Thymic overexpression of Ttg-1 in transgenic mice results in T-cell acute lymphoblastic leukemia/lymphoma

1992 ◽  
Vol 12 (9) ◽  
pp. 4186-4196
Author(s):  
E A McGuire ◽  
C E Rintoul ◽  
G M Sclar ◽  
S J Korsmeyer
Keyword(s):  
Transcription Factors ◽  
T Cell ◽  
Transgenic Mice ◽  
Lymphoblastic Leukemia ◽  
Intermediate Stage ◽  
Proximal Promoter ◽  
Minority Population ◽  
Primary Role ◽  
Double Positive ◽  
Aberrant Expression

T-cell translocation gene 1 (Ttg-1), also called rhombotin, is deregulated upon translocation into the alpha/delta T-cell receptor loci in acute lymphoblastic leukemias bearing the t(11;14)(p15;q11). Ttg-1 encodes a nuclear protein, expressed predominantly in neuronal cells, which belongs to a novel family of transcription factors possessing LIM domains. We utilized the lck proximal promoter to overexpress this candidate oncogene in immature thymocytes of transgenic mice. lckPr Ttg-1 mice develop immature, aggressive T-cell leukemia/lymphomas. Tumor incidence is proportional to the level of Ttg-1 expression. Most tumors contain CD4+8+ cells as well as CD4-8+ cells, which have an immature rather than a mature peripheral phenotype. Ttg-1-induced tumorigenesis preferentially affects a minority population of thymocytes representing an immature CD4-8+ intermediate stage between double-negative CD4-8- cells and double-positive CD4+8+ cells. This model indicates that the aberrant expression of putative transcription factors plays a primary role in the genesis of T-cell acute lymphoblastic leukemias.

scholarly journals Thymic overexpression of Ttg-1 in transgenic mice results in T-cell acute lymphoblastic leukemia/lymphoma.

1992 ◽  
Vol 12 (9) ◽  
pp. 4186-4196 ◽  
Author(s):  
E A McGuire ◽  
C E Rintoul ◽  
G M Sclar ◽  
S J Korsmeyer
Keyword(s):  
Transcription Factors ◽  
T Cell ◽  
Transgenic Mice ◽  
Lymphoblastic Leukemia ◽  
Intermediate Stage ◽  
Proximal Promoter ◽  
Minority Population ◽  
Primary Role ◽  
Double Positive ◽  
Aberrant Expression

T-cell translocation gene 1 (Ttg-1), also called rhombotin, is deregulated upon translocation into the alpha/delta T-cell receptor loci in acute lymphoblastic leukemias bearing the t(11;14)(p15;q11). Ttg-1 encodes a nuclear protein, expressed predominantly in neuronal cells, which belongs to a novel family of transcription factors possessing LIM domains. We utilized the lck proximal promoter to overexpress this candidate oncogene in immature thymocytes of transgenic mice. lckPr Ttg-1 mice develop immature, aggressive T-cell leukemia/lymphomas. Tumor incidence is proportional to the level of Ttg-1 expression. Most tumors contain CD4+8+ cells as well as CD4-8+ cells, which have an immature rather than a mature peripheral phenotype. Ttg-1-induced tumorigenesis preferentially affects a minority population of thymocytes representing an immature CD4-8+ intermediate stage between double-negative CD4-8- cells and double-positive CD4+8+ cells. This model indicates that the aberrant expression of putative transcription factors plays a primary role in the genesis of T-cell acute lymphoblastic leukemias.

scholarly journals EZH2 knockdown upregulates expression of the genes involved in T-ALL cell differentiation

2021 ◽  
Author(s):  
Sahar Safaei ◽  
Behzad Baradaran ◽  
Behzad Mansoori ◽  
Masoumeh Fardi ◽  
Elham Baghbani ◽  
...  
Keyword(s):  
T Cells ◽  
Transcription Factors ◽  
Cell Differentiation ◽  
T Cell ◽  
Lymphoblastic Leukemia ◽  
Leukemia Cell ◽  
Leukemia Cell Line ◽  
Aberrant Expression ◽  
Expression Levels ◽  
Ezh2 Expression

