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1. Cleton-Jansen AM, van Beerendonk HM, Baelde HJ, Bovée JV, Karperien M, Hogendoorn PC: Estrogen signaling is active in cartilaginous tumors: implications for antiestrogen therapy as treatment option of metastasized or irresectable chondrosarcoma. Clin Cancer Res; 2005 Nov 15;11(22):8028-35
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  • [Title] Estrogen signaling is active in cartilaginous tumors: implications for antiestrogen therapy as treatment option of metastasized or irresectable chondrosarcoma.
  • PURPOSE: Chondrosarcoma is a malignant cartilaginous matrix-producing tumor that can be lethal in 10% to 50% of the patients.
  • Surgery is the only effective treatment known as these tumors are notorious refractory to all types of conventional chemotherapy or radiotherapy.
  • To identify a target for therapy, we want to determine whether estrogen signaling is active in chondrosarcoma because estrogen is important in the regulation of longitudinal growth that is initiated by chondrocyte proliferation and differentiation in the epiphyseal growth plate of long bones.
  • EXPERIMENTAL DESIGN: We studied protein expression of the estrogen receptor in 35 cartilaginous tumors as well as mRNA levels for the estrogen receptor and for aromatase, an enzyme for estrogen synthesis and another potential therapeutic target.
  • Dose-response experiments with chondrosarcoma cultured cells were done with estrogen, androstenedione, and exemestane.
  • The aromatase activity assay showed a functional aromatase enzyme in primary chondrosarcoma cultures and in a cell line.
  • Growth of chondrosarcoma cell cultures can be stimulated by adding estrogen or androstenedione, which can be inhibited by exemestane.
  • This observation implicates potential use of targeted drugs that interfere with estrogen signaling, such as those applied for treating breast cancer.
  • [MeSH-major] Bone Neoplasms / drug therapy. Chondrosarcoma / drug therapy. Estrogen Antagonists / therapeutic use. Estrogens / physiology. Signal Transduction
  • [MeSH-minor] Adult. Aged. Androstadienes / pharmacology. Androstenedione / pharmacology. Aromatase / genetics. Aromatase / metabolism. Aromatase Inhibitors / pharmacology. Cell Line, Tumor. Cell Proliferation / drug effects. Dose-Response Relationship, Drug. Female. Gene Expression Regulation, Neoplastic / drug effects. Humans. Male. Middle Aged. Neoplasm Metastasis. RNA, Messenger / genetics. RNA, Messenger / metabolism. Receptors, Estrogen / genetics. Receptors, Estrogen / metabolism

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  • (PMID = 16299232.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androstadienes; 0 / Aromatase Inhibitors; 0 / Estrogen Antagonists; 0 / Estrogens; 0 / RNA, Messenger; 0 / Receptors, Estrogen; 107868-30-4 / exemestane; 409J2J96VR / Androstenedione; EC 1.14.14.1 / Aromatase
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2. Sun X, Wei L, Chen Q, Terek RM: CXCR4/SDF1 mediate hypoxia induced chondrosarcoma cell invasion through ERK signaling and increased MMP1 expression. Mol Cancer; 2010 Jan 26;9:17
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  • [Title] CXCR4/SDF1 mediate hypoxia induced chondrosarcoma cell invasion through ERK signaling and increased MMP1 expression.
  • BACKGROUND: Chondrosarcoma is a disease that does not respond to conventional cytotoxic chemotherapy and expression of MMP1 is a marker for a poor prognosis.
  • The mechanism of increased MMP1 expression in chondrosarcoma is not completely known.
  • Our goal is to identify molecular pathways that could serve as therapeutic targets.
  • Chondrosarcoma become hypoxic as they grow, are capable of eliciting an angiogenic response, and typically metastasize to the lungs.
  • The present study determined the effect of hypoxia and specifically HIF-1a on expression of CXCR4 and MMP1 and their role in chondrosarcoma cell invasion.
  • RESULTS: CXCR4 and its ligand, SDF1, are upregulated in primary chondrosarcoma tumors compared to normal articular cartilage, and CXCR4 was upregulated in chondrosarcoma cell line JJ compared to normal chondrocytes.
  • Hypoxia and specifically HIF-1a increased CXCR4 and MMP1 expression in JJ cell line and chondrosarcoma invasion in vitro.
  • The hypoxia mediated increase in MMP1 expression and chondrosarcoma invasion could be inhibited by siRNA directed at HIF-1a or CXCR4, the CXCR4 inhibitor AMD3100, as well as with ERK inhibitor U0126 and ERK siRNA.
  • CONCLUSIONS: Chondrosarcoma cell invasion is increased by hypoxia induced expression of CXCR4 and MMP1 and is mediated by HIF-1a and ERK.
  • Both invasion and MMP1 can be inhibited with CXCR4 blockade, suggesting that CXCR4/SDF1 signaling may be a therapeutic target for chondrosarcoma.

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  • (PMID = 20102637.001).
  • [ISSN] 1476-4598
  • [Journal-full-title] Molecular cancer
  • [ISO-abbreviation] Mol. Cancer
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / P20 GM104937; United States / NCRR NIH HHS / RR / 1P20RR024484-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Chemokine CXCL12; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Protein Kinase Inhibitors; 0 / RNA, Messenger; 0 / Receptors, CXCR4; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 3.4.24.7 / MMP1 protein, human; EC 3.4.24.7 / Matrix Metalloproteinase 1
  • [Other-IDs] NLM/ PMC2825244
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3. Rozeman LB, Cleton-Jansen AM, Hogendoorn PC: Pathology of primary malignant bone and cartilage tumours. Int Orthop; 2006 Dec;30(6):437-44
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  • [Title] Pathology of primary malignant bone and cartilage tumours.
  • Bone- and cartilage-forming tumours (osteosarcomas and chondrosarcomas) are rare malignant neoplasms.
  • These tumours are clinically aggressive and often need extensive local and/or systemic treatment.
  • Whereas no other treatment but surgery is currently available for chondrosarcomas, osteosarcomas show an approximately 50-80% response rate to adjuvant chemotherapy.
  • In addition, the tumours have a risk of local recurrences adversely affecting the prognosis compared to the primary tumour.
  • In this report we will mainly focus on two of the most prevalent malignant bone tumours, conventional osteosarcoma and conventional chondrosarcoma, and use these to illustrate the problems with the diagnosis of bone sarcomas in general.
  • [MeSH-major] Bone Neoplasms / pathology. Chondrosarcoma / pathology. Osteosarcoma / pathology

