scholarly journals No Evidence of Abnormal Expression of Beta-Catenin and Bcl-2 Proteins in Pilomatricoma as One Clinical Feature of Tetrasomy 9p Syndrome

2021 ◽  
Vol 2021 ◽  
pp. 1-8
Author(s):  
Chariyawan Charalsawadi ◽  
Sasipong Trongnit ◽  
Kanoot Jaruthamsophon ◽  
Juthamas Wirojanan ◽  
Somchit Jaruratanasirikul ◽  
...  
Keyword(s):  
Peripheral Blood ◽  
Chromosomal Abnormalities ◽  
Partial Trisomy ◽  
Chromosome 9 ◽  
Clinical Feature ◽  
Beta Catenin ◽  
Genetic Syndromes ◽  
Ctnnb1 Gene ◽  
Protein Expressions ◽  
Isodicentric Chromosome

Background. Little is currently known about the genetics of pilomatricoma. A number of studies have reported some evidence that this disease may have a genetic association with mutations of CTNNB1 gene or expression of the beta-catenin protein. In this study, we reviewed literatures involving 30 patients with various genetic syndromes that have been linked to pilomatricoma and found that somatic mutations of the CTNNB1 gene were reported in 67% of patients. Pilomatricoma has been reported in patients with chromosome 9 rearrangements, including 4 patients with tetrasomy 9p syndrome and one patient with partial trisomy 9. In addition to beta-catenin, the expression of bcl2 was observed in pilomatricoma. Objectives. To report an additional case of tetrasomy 9p syndrome with concurrent pilomatricoma and to examine whether abnormal protein expressions of the CTNNB1 and/or BCL2 genes were present. Methods. Cytogenetic analysis was carried out on peripheral blood, biopsied skin, and pilomatricoma tissue obtained from a patient with tetrasomy 9p syndrome. Immunohistochemical staining was performed on the pilomatricoma tissue, using beta-catenin and bcl2 monoclonal antibodies. Results. SNP microarray revealed nonmosaic gain of the short arm of chromosome 9. A nonmosaic isodicentric chromosome 9 was identified in the peripheral blood but this rearranged chromosome was detected in only 8.3% of the skin fibroblasts. Chromosomal abnormalities were not detected in the pilomatricoma nor expression of beta-catenin or bcl2 proteins in our patient. Conclusion. Pilomatricoma could be a new clinical feature associated with tetrasomy 9p syndrome; however, we found no evidence of tetrasomy 9p or abnormal beta-catenin or bcl2 proteins of the CTNNB1 and BCL2 genes in our pilomatricoma patient.

scholarly journals Emergence of a B-cell lymphoblastic lymphoma in a patient with B-cell chronic lymphocytic leukemia: evidence for the single-cell origin of the two tumors

Blood ◽  
1991 ◽  
Vol 78 (3) ◽  
pp. 797-804
Author(s):  
V Pistoia ◽  
S Roncella ◽  
PF Di Celle ◽  
M Sessarego ◽  
G Cutrona ◽  
...  
Keyword(s):  
Chronic Lymphocytic Leukemia ◽  
B Cell ◽  
Cell Lines ◽  
Peripheral Blood ◽  
Chromosomal Abnormalities ◽  
Cell Clone ◽  
Lymphoblastic Lymphoma ◽  
Lymphocytic Leukemia ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Chain Gene

A patient is described who presented with a chronic lymphocytic leukemia (CLL) and later developed a lymphoblastic lymphoma. The cells from the CLL were typical mature B lymphocytes as could be assessed by morphologic, cytochemical, and surface marker analyses. The cells from the lymphoblastic lymphoma were immature B cells that expressed CD10, CD20, and HLA-DR markers, but not surface Ig or cytoplasmic mu chains, and were negative for terminal deoxynucleotidyl transferase (TdT). The cells of two continuous cell lines, obtained from the bone marrow and the peripheral blood of the patient, had the same phenotype as the lymphoblastic lymphoma cells, did not contain the Epstein-Barr virus genome, and displayed malignant features in vitro, including the capacity to form colonies in agar. The two cell lines also shared identical chromosomal abnormalities, a finding which suggests that they derived from the same malignant cell already present in vivo. Such chromosomal abnormalities were not seen in the karyotype of the peripheral blood cells at the onset of the disease. Analysis of the Ig heavy chain genes using a DJ-specific probe showed the very same monoclonal rearrangement in the cells from the B-CLL, the lymphoblastic lymphoma and the two cell lines, thus demonstrating their common clonal origin. By contrast, a monoclonal rearrangement of the lambda chain gene locus was found in the B-CLL cells only, a finding consistent with their exclusive capacity to express surface IgM lambda. This patient represents a rare case in whom a chronic lymphoproliferative disorder with mature malignant cells transforms into a lymphoblastic lymphoma characterized by cells frozen at a very early maturational stage. The possible mechanisms leading to such transformation within the same cell clone are discussed.

