The Mechanism of Thymic Lymphomagenesis in Genetically Engineered Mouse Model

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Using T121, we generated a mouse model, in which cytokeratin (K) 18 drives floxed eGFP stop T121 expression. K18 is expressed widely in simple epithelial cells (e.g. prostate luminal cells, mammary gland luminal cells, thymic epithelial cells, etc). Once K18 mouse is crossed to a Cre line, T121 expression will be driving directly under K18 regulation. We have crossed K18 mouse to several different Cre lines (e.g. R26CreER, b-actin Cre, PbCre4, PSACre, and FSPCre). All offspring developed atypical lymphoid hyperplasia, pre-neoplastic, or T-cell lymphoblasts lymphoma. Bone marrow transplantation study showed that thymic mass was developed only in K18 recipient mice with wildtype mice as donors, and no thymic mass developed in wildtype recipient mice with K18 mice as donors, suggesting K18 stroma contribute to the lymphomagenesis in these mice.