May, L.; Gascoyne, R. D.; Connors, J. M.; Troen, G.; Holte, H.; Kvaloy, S.; Dierickx, D.; Verhoef, G.; Delabie, J.; Smeland, E. B.; Jares, P.; Martinez, A.; Lopez-Guillermo, A. (2008). "Stromal Gene Signatures in Large-B-Cell Lymphomas". New England Journal of Medicine 359 (22): 2313–2323. doi:10.1056/NEJMoa0802885. PMID 19038878. edit
^ Schwartz, R. S.; Lenz, G.; Staudt, L. M. (2010). "Aggressive Lymphomas". New England Journal of Medicine 362 (15): 1417–1429. doi:10.1056/NEJMra0807082. PMID 20393178. edit
^ Linderoth, J.; Edén, P.; Ehinger, M.; Valcich, J.; Jerkeman, M.; Bendahl, P. R. O.; Berglund, M.; Enblad, G.; Erlanson, M.; Roos, G. R.; Cavallin-Ståhl, E. (2008). "Genes associated with the tumour microenvironment are differentially expressed in cured versus primary chemotherapy-refractory diffuse large B-cell lymphoma". British Journal of Haematology 141 (4): 423–432. doi:10.1111/j.1365-2141.2008.07037.x. PMID 18419622. edit
^ ^a ^b De Jong, D.; Xie, W.; Rosenwald, A.; Chhanabhai, M.; Gaulard, P.; Klapper, W.; Lee, A.; Sander, B.; Thorns, C.; Campo, E.; Molina, T.; Hagenbeek, A.; Horning, S.; Lister, A.; Raemaekers, J.; Salles, G.; Gascoyne, R. D.; Weller, E. (2008). "Immunohistochemical prognostic markers in diffuse large B-cell lymphoma: Validation of tissue microarray as a prerequisite for broad clinical applications (a study from the Lunenburg Lymphoma Biomarker Consortium)". Journal of Clinical Pathology 62 (2): 128–138. doi:10.1136/jcp.2008.057257. PMID 18794197. edit
^ ^a ^b Choi, W. W. L.; Weisenburger, D. D.; Greiner, T. C.; Piris, M. A.; Banham, A. H.; Delabie, J.; Braziel, R. M.; Geng, H.; Iqbal, J.; Lenz, G.; Vose, J. M.; Hans, C. P.; Fu, K.; Smith, L. M.; Li, M.; Liu, Z.; Gascoyne, R. D.; Rosenwald, A.; Ott, G.; Rimsza, L. M.; Campo, E.; Jaffe, E. S.; Jaye, D. L.; Staudt, L. M.; Chan, W. C. (2009). "A New Immunostain Algorithm Classifies Diffuse Large B-Cell Lymphoma into Molecular Subtypes with High Accuracy". Clinical Cancer Research 15 (17): 5494–5502. doi:10.1158/1078-0432.CCR-09-0113. PMID 19706817. edit
^ Colomo, L.; López-Guillermo, A.; Perales, M.; Rives, S.; Martínez, A.; Bosch, F.; Colomer, D.; Falini, B.; Montserrat, E.; Campo, E. (2002). "Clinical impact of the differentiation profile assessed by immunophenotyping in patients with diffuse large B-cell lymphoma". Blood 101 (1): 78–84. doi:10.1182/blood-2002-04-1286. PMID 12393466. edit
^ ^a ^b Hans, C. P.; Weisenburger, D. D.; Greiner, T. C.; Gascoyne, R. D.; Delabie, J.; Ott, G.; Müller-Hermelink, H. K.; Campo, E.; Braziel, R. M.; Jaffe, E. S.; Pan, Z.; Farinha, P.; Smith, L. M.; Falini, B.; Banham, A. H.; Rosenwald, A.; Staudt, L. M.; Connors, J. M.; Armitage, J. O.; Chan, W. C. (2004). "Confirmation of the molecular classification of diffuse large B-cell lymphoma by immunohistochemistry using a tissue microarray". Blood 103 (1): 275–282. doi:10.1182/blood-2003-05-1545. PMID 14504078. edit
^ Muris, J. J. F.; Meijer, C.; Vos, W.; Van Krieken, J.; Jiwa, N. M.; Ossenkoppele, G. J.; Oudejans, J. J. (2006). "Immunohistochemical profiling based on Bcl-2, CD10 and MUM1 expression improves risk stratification in patients with primary nodal diffuse large B cell lymphoma". The Journal of Pathology 208 (5): 714–723. doi:10.1002/path.1924. PMID 16400625. edit
^ Cultrera JL, Dalia SM (July 2012). "Diffuse large B-cell lymphoma: current strategies and future directions". Cancer Control 19 (3): 204–13. PMID 22710896.
^ http://cornell-lymphoma.com/tag/dlbcl/
^ Sehn LH, Berry B, Chhanabhai M et al. (March 2007). "The revised International Prognostic Index (R-IPI) is a better predictor of outcome than the standard IPI for patients with diffuse large B-cell lymphoma treated with R-CHOP". Blood 109 (5): 1857–61. doi:10.1182/blood-2006-08-038257. PMID 17105812.
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UpToDate Contents

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1. びまん性大細胞型B細胞性リンパ腫の予後 prognosis of diffuse large b cell lymphoma
2. びまん性大細胞型B細胞性リンパ腫の疫学、臨床症状、病理学的特徴、および診断 epidemiology clinical manifestations pathologic features and diagnosis of diffuse large b cell lymphoma
3. 進行期びまん性大細胞型B細胞性リンパ腫の初期治療 initial treatment of advanced stage diffuse large b cell lymphoma
4. 限局期びまん性大細胞B細胞性リンパ腫の初期治療 initial treatment of limited stage diffuse large b cell lymphoma
5. 再発性または難治性のびまん性大細胞型B細胞リンパ腫の治療 treatment of relapsed or refractory diffuse large b cell lymphoma

English Journal

Regulation of the MIR155 host gene in physiological and pathological processes.

