Table 2.

Some prominent growth factors and receptor tyrosine kinases rely on monomeric G-proteins such as Ras and Rho to drive cancer progression. Using the PCAIs to uncouple the functional protein-protein interactions involving G-proteins downstream of the receptors might curtail the excessive signaling from the upstream receptors as K-Ras, Rho, Rac1 and Cdc42 that drive cancer progression are depleted in PCAIs-treated cancer cells [48, 50, 51, 71].

Protein	Cancer type	Aberrations	Incidence rate (%)	References
Epidermal growth factor receptor, EGFR (ErbB-1)	Pancreatic cancer	Overexpression	90	[72]
	Glial tumors	Overexpression	50	[73]
	Non-small cell lung cancer	Amplification and mutation	10	[73, 74]
	Non-small cell lung cancer	Overexpression	40-80	[75]
	Breast	Mutation	60	[53]
	Head and Neck	Amplification	7	[76]
	Colon cancer	Amplification	6	[77]
	Ovarian cancer	Overexpression	64	[78]
HER2 (ErbB-2)	Breast cancers	Overexpression	20-25	[79]
	Colon cancer	Overexpression	15.5	[80]
ErbB-3	Lung	Overexpression	50-70	[81]
	Breast	Overexpression	50-70	[81]
	Colon	Overexpression	50-70	[81]
ErbB-4	Colon	Overexpression	22	[81]
IGF1R	Breast	Amplification	10	[81]
	Melanoma	Amplification	3	[81]
	Prostate cancer risk	Amplification	4.3	[82]
IGF2R	Breast	Mutations	40	[83]
	Hepatocellular	Mutations	80	[84]
	Colorectal	Mutations	5	[85]
bFGF	Prostate	Overexpressed	83	[86]
VEGF	Colon	Overexpression	55.5	[80]
	Ovarian cancer	Overexpression	25	[78]