fms genes


Summary: Family of genes originally isolated from the Susan McDonough strain of feline sarcoma virus (SARCOMA VIRUSES, FELINE). The proto-oncogene fms (c-fms) codes for the MCSF receptor (RECEPTOR, MACROPHAGE COLONY-STIMULATING FACTOR). The oncogene fms (v-fms) codes for ONCOGENE PROTEIN GP140(V-FMS) which is a mutated form of the MCSF. The human c-fms gene is located between 5q33.2 and 5q33.3.

Top Publications

  1. Yao Z, Li P, Zhang Q, Schwarz E, Keng P, Arbini A, et al. Tumor necrosis factor-alpha increases circulating osteoclast precursor numbers by promoting their proliferation and differentiation in the bone marrow through up-regulation of c-Fms expression. J Biol Chem. 2006;281:11846-55 pubmed
    ..Therefore, the first step of TNF-induced osteoclastogenesis is at the level of OCP genesis in the bone marrow, which represents another layer of regulation to control erosive disease. ..
  2. Xie Y, Zhong R, Chen C, Calderwood S. Heat shock factor 1 contains two functional domains that mediate transcriptional repression of the c-fos and c-fms genes. J Biol Chem. 2003;278:4687-98 pubmed
    ..Mapping the structural domains involved in this process should permit further characterization of molecular mechanisms that mediate repression. ..
  3. Castresana J, Barrios C, Gomez L, Kreicbergs A. Amplification of the c-myc proto-oncogene in human chondrosarcoma. Diagn Mol Pathol. 1992;1:235-8 pubmed
    ..The clinical significance of this gene amplification remains to be established. ..
  4. Bertino P, Porta C, Barbone D, Germano S, Busacca S, Pinato S, et al. Preliminary data suggestive of a novel translational approach to mesothelioma treatment: imatinib mesylate with gemcitabine or pemetrexed. Thorax. 2007;62:690-5 pubmed
    ..This study provides a rationale for a novel translational approach to the treatment of mesothelioma which relies on enhancement of tumour chemosensitivity by inhibition of Akt. ..
  5. Bourette R, Grasset M, Mouchiroud G. E2a/Pbx1 oncogene inhibits terminal differentiation but not myeloid potential of pro-T cells. Oncogene. 2007;26:234-47 pubmed
    ..Finally, additional experiments suggested that PU.1 and eight twenty-one transcriptional regulators might be implicated in the mechanisms of oncogenesis by E2a/Pbx1. ..
  6. Padua R, Guinn B, Al Sabah A, Smith M, Taylor C, Pettersson T, et al. RAS, FMS and p53 mutations and poor clinical outcome in myelodysplasias: a 10-year follow-up. Leukemia. 1998;12:887-92 pubmed
    ..005). This study shows that oncogene mutation, indicative of genetic instability, is associated with disease progression and poor survival in MDS. ..
  7. Misawa S, Horiike S, Kaneko H, Kashima K. Genetic aberrations in the development and subsequent progression of myelodysplastic syndrome. Leukemia. 1997;11 Suppl 3:533-5 pubmed
    ..However, patients who showed an NRAS mutation had a shorter survival time once the mutation emerged, similar to that of patients with a TP53 mutation. ..
  8. Gogusev J, Barbey S, Nezelof C. Modulation of c-myc, c-myb, c-fos, c-sis and c-fms proto-oncogene expression and of CSF-1 transcripts and protein by phorbol diester in human malignant histiocytosis DEL cell line with 5q 35 break point. Anticancer Res. 1993;13:1043-7 pubmed
    ..Through this drug-induced modulation, the DEL cell line offers an additional model for studying some of the subtle interrelations existing between a growth factor (CSF-1) and its receptor (c-fms) in the monocyte/macrophage system. ..