scholarly journals Marginal zone B-cell lymphomas of different sites share similar cytogenetic and morphologic features [see comments]

Blood ◽  
1996 ◽  
Vol 87 (1) ◽  
pp. 299-307 ◽  
Author(s):  
J Dierlamm ◽  
S Pittaluga ◽  
I Wlodarska ◽  
M Stul ◽  
J Thomas ◽  
...  
Keyword(s):  
B Cell ◽  
Structural Changes ◽  
Marginal Zone ◽  
Chromosomal Abnormalities ◽  
Molecular Genetic ◽  
Clinical Manifestations ◽  
B Cell Lymphoma ◽  
Partial Trisomy ◽  
Chromosome 1 ◽  
Chromosomal Changes

Clinical, histologic, cytogenetic, and molecular genetic data of 31 patients with extranodal, nodal, and splenic marginal zone B-cell lymphoma (MZBCL) are presented. Despite these variable clinical manifestations, a similar spectrum of morphologic features as well as distinctive immunophenotypic findings were noted. In all cases, a monotypic B-cell proliferation consistently negative for CD5, CD10, and CD23 was found expanding the marginal zone of the B follicle with and without colonization of the follicle centers. Clonal chromosomal abnormalities were detected in 23 of the 31 patients. Recurrent aberrations included whole or partial trisomy 3 (18 cases), trisomy 18 (9 cases), and structural rearrangements of chromosome 1 with breakpoints in 1q21 (9 cases) or 1p34 (6 cases), all of which were seen in extranodal, nodal, as well as splenic MZBCL. Abnormalities of the additional chromosome 3, such as +del(3)(p13),+i(3)(q10), or structural changes involving the distal part of the long arm, were evident in 9 of the 18 cases. All recurrent abnormalities were found in MZBCL more frequently than in other histologic entities of B-cell non-Hodgkin's lymphoma (B-NHL). None of the known lymphoma-associated chromosomal changes or rearrangements of the BCL1, BCL2, BCL3, BCL6, and CMYC genes were detected. We conclude that MZBCL represent a distinct entity of B- NHL with characteristic morphologic and immunophenotypic features and particular chromosomal abnormalities, and that a close histogenetic relationship between extranodal, nodal, and splenic MZBCL is likely, although the clinical presentation may vary.

scholarly journals Distal Partial Trisomy 15q26 and Partial Monosomy 16p13.3 in a 36-Year-Old Male with Clinical Features of Both Chromosomal Abnormalities

2015 ◽  
Vol 145 (1) ◽  
pp. 29-34 ◽  
Author(s):  
Devin M. Cox ◽  
Merlin G. Butler
Keyword(s):  
Intellectual Disability ◽  
Chromosomal Abnormalities ◽  
Receptor Gene ◽  
Partial Trisomy ◽  
Chromosome Translocation ◽  
Fish Analysis ◽  
Partial Monosomy ◽  
Chronic Anemia ◽  
Dysmorphic Features ◽  
History Of

We report a 36-year-old Caucasian male identified with distal partial trisomy 15q and partial monosomy 16p from an unbalanced chromosome translocation detected by microarray and FISH analysis. He had a history of developmental delay and intellectual disability, chronic anemia, tall and slender stature, thoracic scoliosis and lumbar lordosis, and dysmorphic features. The distal partial trisomy 15q included the insulin-like growth factor 1 receptor gene involved with growth, while genes in the distal partial monosomy 16p region are involved with alpha hemoglobin production, intellectual disability, dysmorphic features, and acromegaly. The chromosome derivative found in our patient contains genes known to play a role in his phenotype.

