Analysis of factors associated with postoperative acute kidney injury in patients with colorectal cancer / 中华普通外科杂志

Objective:To investigate factors associated with acute kidney injury(AKI) in postoperative colorectal cancer patients.Methods:The clinical data of 376 colorectal carcinoma (CRC) patients at Department of General Surgery, Affiliated Cancer Hospital of Zhengzhou University from Jan 2018 to Jun 2021 were retrospectively analyzed. Patients were divided into acute kidney injury (AKI) ( n=29) and non-AKI groups ( n=347). The demographic information, perioperative status, laboratory results and other relevant data of the two groups were compared . Binary logistic regression was used to analyze the independent risk factors for postoperative AKI. Results:Twenty-nine CRC patients (7.7%) had postoperative AKI. Binary Logistic regression analysis showed that preoperative hypertension ( OR=3.487, 95% CI: 1.081-11.251, P=0.037), anemia ( OR=3.158, 95% CI: 1.114-8.953, P=0.031), inadequate intraoperative crystalloid infusion ( OR=0.998, 95% CI: 0.997-0.999, P=0.007), low intraoperative mean arterial pressure ( OR=0.915, 95% CI: 0.863-0.970, P=0.003) and moderate to severe postoperative decline in hemoglobin levels ( OR=4.105, 95% CI: 1.487-11.335, P=0.006) were independent risk factors. Conclusion:Preoperative hypertension, anemia, inadequate intraoperative crystalloid infusion, low intraoperative mean arterial pressure, and moderate to severe postoperative decline in hemoglobin levels were independent risk factors for AKI development in colorectal cancer patients.

Periostin regulated by let-7/miR-98 family mediates the apoptosis and epithelial-mesenchymal transition of colon cancer / 中华肿瘤杂志

Objective@#To observe the expressions of periostin (Postn) in colon cancer tissues and cells, and to investigate its biological effect and mechanism in colon cancer cells.@*Methods@#Real-time quantitative polymerase chain reaction (RT-qPCR) and western blot were used to detect the expressions of Postn, let-7a and miR-98 in 20 pairs of colon cancer tissues and adjacent normal tissues, colon cancer cell lines including SW480, HT-29, HCT-116 and human normal colon epithelial cell NCM460. Small interfering RNAs (siRNAs) of Postn, pcDNA3.1-Postn plasmids, let-7a mimic and its negative control let-7a mimic-NC, miR-98 mimic and its negative control miR-98 mimic-NC were transfected into HCT-116 cells. 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2H tetrazolium bromide (MTT) was used to detect cell viability. Flow cytometry was used to detect cell apoptosis. Luciferase reporter gene assay was used to determine the targeting relationship between miRNAs and Postn.@*Results@#Compared with adjacent normal tissues, Postn expression was up-regulated (P<0.05) while let-7a/miR-98 expression was down-regulated (P<0.05) in colon cancer tissues. Compared with NCM460 cells, Postn expression was up-regulated (P<0.05) while let-7a/miR-98 expression was down-regulated (P<0.05) in SW480, HT-29 and HCT-116 cells. In colon cancer tissues, the expression of Postn was negatively correlated with the expressions of let-7a and miR-98 (r=-0.69, P<0.001; r=-0.80, P<0.001). Inhibition of Postn in vitro reduced the viability of HCT-116 cells [(53.73±7.63)%, P<0.05], increased the apoptotic rate [(22.88±3.40)%, P<0.05], enhanced the expression of epithelial-mesenchymal transition (EMT) marker E-cadherin (2.44±0.39, P<0.05), while down-regulated the expressions of N-cadherin and Vimentin (0.44±0.07 and 0.38±0.06, P<0.05). Overexpression of Postn in vitro enhanced the cell viability of HCT-116 cells [(134.41±8.82) %, P<0.05], decreased the expression of E-cadherin (0.55±0.09, P<0.05), increased the expressions of N-cadherin and Vimentin (2.93±0.42 and 2.24±0.34, P<0.05), but had no effect on the apoptotic rate (P>0.05). Overexpression of let-7a or miR-98 partially reversed the biological effects of Postn overexpression in colon cancer cells, which implicated that Postn was a target gene of let-7a/miR-98.@*Conclusions@#Postn is a cancer-promoting molecule of colon cancer, and inhibition of Postn expression can increase the apoptotic rate of colon cancer cells and repress EMT. Postn expression and function is regulated by let-7a/miR-98.

