Cancer

M. Serrano, A.W. Lin, M.E. McCurrach, D. Beach, S.W. Lowe, "Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a," Cell, 88:593-602, March 7, 1997. (Cited in more than 180 papers since publication) Comments by Scott W. Lowe, associate professor, Cold Spring Harbor Laboratory, Cold Spring Harbor, N.Y. Scott W. Lowe and postdoctoral fellow Maria Soengas An unpublished 15-year-old observation of an obscure cell line, dusted off and revisited, helped Sco

Written byPaul Smaglik
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M. Serrano, A.W. Lin, M.E. McCurrach, D. Beach, S.W. Lowe, "Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a," Cell, 88:593-602, March 7, 1997. (Cited in more than 180 papers since publication)

Comments by Scott W. Lowe, associate professor, Cold Spring Harbor Laboratory, Cold Spring Harbor, N.Y.

After Lowe's group shelved its findings, p53 began its rise to prominence as a definitive tumor suppressor.2,3 Few other well-characterized tumor suppressors existed at the time, so Lowe decided to see how p53 interacted with ras. "We imagined that ras would induce p53 and E1A would block this induction," Lowe notes. "When we did the experiment, ras did induce p53, but E1A did it even more."

When Lowe joined Cold Spring Harbor Laboratory in 1995, he decided to revisit exactly why and how. By then, scientists had developed better retroviral gene transfer techniques, which allowed Lowe to do what ...

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