Details

Autor(en) / Beteiligte

• Finch, Andrew
• Prescott, Julia
• Shchors, Ksenya
• Hunt, Abigail
• Soucek, Laura
• Dansen, Tobias B.
• Swigart, Lamorna Brown
• Evan, Gerard I.

Titel

Bcl-x L gain of function and p19 ARF loss of function cooperate oncogenically with Myc in vivo by distinct mechanisms

Ist Teil von

• Cancer cell, 2006, Vol.10 (2), p.113-120

Ort / Verlag

Elsevier Inc

Erscheinungsjahr

2006

Link zum Volltext

Quelle

Free E-Journal (出版社公開部分のみ）

Beschreibungen/Notizen

• Overexpression of Bcl-x L, loss of p19 ARF , and loss of p53 all accelerate Myc oncogenesis. All three lesions are implicated in suppressing Myc-induced apoptosis, suggesting that this is a common mechanism by which they synergize with Myc. However, using an acutely switchable model of Myc-induced tumorigenesis, we demonstrate that each lesion cooperates with Myc in vivo by a distinct mechanism. While Bcl-x L blocks Myc-induced apoptosis, inactivation of p19 ARF enhances it. However, this increase in apoptosis is matched by increased Myc-induced proliferation. p53 inactivation shares features of both lesions, partially suppressing apoptosis while augmenting proliferation. Bcl-x L and p19 ARF loss together synergize to further accelerate Myc oncogenesis. Thus, differing lesions cooperate oncogenically with Myc by discrete mechanisms that can themselves synergize with each other.