MiR-145 inhibits drug resistance to Oxaliplatin in colorectal cancer cells through regulating G protein coupled receptor 98 / 中华胃肠外科杂志

<p><b>OBJECTIVE</b>To predict and identify the target gene of miR-145, and to explore the underlying mechanism of the inhibition of miR-145 on drug resistance to Oxaliplatin (L-OHP) in human colorectal cancer cells.</p><p><b>METHODS</b>L-OHP-resistant human colorectal cancer cell line (HCT116/L-OHP) was established in vitro by exposing to increased concentrations of L-OHP in cell culture medium. MiR-145-mimics and its negative control (NC-miRNA) were transfected into HCT116/L-OHP cells using liposome to establish HCT116/L-OHPover-expressing miR-145 and HCT116/L-OHP. The target genes of miR-145 were predicted by bioinformatic analysis, and validated by dual luciferase activity assay. After determination of G protein coupled receptor 98(GPR98) as target gene, corresponding plasmids were constructed and transfected to establish HCT116/L-OHPover-expressing GPR98 and HCT116/L-OHP. HCT116/L-OHP cells over-expressing both GPR98 and miR-145 (HCT116/L-OHP) were acquired through modification of the binding sites of GPR98 cDNA with miR-145. CCK-8 assay was used to assess the proliferation (A value) and sensitivity to L-OHP (the lower the IC50, the stronger the sensitivity) in HCT116/L-OHP cells. Real-time quantitative PCR was used to measure the mRNA expression of miR-145 and GPR98. Western blot was used to examine the protein expression of GPR98 and drug-resistant associated protein, such as P-glycoprotein (gp), multiple drug-resistance protein 1(MRP1), cancer-inhibition gene PTEN.</p><p><b>RESULTS</b>HCT116/L-OHP cell line was successfully established with ICof (42.34±1.05) mg/L and miR-145 mRNA expression of 0.27±0.04, which was higher than (9.81±0.95) mg/L (t=39.784, P=0.000) and lower than 1.00±0.09 (t=13.021, P=0.000) in HCT116 cells. Based on HCT116/L-OHP cells, HCT116/L-OHPcells were established successfully, with relative miR-145 expression of 10.01±1.05, which was higher than 1.06±0.14 in HCT116/L-OHPand 1.00±0.16 in HCT116/L-OHP (F=161.797, P=0.000). GPR98 was identified to be the target gene of miR-145. The relative mRNA and protein expressions of GPR98 in HCT116/L-OHPcells were 8.48±0.46 and 1.71±0.09, respectively, which were higher than those in HCT116/L-OHP(mRNA: 3.65±0.40, protein: 1.21±0.10) and HCT116/L-OHP (mRNA: 3.49±0.35, protein: 1.22±0.08; all P<0.05). The A value was 1.31±0.10, and the relative protein expressions of P-gp and MRP1 were 1.53±0.18 and 1.49±0.20 in HCT116/L-OHPcells, which were higher than those in HCT116/L-OHP (A value: 0.82±0.08, relative protein expression: 1.00±0.06 and 1.21±0.13, all P<0.05). The A value was 0.89±0.08, and the relative protein expressions of P-gp and MRP were 1.02±0.24 and 1.38±0.25 in HCT116/L-OHPcells, which were higher than those in HCT116/L-OHP(A value: 0.20±0.05, relative protein expression: 0.20±0.07, 0.55±0.10, all P<0.05). The relative protein expression of PTEN in HCT116/L-OHPcells was 0.12±0.03, which was lower than 1.25±0.14 in HCT116/L-OHP cells(P<0.05). In addition, relative protein expressions of P-gp and MRP1 were 1.02±0.24 and 1.38±0.25 in HCT116/L-OHPcells, which were higher than those in HCT116/L-OHPcells (0.20±0.07 and 0.55±0.10), while PTEN expression in HCT116/L-OHPcells was lower as compared to HCT116/L-OHPcells (1.41±0.16 vs. 1.98±0.13, P<0.05).</p><p><b>CONCLUSION</b>MiR-145 inhibits drug resistance to L-OHP of HCT116 cells through suppressing the expression of target gene GPR98.</p>

Detection and clinical significance of myeloid-derived suppressor cells in peripheral blood of patients with rectal carcinoma / 中华胃肠外科杂志

