BACKGROUND: @entity1124 ( @entity1124 ) is a devastating disease hallmarked by limited @entity1 survival. Resistance to chemotherapy, a major cause of treatment failure in @entity1124 @entity1 , is often attributed to Cancer Stem Cells (CSCs). Pancreatic CSCs are a small subset of quiescent cells within a @entity5 represented by surface markers like @entity16533 . These cells are responsible not only for @entity5 recurrence, but also poor prognosis based on their "stem-like" characteristics. At present, conventional therapy is directed towards rapidly dividing @entity1124 cells and thus fails to target the CSC population. METHODS: MIA PaCa-2, S2-013 and AsPC-1 were treated with 12.5 nM @entity9367 (12  T cells) for 7  days. The surviving cells were recovered briefly in drug-free growth media and then transferred to Cancer Stem cell Media (CSM). As a control, untreated cells were also transferred to CSM media (CSM). The 12  T and CSM cells were tested for stemness properties using RNA and protein markers. Low numbers of CSM and 12  T cells were implanted subcutaneously in athymic @entity19 to study their tumorigenic potential. 12  T and CSM cells were sorted for @entity16533 expression and assayed for their colony forming ability and sphere forming ability. Invasiveness of 12  T cells, CSM and MIA PaCa-2 were compared using Boyden chamber assays. RESULTS: Treated 12  T cells displayed increased expression of the surface marker @entity16533 and the drug transporter @entity34736 compared to untreated cells (CSM cells). Both 12  T and CSM cells formed subcutaneous @entity5 in @entity19 confirming their @entity5 -initiating properties. When tested for invasion, 12  T cells had increased invasiveness compared to CSM cells. @entity16533 (+) cells in both CSM and 12  T showed greater colony and sphere forming ability compared to @entity16533 (-) cells from each group. Consistent with these data, when injected subcutaneously in @entity19 , @entity16533 (-) cells from CSM or 12  T did not form any @entity5 whereas @entity16533 (+) cells from both groups showed @entity5 formation at a very low cell number. Despite pre-exposure to @entity9367 in 12  T @entity16533 (+) cells, treatment of @entity5 formed by these cells with @entity68586 , a @entity9367 pro-drug, showed significant @entity5 regression. CONCLUSION: Our results indicated that @entity9367 enhanced and enriched the "stemness" in the @entity1124 cell lines at a low dose of 12.5 nM, but also resulted in the regression of @entity5 derived from these cells.

XXXX effectively eliminates @entity16533 (+) side population in pancreatic cancer.

@entity1 :: ('9606', 'Species') :: ['patients', 'patient'] @entity1124 :: ('MESH:D021441', 'Disease') :: ['Pancreatic Ductal Adenocarcinoma', 'PDAC'] @entity5 :: ('MESH:D009369', 'Disease') :: ['tumor', 'tumors'] @entity19 :: ('10090', 'Species') :: ['mice', 'nude mice'] @entity16533 :: ('19126(Tax:10090)', 'Gene') :: ['CD133'] @entity9367 :: ('MESH:C001899', 'Chemical') :: ['triptolide'] @entity68586 :: ('MESH:C579022', 'Chemical') :: ['Minnelide'] @entity34736 :: ('26357(Tax:10090)', 'Gene') :: ['ABCG2']
@entity68586 :: (MESH:C579022,Chemical) :: ['Minnelide']
