ArticleLeukemia2006
Serpin A1 is overexpressed in ALK+ anaplastic large cell lymphoma and its expression correlates with extranodal dissemination.
Article in Leukemia, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed, 19 citations in OpenAlex.
- Mouse characteristics that affect establishing xenografts from hepatocellular carcinoma patient biopsies in the United States.Cancer medicine · 2022Article
- Tumor cell-specific Serpin A1 expression in vulvar squamous cell carcinoma.Archives of gynecology and obstetrics · 2019Article
- Peptides derived from the dependence receptor ALK are proapoptotic for ALK-positive tumors.Cell death & disease · 2015Article
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Anaplastic large cell lymphoma (ALCL) is a distinct subtype of non-Hodgkin's lymphoma. Most of ALCLs (85%) carry a chromosomal translocation involving different partners in the 5' portion, and the anaplastic lymphoma kinase (ALK) receptor kinase domain in the 3' portion. These translocations induce the ectopic expression of X-ALK proteins, thought to be involved in lymphomagenesis, through the dysregulation of cell proliferation and apoptotic pathways. In the present study, based on several ALK+ and ALK- ALCL cell lines and biopsy specimens, we showed that serpin A1, a secretory glycoprotein, was overexpressed in ALK+ ALCL cell lines and ALK+ tumors at both the transcriptional and translational levels. The crucial role of NPM-ALK in the regulation of serpin A1 expression was further demonstrated by using both ectopic expression and downregulation, by RNA interference, of the NPM-ALK oncogene. In addition, in ALK+ tumors, serpin A1 expression appeared to be correlated with the clinical status of the patients as the serpin A1 mRNA level was higher in patients presenting with extranodal dissemination. These data, together with the pattern of expression of serpin A1 we observed in ALK+ tumors, suggest that serpin A1 has an invasion-promoting effect in ALK+ ALCL.
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