<p><b>OBJECTIVE</b>To study the expression of myeloid-derived suppressor cells (MDSC) in peripheral blood of patients with rectal carcinoma and to preliminarily explore its clinical significance.</p><p><b>METHODS</b>Blood samples from 76 rectal carcinoma patients who underwent surgery in Department of General Surgery, The Affiliated Cancer Hospital, Zhengzhou University between June and October 2013 were collected before operation, postoperative day 10 and 2 years after operation respectively. Flow cytometry was used to detect MDSC percentage in peripheral blood of 76 rectal carcinoma patients and 40 healthy people. The change of MDSC percentage in peripheral blood of rectal carcinoma patients after treatment was investigated. Furthermore, the relationship of peripheral blood MDSC percentage with clinicopathological characteristics was examined.</p><p><b>RESULTS</b>Preoperative MDSC percentage in peripheral blood of 76 rectal carcinoma patients [(3.52±0.68)%] was higher than that of 40 healthy people[(0.92±0.21)%], with significant difference (t=3.026, P=0.005). Preoperative MDSC percentage in peripheral blood of rectal carcinoma patients was significantly related with histological classification (t=2.453, P=0.018), depth of tumor invasion (t=2.051, P=0.035), lymph node metastasis (t=2.328, P=0.022), TNM stage (t=2.529, P=0.016). Univariate analysis showed that TNM stage, histological classification, lymph node metastasis, preoperative MDSC percentage in peripheral blood were the prognostic factors in rectal carcinoma. Multivariate analysis showed that TNM stage (HR=2.535, 95%CI: 0.851 to 4.160, P=0.038) and preoperative MDSC percentage in peripheral blood (HR=3.651, 95%CI: 0.877 to 14.263, P=0.031) were independent prognostic factors of rectal carcinoma. MDSC percentage in peripheral blood of rectal carcinoma patients decreased significantly on the postoperative 10-day [(2.41±0.46)%] compared to that before operation [(3.52±0.68)%], whose difference was statistically significant (t=1.778, P=0.043). During follow-up, tumor recurrence or metastasis was found in 23 patients. MDSC percentage in peripheral blood of rectal carcinoma patients with recurrence or metastasis [(4.37±1.23)%] was higher than that of rectal carcinoma patients without recurrence or metastasis [(2.36±0.35)%] two years after operation, with statistically significant difference (t=1.982, P=0.039).</p><p><b>CONCLUSIONS</b>MDSC percentage in peripheral blood of rectal carcinoma patients is significantly elevated compared to that of healthy people. Increased MDSC percentage indicates poor prognosis and tumor progression in rectal carcinoma patients. Measurement of peripheral blood MDSC percentage may have a potential clinical value in prognosis prediction of rectal carcinoma.</p>

Expression of heat shock protein 27, 60 and 90 in gastric cancer and its clinical value / 中国免疫学杂志

Objective: To investigate the expression of HSP-27,-60 and -90 in gastric cancer and its clinical significance. Methods:66 cases of gastric carcinoma was detected by immunohistochemistry HSP-27,60 and 90 of the expression and clinical significance of combined with clinical and pathological characteristics, tumor cell proliferation and survival analysis of three kinds of heat shock protein expression. Results: HSP-27,-60 and -90 were highly expressed in gastric cancer tissues. HSP-27 expression and tumor size (pT,P=0. 026),organ metastasis (pM,P=0. 046) and pathological staging (P=0. 041),HSP-27 staining intensity and lymph node status were significantly correlated ( pN, P=0. 042 ) . HSP-60 expression was associated with gender ( P=0. 011),and HSP-60 staining intensity was associated with age (P=0. 027) and tumor grade (P=0. 031). There was no correlation between HSP-90 expression and the clinical pathological parameters of this study; however, the intensity of HSP-90 staining was significantly correlated with tumor size (P=0. 020,pT). Single factor analysis showed that HSP-90 was significantly associated with longer survival (P=0. 033). Multivariate analysis demonstrated that HSP-90 was highly expressed as an independent prognostic factor for gastric cancer (P=0. 026). Conclusion: the HSP-27,-60 and -90 and some clinical pathological parameters. These parameters is very important for the treatment of patients with gastric cancer. The high expression of HSP-90 in patients with gastric cancer were inde-pendent prognostic indicators.

