Heymann D. San Diego: Elsevier Google Scholar. Advances in sarcoma genomics and new therapeutic targets.
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Nat Rev Cancer 11 — Targeted therapeutics in treatment of children and young adults with solid tumors: an expert survey and review of the literature. Klin Padiatr — Targeting developmental pathways in children with cancer: what price success? Lancet Oncol 14 :e70—8. Bone sarcomas in pediatrics: progress in our understanding of tumor biology and implications for therapy. Paediatr Drugs 17 — Development of curative therapies for Ewing sarcomas by interdisciplinary cooperative groups in Europe. Rhabdomyosarcoma: current challenges and their implications for developing therapies.
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Cancer Res 64 — Functional and molecular characterization of interleukin-2 transgenic Ewing tumor cells for in vivo immunotherapy. Pediatr Blood Cancer 43 — Keywords: osteosarcoma, Ewing sarcoma, rhabdomyosarcoma, epithelioid sarcoma, targeted therapy, immunotherapy, cell death, preclinical models. The use, distribution or reproduction in other forums is permitted, provided the original author s or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice.
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In the present study, we chose 20 markers reported to be closely associated with normal stem cells such as mesenchymal stem cell and CSCs to identify markers that were enriched in the potential stem-like fraction of GCTB. We hope our findings may provide new insight into the complex mechanisms of GCTBs progression and future clinical applications. In addition, 20 candidate cell surface markers in GCTB28 sphere cells and parental cells were expressed and of these, only ALCAM was significantly different between parental cells and spheres Fig.
A multinucleated giant cell was indicated by red arrow in the left panel. Spheres of GCTB28 had anchorage dependent growth right panel. Error bars represent s. Independent experiments were repeated three times. These data appear in Fig. Surviving cells adhered at the bottom of the culture dish right panel.
There was no difference in migration capacity of either subset Figs. Ten high-power fields were selected for comparison. White arrow indicates severe tibia destruction. Morphology of mice xenograft tissues showed similar pathological features of human GCTB. Green arrow showed multinucleated giant cells. To assess the tumorigenicity of GCTB cells after knockingdown the ALCAM gene, different numbers of GCTB28 cells were injected into the tibial marrow cavity of mice and underwent imaging observation after the first, second, and third month of inoculation.
Ten high power fields were selected for comparison. See also Table S4. White arrow indicates tibia destruction. Patients with tumors with high ALCAM expression had greater risk of tumor recurrence one year after surgery. A number of studies have demonstrated the presence of cancer stem cells in malignant tumors 19 , 20 , 21 , 22 , 23 , 24 , which states that a subpopulation of tumor-initiating cells TICs is more tumorigenic than the rest of the tumor cell population and share many characteristics with tissue stem cells, such as self-renewal and differentiation, and may be highly resistant to therapeutics.
Eradication of CSCs might represent a promising strategy to explore effective therapies of cancer. Accordingly, little is known about what the role of CSCs is in the tumorigenesis and development of benign tumors, and how CSCs in benign tumor are different from their counterparts in malignant tumor.
It is of note that mice xenograft tumor tissues that generated from stromal cells showed the typical polymorphic morphology of human GCTB. We supposed that most of multinucleated giant cells disappeared in vitro culture for the lack of regulation of the in vivo environment factors which promoted multinucleated giant cells apoptosis or dividing into mononuclear stromal cells. However, when mononuclear stromal cells were injected into immunodeficient mice, stromal cells transformed into or multiple stromal cells fused into multinucleated giant cells.
These findings indicated that stromal cells were the predominant force in the onset and development of GCTB. As we know, most benign tumors lack the ability to invade or metastasize as their malignant counterparts. Although GCTB is named for the osteoclastlike giant cells, which have been considered the main culprits in bone destruction, the spindle-like stromal cells are believed the neoplastic element of GCTB 1 , Previous study suggests GCTB stromal cells originate from mesenchymal stem cells MSCs in the bone marrow and exhibit early osteoblastic differentiation 1 , 25 , 26 , 27 , Our data provided the evidence that cancer stem-like cells population were present within the stromal fraction of GCTB.
These results indicate that tumorigenicity of GCTB cells required a strict microenvironment and was highly selective in environmental factors. We hypothesized that GCTB with a high relapse rate and low rate of metastasis might be due to GCTB was more suitable to grow in the bone microenvironment. It is necessary to search for factors related to tumor progression that may predict the clinical outcome of GCTB patients. Jaffe et al. However, the histological staging system of Jaffe and its prognostic value of this grading were controversial.
Previous reports showed that there were no correlation between prognosis and the histological grading of GCTB. Enneking and Campanacci et al. As our findings in the present study, some previous reports showed that there was no correlation between the risk of recurrence and the radiographic grading of GCTB, and the prognostic significance of the clinicoradiological staging systems described Enneking and Campanacci et al. One important aim of this study was to find factors that may be involved in the progression of the GCTBs and to identify potential targets for future diagnosis and therapy.
In addition, it is of special clinical interest that the risk index calculated from expression of ALCAM may be useful in future clinical practice. Cells were treated with a trypsin-EDTA solution.
Cells were washed twice with PBS. Isotype controls were included in all flow cytometry analyses. Flowjo v7. Beta-actin mRNA was used as an internal control. Cell culture medium was changed according to the conventional procedure. Experimental cells were in the logarithmic growth phase. Louis, MO. An EDTA digestion solution 2. Ten microliters of CCK-8 solution were added to each well. Colonies were fixed with methanol and stained with 0. The number of colonies was counted using an inverted microscope. Cells that moved to the bottom surface of the chamber were stained with 0.
Skyscan in vivo X-ray microtomograph Skyscan Inc. During 2—12 weeks, these mice were anesthetized for fluorescence detection using in vivo imaging system. After these mice were sacrificed, the lungs were rapidly removed, fixed, paraffin-embedded, and sectioned for histopathological examination. Negative controls, in which the primaryantibody was omitted, were also included in each run. In the present study, sampling and data collection of the clinical cases were from our institutes. Among the samples, 28 cases of clinical tumors and corresponding tumor-adjacent normal tissue were used to study the expression of ALCAM.
Survival analysis of the patients was conducted using Kaplan—Meier method and log rank test. Wulling, M. The nature of giant cell tumor of bone. Cancer Res. Schajowicz, F.
ALCAM + stromal cells: role in giant cell tumor of bone progression | Cell Death & Disease
A commentary on the second edition. Cancer 75 , — Rock, M. Secondary malignant giant-cell tumor of bone. Clinicopathological assessment of nineteen patients. Bone Jt. Feigenberg, S.
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Radiation therapy for giant cell tumors of bone. Ruka, W. The megavoltage radiation therapy in treatment of patients with advanced or difficult giant cell tumors of bone. Enneking, W. A system of staging musculoskeletal neoplasms. Campanacci, M. Giant-cell tumor of bone. Errani, C. Giant cell tumor of the extremity: A review of cases from a single institution.
Cancer Treat. Klenke, F. Giant cell tumor of bone: risk factors for recurrence. Balke, M.