Table 1.

Involvement of oncogenes and gatekeeper tumor suppressor genes in genetic instability.

Oncogene or Tumor suppressor gene	Involvement in tumors	Type of genetic instability associated with dysfunction	Putative mechanism for genetic instability
myc	Overexpression (amplification, translocation, or most often, indirect)	s-CIN	Overreplication (S phase stimulation)
ras	Mutation altering the aminoacid sequence Overexpression	s-CIN w-CIN?	Overreplication Control myc activity? Centrosome amplification through cyclin D1
Cyclin D1	Overexpression (amplification, translocation, or most often, indirect)	s-CIN w-CIN?	Overreplication (S phase stimulation) Centrosome amplification
Cyclin E	Overexpression (amplification, or most often, indirect)	s-CIN	Impairment of S phase progression Forcing premature S phase entry under conditions of nucleotide deficiency
p53 mutant and p53 wild-type	Mutation altering the aminoacid sequence + overexpression Lack of expression	s-CIN, w-CIN	Overreplication (control of myc ?) Loss of mitotic checkpoint Centrosome amplification Tolerance to aneuploidy
APC	Lack of expression (most often)	s-CIN? w-CIN	Control of myc through b-catenin Role in chromosome segregation
Rb	Lack of expression (gene inactivation, or most often, indirect)	w-CIN s-CIN?	Forcing premature S phase entry under conditions of nucleotide deficiency Centrosome amplification

^?is used when the corresponding type of genetic instability, although predictable, has not been clearly demonstrated