Effects and mechanism of silent information regulator of transcription 1 in the drug-resistance of colonic cancer / 中华消化外科杂志

Objective To investigate the effects of mechanism of silent information regulator of transcription 1 (SIRT1) in the drug-resistance of colonic cancer.Methods The clinical data of 25 colonic cancer patients with 5-Fu-resistance and 30 colonic cancer patients with chemosensitivity who were admitted to the Henan Tumor Hospital from December 2012 to December 2013 were retrospectively analyzed.The specimens of colonic cancer were collected for study.(1) The protein expression of SIRT1 in patients with drug-resistance or chemotherapeutic sensitivity was tested by immunohistochemical staining.The protein expression of SIRT1 in the HCT116 and HCT1 16/5-FU cells was detected by Western blot.(2)HCT116/5-FU cells were interfered by siRNA and divided into the blank control group (cells untreated),the empty vector group (cells treated by siRNA) and the SIRT1 silence group (cells treated by SIRT1 siRNA).The protein expression of the HCT116/5-FU cells were inhibited by the c-Jun N-terminal kinase (JNK) and then divided into the SP600125 group [cells were treated by JNK signaling pathway inhibitor SP60012 (concentration:30 μmol/L)for 12 hours],the DMSO group [cells were treated by DMSO (cells were treated by 0.1％ DMSO for 12 hours] and the control group (cells were treated by cell culture media).(3) Serine in the SIRT1 ser47 was mutated to alanine or aspartic acid,and mutations S47A (S47A group,serine to alanine) and S47D (S47D group,serine to aspartic acid) ; Untransfected HCT116/5-FU cells were in the S47 wild type group,and apCMV-3Tag-3 cells transfected by empty vector were served as negative control; all the HCT116/5-FU cells were interfered by 5-FU (concentration:8 μmol/L) for 12 hours.HTC116 cells and HTC116/5-FU cells were treated by SIRT1 inhibitor resveratrol at concentrations of 0,1,10,50,100 nmol/L and SIRT1 activator niacinamide at concentrations of 0,1,2,3,4,5 ng/L.Cell proliferation was detected by MTF.(4) Cell apoptosis was detected by flow cytometry.(5) The expressions of related genes were detected by real-time PCR.(6)The expressions of related proteins were detected by western blot.The count data were analyzed using the chi-square test.The measurement data with normal distribution were presented as (x) ± s.The comparison among groups were analyzed using the one-way analysis of variance and LSD-t test.The pairwise comparisons were analyzed using the t text.Results (1) The results of immunohistochemical staining were as follows.The positive expressions of SIRT1 in patients with chemotherapeutic sensitivity and drug-resistance were 16.7％ (5/30) and 92.0％ (23/25),respectively,with significant difference (x2 =30.965,P ＜ 0.05).The relative mRNA and protein expressions of SIRT1 in HCT116/5-FU cells with drug-resistance were 1.870 ± 0.100 and 1.660 ± 0.109,which were significantly higher than 1.000 ± 0.070 and 1.000 ± 0.050 in HCT116/5-FU cells without drug-resistance (t =11.721,8.963,P ＜ 0.05).(2) The results of MTT were as follows.The proliferation rates of HCT116/5-FU cells treated by resveratrol at concentrations of 0,1,10,50 nmol/L were 100％ ±12％,105％± 14％,129％ ± 10％ and 144％ ± 17％,which were significantly higher than 41％ ± 10％,49％ ±11％,74％ ± 16％ and 105％ ± 17％ of HCT116 cells which were treated by reseratrol at the same contrations (t =8.226,-7.236,6.673,3.510,P ＜0.05).The proliferation rates of HCT116/5-FU cell treated by niacinamide at concentrations of 0,1,2 ng/L were 87％ ± 12％,78％ ± 12％,69％ ± 11％,which were significantly higher than 36％ ± 6％,32％± 5％,30％± 6％ of HCT116 cells which were treated by niacinamide at the same concentrations (t =-8.593,-8.006,-7.000,P ＜ 0.05).The proliferation rates of HCT116/5-FU cells in the blank control group,the empty vector group and the SIRT1 silence group were 100％± 8％,99％ ±9％,37％ ± 6％,with significant differences among the 3 groups (F =66.597,P ＜ 0.05),and the proliferation rate of HCT116/5-FU cells in the SIRT1 silence group was significantly lower than that in the blank control group (t =10.113,P ＜0.05).(3) The results of flow cytometry were as follows.The apoptotic rates of HCT116/5-FU cells in the SIRT1 silence group,the empty vector group and the blank control group were 60％ ± 5％,36％ ± 4％,35％ ±4％,with significant differences among the 3 groups (F =36.549,P ＜ 0.05),and the apoptotic rates of HCT1 16/5-FU cells in the SIRT1 silence group were significantly higher than that in the blank control group and the empty vector group (t =-7.215,-7.084,P ＜0.05).(4)The results of RT-PCR were as follows.The relative expression rates of P-gp mRNA in the HCT116/5-FU cells in the SIRT1 silence group,the empty vector group and the blank control group were 0.320 ± 0.030,0.990 ± 0.060,1.000 ± 0.090,with significant differences among the 3 groups (F =10.107,P ＜ 0.05),and the relative expression rate of P-gp mRNA in the SIRT1 silence group was significantly lower than that in the blank control group (t =11.463,P ＜ 0.05).The relative expression rates of P-gp mRNA in the HCT116/5-FU cells in the SP600125 group,the DMSO group and the control group were 0.240 ±.0.040,0.990 ± 0.100,1.000 ± 0.070,with significant difference among the 3 groups (F =19.002,P＜0.05),and the relative expression rates of P-gp mRNA in the SP600125 group was significantly lower than that in the control group (t =7.301,P ＜0.05).(5) The results of western blot were as follows.The relative expression rates of p-JNK protein in the HCT116/5-FU cells in the blank control group,the empty vector group and the SIRT1 silence group were 1.000 ± 0.090,1.090 ± 0.020,0.080 ± 0.010,with significant difference among the 3 groups (F =12.130,P ＜ 0.05).The ratios of p-SIRT1-S27/T-SIRT1,p-SIRT1-T530/T-SIRT1,p-SIRT1-S47/T-SIRT1 were 1.158 ±0.140,1.209 ±0.150,3.760 ±0.150 in HCT116 cells treated by 5-FU,and 1.120 ±0.109,1.130 ±0.100,2.160 ±0.110 in HCT116 cells treated by DMSO,with significant differences (F =9.763,10.261,P ＜0.05).The ratios of p-SIRT1-S47/T-SIRT1 in HCT116 cells treated by 5-FU and DMSO were 3.760 ± 0.150 and 2.160 ± 0.110,which were significantly higher than 0.940 ± 0.040 and 1.121 ± 0.110 in HCT116/5-FU cells (t =14.721,21.335,P ＜ 0.05).(6) The proliferation rates of HCT116/ 5-FU cells in the S47 wild type group,the negative control group,the S47A group and the S47D group were 41％± 31％,39％ ± 4％,64％ ± 2％ and 26％ ± 5％,with significant differences among the 4 groups (F =6.371,P ＜ 0.05).Conclusions SIRT1 promotes the proliferation of drug-resistant colonic cancer cells and increases the expression of P-gp via JNK signaling pathway,there by enhances cellular drug resistance.SIRT1 S47 is the critical site for 5-FU-resistance in HCT116/5-FU cells.

