Expression of keratinocyte growth factor and its receptor in human breast cancer

Bansal, G S; Cox, H C; Marsh, Sharon; Gomm, Jennifer J.; Yiangou, C; Luqmani, Y. A.; Coombes, R. Charles; Johnston, C L

doi:10.1038/bjc.1997.269

Cited by 48 publications

(42 citation statements)

References 39 publications

(44 reference statements)

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“…The fact that FGFR2IIIb, the receptor that specifically binds KGF, 39,40 is present on breast cancer cell lines 41 and that there are reports of increased proliferation and migration in various tumor cells in response to KGF, [42][43][44][45] stresses the necessity to rule out any negative effect this growth factor might have in breast cancer patients. In view of a recent publication, revealing that 4T1 cells express mRNA of FGFR2IIIb, 46 prompted us to study the effect of KGF treatment in mice bearing this tumor.…”

Section: Discussionmentioning

confidence: 99%

Graft-versus-tumor effects on murine mammary carcinoma in a model of nonmyeloablative haploidentical stem cell transplantation

Vanclée

Gelder

Schouten

et al. 2006

Bone Marrow Transplant

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Despite a slight decrease in mortality over the last decade, breast cancer still remains a leading cause of cancerrelated death in women. Although anti-tumor effects have been observed after allogeneic stem cell transplantation (SCT), this treatment is not standard care owing to graftversus-host disease (GVHD) and scarcity of suitable donors. With the aim of reducing treatment-related mortality and increasing donor availability in clinical situations, we developed a preclinical mouse model that combines nonmyeloablative conditioning with the use of haploidentical donor-recipient pairs. To mimic active disease, CB6F1 mice were inoculated with 5 Â 10 4 4T1 mammary carcinoma cells 10 days before transplantation. Keratinocyte growth factor (KGF) was used as GVHD prophylaxis. Syngeneic (CB6F1) SCT did not cure any of the mice and KGF treatment did not influence tumor development. After transplantation with haploidentical (B6CBAF1) bone marrow and splenocytes, however, tumor outgrowth was reduced and long-term disease-free survival (43 months) was observed in 9/18 (50%) (P ¼ 0.0011) of the animals. We conclude that in a model of murine breast cancer, a graft-versus-tumor effect can be induced by a nonmyeloablative haploidentical SCT procedure.

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Section: Discussionmentioning

confidence: 99%

Graft-versus-tumor effects on murine mammary carcinoma in a model of nonmyeloablative haploidentical stem cell transplantation

Vanclée

Gelder

Schouten

et al. 2006

Bone Marrow Transplant

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“…Production of both FGF-2 and its receptors is induced during the di erentiation of rat or human mammary epithelial cells into myoepithelial cells (Barraclough et al, 1990;Fernig et al, 1990;Ke et al, 1993). The FGFR-2 IIIb receptor which binds FGF-1, FGF-3 and FGF-7 is present on human mammary myoepithelial and epithelial cells (Bansal et al, 1997).…”

Section: In Vitro Invasive Propertiesmentioning

confidence: 99%

FGF-3 and FGF-4 elicit distinct oncogenic properties in mouse mammary myoepithelial cells

et al. 1998

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Fibroblast Growth Factors 3 (FGF-3) and 4 (FGF-4) were compared for the e ects they each exert on EF43 mouse cells. This non-transformed mammary cell line appears to be myoepithelial mainly because it expresses a-smooth muscle actin. The EF43 cells were infected with similar vectors that carry either the short fgf-3 sequence (the product of which goes into the secretory pathway), fgf-4 or the selection gene only as control. In syngeneic animals, EF43.fgf-3 cells were tumorigenic only when orthotopically implanted whereas EF43.fgf-4 cells invariably gave rise to aggressive tumors. However, both tumor types were metastatic as evidenced by the blue micrometastases observed when the implanted cells expressed lacZ. In vitro, the FGF-3 producing cells were strongly invasive in matrigel coated chambers whereas the EF43.fgf-4 cells only were invasive in type I-collagen gels. Interestingly, FGF-3 production greatly stimulated the synthesis of pro-MMP-9 (Matrix Metalloprotease-9) and, to a lesser extent, that of pro-MMP-2. FGF-3 also up-regulated the production of plasminogen activators. In contrast, FGF-4 had no e ect on these secretions and the medium conditioned by the EF43.fgf-4 cells displayed the largest plasminogen activator ± inhibitor activity. These results show that FGF-3 and FGF-4 have distinct mechanisms of action on myoepithelial cells.

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“…In contrast, the fgf-7 expression level measured in the non-malignant breast is conserved in the malignant tissue. This FGF-7 is mainly produced by the fibroblasts but could influence the progression of breast cancer because of the presence of its specific receptor, FGFR-2 IIIb, on the epithelial cells [18]. FGF-3 has not been detected in breast cancer; however, it also binds to FGFR-2 IIIb, so it could induce similar disregulation in the mammary tissue growth as do FGF-7 or FGF-10.…”

Section: Introductionmentioning

confidence: 99%

Progression in MCF-7 breast cancer cell tumorigenicity: compared effect of FGF-3 and FGF-4

Hajitou

Deroanne

Noël

et al. 2000

Breast Cancer Res Treat

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SummaryThe transforming properties of fibroblast growth factor 3 (FGF-3) were investigated in MCF7 breast cancer cells and compared to those of FGF-4, a known oncogenic product. The short form of fgf-3 and the fgf-4 sequences were each introduced with retroviral vectors and the proteins were only detected in the cytoplasm of the infected cells, as expected. In vitro, cells producing FGF-3 (MCF7.fgf-3) and FGF-4 (MCF7.fgf-4) displayed an amount of estrogen receptors decreased to around 45% of the control value. However, MCF7.fgf-3 cell proliferation remained responsive to estradiol supply. The sensitivity of the MCF7.fgf-4 cells, if existant, was masked by the important mitogenic action exerted by FGF-4. In vivo, the MCF7.fgf-3 and MCF7.fgf-4 cells gave rise to tumors under conditions in which the control cells were not tumorigenic. Supplementing the mice with estrogen had the paradoxical effect of totally suppressing the start of the FGF-3 as well as the FGF-4 tumors. Tumorigenicity in the presence of matrigel was similar for MCF7.fgf-3 and control cells and was increased by estrogen supplementation. Once started, the MCF7.fgf-4 tumors grew with a characteristic high rate. Remarkably, FGF-4 but not FGF-3, stimulated the secretion of vascular endothelial growth factor (VEGF 165 ) without altering the steady-state level of its mRNA, suggesting a possible regulation of VEGF synthesis at the translational level in MCF7 cells. The increased VEGF secretion is probably involved in the more aggressive phenotype of the MCF7.fgf-4 cells while a decreased dependence upon micro-environmental factors might be part of the increased tumorigenic potential of the MCF7.fgf-3 cells.

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Expression of keratinocyte growth factor and its receptor in human breast cancer

Cited by 48 publications

References 39 publications

Graft-versus-tumor effects on murine mammary carcinoma in a model of nonmyeloablative haploidentical stem cell transplantation

Graft-versus-tumor effects on murine mammary carcinoma in a model of nonmyeloablative haploidentical stem cell transplantation

FGF-3 and FGF-4 elicit distinct oncogenic properties in mouse mammary myoepithelial cells

Progression in MCF-7 breast cancer cell tumorigenicity: compared effect of FGF-3 and FGF-4

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