ArticleThe American journal of pathology2003
Expression of Bcl-2 and Bcl-xL in cutaneous and bone marrow lesions of mastocytosis.
Article in The American journal of pathology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 44 citations in OpenAlex.
- Impact of Molecular Evaluations in the Biology, Diagnosis, and Prognostication of Patients With Mastocytosis.The journal of allergy and clinical immunology. In practice · 2026Review
- Mastocytosis.Nature reviews. Disease primers · 2025Review
- Mast Cells in the Skin: Defenders of Integrity or Offenders in Inflammation?International journal of molecular sciences · 2021Review
- Recent Advances in the Molecular Biology of Systemic Mastocytosis: Implications for Diagnosis, Prognosis, and Therapy.International journal of molecular sciences · 2020Review
- Preclinical human models and emerging therapeutics for advanced systemic mastocytosis.Haematologica · 2018Review
- Controlling Mast Cell Activation and Homeostasis: Work Influenced by Bill Paul That Continues Today.Frontiers in immunology · 2018Review
- IL-33/ST2 axis promotes mast cell survival via BCLXL.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Development of selective inhibitors for anti-apoptotic Bcl-2 proteins from BHI-1.Bioorganic & medicinal chemistry · 2007Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mastocytosis is a rare disease characterized by accumulation of mast cells in tissues. To investigate whether an altered regulation of mast cell apoptosis might be involved in the pathogenesis of mastocytosis, expression of the apoptosis-preventing molecules bcl-2 and bcl-xL was studied by immunohistochemistry in skin and bone marrow lesions of mastocytosis patients. In addition, reverse transcription-polymerase chain reaction was used to investigate levels of bcl-2 and bcl-xL mRNA in cutaneous mastocytosis lesions. Since activating mutations of c-kit are known to be associated with some forms of mastocytosis, human mast cell cultures were also stimulated via c-kit and the expression of bcl-2 and bcl-xL was assessed by immunoblotting. In patients with mastocytosis, the expression of bcl-2 protein but not bcl-xL in cutaneous mast cells was significantly enhanced, compared to healthy controls. Evaluating different subgroups of adult and pediatric mastocytosis patients, all groups were found to express significantly increased levels of bcl-2 protein, and none of the patient groups was found to overexpress bcl-xL, with the exception of solitary mastocytomas that showed a tendency for up-regulated bcl-xL protein. Furthermore, the expression of bcl-2 mRNA was significantly enhanced in cutaneous lesions of adult and pediatric patients, while bcl-xL mRNA levels were only slightly increased in pediatric, but not in adult patients with mastocytosis. In contrast to the skin lesions, bone marrow infiltrates of patients with systemic mastocytosis showed only low or absent immunoreactivity for bcl-2, but marked expression of bcl-xL. In vitro, stimulation of two different mast cell culture systems by activation of c-kit resulted in up-regulation of bcl-2 and also in an increase of bcl-xL, although less pronounced. Thus, overexpression of bcl-2 and bcl-xL leading to prolonged survival of mast cells may contribute to the pathogenesis of mastocytosis. Our findings may help to develop new strategies for the treatment of this disease.
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