When cyclin D1 was overexpressed by the Eμ-cyclin D1 transgene, ATA B cells progressed to further diffused lymphoma in aged mice, including in various lymph nodes with accumulation of IgM<sup>hi</sup>IgD<sup>lo</sup>CD5<sup>+</sup>CD23<sup>-</sup>CD43<sup>+</sup> cells, resembling aggressive human mantle cell lymphoma.
It is widely acknowledged that FISH is the most consistently useful test to identify the juxtaposition of the CCND1 and IGH genes in mantle cell lymphoma and is regarded as the 'gold standard'.
A simple antigen retrieval method for the optimal demonstration of cyclin-D1 overexpression in formalin-fixed paraffin-embedded cases of mantle cell lymphoma.
Quantitative monitoring of cyclin D1 expression: a molecular marker for minimal residual disease monitoring and a predictor of the disease outcome in patients with mantle cell lymphoma.
On a genetic level, many cases of mantle cell lymphomas have the t(11;14)(q13;q32) that causes overexpression of cyclin-D1, a protein that can be demonstrated by immunohistochemistry in many examples of mantle cell lymphoma and that can be exploited diagnostically to distinguish mantle cell lymphomas from other low-grade B cell lymphoproliferative disorders.
We surveyed lymphomas to determine the range of expression of the mantle cell lymphoma-associated SOX11 transcription factor and its relation to cyclin D1.
On the other hand, the molecular basis of some of these diseases (eg, the overexpression of the Prad1/CCND1 gene in mantle-cell lymphomas, the relationship between bcl-2 and bax expression in chronic lymphocytic leukemia homeostasis, the role of p53 tumor suppressor gene mutations in chronic lymphocytic leukemia progression) are increasingly well known.
Detection of cyclin D1 overexpression by real-time reverse-transcriptase-mediated quantitative polymerase chain reaction for the diagnosis of mantle cell lymphoma.
Mantle cell lymphoma is a B cell malignancy in which constitutive dysregulation of cyclin D1 and the cell cycle, disruption of DNA damage response pathways, and activation of cell survival mechanisms contribute to oncogenesis.