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  • (PMID = 16944143.001).
  • [ISSN] 0341-2695
  • [Journal-full-title] International orthopaedics
  • [ISO-abbreviation] Int Orthop
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Number-of-references] 35
  • [Other-IDs] NLM/ PMC3172744
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4. Bovée JV, Cleton-Jansen AM, Taminiau AH, Hogendoorn PC: Emerging pathways in the development of chondrosarcoma of bone and implications for targeted treatment. Lancet Oncol; 2005 Aug;6(8):599-607
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  • [Title] Emerging pathways in the development of chondrosarcoma of bone and implications for targeted treatment.
  • Chondrosarcoma is a malignant cartilage-forming tumour of bone, of which distinct clinicopathological subtypes are known.
  • Conventional chondrosarcoma is notorious for its locally aggressive behaviour as well as for its resistance to chemotherapy and radiotherapy; so far surgery is the only effective therapeutic option.
  • During the past 10 years, substantial new insights have been gained about molecular cell biology, molecular cytogenetics, and immunopathology, leading to better understanding of chondrosarcoma development at the molecular level, which will ultimately lead to better clinical understanding and possibly to the development of targeted treatment.
  • [MeSH-major] Bone Neoplasms / physiopathology. Chondrosarcoma / physiopathology

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  • (PMID = 16054571.001).
  • [ISSN] 1470-2045
  • [Journal-full-title] The Lancet. Oncology
  • [ISO-abbreviation] Lancet Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 84
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5. Gelderblom H, Hogendoorn PC, Dijkstra SD, van Rijswijk CS, Krol AD, Taminiau AH, Bovée JV: The clinical approach towards chondrosarcoma. Oncologist; 2008 Mar;13(3):320-9
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  • [Title] The clinical approach towards chondrosarcoma.
  • This review provides an overview of the histopathology, classification, diagnostic procedures, and therapy of skeletal chondrosarcoma.
  • Chondrosarcomas that arise de novo are primary chondrosarcomas, whereas chondrosarcomas developing superimposed on pre-existing benign cartilage neoplasms such as enchondromas or osteochondromas are referred to as secondary chondrosarcomas.
  • Conventional chondrosarcomas can be categorized according to their location in bone into central, peripheral, and juxtacortical chondrosarcomas.
  • Rare subtypes of chondrosarcoma, including dedifferentiated, mesenchymal, and clear cell chondrosarcoma, are discussed as well.
  • Magnetic resonance imaging is necessary to delineate the extent of the intraosseous and soft tissue involvement preoperatively.
  • Computed tomography is especially recommended in the pelvis and other flat bones where it may be difficult to discern the pattern of bone destruction and the presence of matrix mineralization.
  • Wide, en-bloc excision is the preferred surgical treatment in intermediate- and high-grade chondrosarcoma.
  • In low-grade chondrosarcoma confined to the bone, extensive intralesional curettage followed by local adjuvant treatment and filling the cavity with bone graft has promising long-term clinical results and satisfactory local control.
  • Chondrosarcomas are relatively radiotherapy resistant; therefore, doses >60 Gy are needed in attempts to achieve local control after incomplete resection.
  • Chemotherapy is only possibly effective in mesenchymal chondrosarcoma, and is of uncertain value in dedifferentiated chondrosarcoma.
  • Potential new systemic treatment targets are being discussed.
  • [MeSH-major] Bone Neoplasms / therapy. Chondrosarcoma, Mesenchymal / therapy
  • [MeSH-minor] Humans. Mesoderm / pathology. Prognosis. Treatment Outcome

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  • [ErratumIn] Oncologist. 2008 May;13(5):618
  • (PMID = 18378543.001).
  • [ISSN] 1083-7159
  • [Journal-full-title] The oncologist
  • [ISO-abbreviation] Oncologist
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 91
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6. Lagonigro MS, Tamborini E, Negri T, Staurengo S, Dagrada GP, Miselli F, Gabanti E, Greco A, Casali PG, Carbone A, Pierotti MA, Pilotti S: PDGFRalpha, PDGFRbeta and KIT expression/activation in conventional chondrosarcoma. J Pathol; 2006 Apr;208(5):615-23
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  • [Title] PDGFRalpha, PDGFRbeta and KIT expression/activation in conventional chondrosarcoma.
  • Chondrosarcomas represent 20% of all primary bone sarcomas, and many studies have attempted to unravel molecular targets for future development of new therapies.
  • The aim of this study was to investigate the expression/activation of PDGFRalpha, PDGFRbeta and KIT receptor tyrosine kinases (RTKs) as potential therapeutic targets in conventional central primary chondrosarcomas (CCS).
  • PDGFRbeta was expressed but not activated in control healthy joint cartilage, in line with no PDGFB detection.
  • The CCS gene profile described here offers a rationale for the use of RTK inhibitors alone or in combination with chemotherapy, and supports further investigation of RTKs and their downstream signals.
  • [MeSH-major] Bone Neoplasms / metabolism. Chondrosarcoma / metabolism. Neoplasm Proteins / metabolism

