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Results for “Cancer stem cells”

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PubMed2005

Cancer stem cells.

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Acute Disease↗
PubMed2006

[Correlation research between cancer stem cells and the pathological grades of neuroepithelial tumors].

OBJECTIVE: To explore the methods of isolation, culture and identification of brain tumor stem cells (BTSCs) in neuroepithelial tumor tissues in vitro, and to study the correlation between BTSCs and the patholorical grades of neuroepithelial tumors. METHODS: Tumor cells from patients undergoing neuroepithelial tumors excision were acutely dissociated, triturated into single cells, and then seeded into serum-free medium. After the primary brain tumor spheres (BTSs) were generated, they were triturated again and passaged in fresh medium. The expression of Nestin and CD133 of BTSs was detected by immunocytochemistry staining, and the expression of CD133 of tumor specimen sections was detected by immunohistochemistry staining . The expression of CD133 of 46 brain tumors and 5 normal brain tissues were analysed by SABC immunohistochemical staining, and the correlation between the expression and pathological grade of the tumors was analysed. RESULTS: BTSCs from neuroepithelial tumors could be isolated and cultured, and could be generated and passaged in vitro. The expression of Nestin and CD133 could be detected in BTSCs. CD133 could be detected in neuroepithelial tumor tissues, but not in normal brain tissues. There was significant difference between the expression of CD133 and the different grades of tumors (P < 0.01), and there was a positive correlation between the expression of CD133 and the histologic grading of tumors (P < 0.01). CONCLUSION: A small proportion of stem cells have the ability to self-renew in human neuroepithelial tumors, and there is a positive correlation between the expression of CD133 and histologic grading of tumors.

AC133 Antigen↗
PubMed2006

Brain cancer stem-like cells.

Both stem cells and cancer cells are thought to be capable of unlimited proliferation. Moreover, many tumours and cancer cell lines express stem cell markers, including adenosine triphosphate (ATP)-binding cassette transporters, by which the cells pump out specific fluorescent dyes as well as anti-cancer drugs, suggesting either that cancer cells resemble stem cells or that cancers contain stem-like cells. Using the common characteristics of brain tumour cells and neural stem cells, several research groups have succeeded in identifying stem-like cells (cancer stem-like cells) in brain tumours and brain cancer cell lines. The purified cancer stem-like cells, but not the other cancer cells, self-renew and form tumours when transplanted in vivo. Thus, cancer stem-like cells in brain tumours might be a crucial target for anti-brain tumour therapy.

Brain Neoplasms↗
PubMed2005

Spontaneous human adult stem cell transformation.

Human adult stem cells are being evaluated widely for various therapeutic approaches. Several recent clinical trials have reported their safety, showing them to be highly resistant to transformation. The clear similarities between stem cell and cancer stem cell genetic programs are nonetheless the basis of a recent proposal that some cancer stem cells could derive from human adult stem cells. Here we show that although they can be managed safely during the standard ex vivo expansion period (6-8 weeks), human mesenchymal stem cells can undergo spontaneous transformation following long-term in vitro culture (4-5 months). This is the first report of spontaneous transformation of human adult stem cells, supporting the hypothesis of cancer stem cell origin. Our findings indicate the importance of biosafety studies of mesenchymal stem cell biology to efficiently exploit their full clinical therapeutic potential.

Adipose Tissue↗
PubMed2006

Invasive growth: a MET-driven genetic programme for cancer and stem cells.

Metastasis follows the inappropriate activation of a genetic programme termed invasive growth, which is a physiological process that occurs during embryonic development and post-natal organ regeneration. Burgeoning evidence indicates that invasive growth is also executed by stem and progenitor cells, and is usurped by cancer stem cells. The MET proto-oncogene, which is expressed in both stem and cancer cells, is a key regulator of invasive growth. Recent findings indicate that the MET tyrosine-kinase receptor is a sensor of adverse microenvironmental conditions (such as hypoxia) and drives cell invasion and metastasis through the transcriptional activation of a set of genes that control blood coagulation.

Cell Hypoxia↗
PubMed2006

Stem cells and cancer: two faces of eve.

Recent evidence suggests that a subset of cancer cells within some tumors, the so-called cancer stem cells, may drive the growth and metastasis of these tumors. Understanding the pathways that regulate proliferation, self-renewal, survival, and differentiation of malignant and normal stem cells may shed light on mechanisms that lead to cancer and suggest better modes of treatment.

Cell Differentiation↗
PubMed2006

Stem cells and cancer: evidence for bone marrow stem cells in epithelial cancers.

Cancer commonly arises at the sites of chronic inflammation and infection. Although this association has long been recognized, the reason has remained unclear. Within the gastrointestinal tract, there are many examples of inflammatory conditions associated with cancer, and these include reflux disease and Barrettos adenocarcinoma of the esophagus, Helicobacter infection and gastric cancer, inflammatory bowel disease and colorectal cancer and viral hepatitis leading to hepatocellular carcinoma. There are several mechanisms by which chronic inflammation has been postulated to lead to cancer which includes enhanced proliferation in an endless attempt to heal damage, the presence of a persistent inflammatory environment creating a pro-carcinogenic environment and more recently a role for engraftment of circulating marrow-derived stem cells which may contribute to the stromal components of the tumor as well as the tumor mass itself. Here we review the recent advances in our understanding of the contributions of circulating bone marrow-derived stem cells to the formation of tumors in animal models as well as in human beings.