Background: EZH2 (enhancer of zeste 2 polycomb repressive complex 2 subunit), as one of the polycyclic group proteins (PcGs), is an epigenetic regulator that plays a crucial role in the pathophysiology of hematologic malignancies through regulating cell differentiation. Also, it is well known that aberrant expression of specific transcription factors can be involved in the pathogenesis of various cancers. Objective: Herein, we aimed to suppress EZH2 expression in MOLT-4 cells, T-ALL (T cell acute lymphoblastic leukemia) cell line, and evaluate the role of EZH2 on the expression of transcription factors that regulate T cell maturation, differentiation, and apoptosis. Methods: EZH2-siRNA was transfected into MOLT-4 cells, and the expression levels of EZH2, NOTCH1, TCF1, IKZF1, and NFATC1 were measured using real-time PCR. The MTT (3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide) assay was performed to study the effect of EZH2 knockdown on MOLT-4 cell viability. The apoptosis rate of EZH2-siRNA transfected cells was assessed by flow cytometry. The interaction of mentioned genes was investigated using STRING and GO (gene ontology). Results: Our results have shown that EZH2-siRNA transfection can substantially decrease EZH2 expression in MOLT-4 cells. Besides, EZH2 suppression can upregulate NOTCH1, TCF1, IKZF1, and NFATC1 expression levels. EZH2 knockdown does not affect the viability and apoptosis of MOLT-4 cells. The most remarkable protein-protein interaction of EZH2 has been with NOTCH1. Besides, GO analysis has demonstrated that EZH2, NOTCH1, TCF1, IKZF1, and NFATC1 were located within nucleoplasm and can regulate RNA polymerase II-mediated transcription. Conclusion: Our results have shown that MOLT-4 cells harbor increased expression of EZH2 in comparison with normal human T cells. EZH2 knockdown can upregulate the expression of the transcription factors involved in T cell differentiation. Thus, EZH2 can halt the differentiation of immature lymphoblastic T cells.

scholarly journals Lmo2's Oncogenic Function in T-Cell Leukemia Requires Ldb1

Blood ◽  
2015 ◽  
Vol 126 (23) ◽  
pp. 3663-3663
Author(s):  
Liqi Li ◽  
Justin H. Layer ◽  
Claude Warzecha ◽  
Rati Tripathi ◽  
Paul Love ◽  
...  
Keyword(s):  
T Cell ◽  
Transgenic Mice ◽  
Conflicts Of Interest ◽  
Protein Complexes ◽  
Lymphoblastic Leukemia ◽  
Conditional Knockout ◽  
Lim Domain ◽  
Double Positive ◽  
Hematopoietic Stem ◽  
T Cell Progenitors

Abstract LIM domain Only-2 (LMO2) is one of the most frequently deregulated oncogenes in T-cell acute lymphoblastic leukemia (T-ALL). LMO2 encodes a small protein with 2 LIM domains that is part of a large multiprotein complex in hematopoietic stem and progenitor cells, where it is required for HSC specification and maintenance. Many of LMO2's protein partners in HSPCs are expressed in T-ALL implying that protein complexes similar to those nucleated by LMO2 in HSPCs also play a role in leukemia. In this study, we analyzed a critical component of the LMO2 associated complex, LIM domain binding1 (LDB1). LDB1 appears to be an obligate partner of LMO2 in HSPCs but it is not required for T-cell development from committed progenitors. LDB1 is concordantly expressed with LMO2 in human T-ALL although its expression is more widespread than LMO2. To further define Ldb1's role in leukemia, we induced its conditional knockout in CD2-Lmo2 transgenic mice. CD2-Lmo2 transgenic mice develop T-ALL with high penetrance and closely model the human disease. We discovered that Lmo2-induced T-ALL was markedly attenuated in penetrance and latency by Ldb1 deletion. Since Lmo2 induces a distinct differentiation arrest in T-cell progenitors prior to leukemic transformation, we analyzed the differentiation of T-cell progenitors in CD2-Lmo2 transgenic/floxed-Ldb1/Lck-Cre mice and in non-Lmo2 transgenics: floxed-Ldb1/Lck-Cre mice. Ldb1 deletion by Lck-Cre was efficient in double negative and double positive T-cell progenitors. In striking contrast, Ldb1 deletion could not be induced in CD2-Lmo2 transgenic T-cell progenitors. Consistent with this finding, T-ALLs that developed in CD2-Lmo2/floxed-Ldb1/Lck-Cre mice had incomplete deletion of Ldb1. These results imply that Ldb1 is a required factor for Lmo2 to induce T-ALL. Lastly, gene expression analysis of Lmo2-induced T-ALLs and ChIP-exonuclease analysis of Ldb1 occupancy in T-ALL suggested that the Lmo2/Ldb1 complex enforced a gene signature similar to that seen in HSPCs and in Early T-cell Precursor ALL. In conclusion, Ldb1 is a required partner for Lmo2 to induce T-ALL. Additionally, the HSPC function of Lmo2/Ldb1 complexes may be recapitulated in T-cell progenitors prior to T-ALL. Disclosures No relevant conflicts of interest to declare.

