Cytogenetic Study of Human Lymphoid T -Cell Lines Derived From Lymphocytic Leukemia
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Huang, C. C.; Hou, Yanfei; Woods, L. K.; Moore, George E.; Minowada, Jun

doi:10.1093/jnci/53.3.655

Cited by 107 publications

(27 citation statements)

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“…An extra band on 14q was described also in one patient with Hodgkin's disease and one with lymphocytic lymphoma (42). Chromosome 14 was involved in a translocation with chromosome 11 in a primary culture from a patient with acute lymphoblastic leukemia (43) and a familial translocation of chromosome 14 was reported in another patient with acute lymphoblastic leukemia (44). The frequent rearrangement of chromosome 14 in human lymphoproliferative disorders suggests that the specificity of the initial chromosome aberration is related to the type of cell characteristic of these human neoplasms.…”

Section: Resultsmentioning

confidence: 86%

Somatic rearrangement of chromosome 14 in human lymphocytes.

McCaw¹,

Hecht²,

Harnden³

et al. 1975

Proc. Natl. Acad. Sci. U.S.A.

229

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Section: Resultsmentioning

confidence: 86%

Somatic rearrangement of chromosome 14 in human lymphocytes.

McCaw¹,

Hecht²,

Harnden³

et al. 1975

Proc. Natl. Acad. Sci. U.S.A.

229

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“…The human TdT positive pre-T (RPMI-8402) cell line (17) was maintained in continuous suspension culture in RPMI-1640 medium supplemented with 10% FBS, 4 mM L-Glutamine, 100 mM Na-Pyruvate, and 25 mM Hepes. Cells were grown at 2.5 x 10s/ml, with more than 98% viability as determined by trypan blue dye exclusion test.…”

Section: Cell Culturesmentioning

confidence: 99%

Involvement of Caspase-3 in the Cleavage of Terminal Transferase

Trubiani

Guarnieri

Paganelli

et al. 2002

Int J Immunopathol Pharmacol

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To investigate the ill vivo role of caspase-3 in Terminal Transferase metabolism DMSO-treated RPMI-8402, a human pre-T cell line was used. In DMSO treated samples 3H·dGTP incorporation and TdT phosphorylation occurs after 4 hours of treatment. After 8 hours cells undergo TdT proteolysis in addition to its inactivation. The cleavage ofTdT into 32· and 58-KDa proteolytic fragments occurred simultaneously with the activation of Caspase-3, but preceded changes associated with the apoptotic process described after 48 hours of treatment. The Caspase-3 peptide inhibitor V, used as a specific inhibitor, prevented TdT proteolysis prolonging its activity and rescued cells from apoptosis. Our experiments suggest that TdT is a nuclear substrate for Caspase-3, the main apoptotic effector protease in many cell types, and that the cleavage of TdT represents a primary step in a signal cascade leading to pre-T cell apoptosis.

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“…In order to identify new genes that might participate in T-cell growth and neoplasia, we cloned the breakpoints of both derivative chromosomes of the t(11;14)(p15;qll) found in the well-characterized T-ALL cell line, RPMI 8402 (26). This translocation involves the BTCR locus at 14qll.…”

Section: D81d82j81 Intermediate Rearrangementmentioning

confidence: 99%

“…We postulate that the protein encoded by this cDNA (termed Ttg-l for T-cell translocation gene 1) may form two zinc fingers similar in structure to those described for several families of DNA-binding proteins (for reviews, see references 5 and 30). qll) (26) was used in this study. This phenotypically immature cell lacks CD3, CD1, CD4, and CD8 but displays CD7 and CD2 (21 (17) and Jurkat (JM) (38), TCR-expressing T-cell lines; Peer (17), a -yb-expressing T-ALL line; -yS CBL and -yb PBL, human T-cell lymphotropic virus type 1-transformed cord blood and peripheral blood lymphocytes, respectively (kindly provided by D. Cohen, National Institutes of Health); HSB-2 (21), CD3-T-ALL; SUDHL-6 and SUDHL-4 (46), mature B-cell lines which bear a t(14;18)(q32;q21); and U937 (51), a monoblastic leukemia cell line.…”

Section: D81d82j81 Intermediate Rearrangementmentioning

confidence: 99%

The t(11;14)(p15;q11) in a T-cell acute lymphoblastic leukemia cell line activates multiple transcripts, including Ttg-1, a gene encoding a potential zinc finger protein.

