Abstract
BackgroundCD133 is a marker that identifies/enriches cancer stem cell implicated in tumor initiation. We hypothesize that changes in the CD133 mRNA expression levels and vascular endothelial growth factor (VEGF) may correlate tumor response in GIST.Methodology/Principal FindingsAfter informed consent, we obtained peripheral blood samples from 24 evaluable patients with gastrointestinal stromal tumors (GIST). There were 7 -paired samples before and after treatment, We measured CD133 mRNA levels by real time RT-PCR method and vascular endothelial growth factor (VEGF) levels by ELISA. All measurements were done in duplicates in two separate experiments. The treatment resulted in significant reduction of CD133 mRNA expression (p = 0.048) as well as the level of VEGF (p = 0.003). The mean CD133 mRNA levels for GIST patients was 615. We found no correlation between the CD133 mRNA levels and VEGF levels. (p = 0.826). Logistic regression analysis suggested a relationship between elevated CD133 mRNA levels and fitted probability of eventual progressive disease (PD) and mixed response at 37% for CD133 mRNA of 2.25, and the probability of eventual PD/MR is 84% for a CD133 of 2072 (p = 0.08).Conclusions/SignificanceCD133 mRNA expression levels in GIST patients measured by real time RT-PCR assay appeared to correlate with tumor response to surgery or imatinib and may be used to predict tumor progression. Additional prospective studies are warranted.
Highlights
Gastrointestinal stromal tumors (GISTs) are a paradigm for the development of personalized treatment for cancer patients
The results showed that the relative amount of CD133 mRNA expression was significantly lower in the post-treated patients as compared to those same pretreated 7 patients (p = 0.048)
We found no correlation between CD133 mRNA levels and plasma vascular endothelial growth factor (VEGF) levels in using Pearson regression analysis, (p = 0.826) (Table 3)
Summary
Gastrointestinal stromal tumors (GISTs) are a paradigm for the development of personalized treatment for cancer patients. Further improvements in GIST treatment may require targeting GIST stem cell populations [1]. Cancer stem cell theory proposed that a subset of cancer cell is responsible for the initiation of drug resistance and tumor progression [2] As this theory has recently gained traction in number of epithelial cancers, cancer stem cells have been identified from tumors of mesenchymal origin [3]. GIST is believed to derive from mesenchymal stem cells of embryonic mesoderm and displays vast array of tissue heterogeneity as cancers of epithelial origin, and hematopoietic systems, which are derived from the embryonic ectoderm and endoderm respectively [4]. CD133 is a marker that identifies/enriches cancer stem cell implicated in tumor initiation. We hypothesize that changes in the CD133 mRNA expression levels and vascular endothelial growth factor (VEGF) may correlate tumor response in GIST
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