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1.  CD133-positive cancer stem cells from Colo205 human colon adenocarcinoma cell line show resistance to chemotherapy and display a specific metabolomic profile 
Genes & Cancer  2014;5(7-8):250-260.
During the past decade, cancer stem-like cells (CSCs) have drawn substantial interest in cancer research since they have been described as major targets to improve treatment of tumors and to prevent recurrence and metastasis. In this paper, we report on the search for CSCs within the Colo205 human adenocarcinoma cell line. We describe that CD133 (prominin) was the only reliable marker for the isolation and characterization of CSCs within a Colo205 cell population. CD133-positive cells displayed many CSC characteristics, such as tumorsphere formation ability, expression of early-stage development markers, high invasiveness, raised tumor initiation potential and resistance to cisplatin chemotherapy treatment. In vitro analyses also highlighted a specific metabolomic profile of CD133-positive cells and we concluded that the chemotherapy resistance of CSCs could be related to the quiescence of such cells associated with their reduced metabolism. Furthermore, in vivo metabolome analyses suggested that a high level of circulating glutathione molecules could also promote treatment resistance. From the perspective of metabolomics, we also discuss the controversial use of serum-free in vitro cultures for CSC enrichment prior to further phenotype characterization.
PMCID: PMC4162140  PMID: 25221643
cancer stem cells; CD133; metabolomics; adenocarcinoma; CE-TOF-MS
2.  The relationship between the type of destructive spondyloarthropathy and its 10 years ago cervical spine alignment 
European Spine Journal  2009;18(6):900-904.
The objective of this retrospective study was to analyze the relationship between the type of destructive spondyloarthropathy (DSA) and its 10 years ago cervical spine alignment. DSA was reported as a serious complication of long-term hemodialysis. Although previous reports in regard to risk factor of DSA dealt with the period of hemodialysis and the patient’s age upon commencement of hemodialysis, we could not find any reports of the relationship between the type of DSA and its 10 years ago cervical spine alignment. In 96 DSA patients who were the subjects of our study, 8 patients were defined as stage 1, 39 patients as stage 2, 5 patients as stage 3 type A, 11 patients as stage 3 type B, and 33 patients as stage 3 type D. The C2/C7 angle of stage 3 type B was statistically low. The number of the abnormal local cervical alignment was larger in stage 3 types A and B. Multivariate analysis revealed that the risk factors of stage 3 types A and B were the C2/C7 angle and the existence of local abnormal alignment. Fifty-four patients were symptomatic due to DSA and treated at our hospital. Forty-four patients were treated conservatively with medications, physiotherapy, or wearing cervical brace. Ten patients underwent surgical treatment. The loss of physiological lordosis of cervical spine promoted the progression of DSA. Furthermore, the number of the abnormalities of local cervical alignment was statistically larger in stage 3 types A and B; they were the crucial factor promoting the progression of DSA stage 3 types A and B.
PMCID: PMC2899660  PMID: 19350288
Destructive spondyloarthropathy (DSA); Hemodialysis; Cervical spine
3.  Novel mode of action of c-kit tyrosine kinase inhibitors leading to NK cell–dependent antitumor effects 
Journal of Clinical Investigation  2004;114(3):379-388.
Mutant isoforms of the KIT or PDGF receptors expressed by gastrointestinal stromal tumors (GISTs) are considered the therapeutic targets for STI571 (imatinib mesylate; Gleevec), a specific inhibitor of these tyrosine kinase receptors. Case reports of clinical efficacy of Gleevec in GISTs lacking the typical receptor mutations prompted a search for an alternate mode of action. Here we show that Gleevec can act on host DCs to promote NK cell activation. DC-mediated NK cell activation was triggered in vitro and in vivo by treatment of DCs with Gleevec as well as by a loss-of-function mutation of KIT. Therefore, tumors that are refractory to the antiproliferative effects of Gleevec in vitro responded to Gleevec in vivo in an NK cell–dependent manner. Longitudinal studies of Gleevec-treated GIST patients revealed a therapy-induced increase in IFN-γ production by NK cells, correlating with an enhanced antitumor response. These data point to a novel mode of antitumor action for Gleevec.
PMCID: PMC489961  PMID: 15286804

Results 1-3 (3)