Function of death associated protein kinase(DAPK) in colorectal cancer chemoresistance / 中华胃肠外科杂志

<p><b>OBJECTIVE</b>To investigate the role of death associated protein kinase(DAPK) in colon cancer drug-resistance.</p><p><b>METHODS</b>Immunohistochemistry was used to detect DAPK expression in colon carcinoma tissues of 61 cases and adjacent tissues of 32 cases. 5-fluorouracil (5-FU)-induced drug-resistant colon cancer cell lines HCT116/5-FU model was established. DAPK-siRNA was transfected into cells to down-regulate the DAPK gene expression (DAPK-siRNA grouyp), FAM-siRNA was transfected as control group, and DAPK over-expression plasmid vectors were constructed to up-regulate the DAPK gene expression(DAPK over-expression group). Real-time quantitative PCR and Western blotting were used to examine the mRNA and protein expression levels of DAPK, multidrug resistance protein (MRP) and P- glycoprotein (P-gp). MTT and flow cytometry were used to detect cell proliferation and apoptosis for cells treated with 5-FU (8 mg/L) and cells without treatment of 5-FU in 3 groups respectively.</p><p><b>RESULTS</b>Positive expression rate of DAPK in colon cancer tissues was significantly lower than that in adjacent normal tissues [18.0% (11/61) vs. 90.6% (29/32), P < 0.05]. Compared with FAM-siRNA group, DAPK mRNA and protein expression levels were significantly lower in DAPK-siRNA group, but significantly higher in DAPK over-expression group (P<0.05). After treatment of 5-FU, cell proliferation was significantly inhibited, but cell apoptosis was significantly increased in DAPK over-expression group compared to FAM-siRNA group (P < 0.05). Cell proliferation and apoptosis were not significantly different between DAPK siRNA and FAM-siRNA groups (all P < 0.05). Compared with FAM-siRNA group, DAPK over-expression could significantly reduce the mRNA and protein levels of MRP and P-gp, whereas DAPK siRNA had no obvious such effects.</p><p><b>CONCLUSION</b>DAPK can inhibit the proliferation and promote the apoptosis in drug-resistant colon cancer cells, and it probably enhances the sensitivity of cancer cells to drugs by down-regulating the mRNA and protein levels of MRP and P-gp.</p>

