Submitted Successfully!
To reward your contribution, here is a gift for you: A free trial for our video production service.
Thank you for your contribution! You can also upload a video entry or images related to this topic.
Version Summary Created by Modification Content Size Created at Operation
1
Gael Roue
 + 2925 word(s) 2925 2021-01-20 02:43:19 |
2 format correct
Dean Liu
 -1337 word(s) 1588 2021-02-01 05:12:05 |

Video Upload Options

Do you have a full video?
Send video materials Upload full video

Confirm

Are you sure to Delete?
Yes No
Cite
If you have any further questions, please contact Encyclopedia Editorial Office.
Roue, G.; Fernández-Serrano, M. B-Cell Lymphoma. Encyclopedia. Available online: https://encyclopedia.pub/entry/6895 (accessed on 27 July 2024).
Roue G, Fernández-Serrano M. B-Cell Lymphoma. Encyclopedia. Available at: https://encyclopedia.pub/entry/6895. Accessed July 27, 2024.
Roue, Gael, Miranda Fernández-Serrano. "B-Cell Lymphoma" Encyclopedia, https://encyclopedia.pub/entry/6895 (accessed July 27, 2024).
Roue, G., & Fernández-Serrano, M. (2021, January 29). B-Cell Lymphoma. In Encyclopedia. https://encyclopedia.pub/entry/6895
Roue, Gael and Miranda Fernández-Serrano. "B-Cell Lymphoma." Encyclopedia. Web. 29 January, 2021.
B-Cell Lymphoma
Edit
This entry is adapted from the peer-reviewed paper 10.3390/cancers13020214

The term B-cell lymphoma encompasses different neoplasms characterised by an abnormal proliferation of lymphoid cells at various stages of differentiation. B-cell lymphoma develops more frequently in older adults and immunocompromised individuals and includes both Hodgkin’s lymphomas (HLs) and most B-cell non-Hodgkin lymphomas (B-NHLs).

immune checkpoint lymphoid neoplasms programmed death 1 cytotoxic T-lymphocyte antigen 4 monoclonal antibodies combination therapies

1. Introduction

The term B-cell lymphoma encompasses different neoplasms characterised by an abnormal proliferation of lymphoid cells at various stages of differentiation. B-cell lymphoma develops more frequently in older adults and immunocompromised individuals and includes both Hodgkin’s lymphomas (HLs) and most B-cell non-Hodgkin lymphomas (B-NHLs). The latter accounts for up to 4% of the globally diagnosed cancers[1]and are characterised by a malignant proliferation of mature or immature B-lymphocytes in lymphoid tissues and extranodal territories such as the gastrointestinal tract, the central nervous system (CNS), or, essentially, any other body organ[2]. Inherited events such as chromosomal translocations, oncogene activation or even certain viral infections such as the Epstein–Barr virus (EBV) may trigger lymphomagenesis[3]. B-NHLs are divided into low and high grades, typically corresponding to indolent (slow-growing) lymphomas and aggressive lymphomas, respectively. Indolent lymphomas include follicular lymphoma (FL), marginal zone lymphoma (MZL), small cell lymphocytic lymphoma (SLL)/chronic lymphocytic leukaemia (CLL) and Waldenström macroglobulinemia (WM). Early-stage indolent B-cell lymphomas can often be treated with radiation alone, with long-term nonrecurrence. Early-stage aggressive disease is treated with chemotherapy and, often, radiation, with a 70–90% curation rate. Aggressive lymphomas include both precursor lymphoid neoplasms and numerous mature B-cell neoplasms like mantle cell lymphoma (MCL), primary effusion lymphoma (PEL), Burkitt lymphoma (BL), diffuse large B-cell lymphoma (DLBCL) and its many subtypes and variants, and unclassifiable B-cell lymphoma, with features intermediate between DLBCL and BL. These entities usually require intensive treatments, with some having a good prospect for a permanent cure[4].

2. Diffuse Large B-Cell Lymphoma

Diffuse large B-cell lymphoma (DLBCL) represents the most common type of B-NHL in Western countries. The 2016 World Health Organization (WHO) classification of lymphoid malignancies recognises several subtypes characterised by unique clinical and pathological features, including primary DLBCL of the central nervous system (PCNSL), primary cutaneous DLBCL, leg type, T-cell/histiocyte-rich large cell lymphoma, and EBV-positive DLBCL of the elderly. Nevertheless, most cases of DLBCL fall into the “not otherwise specified” (NOS) category[4].

