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Published on: May 31, 2011
A recovered avian myelocytomatosis virus that induces lymphomas in chickens: pathogenic properties and their
Abstract:
The avian myelocytomatosis virus MC29 induces neoplastic diseases in chicken, including myelocytomas and tumors of kidney and liver, which are due to the action of the v-myc gene. However, MC29 has never been reported to cause lymphoid tumors, the disease associated with activation of the c-myc gene by the insertion of a lymphoid leukosis virus genome. We have analyzed a recovered MC29 virus, HBI, which has a myc gene containing c-myc sequences, acquired by recombination with the cellular gene, and some v-myc sequences. Inoculation of HBI into chickens resulted in lymphoid tumors independent of the bursa. Antigenically these tumors were made up of T and B cells. Molecular analysis showed HBI proviral DNA in 36 of 39 tumors analyzed, with no obvious alteration of c-myc, and the HBI gag-myc fusion protein, p 108, could be detected in tumor cells. These data are discussed in terms of the mechanism of target-cell specificity for transformation by the myc gene.
Insights
Avian myelocytomatosis virus MC29, typically causing myeloid and other tumors, was found to induce lymphoid tumors in chickens. This novel finding is linked to a hybrid myc gene in the recovered HBI virus.
Area of Science:
- Oncology
- Virology
- Molecular Biology
Background:
- Avian myelocytomatosis virus MC29 (MC29) normally induces myelocytomas and kidney/liver tumors via its v-myc gene.
- Lymphoid tumors in chickens are typically associated with c-myc gene activation by lymphoid leukosis virus integration.
Purpose of the Study:
- To investigate the oncogenic potential of a recovered MC29 virus (HBI) with a hybrid myc gene.
- To determine if HBI can induce lymphoid tumors and elucidate the underlying molecular mechanisms.
Main Methods:
- Analysis of a recombinant MC29 virus (HBI) containing both c-myc and v-myc sequences.
- Inoculation of HBI into chickens to observe tumor development.
- Molecular analysis of tumors, including proviral DNA integration and protein expression.
Main Results:
- HBI inoculation induced lymphoid tumors in chickens, independent of the bursa.
- Tumors comprised both T and B lymphocytes.
- HBI proviral DNA was detected in most tumors, and the HBI gag-myc fusion protein (p108) was present in tumor cells.
Conclusions:
- The hybrid myc gene in HBI can induce lymphoid tumors, expanding the known disease spectrum of MC29.
- These findings offer insights into the target-cell specificity of myc-driven oncogenesis.
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