  9. Paniagua R, Chang A, Mariano M, Stein E, Wang Q, Lindstrom T, et al. c-Fms-mediated differentiation and priming of monocyte lineage cells play a central role in autoimmune arthritis. Arthritis Res Ther. 2010;12:R32 pubmed publisher
    ..These results suggest that c-Fms plays a central role in the pathogenesis of RA by mediating the differentiation and priming of monocyte lineage cells. Therapeutic targeting of c-Fms could provide benefit in RA. ..

More Information


  1. Jenkins B, Grail D, Inglese M, Quilici C, Bozinovski S, Wong P, et al. Imbalanced gp130-dependent signaling in macrophages alters macrophage colony-stimulating factor responsiveness via regulation of c-fms expression. Mol Cell Biol. 2004;24:1453-63 pubmed
  2. Siao C, Fernandez S, Tsirka S. Cell type-specific roles for tissue plasminogen activator released by neurons or microglia after excitotoxic injury. J Neurosci. 2003;23:3234-42 pubmed
    ..We suggest that an approach to attenuate microglia-mediated neuronal death in vivo might be to pharmacologically prevent microglial activation. ..
  3. Tanaka K. [Molecular biology of ovarian cancer]. Gan To Kagaku Ryoho. 1999;26:2162-7 pubmed
    ..Among the genes searched to date for abnormalities related to ovarian cancer, BRCA1 is thought to be the most likely candidate for having a causal relation with the familial ovarian cancer syndrome. ..
  4. Fenaux P, Preudhomme C. [Molecular abnormalities and clonality in myelodysplastic syndromes]. Pathol Biol (Paris). 1997;45:556-60 pubmed
    ..This opens up the promising possibility that transplantation of autologous multipotent stem cells may be an effective therapeutic approach. ..
  5. Andre C, Hampe A, Lachaume P, Martin E, Wang X, Manus V, et al. Sequence analysis of two genomic regions containing the KIT and the FMS receptor tyrosine kinase genes. Genomics. 1997;39:216-26 pubmed
    ..We have conducted a detailed structural analysis of the two loci containing the KIT and FMS genes. The sequence of the approximately 90-kb KIT locus reveals the position and size of the 21 introns and of the 5' ..
  6. Springall F, O Mara S, Shounan Y, Todd A, Ford D, Iland H. c-fms point mutations in acute myeloid leukemia: fact or fiction?. Leukemia. 1993;7:978-85 pubmed
    ..This study suggests that c-fms mutations at codons 301 and 969 are not important in the pathogenesis of AML in the vast majority of patients. ..
  7. French B, Patrick D, Grever M, Trewyn R. Differential effect of 6-ethylmercaptopurine on c-myc expression in wild-type and HGPRT-deficient HL-60 cells. Cancer Chemother Pharmacol. 1990;27:171-7 pubmed
    ..In addition, e6MP inhibits TPA-induced monocytic/macrophage differentiation as characterized by stabilization of c-fms mRNA and cellular adherence. ..
  8. Sierra A, Gottfried Blackmore A, McEwen B, Bulloch K. Microglia derived from aging mice exhibit an altered inflammatory profile. Glia. 2007;55:412-24 pubmed
    ..Gender differences were not overall observed across the treatments (age, LPS). The low but sustained production of pro-inflammatory cytokines by aging microglia may have a profound impact in the brain aging process. ..
  9. Tangir J, Bonafe N, Gilmore Hebert M, Henegariu O, Chambers S. SGK1, a potential regulator of c-fms related breast cancer aggressiveness. Clin Exp Metastasis. 2004;21:477-83 pubmed
    ..This finding may have implications for potential therapeutic interventions aimed at decreasing the aggressiveness of breast cancer cells. ..