DLBCL, like other cancers, develops in a complex tissue environment with a high content of malignant and nonmalignant compartments of the disease, as well as extracellular components that constitute the tumour microenvironment (TME). The cellular and molecular features of TME have a profound prognostic impact[5] and include T-cells, tumour-associated macrophages (TAMs), dendritic cells (DCs), neutrophils, natural killer (NK) cells and stromal cells[6]. DLBCL harbours a non-inflamed phenotype characterised by lack of immune cell infiltration, which could explain the modest efficacy of immune checkpoint blockade therapy in relapsed/refractory (R/R) DLBCL patients[7].

3. Primary Mediastinal B-Cell Lymphoma

Primary mediastinal B-cell lymphoma (PMBL) is a rare but aggressive lymphoma of thymic B-cell origin, accounting for 3% of B-NHLs. Although it presents similar histology to DLBCL, the genetic profile of PMBL is distinct and shares many features with classic Hodgkin lymphoma (cHL, see below) [8]. Patients are generally not cured after first-line treatment, and, after relapse, autologous stem cell transplantation (ASCT) is usually beneficial. However, relapsed/refractory (R/R) PMBL cases have poor outcomes and are often managed like other forms of DLBCL[9].

4. Follicular Lymphoma

Follicular lymphoma (FL) is the second most common B-NHL, accounting for 29–35% of cases. It is a neoplasm of germinal centre B-cells, which display rearrangement of immunoglobulin (Ig) heavy and light chain genes and somatic hypermutation and express common germinal centre markers such as BCL6, AID and CD10[10][11][12]. FL generally presents an indolent clinical course, with median overall survival (OS) of more than 15 years[10][13]. However, about 20% of patients relapse during the first 2 years after treatment, and others evolve into transformed-FL (t-FL), a much more aggressive subtype [10].

The crosstalk between malignant FL cells and the surrounding cells of their TME is driven by some recurrent genetic events[14]. FL is strongly regulated by direct interaction with a germinal centre (GC)-like microenvironment, including myeloid cells, follicular helper T-cells (TFH), and stromal cells, that may orchestrate efficient immune escape mechanisms[15]. The TME of FL also displays deregulation of the extracellular matrix proteins involved in collagen deposition and organization[16]. Cancer-associated fibroblasts (CAFs) are another important FL tumour-promoting actor, providing a niche with high levels of factors involved in B-cell activation and the activation/recruitment of some TME components such as TAMs[17]. The crosstalk between TFH cells and FL cells is orchestrated by the interaction between antigen-loaded MHC class II molecules and antigen-specific T-cell receptors.

5. Burkitt Lymphoma

Burkitt lymphoma (BL) includes a heterogeneous group of highly aggressive malignancies of intermediate-sized B-cells that may be found infiltrating both nodal or extranodal tissues in a diffuse pattern[18]. BL is invariably associated with chromosomal translocations that dysregulate the expression of c-MYC, and, consequently, several downstream genes involved in the control of cellular processes such as cell cycle progression and apoptosis[19]. The malignant cells usually express the B-cell-specific surface markers CD19 and CD20, as well as low-to-intermediate levels of common acute lymphoblastic leukaemia (ALL) antigen (CD10/CALLA)[20].

The complex interplay between BL cells and the TME also regulates lymphomagenesis and provides new insights for target immunotherapies. Like DLBCL, BL tumours harbour a noninflamed environment with low infiltration of immune cells and are usually resistant to immune checkpoint blockade. One of the hallmarks of the TME in BL tumours is the high content of TAMs which contribute to tumour progression through the secretion of cytokines and chemokines, and the expression of immune checkpoint proteins such as programmed death ligand 1 (PD-L1)[21]. The crosstalk between tumour cells, TAMs, PD-1 signalling, viral antigens, and T-cells may result in the high prevalence of M2 macrophages in the TME and contribute to the failed immunity of BL patients[22].

6. Marginal Zone Lymphoma

Marginal zone lymphoma (MZL) originates from memory B-cells at the marginal zone of lymphoid follicles and account for 5–15% of all NHLs[23][24]. Three distinct entities have been described. Splenic (SMZL) and nodal marginal zone lymphoma (NMZL) arise from the follicle marginal zone of the spleen and the lymph nodes, respectively [24][25][26]. Extranodal marginal zone lymphoma (EMZL) of the mucosa-associated lymphoid tissue (MALT) is the most common subtype, accounting for about 60% of MZL cases. This entity is strongly associated with chronic inflammation derived from autoimmune disease or infection, such as Helicobacter pylori. Other tumour sites include eyes and ocular adnexa (13%), skin (9%), lungs (9%) and salivary glands (8%)[23][27][28]. MZLs mostly have indolent clinical courses, although NMZL has a poorer prognosis than other subtypes[25][26][27].