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  • (PMID = 16470538.001).
  • [ISSN] 0022-3417
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Ligands; 0 / Neoplasm Proteins; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor beta
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7. Susa M, Morii T, Yabe H, Horiuchi K, Toyama Y, Weissbach L, Hornicek FJ, Morioka H: Alendronate inhibits growth of high-grade chondrosarcoma cells. Anticancer Res; 2009 Jun;29(6):1879-88
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  • [Title] Alendronate inhibits growth of high-grade chondrosarcoma cells.
  • BACKGROUND: Conventional chemotherapy is ineffective for high-grade chondrosarcomas, highlighting the need for improved chemotherapies.
  • Chondrosarcoma is still therefore considered a surgical disease despite its aggressive features of recurring locally and spreading to the lungs.
  • Bisphosphonates inhibit growth of various cell types, including cancer cells and perhaps chondrosarcoma.
  • MATERIALS AND METHODS: The effect of different concentrations of alendronate on cell proliferation, migration, apoptosis and cytoskeleton reorganization as well as on the regulation of intracellular protein expression were analyzed for the high-grade chondrosarcoma cell line CS-1.
  • These findings may lead to new treatment options for high-grade chondrosarcoma.
  • [MeSH-major] Alendronate / therapeutic use. Bone Density Conservation Agents / therapeutic use. Bone Neoplasms / drug therapy. Cell Proliferation / drug effects. Chondrosarcoma / drug therapy
  • [MeSH-minor] Blotting, Western. Cell Adhesion / drug effects. Cell Movement / drug effects. Fluorescent Antibody Technique. Humans. Male. Middle Aged. Proteome / analysis. Tumor Cells, Cultured


8. Chen C, Zhou H, Xu L, Xu D, Wang Y, Zhang Y, Liu X, Liu Z, Ma D, Ma Q, Chen Y: Recombinant human PDCD5 sensitizes chondrosarcomas to cisplatin chemotherapy in vitro and in vivo. Apoptosis; 2010 Jul;15(7):805-13
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  • [Title] Recombinant human PDCD5 sensitizes chondrosarcomas to cisplatin chemotherapy in vitro and in vivo.
  • Clinical management of chondrosarcoma remains a challenging problem, largely due to the toxicity and resistance of this tumor to conventional chemotherapy.
  • Programmed Cell Death 5 (PDCD5) is a protein that accelerates apoptosis in different cell types in response to various stimuli, and has been shown to be down-regulated in many cancer tissues.
  • In this study, mRNA and protein levels of PDCD5 were found to be up-regulated in cisplatin-treated SW1353 chondrosarcoma cells compared with untreated cells.
  • Recombinant human PDCD5 (rhPDCD5) was also shown to sensitize chondrosarcoma cells to cisplatin-based chemotherapy, with inhibition of cell growth and apoptosis detected both in vitro and in vivo.
  • Additionally, cleavage of caspase-9 and caspase-3, as well as the cleavage of poly (ADP-ribose) polymerase (PARP), were detected, suggesting that sensitization of chondrosarcoma cells involves the intrinsic mitochondrial apoptosis pathway.
  • In vivo, the treatment of a xenograft model of chondrosarcoma with rhPDCD5 and cisplatin significantly inhibited tumor cell proliferation and induced apoptosis compared to treatment with cisplatin alone.
  • Overall, these data provide a theoretical basis for the administration of rhPDCD5 and cisplatin for the treatment of patients with chondrosarcoma.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Apoptosis. Apoptosis Regulatory Proteins / therapeutic use. Bone Neoplasms / drug therapy. Chondrosarcoma / drug therapy. Cisplatin / therapeutic use. Neoplasm Proteins / therapeutic use
  • [MeSH-minor] Animals. Cell Line, Tumor. Cytochromes c / metabolism. Female. Humans. Mice. Mice, Inbred BALB C. Mice, Nude. Recombinant Proteins / pharmacology. Recombinant Proteins / therapeutic use. Xenograft Model Antitumor Assays. bcl-2-Associated X Protein / metabolism

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  • (PMID = 20349137.001).
  • [ISSN] 1573-675X
  • [Journal-full-title] Apoptosis : an international journal on programmed cell death
  • [ISO-abbreviation] Apoptosis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Neoplasm Proteins; 0 / PDCD5 protein, human; 0 / Recombinant Proteins; 0 / bcl-2-Associated X Protein; 9007-43-6 / Cytochromes c; Q20Q21Q62J / Cisplatin
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9. Kollert M, Basten O, Delling G, Bockmühl U: [Clear cell chondrosarcoma of the larynx. A rare tumor in an uncommon location]. HNO; 2005 Apr;53(4):357-60
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  • [Title] [Clear cell chondrosarcoma of the larynx. A rare tumor in an uncommon location].
  • [Transliterated title] Klarzellchondrosarkom des Larynx. Ein sehr seltener Tumor in einer aussergewöhnlichen Lokalisation.
  • Clear cell chondrosarcoma is a rare bone tumor of low malignancy.
  • So far, there have only been three cases of clear cell chondrosarcoma of the larynx published in the literature.
  • Extended biopsies were taken and histology revealed a clear cell chondrosarcoma.
  • The therapy of choice for this tumor is wide surgical resection.
  • Additional radio- and/or chemotherapy are not recommended.
  • Histologically, the clear cell chondrosarcoma can be easily confused with the highly malignant osteosarcoma or the conventional chondrosarcoma, both requiring more aggressive treatment.
  • Thus, clear cell chondrosarcoma should be kept in mind and, when necessary, a reference histology by a bone tumor register should be requested.
  • [MeSH-major] Chondrosarcoma / diagnosis. Chondrosarcoma / surgery. Dyspnea / diagnosis. Laryngeal Neoplasms / diagnosis. Laryngeal Neoplasms / surgery. Laryngostenosis / diagnosis. Sarcoma, Clear Cell / diagnosis. Sarcoma, Clear Cell / surgery