  10. Sapi E. The role of CSF-1 in normal physiology of mammary gland and breast cancer: an update. Exp Biol Med (Maywood). 2004;229:1-11 pubmed
  11. Manome H, Aiba S, Tagami H. Simple chemicals can induce maturation and apoptosis of dendritic cells. Immunology. 1999;98:481-90 pubmed
  12. Spencker T, Neumann D, Strasser A, Resch K, Martin M. Lineage switch of a mouse pre-B cell line (SPGM-1) to macrophage-like cells after incubation with phorbol ester and calcium ionophore. Biochem Biophys Res Commun. 1995;216:540-8 pubmed
    ..The high efficiency and speed of differentiation in this cellular system makes SPGM-1 a highly suitable model for studying the phenomenon of lineage switching during hemopoesis. ..
  13. Michaelson M, Bieri P, Mehler M, Xu H, Arezzo J, Pollard J, et al. CSF-1 deficiency in mice results in abnormal brain development. Development. 1996;122:2661-72 pubmed
    ..The effects of CSF-1 on cultured embryonic neural cells, the developmentally appropriate expression of CSF-1 and its receptor, and the neurological abnormalities in op/op mice suggest a role for CSF-1 in brain development. ..
  14. Baker A, Ball S, McGlynn H, Whittaker J, Burnett A, Padua R. A C-terminal FMS mutation in a patient with B-cell malignancy. Leukemia. 1995;9:155-8 pubmed
    ..However, the presence of other mutations not detected using this type of analysis cannot be excluded. ..
  15. Cross M, Csar X, Wilson N, Manes G, Addona T, Marks D, et al. A novel 110 kDa form of myosin XVIIIA (MysPDZ) is tyrosine-phosphorylated after colony-stimulating factor-1 receptor signalling. Biochem J. 2004;380:243-53 pubmed
    ..The phosphorylation of p110 myosin XVIIIA by CSF-1 may alter its cellular localization or target its association with other proteins. ..
  16. Metcalf D, Nicola N, Gough N, Elliott M, McArthur G, Li M. Synergistic suppression: anomalous inhibition of the proliferation of factor-dependent hemopoietic cells by combination of two colony-stimulating factors. Proc Natl Acad Sci U S A. 1992;89:2819-23 pubmed
    ..This phenomenon of synergistic suppression may have relevance for the future clinical use of combinations of CSFs, because a potentially similar suppression is also observable with some normal macrophage progenitor cells. ..
  17. DeKoter R, Walsh J, Singh H. PU.1 regulates both cytokine-dependent proliferation and differentiation of granulocyte/macrophage progenitors. EMBO J. 1998;17:4456-68 pubmed
    ..1 into mutant progenitors restores responsiveness to myeloid-specific cytokines and development of mature granulocytes and macrophages. Thus PU.1 controls myelopoiesis by regulating both proliferation and differentiation pathways. ..
  18. Biskobing D, Rubin J. 1,25-Dihydroxyvitamin D3 and phorbol myristate acetate produce divergent phenotypes in a monomyelocytic cell line. Endocrinology. 1993;132:862-6 pubmed
    ..1,25-(OH)2D3-induced phenotypic changes may, therefore, involve modulation of the M-CSF effect. ..
  19. Ilaria R. Tyrosine kinases in AML: where do they fit in?. Leuk Res. 2004;28:217-8 pubmed
  20. Felgner J, Kreipe H, Heidorn K, Jaquet K, Heuss R, Zschunke F, et al. Lineage-specific methylation of the c-fms gene in blood cells and macrophages. Leukemia. 1992;6:420-5 pubmed
  21. Roussel M, Sherr C. Oncogenic potential of the c-FMS proto-oncogene (CSF-1 receptor). Cell Cycle. 2003;2:5-6 pubmed
  22. Follows G, Tagoh H, Lefevre P, Hodge D, Morgan G, Bonifer C. Epigenetic consequences of AML1-ETO action at the human c-FMS locus. EMBO J. 2003;22:2798-809 pubmed
    ..Our experiments provide for the first time a direct insight into the chromatin structure of an AML1-ETO-bound target gene. ..
