S100A9 promotes glycolytic activity in HER2-positive breast cancer to induce immunosuppression in the tumour microenvironment.

Purpose: The purpose of this study was to investigate the correlation between S100 calcium binding protein A9 (S100A9), tumour glycolysis and tumour infiltrating lymphocytes (TIL) in human epidermal growth factor receptor 2 (HER2) - positive breast cancer (BRCA). Materials and methods: A total of 667 BRCA patients in Xiangya Hospital of Central South University were enrolled in this study. Haematoxylin and eosin (H&E) staining were used to count TIN in tissues. Human breast cancer cell lines (SK-BR-3 cells and BT474 cells) were transfected with S100A9 specific small interfering RNA (siRNA). The expressions of S100A9, glycolytic enzymes and lymphocyte markers were detected by immunohistochemistry (IHC) staining, Western blot and immunofluorescence. Lactate production, glucose consumption and the extracellular acidification rate (ECAR) were detected to assess glycolysis activity. Results: S100A9 was significantly overexpressed in HER2+ cases. The expressions of phosphoglycerol kinase 1 (PGK1), lactate dehydrogenase A (LDHA) and enolase α (ENO1) were significantly up-regulated in S100A9 dominant tissues. The expressions of PGK1, LDHA and ENO1 detected in S100A9 silenced cell lines were significantly down-regulated. Moreover, S100A9 silencing significantly altered lactate production, glucose uptake and ECAR levels in HER2+ cell lines. Co-expression of S100A9 and c-Myc was detected in HER2+ tissues. The absence of S100A9 greatly hindered ß-catenin expression in cell lines, which later induced the phosphorylation of c-Myc.The amount of TILs in cases with abundant S100A9 and LDHA was much greater than in cases with low S100A9 levels and poorer LDHA. TIL deficiency and elevated S100A9 intensity are factors affecting the survival rate of HER2+ BRCA cases. Conclusions: S100A9 overexpression upregulated the glycolysis activity of tumour cells through the c-Myc-related pathway, suppressing lymphocyte infiltration in the tumour stroma, affecting the efficacy of immune regulation and long-term survival of patients.

The prognostic effect of HER2 heterogeneity and YAP1 expression in HER2 positive breast cancer patients: a retrospective study.

Background: This study sought to estimate the prognostic effect of intratumoral heterogeneity (ITH) and Yes-associated protein 1 (YAP1) intensity in human epidermal growth factor receptor 2 (HER2) positive breast cancer patients. We also investigated individualized adjuvant therapy for YAP1-sufficient patients and HER2 heterogeneous patients. Methods: The relationship between prognostic outcomes and clinicopathological variables in 1,650 retrieved breast cancer patients was evaluated. The HER2 intensity and YAP1 expression in HER2-ITH and non-ITH (NITH) patients were also estimated. All patients were followed-up, regardless of whether or not they received intensive treatment, to explore individualized adjuvant therapy for YAP1-sufficient patients and HER2 heterogeneous patients. Results: Over-expression and nuclear localization of YAP1 were significant in HER2-ITH patients. The over-expression of YAP1 and the presence of ITH affected the prognosis of HER2 positive patients. YAP1 intensity and lymph nodes metastases was more obviously affected the survival of HER2-ITH patients, while the prognosis of NITH patients were correlated with clinical Tumor-Node-Metastasis (cTNM) stage and lymph-vascular space invasion (LVSI) status. HER2-NITH patients and YAP1-insufficient patients benefited from a combination of Trastuzumab and Pertuzumab/Lapatinib, while Capecitabine significantly decreased the relapse risk of ITH patients and YAP1-sufficient patients. Conclusions: YAP1 overexpression and nuclear localization was usually observed in HER2-ITH patients. For HER2-NITH patients, an advanced stage of cTNM and LVSI status increased the recurrent risk, and intensified Pertuzumab or Lapatinib treatment (combination with Trastuzumab) improved their survival. For HER2-ITH patients, the overexpression of YAP1 and pathological lymph nodes (pLN) metastases increased recurrent risk, and intensified Capecitabine treatment improved their survival. YAP1 overexpression contributed to a poor prognostic outcome, especially when HER2 signal intensity was insufficient.

YAP1/MMP7/CXCL16 axis affects efficacy of neoadjuvant chemotherapy via tumor environment immunosuppression in triple-negative breast cancer.

