Table 1.

Some prominent G-protein cancer drivers and their incidence rates in human cancers. K-Ras, RhoA, Rac1 and Cdc42 are depleted in cancer cells treated with PCAIs resulting in loss of cancer progression phenomena such as cell viability, cytoskeletal organization, cell shape, motility and invasion, consistent with loss of their biological functions [24, 46-51].

Protein	Cancer type	Aberrations (type of alteration)	Incidence rates (%)	References
K-Ras	Pancreatic cancer	Mutation	90	[52]
	Non-small cell lung cancer	Mutation	30-35	[52]
	Breast	Mutation	5	[53]
	Colorectal cancer	Mutation	30-54	[52, 54]
	Eleven most common cancers	Mutation	14.3	[55]
N-Ras	Human cutaneous melanoma	Mutation	94	[56]
	Acute myelogenous leukemia (AML)	Mutation	59	[57]
H-Ras	Bladder urothelial	Mutations	57	[58]
RhoA	Colon	Overexpression	95	[59]
	Lung	Overexpression	95	[59]
RAC1	Breast	Overexpression	70	[59, 60]
		Mutation	50	[61, 62]
	Lung	Overexpression	50	[63]
	Melanoma	Mutation	5	[56]
Rac2	Melanoma	Mutation	10	[56]
Cdc42	Breast	Overexpression	95	[59]
	Colorectal	Overexpression	60	[64]
	Melanoma	Mutation	5	[56]