  23. Macary C, Chauvin C, Thelu J, Oury B, Santoro F, Ambroise Thomas P. [Detection of homologous oncogene sequences in the genome of Plasmodium falciparum]. C R Acad Sci III. 1991;312:37-42 pubmed
    ..The oncogene study will allow an understanding of the biology of the parasite and particularly the host-parasite relationships which allow P. falciparum to develop, keeping the established harmony between the parasite and his host. ..
  24. Goto T, Nishimura J. [Activation of protooncogenes by point mutations in hematological malignancies]. Nihon Rinsho. 1992;50:1335-40 pubmed
    ..Furthermore, mutations in the 3' border of the exon 1 of c-myc are frequent, and may play an additional role in pathogenesis of Burkitt lymphoma. ..
  25. Rowley P, Farley B, Giuliano R, LaBella S, Leary J. Induction of the fms proto-oncogene product in HL-60 cells by vitamin D: a flow cytometric analysis. Leuk Res. 1992;16:403-10 pubmed
  26. Pfeilstöcker M, Grill R, Koller E, Krieger O, Pittermann E, Karlic H. FMS hemizygosity in myeloid dysplasia and acute myeloid leukemia with chromosomal aberration del(5)(q) demonstrated by polymerase chain reaction. J Mol Med (Berl). 1995;73:403-7 pubmed
    ..PCR-based analysis can be used for primary diagnosis in addition to cytogenetic evaluation and for follow-up in patients with del(5)(q) aberration. ..
  27. Panterne B, Hatzfeld A, Sansilvestri P, Cardoso A, Monier M, Batard P, et al. IL-3, GM-CSF and CSF-1 modulate c-fms mRNA more rapidly in human early monocytic progenitors than in mature or transformed monocytic cells. J Cell Sci. 1996;109 ( Pt 7):1795-801 pubmed
    ..These results suggest that oncogene expression can be regulated much more rapidly in immature progenitors than was previously observed in mature cells or transformed cell lines. ..
  28. Ross I, Dunn T, Yue X, Roy S, Barnett C, Hume D. Comparison of the expression and function of the transcription factor PU.1 (Spi-1 proto-oncogene) between murine macrophages and B lymphocytes. Oncogene. 1994;9:121-32 pubmed
    ..1 expression. The data suggest that differences in nuclear PU.1 expression and function between macrophages and B cells may play a role in lineage divergence. ..
  29. Storga D, Pecina Slaus N, Pavelic J, Pavelic Z, Pavelic K. c-fms is present in primary tumours as well as in their metastases in bone marrow. Int J Exp Pathol. 1992;73:527-33 pubmed
    ..Our results showed that c-fms product is confined, not only to some normal, but also to the variety of malignant cells of different origin. ..
  30. McArthur G, Metcalf D, Rakar S, Johnson G. Overexpression of C-FMS in the myeloid cell line FDC-P1 induces transformation that dissociates M-CSF-induced proliferation and differentiation. Leukemia. 1995;9:68-76 pubmed
    ..The data indicate that transformation of c-fms expressing cells results in a variety of phenotypes with dissociation of M-CSF induced proliferation and differentiation in different cell lines. ..
  31. Haller H, Behrend M, Park J, Schaberg T, Luft F, Distler A. Monocyte infiltration and c-fms expression in hearts of spontaneously hypertensive rats. Hypertension. 1995;25:132-8 pubmed
    ..We suggest that mononuclear cell recruitment and induction of c-fms may play a role in the development of hypertension-associated myocardial hypertrophy. ..
  32. Alterman R, Stanley E. Colony stimulating factor-1 expression in human glioma. Mol Chem Neuropathol. 1994;21:177-88 pubmed
    ..We conclude that coexpression of CSF-1 and its receptor in some human gliomas hints at a possible autocrine or paracrine growth stimulatory role for CSF-1; however, its function in the mammalian CNS remains to be elucidated. ..
