Pain and functional outcomes of the sacroiliac joint after platelet-rich plasma injection: a descriptive review.

The purpose of this manuscript is to highlight and review the status of literature regarding efficacy of platelet-rich plasma (PRP) in the treatment of sacroiliac joint (SIJ) dysfunction. A review of the literature on PRP interventions on the SIJ or ligaments was performed. Seven studies had improvements in their respective primary end point and demonstrated a strong safety profile without any serious adverse events.

Temozolomide competes for P-glycoprotein and contributes to chemoresistance in glioblastoma cells.

Chemotherapeutic resistance can occur by P-glycoprotein (P-gp), a 12-transmembrane ATP-dependent drug efflux pump. Glioblastoma (GBM) has poor survival rate and uniformly acquired chemoresistance to its frontline agent, Temozolomide (TMZ). Despite much effort, overcoming TMZ resistance remains a challenge.

T/Th17 polarization by distinct subsets of breast cancer cells is dictated by the interaction with mesenchymal stem cells.

Breast cancer (BC) cells (BCCs) exist within a hierarchy beginning with cancer stem cells (CSCs). Unsorted BCCs interact with mesenchymal stem cells (MSCs) to induce regulatory T cells (T). This study investigated how distinct BCC subsets interacted with MSCs to polarize T-cell response, T versus T helper 17 (Th17).

Temozolomide resistance in glioblastoma occurs by miRNA-9-targeted PTCH1, independent of sonic hedgehog level.

Glioblastoma Multiforme (GBM), the most common and lethal adult primary tumor of the brain, showed a link between Sonic Hedgehog (SHH) pathway in the resistance to temozolomide (TMZ). PTCH1, the SHH receptor, can tonically represses signaling by endocytosis. We asked how the decrease in PTCH1 in GBM cells could lead to TMZ-resistance.

High expression of miR-9 in CD133 glioblastoma cells in chemoresistance to temozolomide.

Glioblastoma Multiforme (GBM), a uniformly lethal stage IV astrocytoma, is currently treated with a combination of surgical and radiation therapy as well as Temozolomide (TMZ) chemotherapy. Resistance to TMZ is rapidly acquired by GBM cells and overcoming this resistance has been an area of signi?cant research. GBM 'cancer stem cells' (CSC) also known as 'cancer initiating cells' are often positively selected by CD133 expression and TMZ resistance.

Temozolomide resistance in glioblastoma cells occurs partly through epidermal growth factor receptor-mediated induction of connexin 43.

Glioblastoma Multiforme (GBM) is an aggressive adult primary brain tumor with poor prognosis. GBM patients develop resistance to the frontline chemotherapy, temozolomide (TMZ). As the connexins (Cx) have been shown to have a complex role in GBM, we investigated the role of Cx43 in TMZ resistance.