Objective To discuss the role of oxidative stress (OS) and estrogen receptor (ER) levels in ectopic endome-trium in patients with pelvic pain. Methods The ectopic endometrium was taken from patients with mild, moderate and se-vere pelvic pain, and samples were divided into mild group (n=29), moderate group (n=34) and severe group (n=26). The nor-mal samples of endometrium (n=30) were used as control group. Xanthine oxidase method was used to detect the level of su-peroxide dismutase (SOD), thiobarbituric acid colorimetric method was used to detect the level of malondialdehyde (MDA) and immunohistochemistry was used to detect the level of estrogen receptor (ER). The correlation of MDA, SOD and ER lev-els was analysed between three ectopic endometrium groups. Results The SOD levels were significantly lower and MDA and ER levels were significantly higher in three ectopic endometrium groups than those in control group (P<0.05). The SOD levels were decreased, while MDA and ER levels were gradually increased with increased pain intensity in three groups of ec-topic endometrium (P<0.05). There was no correlation between MDA level and ER level in mild group (P>0.05). A posi-tive correlation was found between MDA and ER levels in moderate and severe groups (P<0.05). There was no relationship between SOD and ER levels in three ectopic endometrium groups (P>0.05). Conclusion Over-expression of OS and ER presents in ectopic endometrium, and both participate in the occurrence of pelvic pain, and create synergies in pelvic pain of ectopic endometrium.

Objective To study the role of epidermal growth factor (EGF),epidermal growth factor receptor(EGFR),extracellular signal-regulated kinase 1/2 (p-ERK1/2) in the pathogenesis of endometriosis under estrogen deprivation conditions.Methods The estrogen was quickly-stripped in medium and the female nude mice were castrated by bilateral oophorectomy to build estrogen deprivation in vitro and in vivo experimental models,respectively.(1) In vitro experiments:according to different treatments the estrogen deprived ectopic endometrial cells were classified into 4 groups:①EGF group:the ectopic endometrial cells were cultured for 72 hours with different concentrations of EGF (0.01,0.1,1,10,50,100 ng/ml),the results of EGF group were represented by the result of cells treated by 10 ng/ml EGF cultured for 72 hours ; ②EGF + PD98059 group:the ectopic endometrial cells were cultured for 72 hours with 5 × 10-2 mol/L PD98059 (inhibitor of ERK),followed by a cultivation for 72 hours treated by 10 ng/ml EGF + 5 × 10-2 mol/L PD98059 ; ③EGF + ICI182780 group:the ectopic endometrial cells were cultured for 72 hours with 10-6 mol/L ICI182780 [inhibitor of estrogen receptor(ER)],followed by a cultivation for 72 hours treated by 10 ng/ml EGF + 10-6 mol/L ICI182780; ④Blank control group:the ectopic endometrial cells were cultured with no treatment.The proliferation activity of ectopic endometrial cells in all groups after treatment were examined by methyl thiazolyl tetrazolium (MTT) method represented by absorbance value (A).The expression of p-ERK1/2 protein were detected by western blot.(2) In vivo experiments:64 female nude mice were randomly divided into control and castration groups (both n =32) using random number chart.The mice in castration group were castrated by bilateral oophorectomy on 3 weeks after the endometriosis model was established.The levels of EGF,EGFR,p-ERK1/2 protein in ectopic lesions of both groups were measured on 4,6,8 and 10 weeks after the endometriosis model was established by western blot.Results (1) The proliferation activity of ectopic endometrial cells:the proliferation activity of ectopic endometrial cells treated by different concentrations of EGF (0.01,0.1,1,10,50,100 ng/ml) for 72 hours were 0.310 ± 0.010,0.340 ± 0.020,0.670 ± 0.010,0.980 ± 0.030,1.360 ± 0.020,1.670 ± 0.020,respectively,the proliferation activity was increased along with of EGF concentrations.The proliferation activity was 0.680 ± 0.030 at EGF + PD98059 group,the differences exhibited significant difference when compared with that at EGF group with 100 ng/ml for 72 hours(P ＜0.01).The proliferation activity of EGF + ICI182780 and blank control groups were 0.330 ±0.030 and 0.310 ±0.030,respectively,which did not reached statistical differences(P ＞ 0.05).(2) The expression of EGF,EGFR,pERK1/2 protein:① In vitro experiments:the levels of p-ERK1/2 protein in EGF and blank control groups were 0.670 ± 0.020 and 0.600 + 0.010,respectively,which reached statistical differences (P ＜ 0.05).The level of p-ERK1/2 protein in EGF + PD98059 group was 0.610 ± 0.020,which exhibited significant differences with that at blank control group(P ＞ 0.05).② In vivo experiments:at 4,6 and 8 weeks after the endometriosis models were established,the expression of EGF protein in the ectopic lesions of castration group and control group were (0.530±0.015 versus 0.610 ±0.015),(0.400 ±0.029 versus 0.620 ±0.018),(0.560 ±0.026versus 0.630 ± 0.021),respectively,the levels of EGFR protein were (0.500 ± 0.030 versus 0.640 ±0.030),(0.470 ± 0.020 versus 0.630 ± 0.020),(0.510 ± 0.030 versus 0.610 ± 0.020) respectively,and the level of p-ERK1/2 protein were (0.500 ± 0.020 versus 0.580 ± 0.020),(0.490 ± 0.020 versus 0.580 ±0.020),(0.570 ±0.020 versus 0.590 0.020),respectively.The difference of EGF,EGFR,pERK1/2 protein expression levels between two groups did not exhibited significant difference(P ＜ 0.01,P ＜0.01,P ＜0.05).At 10 weeks after the endometriosis models were established,the levels of EGF protein in castration group and control group were both 0.620 ± 0.020,the levels of EGFR protein were both 0.610 ±0.020,and the level of p-ERK1/2 protein were 0.590 ±0.010 and 0.600 ± 0.020.No statistical difference (P ＞0.05) was found between those two groups (P ＞ O.05).Conclusions EGF could stimulate the proliferation of ectopic endometrial cells by activating the ERK pathway under estrogen deprivation conditions.The inhibition of EGF signaling system in ectopic lesions was alleviated along with the prolongation of the period of estrogen deprivation.

