Identification of subtype-specific genomic alterations in aggressive adult T-cell leukemia/lymphoma

Oshiro, Aya; Tagawa, Hiroyuki; Ohshima, Koichi; Karube, Kennosuke; Uike, Naokuni; Tashiro, Yoshihiko; Utsunomiya, Atae; Masuda, Masato; Takasu, Nobuyuki; Nakamura, Shigeo; Morishima, Yasuo; Seto, Masao

doi:10.1182/blood-2005-09-3801

Cited by 139 publications

(130 citation statements)

References 34 publications

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“…We and others reported high levels of BCL11B mRNA expression in the majority of T-ALL and T-cell leukemia/lymphoma cell lines Przybylski et al, 2005). Furthermore, BCL11B overexpression was found in the acute type of ATLL in contrast to no or low expression of the gene in the lymphoma type (Oshiro et al, 2006). Thus, although the mechanisms are not clear, Bcl11b seems to be implicated in the process of oncogenesis.…”

Section: Introductionmentioning

confidence: 73%

Inhibition of BCL11B expression leads to apoptosis of malignant but not normal mature T cells

et al. 2006

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The B-cell chronic lymphocytic leukemia (CLL)/lymphoma 11B gene (BCL11B) encodes a Kru¨ppel-like zincfinger protein, which plays a crucial role in thymopoiesis and has been associated with hematopoietic malignancies. It was hypothesized that BCL11B may act as a tumorsuppressor gene, but its precise function has not yet been elucidated. Here, we demonstrate that the survival of human T-cell leukemia and lymphoma cell lines is critically dependent on Bcl11b. Suppression of Bcl11b by RNA interference selectively induced apoptosis in transformed T cells whereas normal mature T cells remained unaffected. The apoptosis was effected by simultaneous activation of death receptor-mediated and intrinsic apoptotic pathways, most likely as a result of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) upregulation and suppression of the Bcl-xL antiapoptotic protein. Our data indicate an antiapoptotic function of Bcl11b. The resistance of normal mature T lymphocytes to Bcl11b suppression-induced apoptosis and restricted expression pattern make it an attractive therapeutic target in T-cell malignancies.

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Section: Introductionmentioning

confidence: 73%

Inhibition of BCL11B expression leads to apoptosis of malignant but not normal mature T cells

et al. 2006

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“…All these aberrations, except for 1p36.33-32 gain, were also recurrently found and at higher frequencies in lymphoma type ATLL (Table 2). 8,9 Although its genomic profile shows considerable overlap with that of lymphoma type ATLL, cutaneous type ATLL possesses a specific aberration such as 1p36 gain. It was reported that this gain is frequently found in some solid tumors, and in hematological malignancies it has been detected in several MF cases with large cell transformation.…”

Section: Discussionmentioning

confidence: 99%

“…8 Briefly, 5 lg of genomic DNA was digested with EcoRI and size-fractionated on a 0.7% agarose gel. The gel was sequentially immersed for 30 min each in 0.25 M HCl, 1.5 M NaCl/0.5 M NaOH and 0.5 M Tris (pH 7.4)/1.5 M NaCl.…”

Section: Southern Blotmentioning

confidence: 99%

“…8,9 DNA extraction DNA was extracted from frozen tissue using the standard proteinase K treatment and phenol-chloroform extraction. Normal DNA was obtained from the peripheral blood of healthy male donors.…”

Section: Patient Samples and Case Selectionmentioning

confidence: 99%

“…8 So far, however, no study has been conducted of the genomic profiles of cutaneous type ATLL. In the study reported here we analyzed these genomic profiles by means of array CGH and related our findings to the clinical features.…”

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confidence: 99%

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Cutaneous type adult T‐cell leukemia/lymphoma is a characteristic subtype and includes erythema/papule and nodule/tumor subgroups

Miyata

Yonekura

Utsunomiya

et al. 2010

Intl Journal of Cancer

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We first analyzed the genomic profile of cutaneous type adult T-cell leukemia/lymphoma (ATLL) in an attempt to clarify its clinical and biological characteristics. Genomic gains of 1p, 7q and 18q and loss of 13q were frequently detected. Gain of 1p36.33-32 or loss of 13q33.1-3 indicated poor prognosis. Among cases with generalized lesions, erythema/papule or nodule/tumor cases showed a distinct genomic profile, indicating that these 2 groups were biologically different and developed via different genetic pathways. Furthermore, cases with generalized nodule/tumor lesions tended to progress to aggressive ATLL.

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Mature B‐ and T‐cell Neoplasms and Hodgkin Lymphoma

Siebert

2010

Cancer Cytogenetics

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Identification of subtype-specific genomic alterations in aggressive adult T-cell leukemia/lymphoma

Abstract: 1q, 2p, 4q, 7p, and 7q, and losses of 10p, 13q, 16q, and 18p,

Cited by 139 publications

References 34 publications

Inhibition of BCL11B expression leads to apoptosis of malignant but not normal mature T cells

Inhibition of BCL11B expression leads to apoptosis of malignant but not normal mature T cells

Cutaneous type adult T‐cell leukemia/lymphoma is a characteristic subtype and includes erythema/papule and nodule/tumor subgroups

Mature B‐ and T‐cell Neoplasms and Hodgkin Lymphoma

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