ArticleInternational journal of clinical and experimental pathology2011
NPM-ALK and the JunB transcription factor regulate the expression of cytotoxic molecules in ALK-positive, anaplastic large cell lymphoma.
Article in International journal of clinical and experimental pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 28 citations in OpenAlex.
- miR-939 acts as tumor suppressor by modulating JUNB transcriptional activity in pediatric anaplastic large cell lymphoma.Haematologica · 2021Article
- AP-1 family transcription factors: a diverse family of proteins that regulate varied cellular activities in classical hodgkin lymphoma and ALK+ ALCL.Experimental hematology & oncology · 2021Review
- The Cellular Origins of Breast Implant-Associated Anaplastic Large Cell Lymphoma (BIA-ALCL): Implications for Immunogenesis.Aesthetic surgery journal · 2019Article
- The c-Jun and JunB transcription factors facilitate the transit of classical Hodgkin lymphoma tumour cells through GScientific reports · 2018Article
- [Expressions and clinical significance of GAS1, IL-1RAP and PRF1 in patients with ALK positive anaplastic large cell lymphoma].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2018Article
- Expression patterns of the activator protein-1 (AP-1) family members in lymphoid neoplasms.Clinical and experimental medicine · 2017Review
- Challenging perspectives on the cellular origins of lymphoma.Open biology · 2016Article
- Anaplastic large cell lymphoma arises in thymocytes and requires transient TCR expression for thymic egress.Nature communications · 2016Article
- Article
- Anaplastic lymphoma kinase: Role in cancer and therapy perspective.Cancer biology & therapy · 2015Review
- Expression of granzyme B sensitizes ALK+ ALCL tumour cells to apoptosis-inducing drugs.Molecular cancer · 2014Article
- Mechanistic insight into ALK receptor tyrosine kinase in human cancer biology.Nature reviews. Cancer · 2013Review
- Cleavage of the JunB transcription factor by caspases generates a carboxyl-terminal fragment that inhibits activator protein-1 transcriptional activity.The Journal of biological chemistry · 2013Article
- Article
- NPM-ALK: The Prototypic Member of a Family of Oncogenic Fusion Tyrosine Kinases.Journal of signal transduction · 2012Article
- ALK Signaling and Target Therapy in Anaplastic Large Cell Lymphoma.Frontiers in oncology · 2012Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Anaplastic lymphoma kinase-positive, anaplastic large cell lymphoma (ALK+ ALCL) is an aggressive non-Hodgkin lymphoma of T/null immunophenotype that is most prevalent in children and young adults. The normal cellular counterpart of this malignancy is presumed to be the cytotoxic T lymphocyte (CTL), and this presumption is partly based on the observation that these tumour cells often express cytotoxic granules containing Granzyme B (GzB) and Perforin. Chromosomal translocations involving the gene encoding for the ALK tyrosine kinase are also characteristic of ALK+ ALCL, and the resulting fusion proteins (e.g. NPM-ALK) initiate signalling events important in ALK+ ALCL pathogenesis. These events include the elevated expression of JunB; an AP-1 family transcription factor that promotes ALK+ ALCL proliferation. In this report we demonstrate that JunB is a direct transcriptional activator of GzB and that GzB transcription is also promoted by NPM-ALK. We found that Perforin expression was not regulated by JunB, but was promoted by NPM-ALK in some cell lines and inhibited by it in others. In conclusion, our study makes the novel observation that signalling through NPM-ALK and JunB affect the expression of cytotoxic molecules in ALK+ ALCL. Moreover, these findings demonstrate the expression of GzB and Perforin in this lymphoma is not solely due its presumed CTL origin, but that oncogenic signalling is actively influencing the expression of these proteins.
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Identifiers
21326808PMC3037198W20400078What OpenQuestion holds
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