The HOX11/TLX1 Transcription Factor Oncogene Induces Chromosomal Aneuploidy in T-ALL.

Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 142-142 ◽  
Author(s):  
Kim De Keersmaecker ◽  
Pedro Jose Real Luna ◽  
Giusy Della Gatta ◽  
Teresa Palomero ◽  
Mireia Castillo ◽  
...  
Keyword(s):  
Gene Expression ◽  
Transcription Factor ◽  
T Cell ◽  
Transgenic Mice ◽  
Target Genes ◽  
Cell Transformation ◽  
Double Positive ◽  
Aberrant Expression ◽  
On Chip ◽  
Gains And Losses

Abstract Abstract 142 T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive malignancy associated with the activation of transcription factor oncogenes. TLX1/HOX11 was originally isolated from the recurrent t(10;14)(q24;q11) in T-ALL and is aberrantly expressed in 5% to 10% of pediatric and up to 30% of adult T-ALL cases. Tlx1 plays an important role during embryonic development and acts as a master transcriptional regulator necessary for the genesis of the spleen. TLX1 positive T-ALLs have a distinct gene expression profile resembling that of thymocytes blocked at the early double positive stage of development. This observation supports the hypothesis that aberrant expression of TLX1 contributes to the pathogenesis of T-ALL by interfering with critical transcriptional regulatory networks involved in cell proliferation, differentiation and survival during T-cell development. However, the identity of such oncogenic pathways and the mechanisms though which they operate are still largely unknown. In order to gain further insight into the mechanisms of transformation induced by TLX1, we generated a transgenic model of TLX1 induced T-ALL. In this model, a human TLX1 cDNA was expressed in developing thymocytes under the control of the proximal LCK promoter. TLX1 transgenic mice displayed a specific defect in T-cell development characterized by reduced thymic size and cellularity with increased apoptosis and a differentiation arrest at the CD4/CD8 double negative, CD25/CD44 double positive stage of differentiation (DN2 thymocytes). Long term follow up revealed that TLX1 transgenic mice develop tumors with a median latency of 29 weeks. TLX1 induced leukemias are characterized by increased thymic size and diffuse infiltration of bone marrow, spleen and peripheral organs by lymphoblasts expressing T-cell markers. Analysis of TCRβ expression and transplantation into isogenic recipients demonstrated that TLX1 tumors are clonal and transplantable. Microarray gene expression profiling of mouse and human T-ALLs showed that tumors from TLX1 transgenic mice have a gene expression signature that is highly related to that of human T-ALLs with aberrant expression of TLX1. Moreover, ChIP-on-chip analysis of promoters bound by TLX1 showed this genetic program is dominated by the downregulation of TLX1 direct target genes. Mutation profiling of T-cell oncogenes and array CGH analysis in mouse TLX1 tumors demonstrated the presence of cooperative mutations including Pten deletions, activating mutations in Notch1 and loss of Bcl11b. Strikingly, SKY analysis and array CGH revealed that 80% of TLX1 induced tumors had numerical chromosomal abnormalities including a high frequency of trisomy 15. Analysis of gene expression of ChIP-on-chip TLX1 direct target genes in double negative thymocytes from preleukemic mice showed downregulation of genes primarily involved in the control of chromosomal segregation during mitosis such as Bub1, Brca2, Chek1, Kntc1, Kif23, CenpE and Plk1. These data suggest that aberrant TLX1 expression directly promotes aneuploidy and contributes to T-cell transformation by interfering with the expression of genes responsible for chromosomal segregation during mitosis. Importantly, T-cell lymphoblasts from TLX1 transgenic mice failed to undergo a mitotic cell cycle arrest after treatment with taxol, a cell cycle inhibitor that interferes with microtubule remodeling during mitosis. Strikingly, karyotype analysis of a series of 59 pediatric T-ALLs demonstrated a high frequency of chromosomal gains and losses in TLX1 and TLX3 positive human T-cell tumors compared with other genetic subgroups of T-ALL (P <0.001). Thus, aberrant expression of TLX1 in T-cell precursors seems to impair the function of the mitotic checkpoint and facilitate the acquisition of chromosomal gains and losses during T-cell transformation. These results establish for the first time a mechanistic link between the activity of a leukemogenic transcription factor oncogene and the development of chromosomal aneuploidy in the pathogenesis of human leukemia. Disclosures: Ferrando: Merck, Pfizer: Research Funding.

