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

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

Cancer Study Type GNASb (%c) GNASa,b RASb RASb 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
  1. 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
  2. bActivating alleles of GNAS and/or KRAS
  3. c% GNAS activating alleles with two or more occurrences in the cancer cohort