Comparative genomic hybridization analysis of primary cutaneous B‐cell lymphomas: Identification of common genomic alterations in disease pathogenesis

Mao, Xin; Lillington, Debra M.; Child, Fiona; Russell‐Jones, Robin; Young, Bryan D.; Whittaker, Sean

doi:10.1002/gcc.10104

Cited by 93 publications

(112 citation statements)

References 74 publications

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“…This may partly be explained by the irreversible nature of the increased methylation of the p16 promoter. Loss of JunB is frequently observed in human tumors of the B-lymphoid lineage, and its gene is silenced in advanced stages of myeloid leukemia (Mao et al, 2002;Szremska et al, 2003;Yang et al, 2003). We propose that any therapeutic strategy that aims at elevating JunB expression is doomed to fail.…”

Section: Discussionmentioning

confidence: 99%

JunB is a gatekeeper for B-lymphoid leukemia

et al. 2007

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Loss of JunB has been observed in human leukemia and lymphoma, but it remains unknown, whether this loss is relevant to disease progression. Here, we investigated the consequences of JunB deficiency using Abelson-induced B-lymphoid leukemia as a model system. Mice deficient in JunB expression succumbed to Abelson-induced leukemia with increased incidence and significantly reduced latency. Similarly, bcr/abl p185-transformed JunB-deficient (junB D/D ) cells induced leukemia in RAG2 À/À mice displaying a more malignant phenotype. These observations indicated that cell intrinsic effects within the junB D/D tumor cells accounted for the accelerated leukemia development. Indeed, explantated bcr/abl p185 transformed junB D/D cells proliferated faster than the control cells. The proliferative advantage emerged slowly after the initial transformation process and was associated with increased expression levels of the cell cycle kinase cdk6 and with decreased levels of the cell cycle inhibitor p16 INK4a . These alterations were due to irreversible reprogramming of the cell, because -once established -accelerated disease induced by junB D/D cells was not reverted by re-introducing JunB. Consistent with this observation, we found that the p16 promoter was methylated. Thus, JunB functions as a gatekeeper during tumor evolution. In its absence, transformed leukemic cells acquire an enhanced proliferative capacity, which presages a more malignant disease.

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Section: Discussionmentioning

confidence: 99%

JunB is a gatekeeper for B-lymphoid leukemia

et al. 2007

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“…[48][49][50][51][52] The candidate target gene at 13q31 was c13orf25. 50 Similar to the BIC gene, transcripts of c13orf25 were unlikely to encode for a protein as predicted ORFs were short (o70 amino acids) and not conserved in closely related species.…”

Section: Mir-17-92 Polycistronmentioning

confidence: 99%

The role of microRNAs in normal hematopoiesis and hematopoietic malignancies

et al. 2006

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“…Gene-specific genomic microarray (array CGH) analysis was performed on the same genomic DNA sample from patient 3183, using an Array300 chip (Abbot Diagnostics, UK) and the GenoSensor Reader System (Abbot Diagnostics, UK) as previously reported. 13 This array allows identification of copy number changes to 287 genes commonly altered in human tumors.…”

Section: To the Editormentioning

confidence: 99%