BACKGROUND: To evaluate the association of potential YAP1/MMP7/CXCL16 axis and tumor infiltrating lymphocytes (TILs) related chemo-response in triple-negative breast cancer (TNBC) patients. METHODS: We estimated the messenger RNA (mRNA) expression levels of Yes-associated protein 1 (YAP1), MMP7, and CXCL16 in paired TNBC tumor/para-tumor tissues by quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR), and performed statistical analysis according to neoadjuvant chemotherapy (NAC) response. Based on The Cancer Genome Atlas (TCGA) data, we noticed outstanding expression of MMP7/CXCL16 in TNBC cases, as well as associations between MMP7/CXCL16 and HIPPO-YAP1-relevant kinases. We also performed gene set enrichment analysis (GSEA) between MMP7/CXCL16 and YAP1-associated pathways. Western blotting assay was employed to evaluate YAP1/MMP7/CXCL16 expression in vitro and their modulation sequence. Logistic model stepwise regression analysis was used to assess YAP1, MMP7, CXCL16, and TILs as therapeutic predictors. Residual cancer burden (RCB) score was calculated and statistically analyzed according to intensity of these variables, and receiver operating characteristic (ROC) curve also showed their predictive value in NAC response. Recruitment efficacy for CD4+/CD8+ TIL cells (TCGA data) as well as quantified TIL cells density were both explored according to YAP1, MMP7, and CXCL16 expression level. RESULTS: Up-regulation of YAP1/MMP7 and down-regulation of CXCL16 were both significant in TNBC cases with poor NAC response. Inhibition of YAP1 induced down-regulation of MMP7 and up-regulation of CXCL16, whereas inhibition of MMP7 also induced up-regulation of CXCL16. It was also shown that MMP7/CXCL16 was enriched in the YAP1-related pathway. Activation of the YAP1/MMP7/CXCL16 axis obviously affected RCB of TNBC cases. The ROC curve also supported the predictive value of YAP1/MMP7/CXCL16 axis and TILs density in NAC response prospect. The density of TILs, meanwhile, demonstrated a strong link with the YAP1/MMP7/CXCL16 axis. Over expression of YAP1/MMP7 significantly suppressed recruitment of CD4+/CD8+ TILs, while CXCL16 over expression had a beneficial impact on anti-tumor immune. CONCLUSIONS: Over expression of causes up-regulation of MMP7 and down-regulation of CXCL16, which suppressed CD4+/CD8+ TILs recruitment and indirectly affected NAC response of TNBC patients.

lncRNA MIR503HG inhibits cell proliferation and promotes apoptosis in TNBC cells via the miR-224-5p/HOXA9 axis.

Triple-negative breast cancer (TNBC) is a highly invasive subtype of breast cancer. This study investigated the molecular mechanism and influences of MIR503HG, miR-224-5p, and homeobox A9 (HOXA9) on TNBC cell growth and migration. Dual-luciferase reporter gene and RNA immunoprecipitation were performed to examine the regulation of MIR503HG, miR-224-5p, and HOXA9. Cell proliferation, apoptosis, migration, and invasion were evaluated by colony formation, flow cytometry, and Transwell assays. Finally, nude mice were employed to investigate the influence of MIR503HG on TNBC tumor growth. HOXA9 protein levels were detected by immunohistochemical staining. MIR503HG and HOXA9 expression were reduced in TNBC, while miR-224-5p was increased. Overexpression of MIR503HG or HOXA9 reduced the cell migration ability and proliferation and promoted apoptosis, and knockdown of MIR503HG or overexpression of miR-224-5p exhibited the opposite effects. Furthermore, MIR503HG promoted HOXA9 expression by inhibiting miR-224-5p. Overexpression of miR-224-5p reversed the effects of MIR503HG overexpression on TNBC cells, while overexpression of HOXA9 reversed the effect of MIR503HG knockdown. Additionally, an in vivo study proved that MIR503HG inhibited TNBC tumor growth via the miR-224-5p/HOXA9 axis. MIR503HG inhibited cell proliferation and promoted the apoptosis of TNBC cells via the miR-224-5p/HOXA9 axis, which may function as a novel target for the treatment of TNBC.

Long non-coding RNA MIR100HG promotes the migration, invasion and proliferation of triple-negative breast cancer cells by targeting the miR-5590-3p/OTX1 axis.