  33. Mouchiroud G, Bourette R, Blanchet J. Expression of functional human CSF-1 receptors on mouse bone marrow erythroid progenitor cells. C R Acad Sci III. 1993;316:1290-6 pubmed
  34. Jaeger U, Panzer S, Bartram C, Haas O, Volc Platzer B, Graninger W, et al. Autoimmune-thrombocytopenia and SLE in a patient with 5q-anomaly and deletion of the c-fms oncogene. Am J Hematol. 1994;45:79-80 pubmed
    ..This case report suggests that SLE can occur in patients with MDS and that a concomitant autoimmune-thrombocytopenia may mask the typical signs of the 5q- syndrome. ..
  35. Jekic B, Novakovic I, Lukovic L, Kuzmanovic M, Popovic B, Milasin J, et al. Lack of TP53 and FMS gene mutations in children with myelodysplastic syndrome. Cancer Genet Cytogenet. 2006;166:163-5 pubmed
    ..Our results suggest that molecular mechanisms of MDS evolution in children are different from those in adults. ..
  36. Flick M, Sapi E, Kacinski B. Hormonal regulation of the c-fms proto-oncogene in breast cancer cells is mediated by a composite glucocorticoid response element. J Cell Biochem. 2002;85:10-23 pubmed
  37. Dubreuil P, Forrester L, Rottapel R, Reedijk M, Fujita J, Bernstein A. The c-fms gene complements the mitogenic defect in mast cells derived from mutant W mice but not mi (microphthalmia) mice. Proc Natl Acad Sci U S A. 1991;88:2341-5 pubmed
    ..Furthermore, they suggest that mi encodes a protein necessary for transducing signals mediated by way of either the c-kit or c-fms receptor. ..
  38. Krysinska H, Hoogenkamp M, Ingram R, Wilson N, Tagoh H, Laslo P, et al. A two-step, PU.1-dependent mechanism for developmentally regulated chromatin remodeling and transcription of the c-fms gene. Mol Cell Biol. 2007;27:878-87 pubmed
    ..The two-step mechanism of developmental gene activation that we describe here may be utilized to regulate gene activity in a variety of developmental pathways. ..
  39. Kimura T, Azuma C, Saji F, Tokugawa Y, Takemura M, Miki M, et al. The biological effects of macrophage-colony-stimulating factor induced by progestin on growth and differentiation of endometrial adenocarcinoma cells. Int J Cancer. 1991;49:229-33 pubmed
    ..These effects of M-CSF on endometrial cancer cells are similar to those of progestins, so the effects of progestins on these cells are, at least in part, probably mediated by M-CSF in an autocrine or paracrine manner. ..
  40. Oghiso Y, Yamada Y, Ando K, Ishihara H, Shibata Y. Differential induction of prostaglandin E2-dependent and -independent immune suppressor cells by tumor-derived GM-CSF and M-CSF. J Leukoc Biol. 1993;53:86-92 pubmed
    ..These results suggest that two distinctly different suppressor cells developed under hemopoiesis of myelomonocytic lineage cells are regulated differentially by the two macrophage growth factors, M-CSF and GM-CSF. ..
  41. Rosnet O, Mattei M, Marchetto S, Birnbaum D. Isolation and chromosomal localization of a novel FMS-like tyrosine kinase gene. Genomics. 1991;9:380-5 pubmed
    ..We have localized the human FLT3 gene to chromosome 13, band q12, and its mouse homolog to chromosome 5, region G. ..
  42. Martin M, Strasser A, Baumgarth N, Cicuttini F, Welch K, Salvaris E, et al. A novel cellular model (SPGM 1) of switching between the pre-B cell and myelomonocytic lineages. J Immunol. 1993;150:4395-406 pubmed
    ..This inducible, rapid switch of virtually the entire population provides a unique model for the molecular analysis of mechanisms involved in cell-fate determination. ..