McGuire¹,

Hockett²,

Pollock³

et al. 1989

Mol. Cell. Biol.

205

109

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Interchromosomal translocations within lymphoid neoplasms frequently involve the antigen receptor genes. We cloned the breakpoints of the t(l1;14)(p15;q11) in a CD3-negative T-cell acute lymphoblastic leukemia cell line (RPMI 8402) in order to identify new genes potentially involved in T-cell neoplasia. An extensive comparison of both breakpoints and their germ line counterparts indicated that an inadvertant recombinasemediated break at chromosome segment llplS recombined with the 6 T-cell receptor at 14qll. The derivative 11 breakpoint resembles a coding joint in which llplS rather than a variable region was introduced 5' to a D81D82J81 intermediate rearrangement. Conversely, the derivative 14 breakpoint corresponds to a signal joint between the 5' heptamer-spacer-nonamer recombinational signal of Dr, and an isolated heptamer at llplS.Multiple, apparently distinct transcripts were found flanking both breakpoints of 8402. RNAs of 3.5, 4.4, 1.4, and 8.0 kilobases originating from either side of the derivative 14 breakpoint were highly expressed in 8402 compared with other cells. This suggests that this translocation deregulated multiple genes and provides the opportunity to assess any multifactorial contribution they may have to malignancy. We cloned and sequenced several cDNAs representing the 1.4-kilobase transcript (termed Ttg-1 [T-cell translocation gene 1]) from an 8402 library. The predicted protein of 156 amino acids contained two internal repeats which could potentially form zinc fingers.Chromosomal translocations are frequently found in malignant cells but not in their normal cellular counterparts. Moreover, unique translocations are associated with histologically and phenotypically distinct neoplasms (43,56, 57). Lymphoid malignancies often possess translocations at the chromosomal sites of the antigen receptor genes, immunoglobulin genes in B-cell neoplasms, or T-cell receptor (TCR) genes in T-cell neoplasms (for a review, see reference 31). These genes normally rearrange during development to assemble separate variable (V), joining (J), and, at times, diversity (D) segments into a contiguous V(D)J coding joint. A site-specific recombinase cleaves at conserved heptamerspacer-nonamer signal sequences, which flank the coding regions of these gene segments (33,53), removing the intervening DNA segments and ligating the signal sequences to each other to generate extrachromosomal circles (22,41). These genes prove to be the most frequent sites for illegitimate recombinations with nonhomologous chromosomes in lymphoid neoplasms (31).Genes located at the sites of such translocations appear to directly participate in the development or maintenance of the malignant phenotype (29). Interchromosomal translocations can deregulate these candidate oncogenes by a variety of mechanisms. Transcriptional activation due to the introduction of enhancer elements has been shown for c-myc in a transgenic mouse model (1). Disruption of normal transcription by acquired somatic mutation has been noted for c-myc in the t(8;14)(q...

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Cytogenetic Study of Human Lymphoid T -Cell Lines Derived From Lymphocytic Leukemia 2

Cited by 107 publications

References 0 publications

Somatic rearrangement of chromosome 14 in human lymphocytes.

Somatic rearrangement of chromosome 14 in human lymphocytes.

Involvement of Caspase-3 in the Cleavage of Terminal Transferase

The t(11;14)(p15;q11) in a T-cell acute lymphoblastic leukemia cell line activates multiple transcripts, including Ttg-1, a gene encoding a potential zinc finger protein.

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