The course of MZL disease is strongly influenced by the TME, and this latter may therefore represent a promising strategy for early diagnosis and therapy choice. SMZL cells are supported by immune cells such as mast cells and macrophages, which may be recruited by tumour cells through the secretion of cytokines and chemokines[29]. The TME components of SMZL can regulate stromal cell proliferation, angiogenesis, extracellular matrix remodelling, and induction of adhesion molecule expression[29]. The chronic inflammation of MALT lymphomas not only triggers B-cell growth but also recruits T-cells, macrophages and neutrophils to the site of inflammation, which contribute to genetic aberrations, DNA damage and genetic instability of the B-cells during somatic hypermutation and class-switching recombination[30].

7. Mantle Cell Lymphoma

Mantle cell lymphoma (MCL) originates from B-cells, a proportion of them being antigen-experienced B-cells, in the mantle zone of lymph nodes. MCL is usually diagnosed as a late-stage disease and may be observed in both the gastrointestinal tract and bone marrow[31]. The diagnosis of MCL is mainly performed by a microscopic evaluation of a biopsy, although the detection of chromosomal translocation t (11:14), with the consequent cyclin D1 expression, is considered the molecular hallmark[32].

The crosstalk between MCL tumour cells and its microenvironment has a central role in disease expansion[33]. MCL cells have shown constitutive expression of PD-1 and its ligand PD-L1, which converts it into an interesting candidate for immunotherapy targeting this checkpoint[34]. Aggressive MCL cases are characterised by a low number of T-cells [35] and a high frequency of regulatory T-cells (Treg)[36]. Moreover, follicular dendritic cells (FDCs) have been shown to support MCL cell survival through a cell–cell interaction mechanism[37]. Autocrine and paracrine secretion of soluble factors could also have an important role within the MCL TME. Interestingly, the blood of MCL patients contains high levels of several cytokines and chemokines, such as IL-8, CCL3 and CCL4, which are correlated with poor survival[38].

8. Classical Hodgkin Lymphoma

Classical Hodgkin lymphoma (cHL) is a neoplasm derived from B-cells and is mainly constituted by a small number of neoplastic mononuclear cells, i.e., Hodgkin cells, and multinucleated Reed–Sternberg (HRS) cells. cHL accounts for 15–25% of all lymphomas and represents the most common lymphoma subtype in children and young adults in the Western world. The cell of origin (COO) is nowadays unequivocally considered to be a (post)germinal centre B-cell[39]. Several genetic alterations, targeting a few pathways, have been identified, but none of them can be considered “dominant”. The affected pathways include NF-κB and JAK-STAT, whose aberrant activation fuel HRS cells with proliferative and antiapoptotic stimuli[40]. Moreover, the LMP1 protein, encoded by EBV that often latently infects HRS cells, likely contributes to NF-κB signalling since LMP1 mimics constitutively active CD402 [41].

Genetic lesions of NF-κB pathway genes largely contribute to aberrant activation of this cascade in a cell-intrinsic manner and/or by amplifying signals from the microenvironment[42]. In addition, HRS cells are outnumbered by reactive cells in the TME, including T- and B-lymphocytes, eosinophils, macrophages, mast cells, plasma cells and stromal cells[43][44].