Biallelic transcriptional activation of oncogenic transcription factors in T-cell acute lymphoblastic leukemia

Blood ◽  
2004 ◽  
Vol 103 (5) ◽  
pp. 1909-1911 ◽  
Author(s):  
Adolfo A. Ferrando ◽  
Sabine Herblot ◽  
Teresa Palomero ◽  
Mark Hansen ◽  
Trang Hoang ◽  
...  
Keyword(s):  
Transcription Factors ◽  
T Cell ◽  
Transcriptional Activation ◽  
Lymphoblastic Leukemia ◽  
Chromosomal Rearrangements ◽  
Regulatory Elements ◽  
Leukemic Cells ◽  
Aberrant Expression ◽  
Transcriptional Regulatory Elements ◽  
Highly Active

Abstract Aberrant expression of transcription factor oncogenes such as HOX11, HOX11L2, TAL1/SCL, LYL1, LMO1, and LMO2 can be detected in lymphoblasts from up to 80% of patients with acute T-cell lymphoblastic leukemia (T-ALL). Transcriptional activation of these oncogenes in leukemic cells typically results from chromosomal rearrangements that place them next to highly active cis-acting transcriptional regulatory elements. However, biallelic activation of TAL1 in some T-ALL cases has been previously proposed. We have used allele-specific mRNA analysis to show that trans-acting mechanisms leading to biallelic overexpression of TAL1 are involved in 10 (42%) of 24 TAL1+ informative T-ALL cases, 2 (17%) of 12 HOX11+ informative cases, and 7 (64%) of 11 LMO2+ informative cases. We propose that aberrant expression of oncogenic transcription factors in a significant fraction of T-ALLs may result from loss of the upstream transcriptional mechanisms that normally down-regulate the expression of these oncogenes during T-cell development.

scholarly journals CD45-null transgenic mice reveal a positive regulatory role for CD45 in early thymocyte development, in the selection of CD4+CD8+ thymocytes, and B cell maturation.

1996 ◽  
Vol 183 (4) ◽  
pp. 1707-1718 ◽  
Author(s):  
K F Byth ◽  
L A Conroy ◽  
S Howlett ◽  
A J Smith ◽  
J May ◽  
...  
Keyword(s):  
Signal Transduction ◽  
T Cell ◽  
B Cells ◽  
Transgenic Mice ◽  
B Cell ◽  
T Cell Development ◽  
Cell Development ◽  
Cross Linking ◽  
Thymocyte Development ◽  
Double Positive

The CD45 transmembrane glycoprotein has been shown to be a protein phosphotyrosine phosphatase and to be important in signal transduction in T and B lymphocytes. We have employed gene targeting to create a strain of transgenic mice that completely lacks expression of all isoforms of CD45. The spleens from CD45-null mice contain approximately twice the number of B cells and one fifth the number of T cells found in normal controls. The increase in B cell numbers is due to the specific expansion of two B cell subpopulations that express high levels of immunoglobulin (IgM) staining. T cell development is significantly inhibited in CD45-null animals at two distinct stages. The efficiency of the development of CD4-CD8- thymocytes into CD4+ CD8+ thymocytes is reduced by twofold, subsequently the frequency of successful maturation of the double positive population into mature, single positive thymocytes is reduced by a further four- to fivefold. In addition, we demonstrate that CD45-null thymocytes are severely impaired in their apoptotic response to cross-linking signals via T cell receptor (TCR) in fetal thymic organ culture. In contrast, apoptosis can be induced normally in CD45-null thymocytes by non-TCR-mediated signals. Since both positive and negative selection require signals through the TCR complex, these findings suggest that CD45 is an important regulator of signal transduction via the TCR complex at multiple stages of T cell development. CD45 is absolutely required for the transmission of mitogenic signals via IgM and IgD. By contrast, CD45-null B cells proliferate as well as wild-type cells to CD40-mediated signals. The proliferation of B cells in response to CD38 cross-linking is significantly reduced but not abolished by the CD45-null mutation. We conclude that CD45 is not required at any stage during the generation of mature peripheral B cells, however its loss reveals a previously unrecognized role for CD45 in the regulation of certain subpopulations of B cells.

