Bladder cancer stem (initiating) cell has not been isolated now, and no one verified its persistence experimentally. The aim of this study was to conclude the persistence of bladder cancer stem (initiating) cell in human primary bladder cancer and investigate the possibility of EMA(-) CD44v6(+) as markers of bladder cancer stem (initiating) cell. Genes differentially expressed between normal urothelium and low malignant bladder cancer were identified by DNA array assay. Overpressed stem cell related genes, Bmi-1 and EZH2, were verified by immunohistochemistry. Side population cells in bladder cancer were found under fluorescence microscope. The value of 28 potential surface markers of bladder cancer stem (initiating) cell for isolating them were judged by immunohistochemistry. Both EMA(-) and CD44v6(+) cells located in basal layer (potential location of stem cells). After gathering the CD44v6(+) cells and EMA(-) cells by magnetic cell sorting, their ability for colony-forming, self-renewal and extensive proliferation were assayed by cells culture. Both EMA(-) cells and CD44v6(+) cells posses the ability for colony-forming, self-renewal and proliferation. We conclude the persistence of bladder cancer stem (initiating) cell. Bladder cancer stem (initiating) cell might be among EMA(-) CD44v6(+) subset. Our strategies for isolating bladder cancer stem (initiating) cell might be useful for isolating other undetermined epithelial cancer stem cell, especially those in well-differentiated cancers.

Cancer stem cells (CSCs) have been positively identified and successfully isolated from some but not all cancers. The studies on CSCs to date suggest that these cells are rare among the tumor cell population, and they are capable of self-renewing and maintaining tumor growth and heterogeneity. Therapies aimed at CSCs have shown some promise, but their further development will require a more thorough understanding of the biology of CSCs and methods for identifying and isolating this cell subpopulation. This review examines what is known to date regarding the similarities and differences between cancer and somatic stem cells: CSC surface marker development and cell isolation (including a model isolation from our lab), the frequency, potential origin, and signal transduction of CSCs, and the current state of CSC-targeting therapeutic strategies.

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Background:Pancreaticoduodenectomy remains a major undertaking. A preoperative blood test, which could confidently predict the benefits of surgery would improve the selection of pancreatic cancer patients for surgery. This study aimed to identify protein biomarkers prognostic for long-term survival and to validate them with clinico-pathological information.Methods:Serum from 40 preoperative patients was used to train for predictive biomarkers using surface-enhanced laser desorption/ionisation time-of-flight mass spectrometry (SELDI), and the results were verified on 21 independent samples. Two predictive proteins were identified by tryptic peptide mass fingerprinting and sequencing, and validated on serum from another 57 patients by enzyme-linked immunosorbent assay (ELISA). The influence of these proteins on growth and invasion of two cancer cell lines was tested in-vitro.Results:The SELDI panel of m/z 3700, 8222 and 11 522 peaks predicted <12 months' survival (ROC AUC: 0.79, 0.64–0.90; P<0.039). When CA19-9 was added, the ROC AUC increased to 0.95 (0.84–0.99; P<0.0001). The six subjects in the verification group who died within 12 months were correctly classified. The m/z 8222 and 11 522 proteins were identified as Serum ApoC-II and SAA-1, respectively. In the validation samples, ELISA results confirmed that ApoC-II was predictive of survival (Kaplan–Meier P<0.009), but not SAA-I. ApoC-II, CA19-9 and major-vessel involvement independently predicted survival. ApoC-II and SAA-1 increased cell growth and invasion of both cancer cell lines.Conclusion:Serum ApoC-II, CA19-9 and major-vessel invasion independently predict survival and improves selection of patients for pancreaticoduodenectomy.

Ovarian metastasis originating from bronchioloalveolar carcinoma (BAC) has not been reported previously. We report a 63-year-old Chinese woman who was diagnosed as BAC with pleural metastasis in 1997. Four years later, she complained of vaginal bleeding, and a pelvic mass was discovered by an abdominal computerized tomography scan. Tumor debulking and total hysterectomy with bilateral salpingo-oopherectomy were performed. Pathology disclosed well-differentiated adenocarcinoma, with abundant clear cytoplasm, in the ovaries. Furthermore, immunohistochemical staining revealed that the tumor cells from the ovary and pleura were reactive to thyroid transcription factor 1 (TTF-1) and cytokeratin-7 (CK-7) but were negative for cytokeratin-20 (CK-20). The results of immunohistochemical staining, clinical course, and pathological features were compatible with the diagnosis of BAC with ovarian metastasis. In conclusion, to investigate the primary site of a metastatic ovarian cancer, clinicians should not forget the lungs since the incidence of lung cancer in females is increasing. Moreover, a monoclonal antibody panel for TTF-1, CK-7, and CK-20 may facilitate discrimination between primary and metastasized ovarian adenocarcinomas and/or identifying tumors of pulmonary origin.