BACKGROUND: As an aggressive subtype of breast cancer with a high risk of recurrence, triple-negative breast cancer (TNBC) lacks available treatment targets. LncRNA MIR100HG promotes cell proliferation in TNBC. However, few studies have investigated the molecular mechanism of MIR100HG in TNBC. Thus, additional in-depth investigations are needed to unravel its associated regulatory mechanism. METHODS: MIR100HG and miR-5590-3p expression in TNBC tissue samples and cell lines was detected by RT-qPCR. Flow cytometry, transwell, wound-healing, CCK8 and colony formation assays were performed to analyse cell apoptosis, cell cycle, invasion, migration and proliferation. The protein expression of orthodenticle homeobox 1 (OTX1) and proteins in the ERK/MAPK signalling pathway were assessed by western blot analysis. Bioinformatics and luciferase assay were performed to predict and validate the interaction between MIR100HG and miR-5590-3p as well as OTX1 and miR-5590-3p. RNA immunoprecipitation (RIP) was used to detect the interaction between MIR100HG and miR-5590-3p. Subcutaneous tumour growth was observed in nude mice. Immunohistochemistry (IHC) analysis was used to assess OTX1 expression in tumour tissues. RESULTS: MIR100HG expression was upregulated, whereas that of miR-5590-3p was downregulated in TNBC. MIR100HG was shown to directly interact with miR-5590-3p. Furthermore, MIR100HG knockdown could promote TNBC cell apoptosis and cell cycle arrest in G0/G1 phase while inhibiting migration, invasion and proliferation. Furthermore, miR-5590-3p inhibition showed the opposite results and could reverse the effect of MIR100HG knockdown in TNBC cells. MiR-5590-3p downregulated the ERK/MAPK signalling pathway, suppressed the migration, invasion and proliferation of TNBC cells and promoted their apoptosis and cell cycle arrest in G0/G1 phase by targeting OTX1. In addition, MIR100HG knockdown inhibited OTX1 expression by upregulating miR-5590-3p in vivo, thereby inhibiting tumour growth. CONCLUSIONS: MIR100HG promotes the progression of TNBC by sponging miR-5590-3p, thereby upregulating OTX1, suggesting a new potential treatment target for TNBC.

Identification of Candidate Genes Associated with Breast Cancer Prognosis.

Breast cancer (BC) is the most malignant tumor in women. The molecular mechanisms underlying tumorigenesis still need to be further elucidated. It is necessary to investigate novel candidate genes involved in breast cancer progression and prognosis. In this study, we commit to explore candidate genes that associate with prognosis and therapy in BC by a comprehensive bioinformatic analysis. Four GEO datasets (GSE5764, GSE7904, GSE20711, and GSE29431) and the BC-related transcriptome data in TCGA database were downloaded and used to identify the differently expressed genes (DEGs). The function of DEGs was analyzed by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways enrichment analysis. The protein-protein interaction (PPI) network of DEGs was constructed to identify hub genes. Prognostic candidate genes were identified through survival analysis. In addition, potential therapeutic targets were identified by constructed gene-drug interaction network through Comparative Toxicogenomics Database. A total of 547 DEGs (302 up and 245 down) were identified. Three core-subnetwork and 25 hub genes were identified in PPI network. Seven genes (namely COL12A1, QPRT, MRPL13, KRT14, KRT15, LAMB3, and MYBPC1) were identified as crucial prognostic candidate genes, which significantly associated with breast cancer overall survival. Furthermore, two representative candidate genes (COL12A1 and LAMB3) were optionally chosen for verification by reverse transcription and quantitative real-time polymerase chain reaction (RT-PCR). What's more, the gene-drugs interaction analysis indicates several antitumor drugs that could affect the expression of these prognostic markers, such as doxorubicin, cisplatin, and tamoxifen. These results identified seven crucial candidate genes that may serve as prognosis biomarkers and novel therapeutic targets of breast cancer, which may facilitate further understanding the molecular pathogenesis and providing potential therapeutic strategies for BC.

Association of Single-Nucleotide Polymorphisms in Monoubiquitinated FANCD2-DNA Damage Repair Pathway Genes With Breast Cancer in the Chinese Population.

