TY - JOUR
T1 - Deregulation of cyclin E meets dysfunction in p53
T2 - Closing the escape hatch on breast cancer
AU - Barton, Michelle Craig
AU - Akli, Said
AU - Keyomarsi, Khandan
PY - 2006/12
Y1 - 2006/12
N2 - In this review, we focus on pathways intersecting through p53 and cyclin E, highlighting how oncogenic effects of cyclin E deregulation, especially overexpression of shortened or low molecular weight (LMW) forms of cyclin E protein, are amplified by loss of regulatory control through p53 to promote tumor development. Expression of cyclin E protein promotes progression into S-phase, an activity opposed by p53-regulated activation of checkpoint controls or apoptosis. Loss of p53 function is an escape hatch by which tumor cells, initiated by a number of means including cyclin E deregulation, can avoid cell cycle arrest or cell death and progress through further stages of unchecked deregulation and growth. To determine how this escape hatch is opened and, ultimately, how to close it, we must understand the networks of normal signaling and processing in a cell and where they intersect.
AB - In this review, we focus on pathways intersecting through p53 and cyclin E, highlighting how oncogenic effects of cyclin E deregulation, especially overexpression of shortened or low molecular weight (LMW) forms of cyclin E protein, are amplified by loss of regulatory control through p53 to promote tumor development. Expression of cyclin E protein promotes progression into S-phase, an activity opposed by p53-regulated activation of checkpoint controls or apoptosis. Loss of p53 function is an escape hatch by which tumor cells, initiated by a number of means including cyclin E deregulation, can avoid cell cycle arrest or cell death and progress through further stages of unchecked deregulation and growth. To determine how this escape hatch is opened and, ultimately, how to close it, we must understand the networks of normal signaling and processing in a cell and where they intersect.
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U2 - 10.1002/jcp.20818
DO - 10.1002/jcp.20818
M3 - Short survey
C2 - 17001684
AN - SCOPUS:33750520135
SN - 0021-9541
VL - 209
SP - 686
EP - 694
JO - Journal of Cellular Physiology
JF - Journal of Cellular Physiology
IS - 3
ER -