Infants with Cleft Lip/Cleft Palate

1988 ◽  
Vol 9 (10) ◽  
pp. 331-334
Author(s):  
Lorraine Suslak ◽  
Franklin Desposito
Keyword(s):  
New York ◽  
Cleft Palate ◽  
Cleft Lip ◽  
Cleft Lip And Palate ◽  
Chromosomal Abnormalities ◽  
Single Gene ◽  
Autosomal Recessive Inheritance ◽  
Racial Groups ◽  
Genetic Syndromes ◽  
Equal Distribution

A cleft of the lip and/or palate occurs approximately once in 750 live births with some variability among various racial groups. As an isolated defect, cleft lip with or without cleft palate is etiologically distinct from cleft palate alone. More than 250 clefting syndromes, most of them relatively uncommon, have been described. In 1970, less than 3% of all cases of cleft lip and/or palate were thought to be associated with identifiable syndromes. A recent survey from a major cleft palate center in New York showed that 30% of patients had recognizable conditions. Some of these included genetic syndromes and others like the charge association or those related to environmental agents were sporadic. Another 30% of cases had one or more associated anomalies, although a specific syndromic diagnosis or etiologic basis could not be identified. The remaining 40% had isolated clefts. A summary of syndromes with cleft lip and palate by etiology is given in Table 1. Approximately, half of the recognized syndromes are due to single-gene disorders with an equal distribution among autosomal dominant and autosomal recessive inheritance. Chromosomal abnormalities account for 18% of the clefting syndromes and would invariably be associated with other malformations, delayed development, and poor prognosis.

scholarly journals Detection by enzymatic amplification of bcr-abl mRNA in peripheral blood and bone marrow cells of patients with chronic myelogenous leukemia

Blood ◽  
1989 ◽  
Vol 73 (6) ◽  
pp. 1735-1741 ◽  
Author(s):  
W Lange ◽  
DS Snyder ◽  
R Castro ◽  
JJ Rossi ◽  
KG Blume
Keyword(s):  
Bone Marrow ◽  
Chronic Myelogenous Leukemia ◽  
Peripheral Blood ◽  
Bone Marrow Cells ◽  
Philadelphia Chromosome ◽  
Chromosome 9 ◽  
Myelogenous Leukemia ◽  
Enzymatic Amplification ◽  
Polymerase Chain ◽  
Marrow Cells

Abstract The Philadelphia chromosome of chronic myelogenous leukemia (CML) patients is caused by a translocation of the c-abl gene from chromosome 9 to the breakpoint cluster region (bcr) on chromosome 22. A new bcr- abl mRNA is expressed in these cases. We have developed a modified polymerase chain reaction (PCR) for the detection of this mRNA. The method is extremely sensitive, reliable, and relatively fast. The analysis of peripheral blood or bone marrow cells from CML patients treated with chemotherapy shows that the two possible mRNAs are expressed in various combinations. Our results show that even after myeloablative therapy for bone marrow transplantation bcr-abl mRNAs are still expressed. Further studies, however, are necessary to determine the clinical relevance of a small number of persisting cells expressing the bcr-abl mRNA.

Relative increase in leukemia-specific DNA in peripheral blood plasma from patients with acute myeloid leukemia and myelodysplasia

Blood ◽  
2004 ◽  
Vol 103 (7) ◽  
pp. 2799-2801 ◽  
Author(s):  
Anna Rogers ◽  
Youngson Joe ◽  
Taghi Manshouri ◽  
Amanda Dey ◽  
Iman Jilani ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
X Chromosome ◽  
Peripheral Blood ◽  
Myeloid Leukemia ◽  
Chromosomal Abnormalities ◽  
Residual Disease ◽  
X Chromosome Inactivation ◽  
Relative Increase ◽  
Chromosome Inactivation ◽  
Acute Myeloid

