Cell cycle genes in a mouse mammary hyperplasia model.
Human mammary epithelial cells emerge spontaneously from senescence, exhibiting eroding telomeric sequences, and ultimately enter crisis to generate the type of chromosomal abnormalities seen in early stages of breast cancer. In a mouse mammary tumor model, the spontaneous escape of senescence can be observed as an increase in DNA synthesis that is reflected by alterations in the cell cycle profile and increases in the expression levels and activities of cell cycle molecular components. This review provides an overview of gene alterations in the cell cycle components in mouse mammary hyperplasia.
Said
Thenaa K
TK
Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas 77030, USA. tsaid@bcm.tmc.edu
Medina
Daniel
D
D000818:Animals; D001940:Breast / Q000473:pathology; D001943:Breast Neoplasms / Q000235:genetics* / Q000503:physiopathology*; D002453:Cell Cycle / Q000235:genetics*; D018797:Cell Cycle Proteins / Q000235:genetics / Q000494:pharmacology; D002869:Chromosome Aberrations; D050760:Cyclin-Dependent Kinase Inhibitor p27; D016213:Cyclins / Q000235:genetics / Q000494:pharmacology; D004247:DNA / Q000096:biosynthesis; D004195:Disease Models, Animal; D004847:Epithelial Cells; D005260:Female; D006801:Humans; D006965:Hyperplasia; D008321:Mammary Glands, Animal / Q000473:pathology*; D015674:Mammary Neoplasms, Animal / Q000235:genetics* / Q000503:physiopathology*; D051379:Mice; D025521:Tumor Suppressor Proteins / Q000235:genetics / Q000494:pharmacology
C493961:Cdkn1b protein, mouse; D018797:Cell Cycle Proteins; D016213:Cyclins; D025521:Tumor Suppressor Proteins; D050760:Cyclin-Dependent Kinase Inhibitor p27; D004247:DNA