References

  1. Fisher, S.G.; Fisher, R.I. The epidemiology of non-Hodgkin’s lymphoma. Oncogene 2004, 23, 6524–6534.
  2. Goldin, L.R.; Landgren, O. Autoimmunity and lymphomagenesis. Int. J. Cancer 2009, 124, 1497–1502.
  3. Basso, K.; Dalla-Favera, R. Germinal centres and B cell lymphomagenesis. Nat. Rev. Immunol. 2015, 15, 172–184.
  4. Quintanilla-Martinez, L. The 2016 updated WHO classification of lymphoid neoplasias. Hematol. Oncol. 2017, 35, 37–45.
  5. Coussens, L.M.; Werb, Z. Inflammation and cancer. Nature 2002, 420, 860–867.
  6. Tamma, R.; Ranieri, G.; Ingravallo, G.; Annese, T.; Oranger, A.; Gaudio, F.; Musto, P.; Specchia, G.; Ribatti, D. Inflammatory Cells in Diffuse Large B Cell Lymphoma. J. Clin. Med. 2020, 9, 2418.
  7. Ansell, S.M.; Minnema, M.C.; Johnson, P.; Timmerman, J.M.; Armand, P.; Shipp, M.A.; Rodig, S.J.; Ligon, A.H.; Roemer, M.G.M.; Reddy, N.; et al. Nivolumab for relapsed/refractory diffuse large B-cell lymphoma in patients ineligible for or having failed autologous transplantation: A single-arm, phase II study. J. Clin. Oncol. 2019, 37, 481–489.
  8. Dunleavy, K.; Wilson, W.H. Primary mediastinal B-cell lymphoma and mediastinal gray zone lymphoma. Blood 2014, 125, 33–40.
  9. Kuruvilla, J.; Pintilie, M.; Tsang, R.; Nagy, T.; Keating, A.; Crump, M. Salvage chemotherapy and autologous stem cell transplantation are inferior for relapsed or refractory primary mediastinal large B-cell lymphoma compared with diffuse large B-cell lymphoma. Leuk. Lymphoma 2008, 49, 1329–1336.
  10. Carbone, A.; Roulland, S.; Gloghini, A.; Younes, A.; von Keudell, G.; López-Guillermo, A.; Fitzgibbon, J. Follicular lymphoma. Nat. Rev. Dis. Prim. 2019, 5, 83.
  11. Jaffe, E.S.; Harris, N.L.; Swerdlow, S.H.; Ott, G.; Nathwani, B.N.; de Jong, D.; Yoshino, T.; Spagnolo, D.; Gascoyne, R.D. Follicular lymphoma. In WHO Classification of Tumours of Haematopoietic and Lymphoid Tissues; Swerdlow, S.H., Campo, E., Harris, N.L., Jaffe, E.S., Pileri, S.A., Stein, H., Thiele, J., Eds.; IARC Press: Lyon, France, 2017; pp. 266–277.
  12. Freedman, A.; Jacobsen, E. Follicular lymphoma: 2020 update on diagnosis and management. Am. J. Hematol. 2020, 95, 316–327.
  13. Apostolidis, J.; Mokhtar, N.; Al Omari, R.; Darweesh, M.; Al Hashmi, H. Follicular lymphoma: Update on management and emerging therapies at the dawn of the new decade. Hematol. Oncol. 2020, 38, 213–222.
  14. Amin, R.; Mourcin, F.; Uhel, F.; Pangault, C.; Ruminy, P.; Dupré, L.; Guirriec, M.; Marchand, T.; Fest, T.; Lamy, T.; et al. DC-SIGN-expressing macrophages trigger activation of mannosylated IgM B-cell receptor in follicular lymphoma. Blood 2015, 126, 1911–1920.
  15. Amé-Thomas, P.; Tarte, K. The yin and the yang of follicular lymphoma cell niches: Role of microenvironment heterogeneity and plasticity. Semin. Cancer Biol. 2014, 24, 23–32.
  16. Sangaletti, S.; Tripodo, C.; Portararo, P.; Dugo, M.; Vitali, C.; Botti, L.; Guarnotta, C.; Cappetti, B.; Gulino, A.; Torselli, I.; et al. Stromal niche communalities underscore the contribution of the matricellular protein SPARC to B-cell development and lymphoid malignancies. Oncoimmunology 2014, 3, e28989.
  17. Lamaison, C.; Tarte, K. Impact of B cell/lymphoid stromal cell crosstalk in B-cell physiology and malignancy. Immunol. Lett. 2019, 215, 12–18.
  18. Giulino-Roth, L.; Cesarman, E. Molecular biology of burkitt lymphoma. Burkitt’s Lymphoma 2013, 18, 211–226.