OBJECTIVE: The aim of the study was to estimate breast cancer risk conferred by individual single-nucleotide polymorphisms of breast cancer susceptibility genes. METHODS: We analyzed the 48 tagging single-nucleotide polymorphisms of 8 breast cancer susceptibility genes involved in the monoubiquitinated FANCD2-DNA damage repair pathway in 734 Chinese women with breast cancer and 672 age-matched healthy controls. RESULTS: Forty-five tagging single-nucleotide polymorphisms were successfully genotyped by SNPscan, and the call rates for each tagging single-nucleotide polymorphisms were above 98.9%. We found that 13 tagging single-nucleotide polymorphisms of 5 genes ( Parter and localizer of Breast cancer gene2 ( PALB2), Tumour protein 53 ( TP53), Nijmegen breakage syndrome 1, Phosphatase and tensin homolog deleted from chromosome 10 ( PTEN), and Breast cancer gene 1 ( BRCA1-interacting protein 1)) were significantly associated with breast cancer risk. A total of 5 tagging single-nucleotide polymorphisms (rs2299941 of PTEN, rs2735385, rs6999227, rs1805812, and rs1061302 of Nijmegen breakage syndrome 1) were tightly associated with breast cancer risk in sporadic cases, and 5 other tagging single-nucleotide polymorphisms (rs1042522 of TP53, rs2735343 of PTEN, rs7220719, rs16945628, and rs11871753 of BRCA1-interacting protein 1) were tightly associated with breast cancer risk in familial and early-onset cases. CONCLUSIONS: Some of the tagging single-nucleotide polymorphisms of 5 genes ( PALB2, TP53, Nijmegen breakage syndrome 1, PTEN, and BRCA1-interacting protein 1) involved in the monoubiquitinated FANCD2-DNA damage repair pathway were significantly associated with breast cancer risk.

Relative dose intensity and therapy efficacy in different breast cancer molecular subtypes: a retrospective study of early stage breast cancer patients treated with neoadjuvant chemotherapy.

To investigate the relationship between chemotherapy dose intensity and therapy efficacy of different molecular subtypes. Clinical and pathological features of the patients with breast cancer were retreived from the hospital records. 315 patients were analyzed (251 showed clinical response, 38 acquired pCR). Patients with positive ER status, negative PR status, higher Ki67 level and higher RTDI had better therapy response. 13.5 and 84.5 % were identified the benchmark of Ki67 and RTDI, respectively. As the result of interior-subgroup comparison, luminal subgroups acquired better response rate when RTDI ≥ 84.5 %. In patients of luminal breast cancer, tumor size change arose from increasing of dose intensity and finally showed reached a plateau after RTDI ≥ 95 % (r (2) = 0.303, p < 0.001). As the result of intersubgroup comparison, TNBC patients were more likely to acquired better clinical and pathology response when RDTI < 84.5 %. Ki67 change arose sharply from increasing of dose intensity when RDTI < 84.5 % (r (2) = 0.656, p < 0.001), whereas the regression curve showed a terminal plateau in patients of RDTI ≥ 84.5 % (r (2) = 0.427, p < 0.001). Given lower RTDI, luminal patients are less likely to achieve response, and TNBC patients are associated with higher response rate. Dissimilar of therapy efficacy between luminal subtype and TNBC becomes inconspicuous as RTDI rises. Chemosensitivity may associate with dose intensity, especially in luminal subtypes, and tailored therapeutic strategies should be considered.

Associations between body mass index and molecular subtypes as well as other clinical characteristics of breast cancer in Chinese women.

