Deregulation of c-
            <i>myc</i>
            by Translocation of the α-Locus of the T-Cell Receptor in T-Cell Leukemias

Erikson, Jan; Finger, Lawrence R.; Sun, Lee K.; Ar-Rushdi, Abbas; Nishikura, Kazuko; Minowada, Jun; Emanuel, Beverly S.; Nowell̀, Peter C.; Croce, Carlo M.

doi:10.1126/science.3486470

Cited by 196 publications

(99 citation statements)

References 11 publications

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“…Experiments were conducted with the human hairy cell leukemia cell line, JOK-1, 36 the human chronic lymphocytic leukemia cell line SKW-3, 37 and two human adult T cell leukemia cell lines, ED-40810(−) 38 and SALT-3. 39 All these cell lines were kindly provided by the Fujisaki Cell Center of Hayashibara Institute of Biochemical Science.…”

Section: Cell Linesmentioning

confidence: 99%

In vitro cytotoxic effects of fludarabine (2-F-ara-A) in combination with commonly used antileukemic agents by isobologram analysis

et al. 2000

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Fludarabine phosphate (2-F-ara-AMP) is an adenine nucleoside analogue that shows significant activity against chronic lymphocytic leukemia and indolent lymphoma. We assessed the cytotoxic interaction produced by the combination of the active metabolite of fludarabine phosphate, fludarabine (9-␤-D-arabinofuranosyl-2-fluoroadenine, 2-F-ara-A), and some commonly used antileukemic agents against human hairy cell leukemia cell line JOK-1, human chronic lymphocytic leukemia cell line SKW-3, and adult T cell leukemia cell lines ED-40810 (−) and SALT-3. The leukemia cells were exposed simultaneously to 2-F-ara-A and to the other agents for 4 days. Cell growth inhibition was determined using MTT reduction assay.

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Section: Cell Linesmentioning

confidence: 99%

In vitro cytotoxic effects of fludarabine (2-F-ara-A) in combination with commonly used antileukemic agents by isobologram analysis

et al. 2000

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“…4a), we searched for translocation targets in the public domain and identified the T-cell antigen receptor (TCR)-α/δ (Tcra/Tcrd) cluster on chromosome 14qC2 and c-myc on chromosome 15qD3 as potential candidates. A similar translocation of t(8;14) is known to be associated with a subset of human T-ALL 16 . Using two-colour FISH analysis with validated bacterial artificial chromosome (BAC) clones ( Supplementary Fig.…”

mentioning

confidence: 99%

Multi-genetic events collaboratively contribute to Pten-null leukaemia stem-cell formation

Guo¹,

Lasky²,

Chang³

et al. 2008

Nature

222

261

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Cancer stem cells, which share many common properties and regulatory machineries with normal stem cells, have recently been proposed to be responsible for tumorigenesis and to contribute to cancer resistance 1 . The main challenges in cancer biology are to identify cancer stem cells and to define the molecular events required for transforming normal cells to cancer stem cells. Here we show that Pten deletion in mouse haematopoietic stem cells leads to a myeloproliferative disorder, followed by acute T-lymphoblastic leukaemia (T-ALL). Self-renewable leukaemia stem cells (LSCs) are enriched in the c-Kit mid CD3 + Lin − compartment, where unphosphorylated β-catenin is significantly increased. Conditional ablation of one allele of the β-catenin gene substantially decreases the incidence and delays the occurrence of T-ALL caused by Pten loss, indicating that activation of the β-catenin pathway may contribute to the formation or expansion of the LSC population. Moreover, a recurring chromosomal translocation, T(14;15), results in aberrant overexpression of the c-myc oncogene in c-Kit mid CD3 + Lin − LSCs and CD3 + leukaemic blasts,

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“…32 Yet, MYC is up-regulated by translocations in Burkitt's lymphoma and mature B cell and T cell ALL, and by amplification or other mechanisms in AML and in several solid tumors. 29,[33][34][35][36] Like ETV6 (see above), its partner in the t(12;21) translocation, AML1, was found to be over-expressed. The translocation t(12;21)(p13;q22), resulting in the production of a chimeric ETV6-AML1 protein, is present in about 25% of children with B-lineage ALL.…”

Section: Discussionmentioning

confidence: 99%

Expression of myeloid-specific genes in childhood acute lymphoblastic leukemia – a cDNA array study

et al. 2002

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Several specific cytogenetic changes are known to be associated with childhood acute lymphoblastic leukemia (ALL), and many of them are important prognostic factors for the disease. Little is known, however, about the changes in gene expression in ALL. Recently, the development of cDNA array technology has enabled the study of expression of hundreds to thousands of genes in a single experiment. We used the cDNA array method to study the gene expression profiles of 17 children with precursor-B ALL. Normal B cells from adenoids were used as reference material. We discuss the 25 genes that were most over-expressed compared to the reference. These included four genes that are normally expressed only in the myeloid lineages of the hematopoietic cells: RNASE2, GCSFR, PRTN3 and CLC. We also detected over-expression of S100A12, expressed in nerve cells but also in myeloid cells. In addition to the myeloid-specific genes, other over-expressed genes included AML1, LCP2 and FGF6. In conclusion, our study revealed novel information about gene expression in childhood ALL. The data obtained may contribute to further studies of the pathogenesis and prognosis of childhood ALL.

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Deregulation of c- myc by Translocation of the α-Locus of the T-Cell Receptor in T-Cell Leukemias

Cited by 196 publications

References 11 publications

In vitro cytotoxic effects of fludarabine (2-F-ara-A) in combination with commonly used antileukemic agents by isobologram analysis

In vitro cytotoxic effects of fludarabine (2-F-ara-A) in combination with commonly used antileukemic agents by isobologram analysis

Multi-genetic events collaboratively contribute to Pten-null leukaemia stem-cell formation

Expression of myeloid-specific genes in childhood acute lymphoblastic leukemia – a cDNA array study

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