Predominant p53 G -> A transition mutation and enhanced cell proliferation in uterine sarcomas of CBA mice treated with 1,2-dimethylhydrazine
TOXICOLOGIC PATHOLOGY, 26(3), 367–374.
By:
L. Trukhanova*, H. Hong*, R. Sills*, A. Bowser*, B. Gaul*, G. Boorman*, V. Turusov*, T. Devereux*, D. Dixon *
author keywords: tumor suppressor gene; ras proto-oncogene; malignant fibrous histiocytoma; stromal sarcoma; undifferentiated sarcoma; estrogen receptor; desmin
MeSH headings : 1,2-Dimethylhydrazine; Animals; Cell Division; Desmin / analysis; Female; Genes, p53 / genetics; Immunohistochemistry; Mice; Mice, Inbred CBA; Point Mutation; Polymorphism, Single-Stranded Conformational; Proliferating Cell Nuclear Antigen / analysis; Receptors, Estrogen / analysis; Sarcoma, Experimental / chemistry; Sarcoma, Experimental / genetics; Sarcoma, Experimental / pathology; Tumor Suppressor Protein p53 / analysis; Uterine Neoplasms / chemically induced; Uterine Neoplasms / chemistry; Uterine Neoplasms / genetics; Uterine Neoplasms / pathology
TL;DR:
The data suggest that DMH-induced uterine sarcomas are not consistent with smooth muscle cell origin and that a subset of these tumors, specifically DMh-induced malignant fibrous histiocytomas, have unique p 53 G:C→A:T transitions and a high proliferative rate.
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