ArticleCancer genetics and cytogenetics2006
Recurrent genomic imbalances in primary effusion lymphomas.
Article in Cancer genetics and cytogenetics, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed.
- MicroRNA-34a promotes genomic instability by a broad suppression of genome maintenance mechanisms downstream of the oncogene KSHV-vGPCR.Oncotarget · 2016Article
- Interleukin 1 receptor-associated kinase 1 (IRAK1) mutation is a common, essential driver for Kaposi sarcoma herpesvirus lymphoma.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- A novel mechanism inducing genome instability in Kaposi's sarcoma-associated herpesvirus infected cells.PLoS pathogens · 2014Article
- A protein array screen for Kaposi's sarcoma-associated herpesvirus LANA interactors links LANA to TIP60, PP2A activity, and telomere shortening.Journal of virology · 2012Article
- Tumor suppressor genes FHIT and WWOX are deleted in primary effusion lymphoma (PEL) cell lines.Blood · 2011Article
- Genome wide DNA-profiling of HIV-related B-cell lymphomas.British journal of haematology · 2010Article
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4 authors.
Funding
Abstract
Primary effusion lymphomas (PEL) form a subset of AIDS-related lymphomas and usually have a poor prognosis. Although Kaposi's sarcoma-associated herpes virus (KSHV) is often associated with PEL, very little is known about the exact mechanisms or causative effects of these associations. We investigated the chromosomal imbalances in six KSHV-positive PEL cell lines using comparative genomic hybridization analysis. We defined the shortest regions of overlaps for genomic gains on six chromosomes: 1q31, 4q31 approximately q33, 7q10 approximately q21, 8q21.1, 12q0 approximately q23, and Xp11 approximately q21. The recurrent nature of the gains found in these chromosomal regions suggests that these imbalances play roles in the pathogenesis of PEL.
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Registered trials
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