  19. Gerbitz, A.; Mautner, J.; Geltinger, C.; Hörtnagel, K.; Christoph, B.; Asenbauer, H.; Klobeck, G.; Polack, A.; Bornkamm, G.W. Deregulation of the proto-oncogene c-myc through t(8;22) translocation in Burkitt’s lymphoma. Oncogene 1999, 18, 1745–1753.
  20. Sigaux, F.; Berger, R.; Bernheim, A.; Valensi, F.; Daniel, M.T.; Flandrin, G. Malignant lymphomas with band 8q24 chromosome abnormality: A morphologic continuum extending from Burkitt’s to immunoblastic lymphoma. Br. J. Haematol. 1984, 57, 393–405.
  21. Pham, L.V.; Pogue, E.; Ford, R.J. The role of macrophage/B-cell interactions in the pathophysiology of B-cell lymphomas. Front. Oncol. 2018, 8, 147.
  22. Granai, M.; Mundo, L.; Akarca, A.U.; Siciliano, M.C.; Rizvi, H.; Mancini, V.; Onyango, N.; Nyagol, J.; Abinya, N.O.; Maha, I.; et al. Immune landscape in Burkitt lymphoma reveals M2-macrophage polarization and correlation between PD-L1 expression and non-canonical EBV latency program. Infect. Agents Cancer 2020, 15, 28.
  23. Sindel, A.; Al-Juhaishi, T.; Yazbeck, V. Marginal Zone Lymphoma: State-of-the-Art Treatment. Curr. Treat. Options Oncol. 2019, 20, 90.
  24. Leslie, L.A.; Feldman, T.A.; McNeill, A.; Timberg, M.; Iida, H.; Goy, A.H. Contemporary management of nodal and primary splenic marginal zone lymphoma. Expert Rev. Hematol. 2019, 12, 1011–1022.
  25. Piris, M.A.; Isaacson, P.G.; Swerdlow, S.H.; Thieblemont, C.; Pittaluga, S.; Rossi, D.; Harris, N.L. Splenic marginal zone lymphoma. In WHO Classification of Tumours of Haematopoietic and Lymphoid Tissues; Swerdlow, S.H., Campo, E., Harris, N.L., Jaffe, E.S., Pileri, S.A., Stein, H., Thiele, J., Eds.; IARC Press: Lyon, France, 2017; pp. 223–225.
  26. Campo, E.; Pileri, S.A.; Jaffe, E.S.; Nathwani, B.N.; Stein, H.; Müller-Hermelink, H.K. Nodal marginal zone lymphoma. In WHO Classification of Tumours of Haematopoietic and Lymphoid Tissues; Swerdlow, S.H., Campo, E., Harris, N.L., Jaffe, E.S., Pileri, S.A., Stein, H., Thiele, J., Eds.; IARC Press: Lyon, France, 2017; pp. 263–265.
  27. Cook, J.R.; Isaacson, P.G.; Chott, A.; Nakamura, S.; Müller-Hermelink, H.K.; Harris, N.L.; Swerdlow, S.H. Extranodal marginal zone lymphoma of mucosa-associated lymphoid tissue (MALT lymphoma). In WHO Classification of Tumours of Haematopoietic and Lymphoid Tissues; Swerdlow, S.H., Campo, E., Harris, N.L., Jaffe, E.S., Pileri, S.A., Stein, H., Thiele, J., Eds.; IARC Press: Lyon, France, 2017; pp. 259–262.
  28. Schreuder, M.I.; van den Brand, M.; Hebeda, K.M.; Groenen, P.J.T.A.; van Krieken, J.H.; Scheijen, B. Novel developments in the pathogenesis and diagnosis of extranodal marginal zone lymphoma. J. Hematop. 2017, 10, 91–107.
  29. Franco, G.; Guarnotta, C.; Frossi, B.; Piccaluga, P.P.; Boveri, E.; Gulino, A.; Fuligni, F.; Rigoni, A.; Porcasi, R.; Buffa, S.; et al. Bone marrow stroma CD40 expression correlates with inflammatory mast cell infiltration and disease progression in splenic marginal zone lymphoma. Blood 2014, 123, 1836–1849.
  30. Thieblemont, C.; Bertoni, F.; Copie-Bergman, C.; Ferreri, A.J.M.; Ponzoni, M. Chronic inflammation and extra-nodal marginal-zone lymphomas of MALT-type. Semin. Cancer Biol. 2014, 24, 33–42.
  31. Vose, J.M. Mantle cell lymphoma: 2017 update on diagnosis, risk-stratification, and clinical management. Am. J. Hematol. 2017, 92, 806–813.
  32. Klener, P. Advances in molecular biology and targeted therapy of mantle cell lymphoma. Int. J. Mol. Sci. 2019, 20, 4417.