Abstract Using loss of heterozygosity (LOH) and X-chromosome inactivation, we compared peripheral blood (PB) plasma with bone marrow (BM) cells in detecting genomic abnormalities in patients with acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS). We detected LOH in the PB plasma of all 45 patients who had cytogenetically documented chromosomal abnormalities (5q-, 7-, +8, 17-, or 20-). BM cells from the same patients showed LOH in 89% of patients with MDS and 70% of patients with AML. Posttherapy samples from 16 of these patients demonstrated complete concordance between LOH and cytogenetics in detecting residual disease in 15 samples. Of the 16 samples, 4 showed LOH in plasma with normal BM morphology. Using X-chromosome inactivation, clonality was detectable in 19 (73%) of 26 BM samples, whereas all PB plasma samples showed clonality. These data support the conclusion that PB plasma is enriched by tumor-specific DNA and can replace BM cells for studying genomic abnormalities. (Blood. 2004;103:2799-2801)

Variant Philadelphia Translocation with BCR/ABL Fusion Gene Site In 10q24 In a Case of Chronic Myeloid Leukemia

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 4839-4839
Author(s):  
Rossana Bonomi ◽  
Pablo Lopez ◽  
Daniela Infante ◽  
Isabel Moro ◽  
Victoria Elizondo ◽  
...  
Keyword(s):  
Chronic Myeloid Leukemia ◽  
Peripheral Blood ◽  
Myeloid Leukemia ◽  
Fusion Gene ◽  
Chromosome 9 ◽  
Chromosome 22 ◽  
Fish Analysis ◽  
Signal Pattern ◽  
Ph Chromosome ◽  
Fusion Signal

Abstract Abstract 4839 Introduction. Chronic myeloid leukemia (CML) is characterized by the Philadelphia chromosome (Ph) observed in more than 90% of patients with CML as a result of t(9;22)(q34;q11), leading to the formation of chimeric gene BCR/ABL encoding for proteins with abnormal tyrosine kinase activity. Cytogenetic variants of Ph chromosome can be identifed in 5 to 10% of CML patients, involving additional chromosomes other than 9 and 22. To explain the formation of variant translocations one-step, two-step and multi-step mechanisms have been proposed. Rarely, the variant Ph chromosome results from a BCR insertion on the ABL region and form a BCR/ABL fusion gene, generally mapping to 9q34, instead of the usual location at 22q11. In very few variant Ph cases, the insertion of the BCR/ABL product in a third chromosome was demonstrated. Case Report 28 year-old man, with bilateral central scotoma and gingivorragia. Physical examination: Grade 4 splenomegaly. Peripheral blood count showed hemoglobin concentration 11.5 g/dl, platelet count: 300.000/mm3, and white blood cell count 590.000/mm3. Blood smear: myelemia exhibiting 30% of myeloid blasts. Bone marrow biopsy: panmyelosis showing 20% of myeloid blasts. Cytogenetic analysis by G-banding performed in peripheral blood verified the following karyotype: 46, XY, t(9;22;10)(q34;q11;q24)[20] The analysis of the BCR-ABL fusion gene according to standard protocols detected the presence of the b3a2 isoform. Fluorescence in situ hybridization (FISH) studies using dual color dual fusion probes in metaphases showed a signal pattern 1F2G1R. The fusion signal mapped to 10q24, the red signal to 9q34, and the normal green signal to chromosome 22, while a second low intensity green signal mapped to the Ph chromosome. No signal was observed in der(9). Interphase FISH analysis in nuclei (n=200) presented the same signal pattern. Instead of using whole chromosome probes for 9 and 22, we hybridised probes used to detect DiGiorge syndrome. These probes detect gene control ARSA (spectrum green) localized at 22q13 and Tuple1 at 22q11 (spectrum orange). Two signals, green and orange were identified in normal chromosome 22. Ph chromosome showed the orange signal, whereas the green signal mapped to der(10). Discussion. The localization of the hybrid BCR/ABL gene on chromosomes other than 22q is a rare event wich can only be detected by FISH techniques. When these unusual translocation occurs, the hypothesis most often put forward is that several consecutive chromosome rearrangements have taken place. In the present case the interpretation of karyotypes, FISH data and molecular evidence lead to the following hypothesis: Insertion of the BCR sequence from chromosome 22 to chromosome 9 may have ocurred, producing a BCR/ABL fusion in der(9). The Ph chromosome detected by G-banding showed a different green fluorescence intensity in the metaphase FISH signal pattern with BCR/ABL dual color dual fusion probes, as a result of an insertion on chromosome 9. This first event was followed by the translocation between the derivative 9 and chromosome 10, being the final localization of the BCR/ABL gene in 10q24. FISH analysis using a DiGeorge syndrome probe, supports the hypothesis of a multistep mechanism underlying insertion and translocations events in the present case. The relocation of BCR/ABL fusion sequence on sites other than chromosme 22q11 represent a rare type of variant Ph translocation. At least 21 cases described in the literature, showed fusion gene BCR/ABL located at 9q24. Only 12 patients with variant Ph were reported bearing BCR/ABL on a third chromosome. All of them involved a masked Ph chromosome. To our best knowledge this is the first report showing a variant Ph chromosome detected by G-banding in a CML patient due to a BCR insertion on ABL sequences and exhibiting the fusion signal in a third chromosome. Disclosures: No relevant conflicts of interest to declare.

