In estrogen receptor-positive (ER+) breast cancer cell lines, cyclin D1
and CDK4 & 6 promote phosphorylation of the retinoblastoma protein (Rb), cell cycle progression, and cell proliferation.
Molecular analysis shows that Ki67 expression and low cyclin D1
immuno-histological expression is linked to higher risk of recurrence in children but p27Kip1 expression and p53 over-expression is not associated with higher rate of recurrence.
Interplay between MEK-ERK signaling, cyclin D1
, and cyclin-dependent kinase 5 regulates cell cycle reentry and apoptosis of neurons.
In contrast to cyclin E1 expression, the analysis showed that expression of cyclin D1
, the molecular partner of CDKs 4 and 6 which are the targets of palbociclib, or PI3 kinase, or PIK3CA, mutations were not predictive of efficacy for palbociclib plus hormone therapy.
In the breast cancer cell line, TNF-[alpha] increases cell proliferation through increased NF-[kappa]B caused byincreased cyclin D1
Those lymphoma cells expressed diffuse positive immunohistochemical stain for CD20, CD79a, CD5, and cyclin D1
, but were negative for CD10, CD23, BCL6, and MUM1.
Replication Untreated cells 1 1 Vanadyl sulphate treated cells 0 0 Cyclin D1
This led to the breakdown of the complex formed between CDKs and cyclin D1
and E and decreased phosphorylation inactivation of tumor suppressor protein Rb1.
(1) The genetic hallmark of this lymphoma, considered to be the primary genetic event, is the t(11;14)(q13;q32) translocation between the immunoglobulin H (IgH) gene and the cyclin D1
gene (CCND1), leading to overexpression of the cyclin D1
protein, which is easily detected by immunohistochemistry.
In estrogen receptor-positive breast cancer cell lines, cyclin D1
and CDK4 and 6 promote phosphorylation of the retinoblastoma protein, cell cycle progression, and cell proliferation.
Specifically, cyclin D1
is a multifunctional Gi-phase cyclin that activates ER-mediated transcription of estradiol-responsive genes.
Activation of cyclin D1
and CDK4/6 plays a significant role in the tumorigenesis of HR+/HER2+ breast cancer [37, 76, 84].