scholarly journals Specific expression of the human CD4 gene in mature CD4+ CD8- and immature CD4+ CD8+ T cells and in macrophages of transgenic mice

1994 ◽  
Vol 14 (2) ◽  
pp. 1084-1094
Author(s):  
Z Hanna ◽  
C Simard ◽  
A Laperrière ◽  
P Jolicoeur
Keyword(s):  
T Cells ◽  
T Cell ◽  
Transgenic Mice ◽  
Cd8 T Cells ◽  
Transcription Initiation ◽  
Critical Role ◽  
Regulatory Elements ◽  
T Cell Subsets ◽  
Double Positive ◽  
Specific Expression

The CD4 protein plays a critical role in the development and function of the immune system. To gain more insight into the mechanism of expression of the human CD4 gene, we cloned 42.2 kbp of genomic sequences comprising the CD4 gene and its surrounding sequences. Studies with transgenic mice revealed that a 12.6-kbp fragment of the human CD4 gene (comprising 2.6 kbp of 5' sequences upstream of the transcription initiation site, the first two exons and introns, and part of exon 3) contains the sequences required to support the appropriate expression in murine mature CD4+ CD8- T cells and macrophages but not in immature double-positive CD4+ CD8+ T cells. Expression in CD4+ CD8+ T cells was found to require additional regulatory elements present in a T-cell enhancer fragment recently identified for the murine CD4 gene (S. Sawada and D. R. Littman, Mol. Cell. Biol. 11:5506-5515, 1991). These results suggest that expression of CD4 in mature and immature T-cell subsets may be controlled by distinct and independent regulatory elements. Alternatively, specific regulatory elements may control the expression of CD4 at different levels in mature and immature T-cell subsets. Our data also indicate that mouse macrophages contain the regulatory factors necessary to transcribe the human CD4 gene.

β-Selection Is Associated With the Onset of CD8β Chain Expression on CD4+CD8+ Pre-T Cells During Human Intrathymic Development

Blood ◽  
1999 ◽  
Vol 94 (10) ◽  
pp. 3491-3498 ◽  
Author(s):  
Yolanda R. Carrasco ◽  
César Trigueros ◽  
Almudena R. Ramiro ◽  
Virginia G. de Yébenes ◽  
Marı́a L. Toribio
Keyword(s):  
T Cells ◽  
T Cell ◽  
Control Point ◽  
Intermediate Stage ◽  
Cell Receptor ◽  
Resting Cells ◽  
Double Positive ◽  
Human T Cell ◽  
A Minor

T-cell precursors that undergo productive rearrangements at the T-cell receptor (TCR) β locus are selected for proliferation and further maturation, before TCR expression, by signaling through a pre–TCR composed of the TCRβ chain paired with a pre–TCR (pT) chain. Such a critical developmental checkpoint, known as β-selection, results in progression from CD4−CD8− double negative (DN) to CD4+CD8+ double positive (DP) TCRβ−thymocytes. In contrast to mice, progression to the DP compartment occurs in humans via a CD4+ CD8−intermediate stage. Here we show that the CD4+CD8− to CD4+ CD8+ transition involves the sequential acquisition of the  and β chains of CD8 at distinct maturation stages. Our results indicate that CD8, but not CD8β, is expressed in vivo in a minor subset of DP TCRβ− thymocytes, referred to as CD4+CD8+ pre-T cells, mostly composed of resting cells lacking cytoplasmic TCRβ chain (TCRβic). In contrast, expression of CD8β heterodimers was selectively found on DP TCRβ− thymocytes that express TCRβicand are enriched for cycling cells. Interestingly, CD4+CD8+ pre-T cells are shown to be functional intermediates between CD4+ CD8−TCRβic− and CD4+CD8β+ TCRβic+thymocytes. More importantly, evidence is provided that onset of CD8β and TCRβic expression are coincident developmental events associated with acquisition of CD3 and pT chain on the cell surface. Therefore, we propose that the CD4+CD8+ to CD4+CD8β+ transition marks the key control point of pre-TCR–mediated β-selection in human T-cell development.