BACKGROUND: Several studies have shown a positive association between body mass index (BMI) and the development of hormone receptor-positive breast cancer in postmenopausal women; however, the associations between BMI groups and molecular subtypes have yet to be well defined in premenopausal breast cancer patients. METHODS: A total of 2465 female breast cancer patients diagnosed at our institution were recruited for this study. Clinicopathologic information (including age, body height and weight, as well as tumor subtypes and stages) was collected; analyses of these characteristics and the associations between them were performed. RESULTS: A total of 1951 cases were included in the study. The mean age was 47.3 years, the majority of patients were of normal weight, premenopausal, had stage 2 cancer, and did not present with positive nodes. The prevalence of the luminal A, luminal B, human epidermal growth factor receptor 2+, and triple-negative subtypes were 57.8%, 11.6%, 6.1%, and 24.5%, respectively. There were significant differences in the clinicopathologic features among BMI groups in premenopausal patients. The case-only odds ratio (OR) analysis revealed that normal weight patients tended to have luminal B cancer (OR = 1.4, P = 0.206), and overweight and obese patients tended to have triple-negative cancer in premenopausal patients (OR = 2.8, OR = 3.7, respectively; P < 0.001). CONCLUSION: IN CHINESE WOMEN, BREAST CANCER CAME WITH THESE CHARACTERISTICS: young mean age (premenopause), luminal A subtype, and the majority of them were within a normal weight range. In premenopausal patients, underweight patients tended to have luminal A, lower human epidermal growth factor receptor 2+ expression, stage 1 and no positive node cancer. However, overweight and obese patients tended to have a triple-negative, stage 3, and lymph node metastatic cancer.

Haplotype analysis of eight genes of the monoubiquitinated FANCD2-DNA damage-repair pathway in breast cancer patients.

BACKGROUND: Ten genes are associated with increased susceptibility to inherited breast cancer have also been associated with population breast cancer risk, and all are involved directly or indirectly in the monoubiquitinated FANCD2-DNA damage repair pathway. We analyzed 13 haplotype blocks in eight of these genes to estimate the breast cancer risk conferred by individual haplotypes. METHODS: Haplotype blocks were constructed with 48 tag single-nucleotide polymorphisms (tSNPs) identified in eight breast cancer susceptibility genes, TP53, PTEN, CHEK2, ATM, NBS1, RAD50, BRIP1, and PALB2. Genotyping was performed by SNPscan on 734 female patients and 672 female age-matched controls. RESULTS: Forty-five tSNPs were successfully genotyped by SNPscan, and call rates for each tSNP were above 98.9%. Thirteen haplotype blocks of eight genes were constructed with 41 successfully genotyped tSNPs. We found that seven haplotypes from four haplotype blocks located within three genes (NBS1, PTEN, and BRIP1) were significantly associated with breast cancer risk. Among these, four haplotypes (ATC in block 1 of NBS1, GCCCC and GCCCT in block 2 of NBS1, and GCT in block 2 of BRIP1) were correlated with breast cancer risk in sporadic cases (OR (95% CI) 1.350(1.124-1.623), 0.752(0.584-0.969), 0.803(0.649-0.993), and 0.776(0.604-0.997), respectively), and only one haplotype (GGCCT in block 2 of NBS1) was significantly associated with breast cancer risk in familial and early-onset cases (OR(95% CI) 1.902(1.134-3.191)). CONCLUSIONS: Four haplotypes within two genes (NBS1 and BRIP1) involved in the monoubiquitinated FANCD2-DNA damage-repair pathway are significantly associated with increased sporadic breast cancer risk, while one haplotype within NBS1 is correlated with an increased risk of familial or early-onset breast cancer, indicating that specific haplotypes may be distinct predictors of breast cancer.

[Gynecomastia in 38 children: etiology and treatment].

OBJECTIVE: To summarize the etiology and treatment of gynecomastia in male children. METHODS: The clinical data of 38 boys with gynecomastia at ages of 2-14 years were retrospectively studied. RESULTS: In the 38 cases, 17 cases were identified as adolescent breast hyperplasia, 2 cases were relevant to primary disease, 4 cases were caused by ingestion of drugs containing hormone, and 15 cases did not show identifiable causes and were diagnosed as idiopathic gynecomastia. For the 3 children with breast development in B3 stage, oral rupixiao was administered (1.34 g, tid) for one month. For 16 children at ages of over 12 years with breast development in B2 stage and with obvious clinical symptoms, oral rupixiao was administered (1.34 g, tid) for 3-5 days. The other patients did not receive drug treatment. In a one month to one year follow-up, most of the patients recovered well. CONCLUSIONS: The etiology of gynecomastia in male children includes adolescent breast hyperplasia, ingestion of drugs containing hormone and secondary causes. Most gynecomastia can be attributed to physiological reasons. Only a few children with obvious clinical symptoms need drug treatment.

[Association of CK20 expression with the progression, metastasis and prognosis of breast cancer].

