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      Expression of Cancer Stem Cell Marker CD44 and Its Polymorphisms in Patients with Chronic Gastritis, Precancerous Gastric Lesion, and Gastric Cancer: A Cross-Sectional Multicenter Study in Thailand

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          Abstract

          Here we investigated CD44 protein expression and its polymorphisms in patients with chronic gastritis, precancerous gastric lesions, and gastric cancer; and we evaluated our result with the risk of CD44 protein expression and clinicopathological characteristics. Our results obtained by analyzing 162 gastric cancer patients, 125 chronic gastritis, and 165 precancerous gastric lesions from three study centers in Thailand showed that CD44 expression was significantly higher in patients with precancerous gastric lesions and gastric cancer while patients with chronic gastritis were negative for CD44 staining ( p = 0.036). We further observed the significant association of variant genotype; gastric cancer patients carrying AG or GG of CD44 rs187116 had more increased risk of CD44 expression than wild-type (WT) carriers (AG: odds ratio (OR) = 5.67; 95% CI = 1.57–7.23; p = 0.024 and GG: OR = 8.32; 95% CI = 2.94–11.42; p = 0.016), but no significant difference in the risk of CD44 expression due to polymorphism in patients with precancerous gastric lesions. Our results suggested that CD44 expression could be used as a marker for the prediction of gastric cancer development, particularly in patients with precancerous gastric lesions carrying AG or GG, who were selected to surveillance follow-up for gastric cancer prevention.

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          AACR centennial series: the biology of cancer metastasis: historical perspective.

          Metastasis resistant to therapy is the major cause of death from cancer. Despite almost 200 years of study, the process of tumor metastasis remains controversial. Stephen Paget initially identified the role of host-tumor interactions on the basis of a review of autopsy records. His "seed and soil" hypothesis was substantiated a century later with experimental studies, and numerous reports have confirmed these seminal observations. An improved understanding of the metastatic process and the attributes of the cells selected by this process is critical for the treatment of patients with systemic disease. In many patients, metastasis has occurred by the time of diagnosis, so metastasis prevention may not be relevant. Treating systemic disease and identifying patients with early disease should be our goal. Revitalized research in the past three decades has focused on new discoveries in the biology of metastasis. Even though our understanding of molecular events that regulate metastasis has improved, the contributions and timing of molecular lesion(s) involved in metastasis pathogenesis remain unclear. Review of the history of pioneering observations and discussion of current controversies should increase understanding of the complex and multifactorial interactions between the host and selected tumor cells that contribute to fatal metastasis and should lead to the design of successful therapy. (c)2010 AACR.
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            Cancer stem cells and metastasis.

            Cancer stem cells (CSCs) represent a subpopulation of tumour cells endowed with self-renewal and multi-lineage differentiation capacity but also with an innate resistance to cytotoxic agents, a feature likely to pose major clinical challenges towards the complete eradication of minimal residual disease in cancer patients. Operationally, CSCs are defined by their tumour-propagating ability when serially transplanted into immune-compromised mice and by their capacity to fully recapitulate the original heterogeneity of cell types observed in the primary lesions they are derived from. CSCs were first identified in haematopoietic malignancies and later in a broad spectrum of solid tumours including those of the breast, colon and brain. Notably, several CSC characteristics are relevant to metastasis, such as motility, invasiveness and, as mentioned above, resistance to DNA damage-induced apoptosis. Here, we have reviewed the current literature on the relation between CSCs and metastasis formation. Preliminary studies on cancer cell lines and patient-derived material suggest a rate-limiting role for stem-like cells in the processes of tumour cell dissemination and metastasis formation. However, additional studies are needed to deliver formal proof of their identity as the cell of origin of recurrences at distant organ sites. Nevertheless, several studies have already provided pre-clinical evidence of the efficacy of novel therapies directed against disseminated CSCs.
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              Understanding the cancer stem cell

              The last 15 years has seen an explosion of interest in the cancer stem cell (CSC). Although it was initially believed that only a rare population of stem cells are able to undergo self-renewing divisions and differentiate to form all populations within a malignancy, a recent work has shown that these cells may not be as rare as thought first, at least in some malignancies. Improved experimental models are beginning to uncover a less rigid structure to CSC biology, in which the concepts of functional plasticity and clonal evolution must be incorporated into the traditional models. Slowly the genetic programmes and biological processes underlying stem cell biology are being elucidated, opening the door to the development of drugs targeting the CSC. The aim of ongoing research to understand CSCs is to develop novel stem cell-directed treatments, which will reduce therapy resistance, relapse and the toxicity associated with current, non-selective agents.
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                Author and article information

                Contributors
                Journal
                Biomed Res Int
                Biomed Res Int
                BMRI
                BioMed Research International
                Hindawi
                2314-6133
                2314-6141
                2017
                27 December 2017
                : 2017
                : 4384823
                Affiliations
                1School of Surgery, Institute of Medicine, Suranaree University of Technology, Nakhon Ratchasima 30000, Thailand
                2Suranaree University of Technology Hospital, Nakhon Ratchasima 30000, Thailand
                3School of Family Medicine, Institute of Medicine, Suranaree University of Technology, Nakhon Ratchasima 30000, Thailand
                4Department of Surgery, Surin Hospital, Surin 32000, Thailand
                5Buriram Hospital, Buriram 31000, Thailand
                6School of Oncology, Institute of Medicine, Suranaree University of Technology, Nakhon Ratchasima 30000, Thailand
                7School of Pathology, Institute of Medicine, Suranaree University of Technology, Nakhon Ratchasima 30000, Thailand
                8School of Preclinic, Institute of Science, Suranaree University of Technology, Nakhon Ratchasima 30000, Thailand
                9Faculty of Public Health, Vongchavalitkul University, Nakhon Ratchasima 30000, Thailand
                Author notes

                Academic Editor: Gail B. Mahady

                Author information
                http://orcid.org/0000-0002-1976-9878
                http://orcid.org/0000-0003-2758-9276
                Article
                10.1155/2017/4384823
                5763069
                29445738
                ae28bf56-587a-4242-a4b4-fce8f356c2db
                Copyright © 2017 Taweesak Tongtawee et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 23 August 2017
                : 5 December 2017
                Categories
                Research Article

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