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Tumor induction by immunologically activated murine leukemia virus.
The Journal of Experimental Medicine
|May 1, 1973
Summary
Graft-vs.-host reactions in mice can activate latent murine leukemia virus (MuLV), leading to lymphoreticular tumors. This study shows cell-free extracts from these mice transmit tumors, confirming MuLV
Area of Science:
- Immunology
- Oncology
- Virology
Background:
- A graft-vs.-host reaction (GVHR) can be induced in mice.
- Some mice undergoing GVHR develop lymphoreticular tumors.
- The role of murine leukemia virus (MuLV) in GVHR-induced tumors is unclear.
Purpose of the Study:
- To investigate the oncogenic potential of cell-free extracts (CFEs) from GVHR-induced mice.
- To determine if MuLV activation is associated with tumor development.
- To establish a causal link between MuLV and lymphoreticular tumors post-GVHR.
Main Methods:
- Induced GVHR in CAF(I) and CB6F(1) mice using BALB/cJ spleen cells.
- Prepared CFEs from reticular tissues of mice at various times post-GVHR.
- Inoculated newborn syngeneic mice with CFEs to assess tumor induction.
- Tested CFEs for infectious MuLV (XC assay) and complement-fixing (CF) MuLV antigen.
Main Results:
- 41.4% of CFEs from GVHR mice induced lymphoreticular tumors in recipients.
- Oncogenic potential increased significantly (75%) in CFEs from mice 12-15 months post-GVHR.
- Infectious MuLV and CF MuLV antigen were detected in oncogenic CFEs, particularly later after GVHR induction.
- CFEs from normal mice did not transmit tumors or MuLV.
Conclusions:
- MuLV is activated during the GVHR.
- Activated MuLV is responsible for the development of lymphoreticular tumors.
- GVHR serves as a model for MuLV activation and subsequent oncogenesis.