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  • (PMID = 15316626.001).
  • [ISSN] 0017-6192
  • [Journal-full-title] HNO
  • [ISO-abbreviation] HNO
  • [Language] ger
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Germany
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10. Gadwal SR, Fanburg-Smith JC, Gannon FH, Thompson LD: Primary chondrosarcoma of the head and neck in pediatric patients: a clinicopathologic study of 14 cases with a review of the literature. Cancer; 2000 May 1;88(9):2181-8
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  • [Title] Primary chondrosarcoma of the head and neck in pediatric patients: a clinicopathologic study of 14 cases with a review of the literature.
  • BACKGROUND: Primary chondrosarcoma of the head and neck in the pediatric age group is rare.
  • METHODS: Fourteen cases of chondrosarcoma of the head and neck from patients age 18 years or younger, diagnosed between 1970 and 1997, were retrieved from the Otorhinolaryngic-Head & Neck Tumor Registry of the Armed Forces Institute of Pathology.
  • All tumors were invasive and malignant as determined by radiology and/or histology.
  • All patients were treated by surgery, followed by radiation (n=5) and/or chemotherapy (n=2).
  • CONCLUSIONS: Primary head and neck chondrosarcoma in the pediatric population is typically low grade and occurs in the maxillary sinus or mandible.
  • [MeSH-major] Chondrosarcoma / pathology. Head and Neck Neoplasms / pathology
  • [MeSH-minor] Adolescent. Chemotherapy, Adjuvant. Child. Child, Preschool. Disease-Free Survival. Female. Follow-Up Studies. Headache / diagnosis. Humans. Male. Mandibular Neoplasms / pathology. Maxillary Sinus Neoplasms / pathology. Nasal Obstruction / diagnosis. Neoplasm Invasiveness. Nose Neoplasms / pathology. Prognosis. Radiotherapy, Adjuvant. Retrospective Studies. Rhinitis / diagnosis. Sinusitis / diagnosis

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  • (PMID = 10813732.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] UNITED STATES
  • [Number-of-references] 41
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11. Riedel RF, Larrier N, Dodd L, Kirsch D, Martinez S, Brigman BE: The clinical management of chondrosarcoma. Curr Treat Options Oncol; 2009 Apr;10(1-2):94-106
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  • [Title] The clinical management of chondrosarcoma.
  • Surgical resection represents the primary and preferred treatment modality for individuals with localized disease.
  • Radiation therapy is appropriate for the treatment of positive surgical margins or palliation of disease-related symptoms.
  • The treatment of advanced, metastatic disease is particularly challenging given the recognition that conventional chemotherapy has proven to be largely ineffective.
  • Systemic chemotherapy may be considered in variant forms such as mesenchymal or dedifferentiated chondrosarcomas but high-quality data supporting its use is limited.
  • There is universal agreement, however, that novel treatment strategies are desperately needed.
  • [MeSH-major] Bone Neoplasms / therapy. Chondrosarcoma / therapy
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Chemotherapy, Adjuvant. Clinical Trials as Topic. Disease Management. Humans. Palliative Care. Prognosis. Radiography. Radiotherapy, Adjuvant / methods. Therapies, Investigational. Treatment Outcome

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  • (PMID = 19238552.001).
  • [ISSN] 1534-6277
  • [Journal-full-title] Current treatment options in oncology
  • [ISO-abbreviation] Curr Treat Options Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 39
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12. Lu X, Tang X, Guo W, Ren T, Zhao H: Sorafenib induces growth inhibition and apoptosis of human chondrosarcoma cells by blocking the RAF/ERK/MEK pathway. J Surg Oncol; 2010 Dec 1;102(7):821-6
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  • [Title] Sorafenib induces growth inhibition and apoptosis of human chondrosarcoma cells by blocking the RAF/ERK/MEK pathway.
  • BACKGROUND: Chondrosarcoma represents the second most common primary malignant bone tumor causing significant morbidity due to local recurrence and limited treatment options.
  • Conventional cytotoxic chemotherapy has been proven to be largely ineffective to this sarcoma.
  • Here we report that sorafenib is effective in growth inhibition of chondrosarcoma cell lines in vitro.
  • METHODS: Chondrosarcoma cell lines (SW1353 and CRL7891) were treated with sorafenib.
  • Flow cytometry, DAPI assay, and Western blotting were employed to determine the effects of sorafenib in inhibitory proliferation and induce apoptosis in chondrosarcoma cells in vitro.
  • RESULTS: The results showed that sorafenib effectively inhibited cell growth and induced apoptosis in chondrosarcoma cells, which was concurrent with inhibition of the expression of phospho-MEK and phospho-ERK.
  • CONCLUSIONS: Our findings demonstrate that sorafenib inhibited the Ras/Raf/MAPK pathway in a time- and dose-dependent fashion in chondrosarcoma cell lines SW1353 and CRL7891 and suggest that sorafenib may be a new therapeutic option for patients with chondrosarcoma.
  • [MeSH-major] Apoptosis / drug effects. Benzenesulfonates / pharmacology. Cell Proliferation / drug effects. Chondrosarcoma / drug therapy. Extracellular Signal-Regulated MAP Kinases / antagonists & inhibitors. Mitogen-Activated Protein Kinase Kinases / antagonists & inhibitors. Pyridines / pharmacology. raf Kinases / antagonists & inhibitors
  • [MeSH-minor] Apoptosis Regulatory Proteins / metabolism. Blotting, Western. Bone Neoplasms / drug therapy. Bone Neoplasms / metabolism. Bone Neoplasms / pathology. Cell Line, Tumor. Cyclin D1 / metabolism. Humans. Niacinamide / analogs & derivatives. Phenylurea Compounds. Phosphorylation / drug effects. Protein Kinase Inhibitors / pharmacology. Proto-Oncogene Proteins c-bcl-2 / metabolism. Signal Transduction / drug effects


