Table 2.

Phenotypes of p53 cell cycle arrest and senescence target gene mouse knockout strains

	p53-dependent cell cycle arrest phenotype of null cells	Knockout mouse phenotype	Knockout mouse tumor models	Refs
p21 Cyclin dependent kinase inhibitor 1A	Deficient: G1 cell cycle arrest of MEFs after DNA damage Competent: Senescence of MEFs after serial passage Cell cycle arrest and senescence of MEFs after oncogene expression	Multiple reports: No tumors in >1 year Spontaneous tumors at a mean latency of 16 months	No effect: Breast cancers driven by MMTV- v-Ras Enhanced tumorigenesis: Renal carcinomas driven by Apc loss Pituitary tumors, thyroid tumors, and pheochromocytomas driven by Rb+/− Various tumor types after irradiation Carcinomas after DMBA and TPA treatment Intestinal adenocarcinomas in Csnk1a1-null mice	[57–60, 62–64, 91–94]
Gadd45a Growth arrest and DNA- damage- inducible 45 alpha	Deficient: Cell cycle arrest of MEFs after oncogene expression Cell cycle arrest of keratinocytes after DNA damage	No spontaneous tumors	Enhanced tumorigenesis: Thymic lymphomas after γ-IR Skin carcinomas after UV irradiation Breast cancers driven by MMTV- v-Ras Decreased tumorigenesis: Breast cancers driven by MMTV- Myc	[65–68, 95]
Pml Promyelocytic leukemia	Deficient: Senescence of MEFs after oncogene expression	No spontaneous tumors Increased susceptibility to infection	Enhanced tumorigenesis: Leukemia in cathepsin-G- PML/RARα transgenic mice Papillomas after DMBA and TPA treatment No effect: MMTV-neu driven breast cancers	[69–73]
Ptprv Protein tyrosine phosphatase, receptor type, V	Deficient: G1 arrest of MEFs after DNA damage	No spontaneous tumors (within 1 year)	Enhanced tumorigenesis: Papillomas after DMBA treatment	[74]