The effects of plasma 5-HT content with depressive patients treated by Turtle-Dragon decoction combined with acupuncture / 国际中医中药杂志

Objective To observe HAMD,SDS scores and plasma 5-tT content with Depressive Patients treated by Turtle-Dragon decoction combined with acupuncture.Methods 70 patients were randomly divided into the treatment group and the control group,the treatment group treated with the turtle dragon decoction combined with acupuncture,the control group treated with fluoxetine hydrochloride,all patients before treatment and after treated 8 weeks were measured by HAMD,SDS and detected by plasma 5-HT content.Results Two groups of patients after 8 weeks of treatment,the total effective rate was 80％ in the treatment group,the total effective rate was 85.71％ in the control group,two groups showed no significant difference (x2=0.40,P＞0.05).HAMD and SDS[the treatment group were(9.31 ± 2.10) points,(55.91± 4.13) points,the control group were(9.36±2.28)points,(56.70±3.77)points] scores were significantly lower(P＜0.01) than before treatment[the treatment group were(12.79±2.50)points,(61.54±3.26)points,the control group were(11.89±2.73)points,(62.09±3.24)points] in all the patients,Plasma 5-HT content[the treatment group were (118.62 ± 29.74) ng/ml,the control group were (121.10 ± 30.56) ng/ml] has been significantly improved (P＜0.01) after treatment[the treatment group were(65.97±23.35)ng/ml,the control group were(63.40±21.24) ng/ml] in all the patients.Between the two groups of patients after treatment,the comparison of the HAMD,SDS scores and Plasma 5-HT content was no significant difference (P ＞ 0.05).Conclusion Turtle-Dragon decoction combined with acupuncture can obviously improve the HAMD,SDS scores and plasma 5-HT content with Depressive Patients.Also treatments between two groups have equivalent effects.

Secondary prevention and treatment of precancerous lesions of breast cancer / 国际外科学杂志

ObjectiveTo practice second-level prevention of breast cancer, conduct serial experiments on blocking precancerous change of breast cancer thus reduce its incidence rate. MethodsAfter the segment resection of primary lesions the breast precancerous lesions with ductal hyporplasia (DH) atypical ductal hyperplasia (ADH) and ductal intraepithelial neoplasia (DCIS), lobular intraepithelial neoplasia (LCIS) ,detected hormone receptors ER, PR and c-erbB-2, P53 were detected. With individualized comprehensive treatment, the positive patients with ER and PR was treated with tamoxifen; the postmenopausal patients took anastrozole to reduce the levels of estrogen; the positive patients with c-erbB-2 were treated with chemotherapy and the combined treatment; the patients with preoperative diagnosis of malignant cells were taken with the ipsilateral axillary lymph node dissection; all patients were observed and followed up.ResultsThere were 126 cases of the breast precancerous lesions from 1992 to 2008, including 75 cases of ADH with the positive rates of ER and PR 86.6％, c-erbB-2 1.33％, P53 0; 51 cases of DCIS and LCIS with the positive rates of ER and PR 84.6％, c-erbB-2 4％ ,P53 4％ ; Axillary lymph node reactive hyperplasia were 0/9 - 0/18. ConclusionsBreast precancerous lesions of ADH, DCIS, LCIS are local symptoms of the systemic disease, the segment resection of primary lesions and comprehensive treatment ( endocrine, chemotherapy, radiotherapy) based on immunohistochemical expression are effective through which the incidence rate of breast cancer could be largely controlled or suppressed.