13. Tang GQ, Yan TQ, Guo W, Ren TT, Peng CL, Zhao H, Lu XC, Zhao FL, Han X: (-)-Epigallocatechin-3-gallate induces apoptosis and suppresses proliferation by inhibiting the human Indian Hedgehog pathway in human chondrosarcoma cells. J Cancer Res Clin Oncol; 2010 Aug;136(8):1179-85
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  • [Title] (-)-Epigallocatechin-3-gallate induces apoptosis and suppresses proliferation by inhibiting the human Indian Hedgehog pathway in human chondrosarcoma cells.
  • PURPOSE: Chondrosarcoma is a soft tissue sarcoma with a poor prognosis that is unresponsive to conventional chemotherapy.
  • The regulatory mechanisms for the rapid proliferation of chondrosarcoma cells and the particular aggressiveness of this sarcoma remain poorly understood.
  • In this study, we investigate the effect of epigallocatechin-3-gallate (EGCG) on growth and apoptosis of chondrosarcoma cells.
  • METHODS: The chondrosarcoma cell lines, SW1353 and CRL-7891, were cultured with and without EGCG.
  • Protein expression levels of caspase-3 were unchanged in response to EGCG treatment in chondrosarcoma cells; however, the expression levels of Bcl-2 were significantly decreased and the levels of Bax were significantly increased.
  • CONCLUSIONS: Our findings demonstrate that EGCG is effective for growth inhibition of a chondrosarcoma cell lines in vitro, and suggest that EGCG may be a new therapeutic option for patients with chondrosarcoma.
  • [MeSH-major] Anticarcinogenic Agents / pharmacology. Apoptosis / drug effects. Bone Neoplasms / drug therapy. Catechin / analogs & derivatives. Cell Division / drug effects. Chondrosarcoma / drug therapy
  • [MeSH-minor] Cell Death / drug effects. Cell Survival / drug effects. DNA Primers. Flow Cytometry. Gene Amplification. Humans. Patched Receptors. Patched-1 Receptor. Receptors, Cell Surface / drug effects. Receptors, Cell Surface / genetics

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  • (PMID = 20127255.001).
  • [ISSN] 1432-1335
  • [Journal-full-title] Journal of cancer research and clinical oncology
  • [ISO-abbreviation] J. Cancer Res. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / DNA Primers; 0 / PTCH protein, human; 0 / Patched Receptors; 0 / Patched-1 Receptor; 0 / Receptors, Cell Surface; 8R1V1STN48 / Catechin; BQM438CTEL / epigallocatechin gallate
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14. Chow WA, Bedell V, Gaytan P, Borden E, Goldblum J, Hicks D, Slovak ML: Methylthioadenosine phosphorylase gene deletions are frequently detected by fluorescence in situ hybridization in conventional chondrosarcomas. Cancer Genet Cytogenet; 2006 Apr 15;166(2):95-100
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  • [Title] Methylthioadenosine phosphorylase gene deletions are frequently detected by fluorescence in situ hybridization in conventional chondrosarcomas.
  • Chondrosarcomas are the second most common primary malignant tumor of bone.
  • Chemotherapy for conventional chondrosarcomas is generally ineffective.
  • MTAP-deficient cells are more susceptible than wild-type cells to pharmacologic inhibitors of de novo purine synthesis.
  • Based on these observations, we investigated the frequency of MTAP deletions in conventional, grade II chondrosarcomas by fluorescence in situ hybridization (FISH) analysis: 23 conventional, grade II chondrosarcoma patient samples from the Cleveland Clinic Foundation were analyzed for MTAP deletions.
  • These findings suggest that approximately one-half of conventional, grade II chondrosarcomas may be preferentially sensitive to pharmacologic inhibitors of de novo purine synthesis.
  • [MeSH-major] Chondrosarcoma / enzymology. Chondrosarcoma / genetics. Gene Deletion. Purine-Nucleoside Phosphorylase / genetics

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  • (PMID = 16631464.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.4.2.1 / Purine-Nucleoside Phosphorylase; EC 2.4.2.28 / 5'-methylthioadenosine phosphorylase
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15. Bovée JV, Hogendoorn PC, Wunder JS, Alman BA: Cartilage tumours and bone development: molecular pathology and possible therapeutic targets. Nat Rev Cancer; 2010 Jul;10(7):481-8
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  • [Title] Cartilage tumours and bone development: molecular pathology and possible therapeutic targets.
  • As a group, cartilage tumours are the most common primary bone lesions.
  • They range from benign lesions, such as enchondromas and osteochondromas, to malignant chondrosarcoma.
  • The benign lesions result from the deregulation of the hedgehog signalling pathway, which is involved in normal bone development.
  • These lesions can be the precursors of malignant chondrosarcomas, which are notoriously resistant to conventional chemotherapy and radiotherapy.
  • Cytogenetic studies and mouse models are beginning to identify genes and signalling pathways that have roles in tumour progression, such as hedgehog, p53, insulin-like growth factor, cyclin-dependent kinase 4, hypoxia-inducible factor, matrix metalloproteinases, SRC and AKT, suggesting potential new therapeutic approaches.
  • [MeSH-major] Bone Development. Bone Neoplasms / genetics. Cartilage / pathology. Chondrosarcoma / genetics. Gene Expression Regulation / drug effects. Osteochondroma / genetics
  • [MeSH-minor] Animals. Antineoplastic Agents / therapeutic use. Humans. Mice. Pathology, Molecular


