. Author manuscript; available in PMC: 2017 Jul 1.

Published in final edited form as: Int J Gynecol Pathol. 2016 Jul;35(4):289–300. doi: 10.1097/PGP.0000000000000243

Table 2.

Clinico-pathologic features, distribution of TP53 mutations and mutations in genes recurrently altered in endometrial cancers in TP53-mutant endometrioid and serous endometrial carcinomas.

		Total (n)	Histologic type		p-value
		Total (n)	Endometrioid (n=27)	Serous (n=37)	p-value
Tumor grade	Grade 1	2	2	0	0.0002^**
	Grade 2	8	8	0
	Grade 3	54	17	37
Integrative genomic subtype	CN-high	52	15	37	0.0002^**
	CN-low	1	1	0
	MSI	5	5	0
	POLE	6	6	0
Type of TP53 mutation	Frameshift	7	3	4	0.7030^**
	Missense	49	20	29
	Nonsense	7	4	3
	Splice-site	1	0	1
Hotspot TP53 mutation	No	43	23	20	0.0144^*
Hotspot TP53 mutation	Yes	21	4	17	0.0144^*
ARID1A gene status	Wild-type	57	23	34	0.4427^*
ARID1A gene status	Mutant	7	4	3	0.4427^*
FBXW7 gene status	Wild-type	50	24	26	0.1247^*
FBXW7 gene status	Mutant	14	3	11	0.1247^*
PPP2R1A gene status	Wild-type	52	25	27	0.0578^*
PPP2R1A gene status	Mutant	12	2	10	0.0578^*
PTEN gene status	Wild-type	46	10	36	<0.0001^*
PTEN gene status	Mutant	18	17	1	<0.0001^*

Fisher’s exact test p-value;

^**

Chi-square test p-value.

CN-high, copy-number high (serous-like) integrative genomic subtype; CN-low, copy-number low (endometrioid) integrative genomic subtype; MSI, microsatellite instable (hypermutated) integrative genomic subtype; n, number of TP53-mutant cases; POLE, POLE (ultramutated) integrative genomic subtype. Hotspot TP53 mutations include R175, G245, R248, R249, R273 and R282.