Applicability of Quantum Dots in Breast Cancer Diagnostic and Therapeutic Modalities-A State-of-the-Art Review.

The increasing incidence of breast cancers (BCs) in the world population and their complexity and high metastatic ability are serious concerns for healthcare systems. Despite the significant progress in medicine made in recent decades, the efficient treatment of invasive cancers still remains challenging. Chemotherapy, a fundamental systemic treatment method, is burdened with severe adverse effects, with efficacy limited by resistance development and risk of disease recurrence.

Fractalkine-induced endothelial cell migration requires MAP kinase signaling.

Background/aims: Angiogenesis is a well-established characteristic in the rheumatoid arthritis (RA) synovial pannus. We have previously demonstrated that fractalkine (Fkn/ CX3CL1) expression is significantly increased in the RA joint and that fractalkine induces angiogenesis. In this work we studied mechanisms through which Fkn functions as an angiogenic mediator.

Fractalkine is a novel chemoattractant for rheumatoid arthritis fibroblast-like synoviocyte signaling through MAP kinases and Akt.

Objective: Fibroblast-like synoviocytes (FLS) are a major constituent of the hyperplastic synovial pannus that aggressively invades cartilage and bone during the course of rheumatoid arthritis (RA). Fractalkine (FKN/CX(3)CL1) expression is up-regulated in RA synovium and RA synovial fluid. While RA FLS express the FKN receptor, CX(3)CR1, the pathophysiologic relevance of FKN stimulation of RA FLS is not understood.

A cell-cycle independent role for p21 in regulating synovial fibroblast migration in rheumatoid arthritis.

Rheumatoid arthritis (RA) is characterized by synovial hyperplasia and destruction of cartilage and bone. The fibroblast-like synoviocyte (FLS) population is central to the development of pannus by migrating into cartilage and bone. We demonstrated previously that expression of the cell cycle inhibitor p21 is significantly reduced in RA synovial lining, particularly in the FLS.

p21Cip1 is required for the development of monocytes and their response to serum transfer-induced arthritis.

One of the central functions of cyclin-dependent kinase inhibitors, such as p21, p27, or p16, is to prevent entry into the cell cycle. However, the question remains as to whether they have other functions in the cell. We previously demonstrated that overexpression of p21 in fibroblasts isolated from patients with rheumatoid arthritis decreases the production of pro-inflammatory molecules.