16. Asavamongkolkul A, Waikakul S, Phimolsarnti R, Kiatisevi P, Wangsaturaka P: Endoprosthetic reconstruction for malignant bone and soft-tissue tumors. J Med Assoc Thai; 2007 Apr;90(4):706-17
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  • [Title] Endoprosthetic reconstruction for malignant bone and soft-tissue tumors.
  • BACKGROUND: Nowadays, the results of the management of malignant bone and soft-tissue tumors have been dramatically improved because of the advance in imaging, chemotherapy, radiation therapy, and surgical techniques.
  • Patients can have longer survival times with limb-salvage surgery.
  • Several techniques of reconstruction have been advocated and gained more popularity following malignant tumor resection by using allograft, tumor prostheses, composite allograft prosthesis, or arthrodesis.
  • OBJECTIVE: To report the preliminary results of 32 endoprosthetic reconstructions following malignant bone and soft-tissue tumor resection.
  • MATERIAL AND METHOD: Since September 1988, the authors have performed 188 limb-salvage surgical operations for the treatment of musculoskeletal tumors at Siriraj Hospital.
  • From March 1994 to July 2006, 32 endoprosthetic reconstructions were performed on 30 patients following malignant bone or soft-tissue tumor removal.
  • The diagnosis was conventional osteosarcoma in 16 patients, parosteal osteosarcoma in two patients, chondrosarcoma in two patients, leiomyosarcoma in two patients, failed allograft in two patients and one patient each of periosteal osteosarcoma, Ewing's sarcoma, Gorham's disease, synovial sarcoma, malignant fibrous histiocytoma, metastatic renal cell carcinoma, and prosthetic loosening.
  • Five proximal femurs, 17 distal femurs, 1 total femur 3 proximal tibias, 1 intercalary tibia, 4 proximal humerus and 1 distal humerus were used for reconstruction.
  • RESULTS: The mean follow-up time was 26 months (range 6-128.7).
  • CONCLUSION: Endoprosthetic reconstruction could yield satisfactory results as a wide excision and limb-salvage for patients with malignant bone and soft-tissue tumors.
  • [MeSH-major] Bone Neoplasms / surgery. Limb Salvage. Osteosarcoma / surgery. Sarcoma, Ewing / surgery. Soft Tissue Neoplasms / surgery

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  • (PMID = 17487125.001).
  • [ISSN] 0125-2208
  • [Journal-full-title] Journal of the Medical Association of Thailand = Chotmaihet thangphaet
  • [ISO-abbreviation] J Med Assoc Thai
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Thailand
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17. Chow WA: Update on chondrosarcomas. Curr Opin Oncol; 2007 Jul;19(4):371-6
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  • PURPOSE OF REVIEW: This paper reviews recent molecular, biologic, developmental therapeutic, and clinical findings in conventional and variant chondrosarcomas.
  • Translational research has validated platelet-derived growth factor receptor, estrogen signaling, matrix metalloproteinase-1, histone deacetylase, methylthioadenosine phosphorylase, and vascular endothelial growth factor-A as potential therapeutic targets.
  • Molecular studies have established that extraskeletal myxoid chondrosarcoma is a unique entity defined by the presence of a fusion gene between the orphan nuclear receptor, CHN/NOR1, and a promiscuous partner, most commonly EWSR1.
  • Clinical studies have shown that development of second malignancies is an uncommon but real risk for chondrosarcoma survivors; the benefit of chemotherapy for dedifferentiated chondrosarcomas remains questionable; and late recurrences of clear cell chondrosarcomas emphasize the need for long-term follow up.
  • SUMMARY: Chondrosarcomas are a heterogeneous group of bone and soft tissue tumors.
  • Recent advances in molecular diagnostics, pathobiology, and developmental therapeutics will aid both scientists and clinicians in improving the classification and therapy of this diverse family of cartilaginous tumors.
  • [MeSH-major] Bone Neoplasms. Chondrosarcoma

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  • (PMID = 17545802.001).
  • [ISSN] 1040-8746
  • [Journal-full-title] Current opinion in oncology
  • [ISO-abbreviation] Curr Opin Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 53
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18. Wunder JS, Nielsen TO, Maki RG, O'Sullivan B, Alman BA: Opportunities for improving the therapeutic ratio for patients with sarcoma. Lancet Oncol; 2007 Jun;8(6):513-24
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  • [Title] Opportunities for improving the therapeutic ratio for patients with sarcoma.
  • Limb-sparing surgery delivered at specialised sarcoma centres as part of a multidisciplinary approach has become the standard treatment for most patients and usually provides excellent local control.
  • Preoperative treatment with chemotherapy is most common for patients with bone sarcomas.
  • The ideal sequence of surgery and radiation for local management of soft-tissue sarcoma remains controversial on the basis of early versus late treatment complications, although preoperative radiation can provide the best results for improved long-term function.
  • However, metastatic disease is common, and conventional chemotherapy provides for only a narrow therapeutic window outside of a few responsive pathological subtypes.
  • Targeting underlying molecular events in specific sarcomas can provide for dramatic benefits, as has been seen with imatinib treatment for gastrointestinal stromal tumours and dermatofibrosarcoma protuberans.
  • Trials of agents targeting the cell cycle and angiogenesis in soft-tissue sarcomas, and of those targeting osteoclasts in bone sarcomas, are currently underway.
  • Biological data and preclinical studies support trials using inhibitors of hedgehog signalling in chondrosarcoma, inhibitors of wnt/beta-catenin in osteosarcoma and aggressive fibromatosis, and inhibitors of histone deacetylases in synovial sarcoma and Ewing sarcoma.
  • Research in stem-cell biology and nanotechnology holds promise for additional novel treatment options in the future.
  • [MeSH-major] Bone Neoplasms / therapy. Sarcoma / therapy
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Clinical Trials as Topic. Combined Modality Therapy. Humans

