title: Loss of p53 expression in Myc-induced B lineage tumors.
abstract: Tumors are formed following the accumulation of several genetic changes in genes which normally function to regulate cell growth. As yet it is unclear why multiple mutations are required, which type of alterations can collaborate with each other, and if collaboration is cell-type specific. In our myc transgenic mouse model system both point mutations and loss of mRNA expression for the p53 tumor suppressor gene have been found in the myc-induced B-lineage tumors arising spontaneously in these mice. This demonstrates the collaboration between these two growth control genes in cellular transformation. The observation that alterations in the expression of p53 is a common phenomenon in tumors formed in myc transgenic mice as well as a variety of different types of human tumors suggests that inactivation of the p53 growth control pathway may be required for transformation, and that alterations in p53 itself might be the most efficient way to achieve this inactivation. An analysis of the molecular mechanism for p53 alterations has implications for what kind of factors, both environmental and physiological, can influence tumor formation. The identification of collaboration groups has implications for the process of tumor formation, growth regulation, and will some day be important for the diagnosis of cancer, the prognosis of the individual and the design of specific therapeutic agents for treatment.
authors: Department of Pathology, University of Texas Southwestern Medical Center, Dallas 75235-9072.
authors: R H
authors: RH
authors: Scheuermann
authors: S R
authors: SR
authors: Bauer
mesh_terms: D000818:Animals; D015870:Gene Expression; D016259:Genes, myc; D016393:Lymphoma, B-Cell / Q000209:etiology / Q000235:genetics; D051379:Mice; D008822:Mice, Transgenic; D016133:Polymerase Chain Reaction; D012333:RNA, Messenger / Q000235:genetics; D016159:Tumor Suppressor Protein p53 / Q000235:genetics*
chemical_list: D012333:RNA, Messenger; D016159:Tumor Suppressor Protein p53