These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Jun activation domain-binding protein 1 expression in malignant lymphoma of the thyroid: its linkage to degree of malignancy and p27 expression.
    Author: Ito Y, Yoshida H, Matsuzuka F, Matsuura N, Nakamura Y, Nakamine H, Kakudo K, Kuma K, Miyauchi A.
    Journal: Anticancer Res; 2003; 23(5b):4121-5. PubMed ID: 14666612.
    Abstract:
    BACKGROUND: Jab1 (Jun activation domain-binding protein 1) is known as a coactivator of the AP1 transcription factor, which contributes to carcinoma progression by degrading the p27/Kip1 protein. To date, the clinical significance of jab1 in human carcinoma, including malignant lymphoma, has not been studied in depth. In this study, we investigated jab1 expression in malignant lymphoma of the thyroid. MATERIALS AND METHODS: We immunohistochemically studied jab1 expression for 50 cases of thyroid lymphoma, as well as 10 cases of chronic thyroiditis. RESULTS: Although jab1 was only occasionally expressed in follicular cells in normal follicules, it was diffusely positive in those forming small follicules typical of chronic thyroiditis and malignant lymphoma. In infiltrating lymphocytes in chronic thyroiditis, jab1 was not overexpressed. On the other hand, in malignant lymphomas, jab1 overexpression was observed in 24 cases (48.0%). It was directly linked to MIB-1 labeling index (p < 0.0001), grade of malignancy (p = 0.0130) and aberrant p53 expression (p = 0.0145). Furthermore, an inverse relationship was observed between jab1 and p27 overexpression (p = 0.0130). CONCLUSION: These results suggest that: 1) jab1 plays a role in the regenerating of follicular cells attacked by lymphocytes in chronic thyroiditis and malignant lymphoma, and 2) jab1 contributes to the progression of malignant lymphoma especially with aggressive phenotypes, possibly by degrading p27.
    [Abstract] [Full Text] [Related] [New Search]