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  • [CommentIn] Lancet Oncol. 2007 Aug;8(8):667-8; author reply 668-9 [17679078.001]
  • [ErratumIn] Lancet Oncol. 2007 Aug;8(8):670
  • (PMID = 17540303.001).
  • [ISSN] 1470-2045
  • [Journal-full-title] The Lancet. Oncology
  • [ISO-abbreviation] Lancet Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01-CA47179
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 92
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19. Bertoni F, Bacchini P, Staals EL, Davidovitz P: Dedifferentiated parosteal osteosarcoma: the experience of the Rizzoli Institute. Cancer; 2005 Jun 1;103(11):2373-82
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  • BACKGROUND: Dedifferentiated parosteal osteosarcoma (DPOS) is a variant of osteosarcoma in which a high-grade sarcoma coexists with a conventional parosteal osteosarcoma (c-POS), either at presentation (synchronous type) or at the time of recurrence (metachronous type).
  • The authors reviewed the clinical and radiologic features, histologic sections, treatments, and outcomes in this group of patients with DPOS.
  • Twenty-eight patients underwent surgery, and 18 of those patients received chemotherapy (5 patients received neoadjuvant chemotherapy, and 13 patients received adjuvant).
  • Of the nine patients who died, one patient received no treatment, five patients underwent surgery (with three patients achieving adequate margins) in combination with chemotherapy, and three patients underwent surgery only (with adequate margins achieved).
  • Of the 20 patients who remained alive, 13 patients underwent surgery (with 10 patients achieving adequate margins) in combination with chemotherapy, whereas 7 patients underwent surgery only (all with adequate margins).
  • The prognosis for patients with DPOS was better than the prognosis for patients with dedifferentiated central and dedifferentiated peripheral chondrosarcoma.
  • [MeSH-major] Bone Neoplasms / pathology. Cell Differentiation. Osteosarcoma, Juxtacortical / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Antineoplastic Agents / therapeutic use. Combined Modality Therapy. Female. Follow-Up Studies. Humans. Male. Middle Aged. Prognosis. Retrospective Studies. Survival Rate. Tomography, X-Ray Computed. Treatment Outcome

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  • (PMID = 15852358.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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20. O'Donnell RJ: Compressive osseointegration of tibial implants in primary cancer reconstruction. Clin Orthop Relat Res; 2009 Nov;467(11):2807-12
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  • [Title] Compressive osseointegration of tibial implants in primary cancer reconstruction.
  • Compressive osseointegration technology, which provides immediate, mechanically compliant endoprosthetic fixation, has been adapted for massive proximal tibial reconstructions in an attempt to avoid aseptic failure encountered with conventional stems.
  • Diagnoses included osteosarcoma (12), Ewing sarcoma (two), chondrosarcoma (one), and undifferentiated sarcoma (one).
  • Four patients developed metastatic disease; one patient died of his primary tumor, and another died from a chemotherapy-related malignancy.
  • One patient developed aseptic loosening and underwent revision; the other 15 implants provided stable osseointegration at last followup.
  • Compressive osseointegration technology can thus achieve acceptable short-term endoprosthetic fixation results and may reduce the risk of aseptic loosening reported with conventional tibial stems.
  • LEVEL OF EVIDENCE: Level IV, therapeutic study.
  • [MeSH-major] Bone Neoplasms / surgery. Osseointegration. Reconstructive Surgical Procedures / methods. Tibia / surgery
  • [MeSH-minor] Adolescent. Adult. Arthroplasty, Replacement, Knee / adverse effects. Arthroplasty, Replacement, Knee / methods. Chondrosarcoma / mortality. Chondrosarcoma / pathology. Chondrosarcoma / surgery. Female. Follow-Up Studies. Humans. Limb Salvage / methods. Male. Osteosarcoma / mortality. Osteosarcoma / pathology. Osteosarcoma / surgery. Prostheses and Implants. Prosthesis Design. Prosthesis Failure. Prosthesis Implantation / methods. Retrospective Studies. Risk Assessment. Sarcoma, Ewing / mortality. Sarcoma, Ewing / pathology. Sarcoma, Ewing / surgery. Survival Rate. Treatment Outcome. Young Adult

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  • (PMID = 19653050.001).
  • [ISSN] 1528-1132
  • [Journal-full-title] Clinical orthopaedics and related research
  • [ISO-abbreviation] Clin. Orthop. Relat. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2758992
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21. Staals EL, Bacchini P, Mercuri M, Bertoni F: Dedifferentiated chondrosarcomas arising in preexisting osteochondromas. J Bone Joint Surg Am; 2007 May;89(5):987-93
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Dedifferentiated chondrosarcomas that arise in osteochondromas are extremely rare lesions for which very little information on treatment and outcome is available in the literature.
  • The purpose of the present study was to describe the specific clinical, radiographic, and histologic features of this lesion and to evaluate the oncologic outcome after different treatment strategies.
  • Radiographic studies, histologic slides, and clinical records were reviewed, the features of those studies were tabulated, and prognostic features and the results of treatment were identified.
  • Radiographically, ten lesions appeared as a conventional secondary chondrosarcoma arising in an exostosis, whereas eight showed typical signs of dedifferentiation.
  • The dedifferentiated component was considered to be an osteosarcoma in nine cases (including six cases in which it was osteoblastic and three in which it was fibroblastic), a malignant fibrous histiocytoma in eight, and a fibrosarcoma in one.
  • For the fifteen patients who were managed at the authors' institution, the two and five-year survival rates were 47% and 29%, respectively; the median survival time was fourteen months.
  • Patients who were managed with a combination of surgery and chemotherapy had a better overall survival rate than did those who were managed with surgery alone (p = 0.03).
  • CONCLUSIONS: Dedifferentiated chondrosarcoma arising in a preexisting osteochondroma is an extremely rare lesion with a poor prognosis.
  • In the present small series, overall survival was better when wide surgical resection was combined with adjuvant chemotherapy.
  • [MeSH-major] Bone Neoplasms / pathology. Chondrosarcoma / pathology. Osteochondroma / pathology

