Transforming growth factor‐β (TGF‐β) is a growth modulator that inhibits the proliferation of many epithelial cells through interaction with its receptors, the type I and type II receptors (TGF‐β RI and RII) by activating their serine/threonine kinase activities. Loss of growth inhibition by TGF‐β is thought to contribute to the development of many types of tumors. To examine the roles of TGF‐β1, ‐β2, and ‐β3 and TGF‐β RI and RII in chemically induced mouse lung tumorigenesis, we used immunohistochemical and in situ hybridization analyses to measure the expression of their proteins and mRNAs in A/J mice treated with the carcinogen urethane to induce lung adenomas. Immunostaining for the TGF‐β ligands and receptors was detected in the epithelia of the bronchioles of untreated and treated A/J mice at similar levels. Immunostaining for the TGF‐β ligands and receptors was also detected in adenomas by 2 mo. While immunostaining for TGF‐β1, ‐β2, and ‐β3 and TGF‐β RI in adenomas was detected at levels comparable to those in bronchioles, immunostaining for TGF‐β RII was less intense in adenomas than in bronchioles. Decreased immunostaining for TGF‐β RII in adenomas persisted for at least 8 mo after exposure to urethane, whereas immunostaining for TGF‐β1, ‐β2, and ‐β3 and TGF‐β RI persisted at levels comparable to those in normal bronchioles. In situ hybridization studies conducted with TGF‐β receptor riboprobes showed a corresponding reduction in expression of TGF‐β RII mRNA but not of TGF‐β RI mRNA in adenomas compared with expression in bronchioles. Expression of TGF‐β RII mRNA was also examined in non‐tumorigenic and tumorigenic mouse lung cells; expression of TGF‐β RII mRNA was lower in the tumorigenic cells derived from urethane‐induced lung tumors. These data suggest that a decrease in expression of TGF‐β RII may contribute to autonomous cell growth and may play an important role in mouse lung carcinogenesis induced by urethane. Mol. Carcinog. 22:46–56, 1998. © 1998 Wiley‐Liss, Inc. This article is a US Government work and, as such, is in the public domain in the United States of America.