Results

ERa and total ERP expression was observed in all examined samples ofnormal and ECA. ERp expression was further subdivided into its constituent isoforms. The expression of transcripts for ERpi, ERP2 (Pcx), ERP4, and ERp5 was observed. From these isoforms, only ERp5 differed significantly (P = 0.010) between normal and ECA samples showing an increase in the latter (Table 1). The levels of expression of ERP 1 mRNA and the "wild-type" ERp, also increased, but were not significant. Although the expression of ERp4 in the healthy as well as in ECA was observed, the level of expression was at the detection margins and its quantification

Figure 1. Schematic representation of estrogens.

unreliable. ERp3 expression was at such low levels oftarget gene mRNA, that was neither detected nor reliably quantified.

Table 1. Expression Levels of ERa, ERP Variants, PR, and AR in Human Normal and Neoplastic Endometrium.

Normal P values Endometrium ECA(n = 19) Normal vs (n = 21)___ECA

Normal P values Endometrium ECA(n = 19) Normal vs (n = 21)___ECA

Table 1. Expression Levels of ERa, ERP Variants, PR, and AR in Human Normal and Neoplastic Endometrium.

M ± SD1

Range

M±SD

Range

pW

Genes

Values

Values

M

ERa

1.0 ±0.69

0.28-2.65

0.79 ± 0.47

0.02-1.89

NS2 (0.59)3

ERP

1.0 ±0.61

0.11 —2.49

0.90 ±0.59

0.14-2.46

NS2 (0.62)3

ERpI

1.0 ± 0.74

0.08-3.16

1.56 ± 1.16

0.20-4.76

NS2 (0.12)3

ERp2

1.0 ±0.58

0.14-2.08

0.85 ± 0.48

0.15-1.73

NS2 (0.39)3

ERp3

NE4

-

NE4

-

-

ERP4

5 WE5

-

5 WE5

-

NS2 (0.85)6

ERp5

1.0± 1.07

0.11-4.21

1.95 ± 1.58

0.23 - 5.96

P=0.0103

PR

1.0 ±0.86

0.16-3.43

0.82 ±0.81

0-3.34

NS2 (0.46)3

AR

1.0 ±0.57

0.29-2.10

0.56 ± 0.36

0.04-1,10

P= 0.036s

1 Mean ± SD 2 NS, Not Significant 3 P value, Kruskal-Wallis test

4NE, Not expressed 5 WE, Without expression 6 P value, analysis

1 Mean ± SD 2 NS, Not Significant 3 P value, Kruskal-Wallis test

4NE, Not expressed 5 WE, Without expression 6 P value, analysis

The expression levels of all ER transcripts were additionally analysed in pre and postmenopausal normal endometria, and in two stages of increasing tumor malignancy indicated by the degree of infiltration of myometrium, where < Vi infiltration, was indicated as IC; and Infiltration, as IB (Figure 2). The ERa mRNA expression was increased in normal postmenopausal endometrium as compared to healthy premenopausal samples (P = 0.01) (Figure 3). Besides estrogen, progestagens and androgens affect the biological function ofthe female reproductive tract. Thus, we also assessed the profile of PR and AR mRNA in normal and ECA tissue samples. We observed that the AR mRNA underwent significant (P, 0.036) down-regulation in the ECA samples. With respect to its profile in normal endometrium, the AR was significantly (P, 0.043) up-regulated in the postmenopausal patients. The PR mRNA, on the other hand, showed a decline (P, 0.041) in expression in more malignant ECA (1C), compared to ECA with less or no infiltration of the myometrium (1A and 1B). (Figure 2).

Figure 2. Expression of ERa, ERß5, and PR in relation to FIGO. Myometrium infiltration> V2,was IC;and < // IB. PR down regulation was observed in IC grade (P, 0.0041).
Figure 3. Expression of ERa, ERp, ERpi, Bpcx, ERP5, and AR in pre and postmenopausal endometrium. Significantly increasing ofERa (P, 0.001) and AR (P, 0.0043) in postmenopausal endometrium.

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