Modeling IL7Ra alterations in leukemia. Expression of mutant ILRα or overexpression of wild-type IL7Rα in thymocytes or hematopoietic progenitors can lead to acute lymphoblastic leukemia with a long latency. These in vivo models are excellent tools for understanding receptor biology and test new therapeutics. Attempts to target downstream signaling pathways leading to leukemia will be facilitated by further characterization of the players (wild-type and mutant receptor) involved in each case. The small red dot represents phosphorylation.

Modeling IL7Ra alterations in leukemia. Expression of mutant ILRα or overexpression of wild-type IL7Rα in thymocytes or hematopoietic progenitors can lead to acute lymphoblastic leukemia with a long latency. These in vivo models are excellent tools for understanding receptor biology and test new therapeutics. Attempts to target downstream signaling pathways leading to leukemia will be facilitated by further characterization of the players (wild-type and mutant receptor) involved in each case. The small red dot represents phosphorylation.

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