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Singapore Med J 2003,44(8):12–19. 2. Jaffe HL, Lichtenstein L, Portis RB: Giant cell tumor of the bone. Its pathological apperance, grading, supposed variant and treatment. Arch Pathol 1940, 30:993–1031. 3. Campanacci M, Baldini N, Boriani S, Sudanese A: Giant cell tumor of bone. J Bone and Joint Surg 1987,69(A):106–114. 4. Faisham WI, Zulmi W, Halim AS, Biswal BM, Mutum SS, Ezane AM:

Aggressive giant cell tumor of the bone. Singapore Med J 2006,47(8):631–633. 5. Faisham WI, Zulmi W, Saim AH, Biswal BM: Pulmonary metastases of giant cell tumor of the bone. Med J Malaysia 2004,59(F):78–81.PubMed 6. Scholzen T, Gerdes J: The Ki 67 protein: from the known and the unknown (review). J Cell physiol 2000, 182:311–322.PubMedCrossRef #selleck randurls[1|1|,|CHEM1|]# 7. Rousseau MA, Luca AH, Lazennec JV: Metachronous multicentric giant cell tumor of the bone in the lower limb. Case report and Ki

67 immuno-histochemistry Selleck MK-8931 study. Virchows Arch 2004, 445:79–82.PubMed 8. Matsui F, Ushigome S, Fuji K: Giant cell tumor of bone. Clinicopathologic study of prognostic factors. Pathol Int 1998,48(9):723–729.CrossRef 9. Matsui F, Ushigome S, Fuji K: Giant cell tumor of bone. An immunohistochemical comparative study. Pathol Int 1998,48(5):355–361.CrossRef 10. Gamberi G, Serra M, Ragazzini P: Identification of markers of possible prognostic value in 57 giant cell tumor of the bone. Oncol Rep 2003,10(2):351–356.PubMed Competing interests The authors declare that they have no competing interests. Authors’ contributions FWI is the group leader and the work represents

his idea in correlation the clinical and basic science of GCT. MSA carried out most of the experimental work, literature review and statistical analysis. MDS and SSM, WZ supervised and evaluated the experimental work, clinical evaluation and also contributed in the discussion and preparation of manuscript. All authors have read and approved the final manuscript.”
“Background Peroxisome proliferator-activated receptor γ (PPARγ) belongs to a family of ligand-activated transcription factors. PPARγ is an intracellular sensor for fatty acids and fatty acid derivatives, CYTH4 which in turn act as endogenous ligands for PPARγ. PPARγ and its ligand activators regulate several lipid and glucose metabolism pathways [1]. In humans, PPARγ is expressed in multiple tissues, including the breast, colon, prostate, lung, placenta, and pituitary tissues [2–5]. PPARγ activation is antiproliferative by virtue of its differentiation-promoting effects. For example, ligands activating PPARγ were effective in arresting the growth of dedifferentiated tumor cells in multiple tumor types [2, 4–9], and they promoted differentiation of tumor cells and inhibited spontaneous metastasis in a xenograft model [7]. However, the mechanism by which PPARγ arrests growth has not been completely clarified.

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