<i>CD79B </i>mutations in primary vitreoretinal lymphoma: Diagnostic and prognostic potential

Yonese, Ichiro; Takase, Hiroshi; Yoshimori, Mayumi; Onozawa, Erika; Tsuzura, Akiho; Miki, Tohru; Mochizuki, Manabu; Miura, Osamu; Arai, Ayako

doi:10.1111/ejh.13191

Cited by 64 publications

(56 citation statements)

References 25 publications

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“…Among them, PVRL‐2 and PVRL‐4 showed early progression in the CNS within 2 years after treatment, whereas the others did not. Recently, it was reported that MYD88 L265P and mutations in the ITAM region of CD79B around Y196 were frequently detected in PVRL at rates of approximately 80% and 35%, respectively. As shown in Table 1, our PVRL cases had at least one of these mutations.…”

Section: Resultssupporting

confidence: 52%

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Gene expression profiling of primary vitreoretinal lymphoma

et al. 2020

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This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. AbstractThe characteristics of tumor cells of primary vitreoretinal lymphoma (PVRL) have not been defined, although researches have shown that most cases are of diffuse large B-cell lymphoma (DLBCL). To determine the subtype and biological characteristics of tumor cells of PVRL, we performed a gene expression profiling analysis. RNA was extracted from the vitreous fluid of 7 PVRL patients and from nodal samples of 10 DLBCL patients: 6 of germinal center B-cell (GCB) type and 4 of activated B-cell (ABC) type determined by Hans' criteria. Six PVRL samples showed gene expression profiles that were similar to each other. The patterns were different from those of the ABC-type nodular DLBCL but relatively close to those of the GCB-type nodular DLBCL. Interestingly, all of the 6 examined PVRL samples had either MYD88 L265P or mutation in the immunoreceptor tyrosine-based activation motif (ITAM) region of CD79B. Five PVRL patients with similar gene expression profiles were treated with a standardized regimen: intravitreal administration of methotrexate (MTX) followed by six courses of systemic high doses of MTX. As a result, 2 patients had CD79B mutations and showed early central nervous system (CNS) progression. Patients without CNS progression did not have this mutation. In conclusion, PVRL had unique genetic features: an expression pattern different from ABC-type and relatively close to GCBtype DLBCL. CD79B mutations showed potential to serve as prognostic markers for CNS progression. K E Y W O R D S CD79B, diffuse large B-cell lymphoma, GCB-type DLBCL, gene expression profiling, primary vitreoretinal lymphoma 1418 | ARAI et Al. | MATERIAL S AND ME THODS | PatientsThe patients were diagnosed and treated at Tokyo Medical and Dental University (TMDU) hospital from 2011 to 2018. Samples from the patients whose vitreous RNA could be obtained were analyzed. The study was approved by the ethics board of TMDU and written informed consent was obtained from the patients. | Diagnosis of primary vitreoretinal lymphomaPrimary vitreoretinal lymphoma was diagnosed using the following criteria according to the previous report 2 : (a) typical eye involvement: a cloudy vitreous body and/or subretinal proliferative lesions; (b) presence of lymphoma cells in the vitreous fluid; and (c) clonality of the infiltrating lymphoma cells in the vitreous fluid using either PCR analysis of IgH gene rearrangements or flow cytometry analysis. Patients who had (a) accompanied by either (b) or (c) were diagnosed with VRL. VRL confined to the eyes at diagnosis was defined as PVRL. S U PP O RTI N G I N FO R M ATI O NAdditional supporting information may be found online in the Supporting Information section.

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Section: Resultssupporting

confidence: 52%

“…Interestingly, 6 of 7 patients with vitreous DNA available for analysis had either MYD88 L265P or mutations in the ITAM region of CD79B . It was reported that MYD88 L265P and the mutations in CD79B were frequently detected in PVRL . However, these mutations were reported to be infrequent in GCB‐type DLBCL .…”

Section: Discussionmentioning

confidence: 38%

Gene expression profiling of primary vitreoretinal lymphoma

et al. 2020

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“…2,3,18, The highest prevalence of MYD88(L265P) is found in lymphoplasmacytic lymphoma/WM, with approximately 85% of the patients being affected. 18,[22][23][24][25][26][27][28][29][30][31][32][33][34][35][36][37] In DLBCL, the prevalence of MYD88(L265P) is highest (range, 44% to 73%) in extranodal DLBCL, in immune-privileged sites, 96 such as primary DLBCL of the central nervous system 18,22,23,[86][87][88]96 and primary testicular lymphoma, 22,23,96,108 primary cutaneous DLBCL, leg type, 22,71,89-91 orbital/vitreoretinal DLBCL, 22,97,98 intravascular large B-cell lymphoma, 95 and primary breast DLBCL. 22,99 The high prevalence of MYD88(L265P) in extranodal site-specific lymphomas, lymphoplasmacytic lymphoma, and WM may provide an indication for the origin of these lymphomas.…”

Section: Prevalencementioning

confidence: 99%

MYD88 in the driver’s seat of B-cell lymphomagenesis: from molecular mechanisms to clinical implications

et al. 2019

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“…15 Intriguingly, this genetic subgroup is linked to primary extranodal lymphomas, including lymphomas arising in the central nervous system (CNS), ocular vitreo-retina and testis, all considered 'immune-privileged' sites as they tolerate allografts and permit only selective entrance of immune cells. [16][17][18][19] Importantly, Wilson et al established that ABC DLBCL harboring mutations in CD79B, particularly those with concurrent MYD88 mutations, were highly responsive to treatment with ibrutinib, a selective Bruton's tyrosine kinase (BTK) inhibitor. 20 These observations suggest that (extranodal) lymphomas belonging to the MCD subtype could also be targeted by inhibition of BCR signaling.…”

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confidence: 99%

Towards genomic-based prognostication and precision therapy for diffuse large B-cell lymphoma

Minderman

Pals

2020

haematol

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T he development of precision medicine for diffuse large B-cell lymphoma (DLBCL) is complicated by its great clinical and molecular heterogeneity. Twenty years ago, two distinct cell-of-origin (COO) subtypes were identified based on distinct gene expression profiles that reflect different stages of B-cell development, i.e., germinal center B-cell-like (GCB) and activated B-celllike (ABC) DLBCL. 1 The ongoing revolution in genomics has since shed light on the genetic landscape of these subtypes. Whereas ABC DLBCL is characterized by frequent mutations in nuclear factor-κB (NF-κB) pathway drivers and intermediates, including TNFAIP3, MYD88, CARD11 and CD79B, as well as loss of cell cycle regulators CDKN2A and CDKN2B, GCB DLBCL carry frequent mutations in epigenetic modifiers, such as CREBBP, KMT2D and EZH2. 2,3 GCB DLBCL patients have a more favorable prognosis and a better clinical response to standard R-CHOP immunochemotherapy than those with ABC DLBCL. Nevertheless, the clinical outcome is het-lymphoma

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CD79B mutations in primary vitreoretinal lymphoma: Diagnostic and prognostic potential

Cited by 64 publications

References 25 publications

Gene expression profiling of primary vitreoretinal lymphoma

Gene expression profiling of primary vitreoretinal lymphoma

MYD88 in the driver’s seat of B-cell lymphomagenesis: from molecular mechanisms to clinical implications

Towards genomic-based prognostication and precision therapy for diffuse large B-cell lymphoma

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