The curious case of Gαs gain-of-function in neoplasia

BMC Cancer

Table 1 Activating alleles of Gαs and/or Rαs in cBioPortal cancer cohorts

Cancer Study Type	GNAS^b	(%^c)	GNAS^a,b RAS^b	RAS^b	Percent	Total Samples
AML	0		0	21	(11%)	191
Bladder	0		0	0	(0%)	131
Breast Cohort 1	1		0	6	(1%)	816
Breast Cohort 2	1		0	3	(1%)	482
Renal Clear Cell Carcinoma	0		0	0	(0%)	499
Colorectal Adenocarcinoma	1		0	91	(43%)	212
Head and Neck Squamous Cell	0		0	0	(0%)	279
Diffuse Glioma	0		0	8	(1%)	794
Lung Adenocarcinoma	2	(2%)	2	76	(33%)	230
Lung Squamous Cell Carcinoma	0		0	0	(0%)	178
Pan-Lung Cancer	5	(<1%)	3	232	(20%)	1144
High Grade Serous Ovarian Cancer	0		0	4	(1%)	316
Pancreatic Adenocarcinoma	7	(5%)	3	138	(93%)	149
Prostate Adenocarcinoma	0		0	0	(0%)	333
Stomach Adenocarcinoma	3	(1%)	1	28	(10%)	287
Papillary Thyroid Cancer	0		0	0	(0%)	507
Uterine Endometrial Carcinoma	0		0	51	(21%)	240

^aCoincidence of GNAS and KRAS activating mutations. Among the cancer cohorts from TCGA in cBioPortal [100, 101], pancreatic adenocarcinoma, pan-lung, and stomach cancers had the highest frequencies of activating alleles of Gαs in the absence of KRAS mutations
^bActivating alleles of GNAS and/or KRAS
^c% GNAS activating alleles with two or more occurrences in the cancer cohort

ISSN: 1471-2407