| First Author | Di Carlo E | Year | 1997 |
| Journal | J Pathol | Volume | 182 |
| Issue | 1 | Pages | 76-85 |
| PubMed ID | 9227345 | Mgi Jnum | J:40758 |
| Mgi Id | MGI:892124 | Doi | 10.1002/(SICI)1096-9896(199705)182:1<76::AID-PATH805>3.0.CO;2-B |
| Citation | Di Carlo E, et al. (1997) Interleukin 6 gene-transfected mouse mammary adenocarcinoma: tumour cell growth and metastatic potential. J Pathol 182(1):76-85 |
| abstractText | Cells from the spontaneous metastatic TSA mammary adenocarcinoma of BALB/C mouse were transfected with the murine (interleukin-6) IL6 gene. The clone (TSA-IL6) secreting the largest amount of IL6 displayed an in vitro increased growth rate compared with that of TSA cells transfected with the neomycin resistance gene only (TSA-neo). TSA-IL6 cell colonies consisted mainly of fusiform cells and TSA-neo colonies of polygonal cells. When subcutaneously (s.c.) injected in syngeneic mice, TSA-IL6 cells gave rise to tumours that grew significantly slower than TSA-neo cell tumours. Microscopically, TSA-IL6 tumours displayed a fascicular pattern of growth, associated with a very scanty macrophage infiltrate. S.c. TSA-IL6 tumours were significantly less metastatic than TSA-neo tumours. By contrast, following intravenous (i.v.) challenge, TSA-IL6 cells produced 5-7 times more lung metastases than TSA-neo cells. The i.v. TSA-IL6 cell lung metastases showed a marked macrophage infiltrate and a rich vascularization. The high in vitro TSA-IL6 cell growth rate is attributable to the IL6-induced production of growth factors, some of which possess heparin-binding properties, such as amphiregulin. The differences in vascularization and macrophage infiltrate may underlie the observed differences between s.c. TSA-IL6 tumour growth with low spontaneous metastatic potential and the widespread growth of i.v. metastasis. |
