Mutational analysis of selected high-grade malignancies in a premenopausal gynecologic cancer population: a potential for targeted therapies?

Table 1 Genes mutated in our cohort and found to be significant

Gene	n = 20	p-value 1-tailed	p-value 2-tailed	Targeted Therapy
ASXL1	3 (15%)	0.120	0.022	Sorafenib (CMML with FLT3-ITD mutation and a corresponding ASXL1 mutation) ¹
ALK	2 (10%)	0.010	0.022	Crizotinib (NSCLC with ALK-EML4 fusion transformation) ² ; Ceritinib (NSCLC or other cancers) ³
EGFR	1 (5%)	0.065	0.130	Erlotinib (NSCLC) ⁴ ; Afatinib (NSCLC) ⁵ ; Gefitinib (NSCLC) ⁶
ERBB3	4 (20%)	0.014	0.028	MM-121 (Clinical Trial NSCLC; sensitizes to other chemo) ⁷ ; MM-111 (Clinical Trial Breast Cancer) ⁸ ; U3–1287/AMG-888 (Clinical Trial Metastatic BCA) ⁹
GPR124	4 (20%)	0.014	0.028	miR-138-5p (NSCLC cell lines; sensitizes to chemo) ¹⁰
KMT2D	4 (20%)	0.014	0.130	None currently; Aka MLL2; (Head and Neck cancer biology) ¹¹
NTRK1	2 (10%)	0.109	0.022	Imatinib (Gleevec; GIST) ¹²
AKAP9	5 (25%)	0.050	0.100	None currently; (Breast, Thyroid) ^{13, 14}
ASXL	2 (10%)	0.011	0.241	Sorafenib (CMML with FLT3-ITD mutation and a corresponding ASXL1 mutation) ¹
CMPK1	5 (25%)	0.050	0.100	Deactivation of gemcitabine ¹⁵
MBD1	5 (25%)	0.050	0.100	Drug resistance (Pancreatic Cancer) ¹⁶
ROS1	5 (25%)	0.050	0.100	Crizotinib (NSCLC) ¹⁷

Both 1-tailed and 2-tailed p-values were determined; significant 2-tailed p-values are considered more sensitive; bold items indicate the p-value for genes found to be significant between cohorts