  43. Dairi T, Ohta T, Hashimoto E, Hasegawa M. Self cloning in Micromonospora olivasterospora of fms genes for fortimicin A (astromicin) biosynthesis. Mol Gen Genet. 1992;232:262-70 pubmed
    ..FTM A non-producing strain) in the course of constructing the plasmid vector pMO116. These results clearly show that this novel gene cloning system in Micromonospora is of practical use. ..
  44. Jin D, Jameson S, Reddy M, Schenkman D, Ostrowski M. Alterations in differentiation and behavior of monocytic phagocytes in transgenic mice that express dominant suppressors of ras signaling. Mol Cell Biol. 1995;15:693-703 pubmed
    ..The results indicate that ras action is critical in monocytic cells after these cells have lost the capacity to traverse the cell cycle. ..
  45. Sapi E, Flick M, Gilmore Hebert M, Rodov S, Kacinski B. Transcriptional regulation of the c-fms (CSF-1R) proto-oncogene in human breast carcinoma cells by glucocorticoids. Oncogene. 1995;10:529-42 pubmed
  46. McArthur G, Rohrschneider L, Johnson G. Induced expression of c-fms in normal hematopoietic cells shows evidence for both conservation and lineage restriction of signal transduction in response to macrophage colony-stimulating factor. Blood. 1994;83:972-81 pubmed
    ..These findings provide evidence for both conservation and lineage restriction of signal transduction in normal hematopoietic cells. ..
  47. Li G, Song Y, Wu K, Lin Y, Cao Z, Zheng G. Clone and expression of mutant M-CSF and its receptor from human leukemic cell line J6-1. Leuk Res. 2002;26:377-82 pubmed
    ..COS-7 cells transfected with MAF-J6-1-R show obvious protein tyrosine kinase (PTK) activity. Our present work shows that MAF-J6-1 and its receptor are mutations of M-CSF and its receptor. ..
  48. Hulkower K, Brosnan C, Aquino D, Cammer W, Kulshrestha S, Guida M, et al. Expression of CSF-1, c-fms, and MCP-1 in the central nervous system of rats with experimental allergic encephalomyelitis. J Immunol. 1993;150:2525-33 pubmed
    ..The results support the conclusion that expression of factors that specifically target cells of the monocyte/macrophage series are an important component of the disease process in experimental allergic encephalomyelitis. ..
  49. Chen A, Rohrschneider L. Mechanism of differential inhibition of factor-dependent cell proliferation by transforming growth factor-beta 1: selective uncoupling of FMS from MYC. Blood. 1993;81:2539-46 pubmed
    ..Therefore, FMS and the GM-CSF receptor induce c-myc via signal transduction pathways that differ in that only the former is inhibited by TGF-beta 1. This inhibition may account for the selective growth regulation by TGF-beta 1. ..
  50. Aoki H, Akiyama H, Hosoya H, Souda M, Morioku T, Marunouchi T. Transient expression of M-CSF is important for osteoclast-like cell differentiation in a monocytic leukemia cell line. J Cell Biochem. 1997;64:67-76 pubmed
    ..Furthermore, both dexamethasone and IFN-gamma impaired the attenuation of M-CSF expression, suggesting that the transient expression of M-CSF may be important for the formation of osteoclast-like cells. ..
  51. Alleva D, Askew D, Burger C, Elgert K. Macrophage priming and activation during fibrosarcoma growth: expression of c-myb, c-myc, c-fos, and c-fms. Immunol Invest. 1994;23:457-72 pubmed
    ..The induction of M phi proto-oncogene expression during cancer may put M phi in a primed state, which leads to earlier and stronger production of adverse suppressor and cytotoxic molecules. ..
  52. Ford A, Healy L, Bennett C, Navarro E, Spooncer E, Greaves M. Multilineage phenotypes of interleukin-3-dependent progenitor cells. Blood. 1992;79:1962-71 pubmed