Metaherin Contributes To The Pathogenesis Of Chronic Lymohcytic Leukemia

Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 4130-4130
Author(s):  
Peipei Li ◽  
Xin Wang ◽  
Chen Na ◽  
Lili Feng ◽  
Xueling Ge ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Flow Cytometry ◽  
B Cells ◽  
Signaling Pathway ◽  
Peripheral Blood ◽  
Wnt Signaling Pathway ◽  
Beta Catenin ◽  
Proliferation And Apoptosis ◽  
Normal Controls

Abstract Introduction Dysregulation of proliferation and apoptosis is associated the pathogenesis of CLL. More recently, Metadherin (MTDH) involved in aberrant proliferation, survival, and increased migration, invasiveness, and metastasis of tumor cells, has been demonstrated as a potential crucial mediator of various types of huamn malignancies. MTDH promotes tumor progression by modulating multiple oncogenic signaling pathways (NF-kB, PI3K/Akt and Wnt/beta-catenin). However, there is no report about the role of MTDH in CLL. Since Wnt signaling pathway had been proven to be unusual activated in CLL, the objective of this study was to investigate the role of MTDH in CLL and the relationship between MTDH and Wnt/beta-catenin signaling pathway. Methods Peripheral blood mononuclear cells (PBMCs) came from samples of 31 CLL patients. The characteristics of CLL patients were shown in Table 1. CD19+B cells were selected from peripheral blood of age-matched heathy donor, cord blood, bone marrow and tonsil of normal controls using CD19+ magnetic selection kits and detected the purity with anti-CD19-PE antibody by flow cytometry. Qantitative PCR and Western blot were used to detect the expression of mRNA and protein for MTDH, and the key functional components of Wnt/beta-catenin signaling pathway (beta-catenin and LEF-1). We also measured MTDH level in B cells by flow cytometry after intracellular staining. CLL cell line(MEC-1) were infected by lentivirus to interfer MTDH and the infection efficiencies were determined by fluorescence microscope and flow cytometry. Both primary CLL cells and MEC-1 were exposed to 10ug/ml goat F(ab`)2 anti-human IgM for 48hours to mimic activation of BCR. The proliferation and apoptosis of these cells were evaluated by CCK-8 method and Annexin V kits. Results mRNA of MTDH in PBMCs of 31 CLL patients were overexpression compared with CD19+ B cells coming from 15 age-matched healthy donors (Figure 1A). 27 out of 31 CLL samples were detected MTDH expression in protein level but none in normal controls (Figure 1B). The expression of MTDH was associated with Rai staging of CLL. There were no MTDH detection in CD19+ B cells collected from bone marrow, peripheral blood, tonsil and cord blood, which stand for precursor, mature, germinal center, and lineage B cells, respectively. The transfection efficiency of MEC-1 cells by interfering MTDH expression with Lentivirus was shown in Figure 1C. The level of MTDH knockdown was accompanied with LEF-1 downregulation (Figure 1D, 1E), as well as the downregulation of c-myc and cyclinD1 expression (Figure 1F). siRNA targeting MTDH treatment in MEC-1 decreased the proliferation and increased the apoptosis(Figure 2A, 2B). We further observed that the proliferation and MTDH expression both in CLL cells and MEC-1 were upregulation after stimulation of anti-human IgM (Figure 2C, 2D, 2E). This effect in the proliferation was blocked by MTDH inteference (Figure 2F). Conclusions Our results demonstrated that MTDH is aberrant expression in B cells of CLL patients and correlated with clinical staging of CLL. MTDH was not expression in any subsets of normal B cells. MTDH may exert a preservative role through activation of Wnt signaling pathway. The CLL cell proliferation activation by BCR signaling pathway may be inhibited by MTDH interference. Our findings indicated that MTDH may be a potential therapeutic target of CLL. Disclosures: No relevant conflicts of interest to declare.

