The 5th Edition of the World Health Organization Classification of Hematolymphoid Tumors

Li, Weijie

doi:10.36255/exon-publications-leukemia-who-5th-edition-hematolymphoid-tumors

Cited by 53 publications

(61 citation statements)

References 31 publications

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“…4 This integrated nomenclature allows the grouping of specific types of immunodeficiency-associated lymphomas (such as DLBCL EBV-positive), despite the underlying immunodeficiency/dysregulation, to better define the unique shared pathogenetic mechanisms. 4,9,10 On the other hand, lymphomatoid granulomatosis is no longer considered an immunodeficiency-associated entity. It occurs exclusively in immunocompetent patients, and in the case of an underlying immunodeficiency, it should be considered a subtype of a polymorphic lymphoproliferative disorder.…”

Section: Who Classification Of Tumors 5th Editionmentioning

confidence: 99%

Imaging of Lymphomas Involving the CNS: An Update-Review of the Full Spectrum of Disease with an Emphasis on the World Health Organization Classifications of CNS Tumors 2021 and Hematolymphoid Tumors 2022

Pons-Escoda

Naval‐Baudin²,

Velasco

et al. 2023

AJNR Am J Neuroradiol

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Lymphomas of the CNS are the second most frequent primary brain malignancy in adults after gliomas. Presurgical suspicion of lymphoma greatly impacts patient management. The radiologic features of this tumor have been widely covered in the literature for decades, but under current classifications, mainly corresponding to the most common presentations of the most frequent type: primary diffuse large B-cell lymphoma of the CNS. Nevertheless, rarer presentations of this specific lymphoma and of other World Health Organization lymphoma subtypes with different imaging features are rarely treated. Moreover, important advances in imaging techniques, changing epidemiologic factors with relevant impact on these tumors (eg, immunodeficiency/dysregulation), and recent updates of the World Health Organization Classification of CNS Tumors 2021 and Hematolymphoid Tumors 2022 may have rendered some accepted concepts outdated. In this article, the authors aim to fulfill a critical need by providing a complete update-review, emphasizing the latest clinical-radiologic features of the full spectrum of lymphomas involving the CNS.ABBREVIATIONS: ALK1/ALKÀ ¼ anaplastic lymphoma kinase positive and negative; CLIPPERS ¼ chronic lymphocytic inflammation with pontine perivascular enhancement responsive to steroids; DLBCL ¼ diffuse large B-cell lymphoma; EBV ¼ Epstein-Barr virus; MALT ¼ mucosa-associated lymphoid tissue; NK ¼ natural killer; PSR ¼ percentage of signal recovery; WHO ¼ World Health Organization

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Section: Who Classification Of Tumors 5th Editionmentioning

confidence: 99%

Imaging of Lymphomas Involving the CNS: An Update-Review of the Full Spectrum of Disease with an Emphasis on the World Health Organization Classifications of CNS Tumors 2021 and Hematolymphoid Tumors 2022

Pons-Escoda

Naval‐Baudin²,

Velasco

et al. 2023

AJNR Am J Neuroradiol

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“…Recently, in 2017, revised WHO 4th edition was introduced and the upcoming WHO 5th edition expected to release in 2023 has still incorporated morphology in the classification of AL along with defining genetic abnormalities. 11…”

Section: History and Evolution Of Morphological Classification For Ac...mentioning

confidence: 99%

Role of Morphology in the Diagnosis of Acute Leukemias: Systematic Review

Sekar

Raj

Manivannan

2023

Indian J Med Paediatr Oncol

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The role of hematopathologists in the diagnosis of acute leukemia (AL) starts with the morphological examination of either peripheral blood smear or bone marrow. The morphological hallmark for the myeloblast includes “Auer rods” and “Phi bodies.” The addition of cytochemical stains such as myeloperoxidase, Sudan Black B, periodic acid-Schiff stain, nonspecific esterase, and Perls' stain acts as an important adjunct to the morphological classification in the resource-constrained settings. The recent World Health Organization classification still endorses the utility of morphology which requires the presence of either ≥ 20% lymphoblasts or myeloblasts/or its equivalents (monoblasts, promonocytes, or megakaryoblasts) and integrates it with the clinical features, immunophenotyping (IP), and molecular genetics for making the diagnosis of AL. Morphology can give clue to the specific diagnosis of acute myeloid leukemia (AML) with t(8:21), t(15:17), t(16:16), or inv(16) and this diagnosis can be made irrespective of blasts count if such translocations are demonstrated by molecular tests. There are some interesting findings such as blasts with “hand-mirror” morphology, nuclear cleavage, prominent cytoplasmic vacuoles, pseudo-Chediak-Higashi granules, cup-like nucleus, and other dysplastic features helping in differentiating lymphoid and myeloid leukemias. Transient abnormal myelopoiesis in Down syndrome and hypoplastic AL can be picked up on morphological examination. Bone marrow biopsy would be greatly beneficial and complementary to aspirate smears and is required for diagnosing exact cellularity, topography of cells, dyspoiesis, myelonecrosis, gelatinous marrow transformation, myelofibrosis, and IP can be performed using immunohistochemistry. Morphological examination in AL is not only helpful for diagnosis but also useful for predicting the prognosis in posttherapy cases, AML with myelodysplasia-related changes, therapy-related myeloid neoplasms, and mixed phenotype AL. Hematogones, blastoid mantle cell lymphoma, high grade B cell lymphoid with blastoid morphology, Burkitt leukemia, prolymphocytes in prolymphocytic leukemia, hairy cell leukemia variant, plasmablasts especially in plasmablastic leukemia, or plasma cell leukemia can mimic AL and IP is useful in these situations. Hence, morphology should be considered as a kind of “gold-standard” starting point for the analysis of AL cases. Morphological examination cannot be replaced and advanced tests cannot be used as surrogate for morphology.