Animals↗
PubMed2006

Stem cells and brain cancer.

An increasing body of research is showing that cancers might contain their own stem cells. In fact, cancer cells, like stem cells, can proliferate indefinitely through a deregulated cellular self-renewal capacity. This raises the possibility that some features of tumor cells may be due to cancer stem cells. Stem cell-like cancer cells were isolated from several solid tumors. Now, evidence has shown that brain cancers, such as glioblastomas, medulloblastomas and astrocytomas, also contain cells that may be multipotent neural stem cell-like cells. In this review, we discuss the results of these studies, along with the molecular pathways that could be involved in cancer stem cell physiopathology.

Animals↗
PubMed2006

Roots and stems: stem cells in cancer.

Cancer develops from normal tissues through the accumulation of genetic alterations that act in concert to confer malignant phenotypes. Although we have now identified some of the genes that when mutated initiate tumor formation and drive cancer progression, the identity of the cell population(s) susceptible to such transforming events remains undefined for the majority of human cancers. Recent work indicates that a small population of cells endowed with unique self-renewal properties and tumorigenic potential is present in some, and perhaps all, tumors. Although our understanding of the biology of these putative cancer stem cells remains rudimentary, the existence of such cells has implications for current conceptualizations of malignant transformation and therapeutic approaches to cancer.

Cell Transformation, Neoplastic↗
PubMed2006

Concise review: cancer/testis antigens, stem cells, and cancer.

In the multistep process of cancer development, the concept that cancer stem cells are derived from normal stem cells that have gradually accumulated various genetic and epigenetic defects is gaining strong evidence. A number of investigations have identified molecular markers that, under normal conditions, are responsible for stem cell homeostasis but are also expressed in tumor "stem cell-like" subpopulations. In this regard, it was recently reported that a group of tumor-specific antigens known as cancer/testis antigens (CTAs) are expressed in human MSCs. It has long been stated that in normal tissue these antigens are exclusively expressed in germ cell precursors; however, based on these results, we suggest that CTAs are expressed at earlier stages during embryogenesis. The tumor-restricted expression of CTAs has led to several immunotherapeutic trials targeting some of these proteins. The clinical implications that these trials may have on the normal stem cell pools, as well as the immunologic properties of these cells, is to date poorly studied and should be considered.

Antigens, Neoplasm↗
PubMed1991

Coexpression of the stem cell factor and the c-kit genes in small-cell lung cancer.

Stem cell factor (SCF) is a pluripotent growth factor which is suggested to play an important role in proliferation and differentiation in various types of fetal and adult tissues as the ligand of the c-kit proto-oncogene product. However, very little is known about expression of the SCF gene in human malignancies. We analysed DNA and RNA extracted from 28 cell lines and 16 fresh tumor specimens of lung cancer as well as 24 cancer cell lines of various origin for SCF expression. Now we report that the SCF gene is expressed in a wide variety of human cancers including lung cancer, in marked contrast to c-kit, which is expressed in very few types of cancers. As a consequence, coexpression of both the ligand and the receptor is seen only in small-cell lung cancer, suggesting possible involvement of autocrine stimulation via this ligand-receptor system in the pathogenesis of this aggressive cancer. In addition, this study revealed that the human SCF gene is transcribed into two major forms of alternatively spliced mRNAs with different molar ratio in fetal, adult and malignant tissues.

Base Sequence↗
PubMed2007

The commonality of plasticity underlying multipotent tumor cells and embryonic stem cells.

Aggressive cancer cells and pluripotent stem cells converge in their capacity for self-renewal, proliferation and plasticity. Recent studies have capitalized on these similarities by demonstrating that tumors arise from specific cancer stem cell populations that, in a manner reminiscent of normal stem cells, are able to both self-renew and give rise to a heterogeneous tumor population. This stem cell like function of aggressive cancer cells is likely attributable to the ectopic expression of embryonic factors such as Nodal and Cancer Testis Specific Antigens (CTAs), which maintain a functional plasticity by promoting pluripotency and immortality. During development, the expression of these embryonic factors is tightly regulated by a dynamic array of mediators, including the spatial and temporal expression of inhibitors such as Lefty, and the epigenetic modulation of the genome. In aggressive cancer cells, particularly melanoma, this balance of regulatory mediators is disrupted, leading to the aberrant expression of pluripotency-associated genes. By exposing aggressive cancer cells to embryonic microenvironments, this balance of regulatory mediators is restored, thereby reprogramming tumor cells to a more benign phenotype. These stem cell-derived mediators, as well as the genes they regulate, provide therapeutic targets designed to specifically differentiate and eradicate aggressive cancers.

Cell Lineage↗