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  • (PMID = 17473135.001).
  • [ISSN] 0021-9355
  • [Journal-full-title] The Journal of bone and joint surgery. American volume
  • [ISO-abbreviation] J Bone Joint Surg Am
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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22. Gouin F, Ory B, Rédini F, Heymann D: Zoledronic acid slows down rat primary chondrosarcoma development, recurrent tumor progression after intralesional curretage and increases overall survival. Int J Cancer; 2006 Sep 1;119(5):980-4

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Zoledronic acid slows down rat primary chondrosarcoma development, recurrent tumor progression after intralesional curretage and increases overall survival.
  • Chondrosarcoma is a difficult musculoskeletal tumor to treat.
  • Surgical treatment leads to severe disability, with high rates of local recurrence and life threat.
  • No adjuvant therapy is effective in differentiated chondrosarcomas.
  • Bisphosphonates (BPs) are a class of molecules which is effective in malignant bone diseases.
  • The aim of the present study was to determine the effects of zoledronic acid (ZOL) on chondrosarcoma tumor progression.
  • 100 microg/kg, twice a week) in a rat chondrosarcoma model and in vitro (10(-7)-10(-4) M) on cells derived from this model.
  • Two types of animal models were assessed, the first simulated development after intralesional curettage, the second nonoperative development of the tumor.
  • The results revealed that ZOL slows down primary tumor development, tumor progression after intralesional curretage and increases overall survival.
  • The present study demonstrates for the first time that in addition to surgery, the therapy of chondrosarcoma with BPs might be beneficial.
  • Because of these first results, new therapeutic approaches of chondrosarcoma must be considered, mainly for low grade chondrosarcoma when disabling operation is planned and when only intralesional resection can be undertaken.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Bone Density Conservation Agents / pharmacology. Chondrosarcoma / drug therapy. Chondrosarcoma / surgery. Curettage. Diphosphonates / therapeutic use. Imidazoles / therapeutic use. Neoplasm Recurrence, Local / prevention & control
  • [MeSH-minor] Animals. Apoptosis / drug effects. Caspase 1 / metabolism. Caspase 3. Caspases / metabolism. Cell Cycle / drug effects. Cell Proliferation / drug effects. Chemotherapy, Adjuvant. Disease Progression. Male. Rats. Rats, Sprague-Dawley. Survival Analysis

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  • [Copyright] Copyright 2006 Wiley-Liss, Inc.
  • (PMID = 16570273.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Bone Density Conservation Agents; 0 / Diphosphonates; 0 / Imidazoles; 6XC1PAD3KF / zoledronic acid; EC 3.4.22.- / Casp3 protein, rat; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases; EC 3.4.22.36 / Caspase 1
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23. Schrage YM, Briaire-de Bruijn IH, de Miranda NF, van Oosterwijk J, Taminiau AH, van Wezel T, Hogendoorn PC, Bovée JV: Kinome profiling of chondrosarcoma reveals SRC-pathway activity and dasatinib as option for treatment. Cancer Res; 2009 Aug 1;69(15):6216-22
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Kinome profiling of chondrosarcoma reveals SRC-pathway activity and dasatinib as option for treatment.
  • Chondrosarcomas are notorious for their resistance to conventional chemotherapy and radiotherapy, indicating there are no curative treatment possibilities for patients with inoperable or metastatic disease.
  • We therefore explored the existence of molecular targets for systemic treatment of chondrosarcoma using kinome profiling.
  • Peptide array was performed for four chondrosarcoma cell lines and nine primary chondrosarcoma cultures with GIST882, MSCs, and colorectal cancer cell lines as controls.
  • Activity of kinases was verified using immunoblot, and active Src- and platelet-derived growth factor receptor (PDGFR) signaling were further explored using imatinib and dasatinib on chondrosarcoma in vitro.
  • The AKT1/GSK3B pathway was clearly active in chondrosarcoma.
  • Although imatinib did not show any effect on chondrosarcoma cell cultures, dasatinib showed a decrease in cell viability at nanomolar concentrations in seven of nine chondrosarcoma cultures.
  • In conclusion, using kinome profiling, we found the Src pathway to be active in chondrosarcoma.
  • Moreover, we showed in vitro that the inhibitor of the Src pathway, dasatinib, may provide a potential therapeutic benefit for chondrosarcoma patients who are not eligible for surgery.
  • [MeSH-major] Chondrosarcoma / enzymology. Protein Kinase Inhibitors / pharmacology. Pyrimidines / pharmacology. Thiazoles / pharmacology. src-Family Kinases / metabolism
  • [MeSH-minor] Benzamides. Cell Line, Tumor. Dasatinib. Glycogen Synthase Kinase 3 / metabolism. Humans. Imatinib Mesylate. Jurkat Cells. MAP Kinase Signaling System / drug effects. Piperazines / pharmacology. Proto-Oncogene Proteins c-akt / metabolism. raf Kinases / metabolism. ras Proteins / metabolism

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  • (PMID = 19602594.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Thiazoles; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / src-Family Kinases; EC 2.7.11.1 / AKT1 protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.1 / glycogen synthase kinase 3 beta; EC 2.7.11.1 / raf Kinases; EC 2.7.11.26 / Glycogen Synthase Kinase 3; EC 3.6.5.2 / ras Proteins; RBZ1571X5H / Dasatinib
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