CD7/CD19 Double-Positive T-Cell Acute Lymphoblastic Leukemia

2006 ◽  
Vol 83 (4) ◽  
pp. 324-327
Author(s):  
Shinya Fujisawa ◽  
Fumihiko Tanioka ◽  
Toshihiko Matsuoka ◽  
Takachika Ozawa ◽  
Kensuke Naito ◽  
...  
Keyword(s):  
Acute Lymphoblastic Leukemia ◽  
T Cell ◽  
Lymphoblastic Leukemia ◽  
Double Positive ◽  
Cell Acute Lymphoblastic Leukemia

Differential Expression of the Homeobox Gene MIXL1 in Non Hodgkin (NHL) and Hodgkin Lymphomas (HL).

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 3014-3014
Author(s):  
Elias Drakos ◽  
George Z. Rassidakis ◽  
Wei Guo ◽  
L. Jeffrey Medeiros ◽  
Lalitha Nagarajan
Keyword(s):  
T Cell ◽  
Protein Expression ◽  
B Cell ◽  
Tumor Cells ◽  
Cell Lymphoma ◽  
Lymphoblastic Leukemia ◽  
T Cell Lymphoma ◽  
High Grade ◽  
Intermediate Grade ◽  
Aberrant Expression

Abstract The gene MIXL1 (Mix1 homeobox-like) encodes a paired class homeobox transcription factor involved in early hematopoietic specification during embryogenesis. Previous studies have shown that MIXL1 gene is expressed in hematopoietic cells during adult life (Guo et al. Blood100;1;89–96, 2002). Furthermore 5′ MIXL1 sequences are a target of retroviral insertion in murine T-cell lymphoma (http:RTCGD.ncifcrf.gov), suggesting a selection advantage for aberrant expression of this gene. However, the status of MIXL1 expression in human lymphomas has not been examined. Using a highly specific antibody, we assessed for MIXL1 protein expression in 14 lymphoma cell lines (9 B-cell and 5 T-cell) by immunobloting. MIXL1 was detected predominantly in nuclear extracts of lysates of all cell lines tested, although at a variable level. We also assessed for MIXL1 protein expression in 126 B-cell and 21 T-cell NHLs of various types, as well as 14 Hodgkin lymphomas using immunohistochemical methods. The results of the immunohistochemical studies are summarized in table 1. Once again, MIXL1 immunoreactivity was primarily nuclear in the tumor cells. Based on distribution data (histogram), a 50% cutoff was selected for high versus low MIXL1 expression. Among B-cell tumors, high expression levels of MIXL1 protein were more frequently detected in high-grade NHL and HL compared with low/intermediate grade NHL (p<0.0001, chi-square test). As a continuous variable, the percentage of MIXL1-positive tumor cells was also significantly higher in high-grade B-cell NHL and HL compared with low/intermediate grade NHL (p<0.0001, Kruskal Wallis test). All Hodgkin lymphomas expressed high levels of MIXL1 with 60% to 100% of neoplastic cells being positive for MIXL1. Most T-cell NHLs also expressed high levels of MIXL1. In contrast, most low/intermediate-grade B-cell NHL and multiple myelomas expressed low levels of MIXL1. Frequent overexpression of MIXL1 gene product in most high-grade B-cell NHLs, HL and T-cell NHLs suggests that aberrant expression of MIXL1 may play a role in proliferation, block of differentiation or both. Table 1. HL (n=14) B-NHL (n =126) T-NHL (n =21) N (%) Low/intermediate grade N (%) N (%) Classical HL 12/12(100%) Chronic lymphocytic leukemia /small lymphocytic lymphoma 0/8 (0% T-precursor lymphoblastic leukemia/lymphoma 2/2 (0%) Nodular lymphocyte predominance HL 2/2 (100%) MALT-lymphoma 0/8 (0%) Mycosis fungoides/Sezary syndrome 2/2 (0%) Follicular lymphoma 9/24 (38%) Extranodal NK/T-cell lymphoma, nasal type 3/3 (100%) Mantle cell lymphoma 5/34 (15%) Peripheral T-cell lymphoma, unspecified 6/9 (66% High grade Anaplastic large cell lymphoma 5/5 (100%) B-precursor lymphoblastic leukemia/lymphoma 1/3 (33%) Burkitt lymphoma/leukemia 2/2 (100%) Diffuse large B-cell lymphoma 30/31 (97%) Plasma cell myeloma/plasmacytoma 0/16 (0%)

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