5-Aza-2-Deoxycytidine Regulates Wnt Beta-Catenin Pathway in B Cell Lymphoma

Blood ◽  
2015 ◽  
Vol 126 (23) ◽  
pp. 4810-4810
Author(s):  
Xinyu Li ◽  
Lingyu Geng ◽  
Xiangxiang Zhou ◽  
Kang Lu ◽  
Peipei Li ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
B Cell ◽  
Cell Lines ◽  
Mononuclear Cells ◽  
Conflicts Of Interest ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
Beta Catenin ◽  
Cell Functions ◽  
Protein Expressions

Abstract Introduction: The Wnt/beta-catenin pathway is aberrantly activated in B cell lymphomas, unphosphorylated beta-catenin accumulates and translocates into the nucleus, regulates the expression of c-myc, cyclinD1 and many other target genes which govern fundamental cell functions, such as proliferation, cell cycle regulation and apoptosis. Methylation is a highlight of epigenetic regulation research which also occurred in lymphoma, but the concrete mechanism of how the demethylation drug 5-aza-2-deoxycytidine affect Wnt/beta-catenin pathway is still unknown. This study was designed to illuminate the implications on Wnt/beta-catenin pathway via demethylation 5-aza in B cell lymphoma. Methods: Peripheral blood mononuclear cells (PBMCs) were obtained from samples of 30 primary CLL patients. The PBMCs contained more than 90% of CD19+ B lymphocytes, which were detected by flow cytometry and were referred to as primary CLL cells. The activation of Wnt/beta-catenin pathway and DNMT-1 of B cell lymphoma cells lines (MEC-1, LY8, Jeko-1, Grant519, mino and sp53) and the 30 patients were detected by qPCR and western blot. The expressions of beta-catenin in 20 cases of B cell lymphoma tissues were measured by IHC. The B cell lines and PBMCs from 10 primary CLL patients were given 5-aza-2-deoxycytidine in different concentrations, the effects in the pathway and apoptosis were observed by WB and flow cytometry. Results: The expressions of beta-catenin, c-myc, cyclinD1 and DNMT-1 were aberrantly higher in all cell lines we used ( MEC-1,LY8, Jeko-1, Grant519, mino and sp53 Fig.1-A,B), most primary CLL patients (Fig.1-C), and B cell lymphoma tissues (Fig.1-D). The protein expressions of beta-catenin in MEC-1 were higer than primary CLL patients. 0, 0.5, 1.0, 2.0¦ÌM 5-aza-2-deoxycytidine were given to the B cells lines and PBMCs from primary CLL patients for 48h, beta-catenin were found accumulated, but c-myc and cyclinD1 in the downstream were reduced (Fig.2-A,B,C,D). For further understanding of aberrant accumulation ofbeta-catenin, we extracted the nuclear protein of MEC-1, nuclear beta-catenin protein expressions were found decreased and cytoplasmic were increased (Fig.2-E). After 5-aza treatment, the apoptosis rate increased and caspase pathway were activated (Fig.2-A,F). Conclusions: The enhanced expressions of beta-catenin, c-myc, cyclinD1 in the B cell lines and the B cell lymphoma samples indicated the Wnt/beta-catenin was aberrantly activated. After 5-aza treatment with the cell lines (MEC-1, Jeko-1, LY8) and primary CLL cells, the abnormal accumulation of beta-catenin protein was observed which was discrepancy with previous reports, but the decrease of c-myc and cyclinD1 suggested the pathway was inhibited, apoptosis also occurred. The increase of totalbeta-catenin protein was supposed to be an stress reaction of the 5-aza treatment, however, the redundant beta-catenin protein in B cell lymphoma was speculated to be combined with demethylated genes and resulted in dormancy of this pathway. Our results indicated that 5-aza played a demethylation role through Wnt/beta-catenin pathway in B cell lymphoma. The data are of interest in the context of epigenetic-based therapy in B cell lymphoma. Figure 1. Figure 1. Figure 2. Figure 2. Disclosures No relevant conflicts of interest to declare.

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