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Loss of the TSG101 leucine zipper domain in aggressive non-Hodgkin's lymphomas

Leukemia volume 14, pages 2014–2016 (2000)Cite this article

Non-Hodgkin's lymphomas (NHL) are a heterogeneous group of disease entities with distinctive clinical, morphological, phenotypic, and genetic characteristics. Most aggressive NHLs occur as primary tumors recognized at diagnosis, but they may also develop secondarily from progression of indolent variants. This transformation is associated with a rapidly progressive clinical course and short survival of the patients. The underlying molecular mechanisms involved in the pathogenesis of aggressive lymphomas and the progression of indolent tumors are not well known.

The TSG101 tumor susceptibility gene is a new putative tumor suppressor gene involved in different types of murine and human tumors.1 The functional inactivation of the TSG101 gene caused cellular transformation and formation of metastasis in nude mice.1 Alternatively spliced TSG101 non-coding messages, with loss of coding exons and early termination codons, are frequently detected in many carcinomas without alterations at the DNA level. These non-coding alternatively spliced messages are always coexpressed with a normal transcript in tumor cells, and are also detectable in normal cells at a lower frequency.2

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Acknowledgements

MF and SH were supported by fellowships from the Instituto de Salud Carlos III and CIRIT, respectively. This work was funded by grants FIS98/0313, and CICYT (SAF96/61 and SAF00/169).

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Authors and Affiliations

  1. Centro de Investigación del Cáncer, CSIC-Universidad de Salamanca, Spain

    M Ferrer & PA Lazo

  2. CNBF, Instituto de Salud Carlos III, Majadahonda, Spain

    M Ferrer & PA Lazo

  3. Hematopathology Section, Hosptial Clinic, Universidad de Barcelona, Spain

    S Hernández & E Campo

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  1. M Ferrer
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  2. S Hernández
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  3. E Campo
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  4. PA Lazo
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Ferrer, M., Hernández, S., Campo, E. et al. Loss of the TSG101 leucine zipper domain in aggressive non-Hodgkin's lymphomas. Leukemia 14, 2014–2016 (2000). https://doi.org/10.1038/sj.leu.2401920

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