Elton TS, Selemon H, Elton SM, Parinandi NL.SourceDavis Heart and Lung Research Institute, The Ohio State University, Columbus, OH, USA; College of Pharmacy, Division of Pharmacology, The Ohio State University, Columbus, OH, USA; Department of Medicine, Division of Cardiology, The Ohio State University, Columbus, OH, USA. Electronic address: terry.elton@osumc.edu.
Gene.Gene.2013 Dec 10;532(1):1-12. doi: 10.1016/j.gene.2012.12.009. Epub 2012 Dec 14.
MicroRNAs (miRNAs), a family of small nonprotein-coding RNAs, play a critical role in posttranscriptional gene regulation by acting as adaptors for the miRNA-induced silencing complex to inhibit gene expression by targeting mRNAs for translational repression and/or cleavage. miR-155-5p and miR-155-3
PMID 23246696

Ten-year follow-up of pediatric patients with non-hodgkin lymphoma treated with allogeneic or autologous stem cell transplantation.

Giulino-Roth L, Ricafort R, Kernan NA, Small TN, Trippett TM, Steinherz PG, Prockop SE, Scaradavou A, Chiu M, O'Reilly RJ, Boulad F.SourceDepartment of Pediatrics, Memorial Sloan-Kettering Cancer Center, New York, New York; Department of Pediatrics, Weill Cornell Medical College, New York, New York.
Pediatric blood & cancer.Pediatr Blood Cancer.2013 Dec;60(12):2018-24. doi: 10.1002/pbc.24722. Epub 2013 Aug 30.
BACKGROUND: Autologous or allogeneic hematopoietic stem cell transplant (SCT) is often considered in patients with relapsed or refractory non-Hodgkin lymphoma (NHL) but there are limited data on the use of SCT for the treatment of NHL in the pediatric setting.PROCEDURE: To evaluate the role of SCT f
PMID 24038967

Epidemiology of lymphoid malignancies: last decade update.

Novelli S, Briones J, Sierra J.SourceHematology Service, Hospital de la Santa Creu i Sant Pau, Barcelona, Spain.
SpringerPlus.Springerplus.2013 Dec;2(1):70. Epub 2013 Feb 26.
BACKGROUND: The non-Hodgkin lymphomas are 12th most prevalent cancers in Europe. No recent update in the epidemiology of these lymphomas has been performed in our country. We diagnosed 701 new lymphomas during the period beginning January 1, 2000 and ending December 31, 2009 in our center.FINDINGS:
PMID 23520573

Japanese Journal

分類不能B細胞リンパ腫DLBCL/BL中間型の臨床的特徴と治療

島田和之,中村栄男
血液内科 65(5), 717-721, 2012-11
NAID 40019515750

肺結核の化学療法中に増大した胸郭内diffuse large B-cell lymphoma (DLBCL)の1例

蓑毛祥次郎,橘和延,辻泰佑
結核 87(10), 663-667, 2012-10
NAID 40019469233

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リンク元	「びまん性大細胞型B細胞リンパ腫」「diffuse large-cell lymphoma」「DLCL」
関連記事	「DLB」

「びまん性大細胞型B細胞リンパ腫」

Diffuse large B cell lymphoma
	Classification and external resources
	Micrograph of a diffuse large B cell lymphoma. Field stain.
ICD-10	C83.3
ICD-O:	M9680/3
MeSH	D016403

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英: diffuse large B-cell lymphoma DLBCL

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「diffuse large-cell lymphoma」

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びまん性大細胞型リンパ腫、びまん性大細胞性リンパ腫、びまん性大細胞リンパ腫

関: diffuse histiocytic lymphoma、diffuse large B-cell lymphoma、DLBCL、DLCL、histiocytic lymphoma、large-cell lymphoma

「DLCL」

　　[★]

びまん性大細胞リンパ腫、びまん性大細胞型リンパ腫

関: diffuse large B-cell lymphoma、diffuse large-cell lymphoma、DLBCL

「DLB」

　　[★] レビー小体型認知症 dementia with Lewy body

[Blood1997-1] "A clinical evaluation of the International Lymphoma Study Group classification of non-Hodgkin's lymphoma. The Non-Hodgkin's Lymphoma Classification Project". Blood 89 (11): 3909–3918. 1997. PMID 9166827. edit

[Morton2006-2] Morton, L. M.; Wang, S. S.; Devesa, S. S.; Hartge, P.; Weisenburger, D. D.; Linet, M. S. (2006). "Lymphoma incidence patterns by WHO subtype in the United States, 1992-2001". Blood 107 (1): 265–276. doi:10.1182/blood-2005-06-2508. PMC 1895348. PMID 16150940. edit

[Smith2011-3] Smith, A.; Howell, D.; Patmore, R.; Jack, A.; Roman, E. (2011). "Incidence of haematological malignancy by sub-type: A report from the Haematological Malignancy Research Network". British Journal of Cancer 105 (11): 1684–1692. doi:10.1038/bjc.2011.450. PMC 3242607. PMID 22045184. edit

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[FOOTNOTESwerdlowCampoJaffePileri2008250.E2.80.93251-15] Swerdlow et al. 2008, pp. 250–251.

[FOOTNOTESwerdlowCampoJaffePileri2008234-16] Swerdlow et al. 2008, p. 234.

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[FOOTNOTESwerdlowCampoJaffePileri2008250-40] Swerdlow et al. 2008, p. 250.

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