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“…Diffuse large B-cell lymphoma (DLBCL), the most common subtype of non-Hodgkin's lymphoma, represents a molecularly heterogeneous entity. [1][2][3] DLBCL is potentially curable with immunochemotherapy using rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP), but recurrent or progressive disease occurs in approximately 40% of the patients. 4,5 Attempts to improve the treatment outcome by combining standard immunochemotherapy with promising novel agents targeting specific pathways have encountered difficulties likely due to the biological complexity of DLBCL.…”

Section: Introductionmentioning

confidence: 99%

“…As for the classification of DLBCL, a strategy to categorize DLBCL is based upon the detection of rearrangements of MYC, BCL2 and/ or BCL6 by fluorescent in-situ hybridization (FISH). 2 The most recent revision of the WHO classification of lymphoid neoplasms recognizes the high-grade B-cell double-/triple-hit lymphoma, with MYC rearrangement and BCL2 and/or BCL6 rearrangements, as a particular entity associated with aggressive behavior and inferior outcome. 8 Gene expression profiling allows to distinguish three molecular subtypes based on cell of origin (COO), dividing DLBCL cases into activated B-cell like (ABC), germinal center B-cell like (GCB), and unclassified subtypes.…”

Section: Introductionmentioning

confidence: 99%

Simplified algorithm for genetic subtyping in diffuse large B-cell lymphoma

Shen

Dong

et al. 2023

Sig Transduct Target Ther

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Genetic classification helps to disclose molecular heterogeneity and therapeutic implications in diffuse large B-cell lymphoma (DLBCL). Using whole exome/genome sequencing, RNA-sequencing, and fluorescence in situ hybridization in 337 newly diagnosed DLBCL patients, we established a simplified 38-gene algorithm (termed ‘LymphPlex’) based on the information on mutations of 35 genes and rearrangements of three genes (BCL2, BCL6, and MYC), identifying seven distinct genetic subtypes: TP53Mut (TP53 mutations), MCD-like (MYD88, CD79B, PIM1, MPEG1, BTG1, TBL1XR1, PRDM1, IRF4 mutations), BN2-like (BCL6 fusion, NOTCH2, CD70, DTX1, BTG2, TNFAIP3, CCND3 mutations), N1-like (NOTCH1 mutations), EZB-like (BCL2 fusion, EZH2, TNFRSF14, KMT2D, B2M, FAS, CREBBP, ARID1A, EP300, CIITA, STAT6, GNA13 mutations, with or without MYC rearrangement), and ST2-like (SGK1, TET2, SOCS1, DDX3X, ZFP36L1, DUSP2, STAT3, IRF8 mutations). Extended validation of 1001 DLBCL patients revealed clinical relevance and biological signature of each genetic subtype. TP53Mut subtype showed poor prognosis, characterized by p53 signaling dysregulation, immune deficiency, and PI3K activation. MCD-like subtype was associated with poor prognosis, activated B-cell (ABC) origin, BCL2/MYC double-expression, and NF-κB activation. BN2-like subtype showed favorable outcome within ABC-DLBCL and featured with NF-κB activation. N1-like and EZB-like subtypes were predominated by ABC-DLBCL and germinal center B-cell (GCB)-DLBCL, respectively. EZB-like-MYC+ subtype was characterized by an immunosuppressive tumor microenvironment, while EZB-like-MYC- subtype by NOTCH activation. ST2-like subtype showed favorable outcome within GCB-DLBCL and featured with stromal-1 modulation. Genetic subtype-guided targeted agents achieved encouraging clinical response when combined with immunochemotherapy. Collectively, LymphPlex provided high efficacy and feasibility, representing a step forward to the mechanism-based targeted therapy in DLBCL.

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The 5th Edition of the World Health Organization Classification of Hematolymphoid Tumors

Cited by 53 publications

References 31 publications

Imaging of Lymphomas Involving the CNS: An Update-Review of the Full Spectrum of Disease with an Emphasis on the World Health Organization Classifications of CNS Tumors 2021 and Hematolymphoid Tumors 2022

Imaging of Lymphomas Involving the CNS: An Update-Review of the Full Spectrum of Disease with an Emphasis on the World Health Organization Classifications of CNS Tumors 2021 and Hematolymphoid Tumors 2022

Role of Morphology in the Diagnosis of Acute Leukemias: Systematic Review

Simplified algorithm for genetic subtyping in diffuse large B-cell lymphoma

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