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Previous Volume 355:1037-1046 September 7, 2006 Number 10 Next

	Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

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In many tissues, there are numerous small and inconspicuous neoplastic lesions that rarely become overt cancers. In these small lesions, clonality and oncogenic mutations have been identified. These lesions include established benign tumors such as melanocytic nevi,¹ some that were previously regarded to be of a "reactive" nature,² and even groups of cells that are histologically only marginally abnormal.³ Once they have grown to a certain size, such lesions stop growing appreciably and do not become more aggressive over many years or even decades. For instance, few moles, which are benign tumors of cutaneous melanocytes, grow larger than 1 cm, . . . [Full Text of this Article]

Oncogene-Induced Proliferative Arrest

Aberrant Proliferative Signaling and Disruption of Cell-Cycle Checkpoints

Telomeres, Replicative Senescence, and Disease

Other Mechanisms of Cellular Senescence

Nevi, Melanomas, p16^INK4A, and Senescence

Telomeric Insufficiency, DNA Damage, and Oncogenic Stress

Senescence and Apoptosis

Future Prospects

Source Information

From the Department of Pathology, Vrije University Medical Center (W.J.M.), and the Division of Molecular Genetics, Netherlands Cancer Institute (D.S.P.) — both in Amsterdam.

Address reprint requests to Dr. Mooi at the Department of Pathology, Vrije University Medical Center, De Boelelaan 1117, 1081 HV Amsterdam, the Netherlands, or at wj.mooi@vumc.nl.

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