Establishment and characterization of a villous lymphoma cell line from splenic B-cell lymphoma

Inokuchi, Koiti; Abo, Junko; Takahashi, Hidemi; Miyake, Keisuke; Inokuchi, Sadaki; Dan, Kazuo; Nomura, Takeo

doi:10.1016/0145-2126(95)00059-3

Cited by 11 publications

(6 citation statements)

References 21 publications

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“…Cytogenetic studies and Southern blot analysis of Ig gene rearrangements confirmed the identical origin of the two cell lines. Although a few SMZL cell lines have been reported—one (VL51) from clinically stable SMZL 21 and two (Karpas 1718 and UCH1) from the refractory form of the disease 22 , 23 —the paired availability of our cell lines from a case of SMZL that manifested a long chronic phase before progression to an aggressive clinical course is invaluable in investigating the transformation mechanism of SMZL.…”

Section: Discussionmentioning

confidence: 99%

Differential gene expression profiling linked to tumor progression of splenic marginal zone lymphoma

Higuchi

Hashida

Taniguchi

et al. 2017

Sci Rep

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The genetic events that lead to aggressive transformation of cases of splenic marginal zone lymphoma (SMZL) after the chronic clinical stage have not been well understood. We aimed to find candidate genes associated with aggressive features of SMZL. We have successfully established two SMZL cell lines, designated SL-15 and SL-22, derived from the same patient’s tumor clone in chronic and aggressive phases, respectively. Microarray analysis identified cell cycle-associated genes—specifically PLK1—as the most significantly upregulated in primary aggressive SMZL cells compared with cells from chronic phase. EPHA4 and MS4A1 (CD20) were found to be downregulated dramatically. These gene expression patterns were reproduced in both cell lines. Genetic knockdown of PLK1 resulted in inhibition of cell proliferation and induction of apoptosis in SL-22 cells, which expressed higher levels of PLK1 than SL-15 cells. SL-22 cells needed higher concentrations of chemical PLK1 inhibitors to achieve greater effects. In addition, we found homozygous deletion of the MS4A1 gene as a newly identified molecular mechanism of CD20-negative conversion. Our findings are expected to stimulate further studies on whether PLK1 could be a potential therapeutic target for this tumor. Furthermore, cases with CD20-negatively converted lymphomas should be screened for the genomic loss of MS4A1.

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Section: Discussionmentioning

confidence: 99%

Differential gene expression profiling linked to tumor progression of splenic marginal zone lymphoma

Higuchi

Hashida

Taniguchi

et al. 2017

Sci Rep

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“…Informed consent was obtained from each subject. In addition, four cell lines were used in the study: Karpas‐1718, SL15 and VL51 cell lines, derived from patients with SMZL, and the marginal zone lymphoma (MZL)‐derived cell line SSK41 (Inokuchi et al , ; Daibata et al , ).…”

Section: Methodsmentioning

confidence: 99%

High‐throughput sequencing analysis of the chromosome 7q32 deletion reveals IRF5 as a potential tumour suppressor in splenic marginal‐zone lymphoma

et al. 2012

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Summary Using high‐resolution genomic microarray analysis, a distinct genomic profile was defined in 114 samples from patients with splenic marginal zone lymphoma (SMZL). Deletion or uniparental disomy of chromosome 7q were detected in 42 of 114 (37%) SMZLs but in only nine of 170 (5%) mature B‐cell lymphomas (P < 0·00001). The presence of unmutated IGHV, genomic complexity, 17p13‐TP53 deletion and 8q‐MYC gain, but not 7q deletion, correlated with shorter overall survival of SMZL patients. Mapping studies narrowed down a commonly deleted region of 2·7 Mb in 7q32.1‐q32.2 spanning a region between the SND1 and COPG2 genes. High‐throughput sequencing analysis of the 7q32‐deleted segment did not identify biallelic deletions/insertions or clear pathogenic gene mutations, but detected six nucleotide changes in IRF5 (n = 2), TMEM209 (n = 2), CALU (n = 1) and ZC3HC1 (n = 1) not found in healthy individuals. Comparative expression analysis found a fourfold down‐regulation of IRF5 gene in lymphomas with 7q32 deletion versus non‐deleted tumours (P = 0·032). Ectopic expression of IRF5 in marginal‐zone lymphoma cells decreased proliferation and increased apoptosis in vitro, and impaired lymphoma development in vivo. These results show that cryptic deletions, insertions and/or point mutations inactivating genes within 7q32 are not common in SMZL, and suggest that IRF5 may be a haploinsufficient tumour suppressor in this lymphoma entity.

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“…14 Total cellular DNA was extracted from BM-MNCs by protease K digestion, phenolchloroform extraction, and ethanol precipitation. 15 Reverse-transcription polymerase chain reaction (RT-PCR) for expression analysis of the p51/p63 gene cDNA was prepared from 0.5 g of total RNA using a random hexamer primer according to the our original protocol. 14 cDNA conversion mixture was amplified by PCR.…”

Section: Extraction Of Rna and Dnamentioning

confidence: 99%

Mutation of the p51/p63 gene is associated with blastic crisis in chronic myelogenous leukemia

et al. 2001

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The p51/p63 gene, a novel member of the p53 gene family, has recently been identified at 3q27-9. There are at least six major isotypes of p51/p63 mRNA transcripts. p51A/TAp63␥ has the potential to induce apoptosis and growth suppression in a manner similar to p53, and other isotypes may suppress the p53 and p51A/TAp63␥ genes in a dominant-negative manner. We analyzed the mutation and expression of the p51/p63 gene in 80 cases of chronic myelogenous leukemia (CML) to evaluate its role in blastic transformation. Expression of the p51/p63 gene was detected in 74 cases. The ␣ isotype of p51/p63 transcripts was dominantly expressed in 72 of these 74 cases. There was no correlation between the isotypes of p51/p63 transcripts and the clinical phase. Mutations of the p51/p63 gene were found in six cases. All these mutated cases expressed p51B/TAp63 ␣. In four of the six cases, the mutations were within a limited region (codon 151-170) corresponding to the DNA-binding domain. We hypothesized that this limited region is a hot spot for mutation of the p51/p63 gene. Mutations of the p53 gene were found in four cases of CML in blastic crisis (BC). Frequencies of the p51/p63 and p53 gene mutations were higher in BC (p51/p63 gene, 11.8%; p53 gene, 7.8%) than in the chronic phase (p51/p63 gene, 1.5%; p53 gene, 0%). The p51/p63 gene mutation may act similarly to the p53 gene mutation as a genetic alteration potentially responsible for the progression of CML. Leukemia (2001) 15, 1729-1734.

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Establishment and characterization of a villous lymphoma cell line from splenic B-cell lymphoma

Cited by 11 publications

References 21 publications

Differential gene expression profiling linked to tumor progression of splenic marginal zone lymphoma

Differential gene expression profiling linked to tumor progression of splenic marginal zone lymphoma

High‐throughput sequencing analysis of the chromosome 7q32 deletion reveals IRF5 as a potential tumour suppressor in splenic marginal‐zone lymphoma

Mutation of the p51/p63 gene is associated with blastic crisis in chronic myelogenous leukemia

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