  33. Chiron, D.; Bellanger, C.; Papin, A.; Tessoulin, B.; Dousset, C.; Maiga, S.; Moreau, A.; Esbelin, J.; Trichet, V.; Chen-Kiang, S.; et al. Rational targeted therapies to overcome microenvironment-dependent expansion of mantle cell lymphoma. Blood 2016, 128, 2808–2818.
  34. Harrington, B.K.; Wheeler, E.; Hornbuckle, K.; Smith, L.; Klamer, B.; Zhang, X.; Long, M.; Baiocchi, R.A.; Maddocks, K.; Johnson, A.J.; et al. Modulation of immune checkpoint molecule expression in mantle cell lymphoma. HHS Public Access. 2019, 60, 2498–2507.
  35. Nygren, L.; Wasik, A.M.; Baumgartner-Wennerholm, S.; Jeppsson-Ahlberg, Å.; Klimkowska, M.; Andersson, P.; Buhrkuhl, D.; Christensson, B.; Kimby, E.; Wahlin, B.E.; et al. T-cell levels are prognostic in mantle cell lymphoma. Clin. Cancer Res. 2014, 20, 6096–6104.
  36. Yang, Z.Z.; Novak, A.J.; Stenson, M.J.; Witzig, T.E.; Ansell, S.M. Intratumoral CD4+CD25+ regulatory T-cell-mediated suppression of infiltrating CD4+ T cells in B-cell non-Hodgkin lymphoma. Blood 2006, 107, 3639–3646.
  37. Papin, A.; Le Gouill, S.; Chiron, D. Rationale for targeting tumor cells in their microenvironment for mantle cell lymphoma treatment. Leuk. Lymphoma 2018, 59, 1064–1072.
  38. Sonbol, M.B.; Maurer, M.J.; Stenson, M.J.; Allmer, C.; Laplant, B.R.; Weiner, G.J.; Macon, W.R.; Cerhan, J.R.; Witzig, T.E.; Gupta, M. Elevated soluble IL-2Rα, IL-8, and MIP-1β levels are associated with inferior outcome and are independent of MIPI score in patients with mantle cell lymphoma. Am. J. Hematol. 2014, 89, E223–E227.
  39. Müschen, M.; Rajewsky, K.; Bräuninger, A.; Baur, A.S.; Oudejans, J.J.; Roers, A.; Hansmann, M.L.; Küppers, R. Rare occurrence of classical Hodgkin’s disease as a T cell lymphoma. J. Exp. Med. 2000, 191, 387–394.
  40. Moy, R.H.; Younes, A. Immune Checkpoint Inhibition in Hodgkin Lymphoma. HemaSphere 2018, 2.
  41. Green, M.R.; Monti, S.; Rodig, S.J.; Juszczynski, P.; Currie, T.; O’Donnell, E.; Chapuy, B.; Takeyama, K.; Neuberg, D.; Golub, T.R.; et al. Integrative analysis reveals selective 9p24.1 amplification, increased PD-1 ligand expression, and further induction via JAK2 in nodular sclerosing Hodgkin lymphoma and primary mediastinal large B-cell lymphoma. Blood 2010, 116, 3268–3277.
  42. Yamamoto, R.; Nishikori, M.; Tashima, M.; Sakai, T.; Ichinohe, T.; Takaori-Kondo, A.; Ohmori, K.; Uchiyama, T. B7-H1 expression is regulated by MEK/ERK signaling pathway in anaplastic large cell lymphoma and Hodgkin lymphoma. Cancer Sci. 2009, 100, 2093–2100.
  43. Mottok, A.; Steidl, C. Biology of classical Hodgkin lymphoma: Implications for prognosis and novel therapies. Blood 2018, 131, 1654–1665.
  44. Campo, E.; Pileri, S.A. The Classification of Lymphomas: Updating the WHO Classification. In Postgraduate Haematology: Seventh Edition; Wiley-Blackwell: Hoboken, NJ, USA, 2015; ISBN 9781118853771.
More
© Text is available under the terms and conditions of the Creative Commons Attribution (CC BY) license; additional terms may apply. By using this site, you agree to the Terms and Conditions and Privacy Policy.
Upload a video for this entry
Information
Subjects: Immunology
Contributors MDPI registered users' name will be linked to their SciProfiles pages. To register with us, please refer to https://encyclopedia.pub/register :
Gael Roue
,
Miranda Fernández-Serrano
View Times: 510
Revisions: 2 times (View History)
Update Date: 01 Feb 2021
Table of Contents
    1000/1000
    Hot Most Recent
    Video Production Service
    Feedback