[Objective]To explore the MRI features of the mucinous breast carcinoma and the correlation with biological prognos?tic factors.[Methods]MRI features of 35 pure and 15 mixed mucinous carcinomas were retrospectively analyzed. MR images were reviewed for shape,margin,the signal intensity,enhancement patterns of tumors and DWI features. All the patients were detected by immunohistochemical staining with expression of ER,PR,CerbB-2,Ki-67 and Her-2. Correlations between the pure and mixed mucinous breast carcinoma and prognostic factors were analyzed.[Results]16 oval masses(16/35,45.7%)and 10 circular masses (10/35,28.6%)were found in 35 pure mucinous breast carcinomas with clear boundary(26/35,74.3%)and lobulated shape(31/35,88.6%);9 irregular masses(9/15,60%)were found in mixed mucinous breast carcinomas with unclear boundary(13/15, 86.7%). Very high signal intensity on T2-weighted images was found in 33 pure mucinous carcinomas(33/35,94.3%)and 11 mixed mucinous carcinomas showed mixed signal intensity(11/15,73.3%). Early enhancement rate was(114.7 ± 9.1)% for pure muci?nous carcinomas and(165.6 ± 14.3)%for mixed mucinous carcinomas. 28 pure mucinous tumors demonstrated persistent enhancing pattern on time-signal intensity curve ,7 pure mucinous tumors demonstrated plateau pattern and 7 mixed mucinous carcinomas showed plateau pattern and washout pattern respectively. Mean ADC value was(1.91 ± 0.06)×10-3 mm2/s for pure mucinous carcino?mas and(1.13±0.08)×10-3mm2/s for mixed mucinous carcinomas. There was significant difference with morphology,boundary,T2WI signal,early enhancement rate,time-signal intensity curve,ADC value between pure and mixed mucinous breast carcinoma(P <0.05). There was significant difference between pure and mixed mucinous breast carcinoma with Her-2 and Ki-67 expression(P <0.05).[Conclusion]MRI could identify PMBC and MMBC from the shape,the signal intensity,dynamic enhancement and ADC val?ue,and PMBC had distinctive MRI features. The prognosis of MMBC is worse than that of PMBC form correlation between biological prognostic factors and mucinous breast carcinoma.

Objective:To investigate the value of synthetic MRI quantitative parameters in identifying different molecular types of breast cancer and triple negative breast cancer (TNBC) and non-TNBC.Methods:A retrospective analysis was performed on 208 patients diagnosed with invasive ductal breast cancer in the First Affiliated Hospital of China Medical University from March 2019 to September 2020. All patients underwent synthetic MR examinations and the following quantitative parameters were measured, including tumor diameter, volume, apparent diffusion coefficient (ADC), and corresponding values of T 1, T 2, and proton density (PD). According to the immunohistochemical results, there were 122 cases of progesterone receptor (PR) positive and 86 cases of PR negative, 123 cases of estrogen receptor (ER) positive and 85 cases of ER negative, 79 cases of human epidermal growth factor receptor-2 (HER2) positive and 129 cases of HER2 negative, 149 cases of Ki-67 high expression and 59 cases of Ki-67 low expression; there were 36 cases of TNBC and 172 cases of non-TNBC. Independent samples t test or Mann-Whitney U test were used to compare the quantitative parameters of different molecular types, TNBC and non-TNBC patients. Multivariate logistic regression was used to analyze independent predictors of TNBC, and receiver operating characteristic curve and area under the curve (AUC) were used to evaluate the efficacy of sole and combined parameters in identifying TNBC. Results:T 1 and T 2 values in PR negative breast cancer patients were higher than those in PR positive patients ( t=2.30, Z=2.04, P<0.05); the values of T 1 and T 2 in ER negative patients were higher than those in ER positive patients ( t=2.52, Z=2.48, P<0.05); ADC value and tumor diameter of HER2 positive patients were larger than those in HER2 negative patients ( t=-3.21, Z=-3.22, P<0.05). T 2 value, tumor volume and diameter in patients with Ki-67 high expression were significantly higher than those in patients with Ki-67 low expression ( Z=-3.47, -2.51, -2.84, P<0.05); ADC value in Ki-67 high expression group was less than that in Ki-67 low expression group ( t=3.94, P<0.001). T 1, T 2 values and tumor volume in TNBC patients were higher than those in non-TNBC patients ( t=-3.26, Z=-5.58, Z=-2.02, P<0.05], and ADC value in TNBC patients was lower than that in non-TNBC patients ( t=3.07, P=0.002). Multivariate logistic regression analysis showed that T 2 (OR=1.060, 95%CI 1.028-1.093, P<0.001) and ADC value (OR=0.947, 95%CI 0.911-0.984, P=0.005) were independent predictors of TNBC. The efficacy of each parameter alone and in combination to identify TNBC showed that the T 2 value in the single parameter had the largest AUC (0.759), and there was no significant difference between T 2 value and its combined parameters in the diagnosis of TNBC. Conclusions:The quantitative parameters based on synthetic MRI, especially T 2 value, have value in differentiating different molecular types of breast cancer, TNBC and non-TNBC may be another non-contrast parameter for evaluating tumor aggressiveness beyond ADC value.