Comparison of <scp>CD</scp>20 expression in <scp>B</scp>‐cell lymphoma between newly diagnosed, untreated cases and those after rituximab treatment

Miyoshi, Hiroaki; Sato, Kensaku; Kimura, Yoshizo; Kiyasu, Junichi; Takeuchi, Masanori; Yoshida, Maki; Ichikawa, Ayako; Ishibashi, Yukinao; Nakamura, Yukihiko; Nakashima, Shinji; Niino, Daisuke; Sugita, Yasuo; Ohshima, Koichi

doi:10.1111/j.1349-7006.2012.02307.x

Cited by 26 publications

(26 citation statements)

References 20 publications

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“…Aberrant down-modulation of CD20 protein expression in DLBCL after treatment with Rituximab has been observed in the clinical settings [33][34][35] . Our results showed that Rituximab-mediated downregulation of CD20 is at the protein levels because the levels of CD20 mRNA expression sustained after treatment with Rituximab.…”

Section: Discussionmentioning

confidence: 99%

Novel HDAC inhibitor Chidamide synergizes with Rituximab to inhibit diffuse large B-cell lymphoma tumour growth by upregulating CD20

et al. 2020

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Loss of CD20 is a major obstacle for the retreatment of relapsed/refractory diffuse large B cell lymphoma (DLBCL) with Rituximab-associated regimens. Histone deacetylation causes gene silencing and inhibits CD20 expression. Chidamide is a novel inhibitor for histone deacetylases (HDACs). We hypothesize that Chidamide could overcome Rituximabmediated down-regulation of CD20 and facilitate Rituximab-induced killing. In this study, we determine the mechanism of synergy of Chidamide with Rituximab in DLBCL using in vitro and in vivo models. We found that the levels of CD20 protein surface expression on five DLBCL cell lines were significantly and positively correlated with the sensitivities of cells to Rituximab. Treatment with Rituximab significantly reduced CD20 surface expression at the protein levels. RNA sequencing showed that Chidamide significantly increased expression of more than 2000 transcriptomes in DLBCL cells, around 1000 transcriptomes belong to the cell membrane and cell periphery pathways, including MS4A1. Chidamide significantly increased CD20 surface expression in DLBCL cell lines. Combination with Chidamide significantly synergized Rituximab-induced cell death in vitro and significantly inhibited tumour growth in DLBCL-bearing xenograft mice. A patient with relapsed/refractory DLBCL achieved a complete response after three cycles combined treatment with Chidamide and Rituximab. In conclusion, our data demonstrate for the first time that inhibition of HDACs by Chidamide significantly enhanced Rituximab-induced tumour growth inhibition in vitro and in vivo. We propose that CD20 surface expression should be used clinically to evaluate treatment response in patients with DLBCL. Chidamide is a promising sensitizer for the retreatment of DLBCL with Rituximab.

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Section: Discussionmentioning

confidence: 99%

Novel HDAC inhibitor Chidamide synergizes with Rituximab to inhibit diffuse large B-cell lymphoma tumour growth by upregulating CD20

et al. 2020

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“…We reviewed tissue samples from 22 cases diagnosed as CD5‐positive follicular lymphoma (FL) from 2005 to 2011 and 62 cases diagnosed as FL without CD5 expression, termed control cases, in 2006 in the Department of Pathology, Kurume University. Control cases were included and described in a previous study . Fresh materials were used for flow cytometry (FCM).…”

Section: Methodsmentioning

confidence: 99%

“…Control cases were included and described in a previous study. 13 Fresh materials were used for flow cytometry (FCM). Paraffin-embedded tissues were used for diagnosis and immunohistochemical staining (IHS).…”

Section: Patientsmentioning

confidence: 99%

CD5‐positive follicular lymphoma characterized by CD25, MUM1, low frequency of t(14;18) and poor prognosis

Miyoshi

Sato

Yoshida

et al. 2014

Pathology International

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CD5-positive follicular lymphoma (FL), although rare, has been described in a number of case reports. However, a statistically valid, clinicopathological comparison between CD5-positive FL and CD5-negative FL has never been performed because of its rarity. We statistically compared clinicopathological characteristics of 22 cases of CD5-positive FL, diagnosed by immunohistochemistry, flow cytometry and morphological findings, with those of 62 cases of FL without CD5 expression (control cases). CD5-positive FL patients showed a higher tendency of peripheral blood involvement (P = 0.076) and a higher frequency of CD25 expression (P = 0.0004) and MUM1 protein expression (P = 0.0008), and a lower frequency of t(14;18)(q32;q21) (P = 0.017). The overall survival (OS) curve of CD5-positive FL was significantly worse than that of control cases (P = 0.0266), although progression-free survival curves did not show a significant difference (P = 0.7899). Moreover, CD5 expression was shown to be an independent poor prognostic factor for OS in both univariate analysis [Hazard Ratio (HR), 3.63; P = 0.0464] and multivariate analysis (HR, 57.16; P = 0.0001). CD5-positive FL showed different clinicopathological characteristics from FL lacking CD5 expression. These results suggest that CD5-positive FL should be considered a different type of FL, and its clinicopathological management should be conducted differently.

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“…Mutation analysis was performed as previously described. 16 In brief, exons 4-8 of TP53 were amplified from genomic DNA using PCR. PCR primers used in this study were detailed in the previous study.…”

Section: Mutation Analysis For Tp53mentioning

confidence: 99%

Mutation Analysis for <i>TP53</i> in Chronic-Type Adult T-Cell Leukemia/Lymphoma

Yoshida¹,

Imaizumi

Utsunomiya

et al. 2015

J Clin Exp Hematopathol

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Adult T-cell leukemia/lymphoma (ATLL) is a T-cell neoplasm caused by human T-cell leukemia virus type I (HTLV-I). ATLL is classified into four clinical subtypes based on the clinical manifestation: acute, lymphoma, chronic and smoldering. Approximately half of chronic type ATLL cases progressed to the acute type. We previously demonstrated that genomic alterations related to the cell cycle de-regulation such as CDKN2A and immune escape such as CD58 alteration can serve as predictive biomarkers for acute transformation of the chronic type. Although alteration of TP53, which is known to be a major regulator of cell cycle, has been identified in several types of cancers including acute type ATLL, no copy number alteration of TP53 was found in the chronic type by array comparative genomic hybridization. In the present study, mutation of TP53 was further analyzed by sequencing for these cases as well as HTLV-I carriers with oligo-clonality. However, no TP53 mutation was identified. These results suggested that TP53 mutation plays a role for the later stage of ATLL development.

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Comparison of CD20 expression in B‐cell lymphoma between newly diagnosed, untreated cases and those after rituximab treatment

Cited by 26 publications

References 20 publications

Novel HDAC inhibitor Chidamide synergizes with Rituximab to inhibit diffuse large B-cell lymphoma tumour growth by upregulating CD20

Novel HDAC inhibitor Chidamide synergizes with Rituximab to inhibit diffuse large B-cell lymphoma tumour growth by upregulating CD20

CD5‐positive follicular lymphoma characterized by CD25, MUM1, low frequency of t(14;18) and poor prognosis

Mutation Analysis for <i>TP53</i> in Chronic-Type Adult T-Cell Leukemia/Lymphoma

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