PubMed · 6019866
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M Garbay. 1967-03-04. [Translumbar amputation].. https://pubmed.ncbi.nlm.nih.gov/6019866/
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A spontaneously occurring murine osteosarcoma cell line (POS-1) was inoculated into the footpads of 88 mice. In 59 mice, the tumor-bearing leg was amputated at 1, 3, 5, or 7 weeks after inoculation and the mice sacrificed at 9 weeks. Lung metastasis was observed in 82.6-100% of the mice undergoing leg amputation at 5 or 7 weeks after inoculation. There were no lung metastasis in the mice amputated at 1 or 3 weeks. The serum immunosuppressive acidic protein (IAP) concentration showed a significant increase at 5 or 7 weeks after inoculation (P<0.005 and P<0.0005, respectively). When amputation was done 5 weeks after inoculation, the serum IAP concentration increased further to 5.9 times the pre-amputation level 1 week after the amputation. The IAP concentration increased only 1.3-fold in the control group without inoculation. Thus, a high serum IAP concentration before amputation and a further increase after amputation were indicators of lung metastasis in this mouse model of osteosarcoma.
Following amputation of a urodele limb or teleost fin, the formation of a blastema is a crucial step in facilitating subsequent regeneration. Using the zebrafish caudal fin regeneration model, we have examined the hypothesis that fibroblast growth factors (Fgfs) initiate blastema formation from fin mesenchyme. We find that fibroblast growth factor receptor 1 (fgfr1) is expressed in mesenchymal cells underlying the wound epidermis during blastema formation and in distal blastemal tissue during regenerative outgrowth. fgfr1 transcripts colocalize with those of msxb and msxc, putative markers for undifferentiated, proliferating cells. A zebrafish Fgf member, designated wfgf, is expressed in the regeneration epidermis during outgrowth. Furthermore, we show that a specific inhibitor of Fgfr1 applied immediately following fin amputation blocks blastema formation, without obvious effects on wound healing. This inhibitor blocks the proliferation of blastemal cells and the onset of msx gene transcription. Inhibition of Fgf signaling during ongoing fin regeneration prevents further outgrowth while downregulating the established expression of blastemal msx genes and epidermal sonic hedgehog. Our findings indicate that zebrafish fin blastema formation and regenerative outgrowth require Fgf signaling.
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