AIM: To analyze the expression of CK20 in human breast cancer, and to evaluate the association between its expression and tumor's progression and prognosis. METHODS: 86 cases with breast cancer, 20 cases of benign tumor tissues were examined for the expression of CK20 by immunohistochemical staining. RESULTS: The positive rate of CK20 expression in breast cancer was 80.23% (69/86), which was significantly higher than that in benign tumor tissues of breast [20.00% (4/20), P<0.01]. CK20 expression was associated with the histologic grades (P<0.05) and the pathological types (P<0.01). The expression of CK20 was observed to correlate positively with TNM stages (r=0.86, P<0.05), lymph node status (r=0.73, P<0.05) and HER-2 status (r=0.69, P<0.05), and correlate negatively with ER status (r=-0.58, P<0.05). Moreover, Kaplan Meier curves of overall survival analysis showed a significant difference between CK20 positive groups and negative group (P<0.01). CONCLUSION: The results suggest that the expression of CK20 may be associated with the progression and prognosis of breast cancer.

[Clinical significance of tumor associated glycoprotein-72 expression in pPrimary breast carcinoma].

AIM: To investigate the expression of tumor associated glycoprotein-72 (TAG-72) in primary breast carcinoma, and to evaluate its clinical significance in clinicopathological status and prognosis of patients with primary breast carcinoma. METHODS: 118 patients with primary breast carcinoma were examined for TAG-72 expression by SABC immunohistochemistry. Then, the clinical outcome of the patients after a follow-up of 5 years was determined in 92 out of 118 patients. The correlation of TAG-72 expression in primary breast carcinoma with the prognosis of patients was also analysis. RESULTS: The positive rates of TAG-72 in breast carcinoma tissues were 78.81% (93/118). Clinicopathological parameters of breast carcinoma and clinical outcome of the patients were associated with TAG-72 expression. TAG-72 was expressed more frequently in breast carcinoma tissues with larger neoplastic diameter (P<0.05), higher TNM stage (P<0.05), poorer histological differentiation (P<0.01) and lymph nodes metastasis (P<0.01). Moreover, the survival rate of the patients with breast carcinoma expressing TAG-72 was significantly lower than the patients without TAG-72 expression (P<0.01). CONCLUSION: The results suggest that the expression of TAG-72 may be an important feature of primary breast carcinomas. The detection of this marker with cancerous staging may increase the ability of investigators to predict the prognosis of patients with breast carcinomas.

[Expression of KLK6 protein and mRNA in primary breast cancer and its clinical significance].

AIM: To investigate the expression of KLK6 protein and mRNA in primary breast carcinoma, and to evaluate its clinical significance in clinicopathological status of patients with primary breast carcinoma. METHODS: 88 patients with primary breast carcinoma chosen randomly were examined for KLK6 protein and mRNA expression by SABC immunohistochemistry and RT-PCR, respectively. The association of KLK6 with the clinicopathologic features of the primary breast cancer was also analysis. RESULTS: The positive expression rates of KLK6 protein in breast carcinoma tissues were 78.40% (69/88). Clinicopathological parameters of breast carcinoma were associated with KLK6 protein expression. KLK6 protein was expressed less frequently in breast carcinoma tissues with lymph nodes metastasis (P<0.01) and ER(+) (P<0.05). Additionally, the mean expression level of KLK6 mRNA in cancerous tissues was significantly higher than that in normal tissues (P<0.01). However, KLK6 mRNA expression was negatively correlated with metastasis (P<0.01) and ER status (P<0.01). The expression of KLK6 protein and mRNA in primary breast carcinoma tissues was not associated with that of CerbB-2. CONCLUSION: KLK6 expression in cancerous tissues may play an important role in the invasion and metastasis of primary breast carcinoma. The detection of it along with clinical staging may help to predict the prognosis of patients with primary breast carcinoma.

[Clinical diagnosis of breast cancer with nonpalpable tumor].

OBJECTIVE: To investigate the early diagnosis of breast cancer with nonpalpable tumor. METHODS: Forty-six cases of clinical nonpalpable tumor were examined by mammography and sonography.The cases of nipple discharge were also examined by fiberoptic ductoscopy. RESULTS: Breast cancer in 46 cases was diagnosed by pathological examination. Of them, 34 diagnosed with breast cancer were found with nodus, calcification or confused structure, and so on, 5 were considered benign tumor, and 7 were not found lesion by mammography. Thirty-one cases were diagnosed with breast cancer, 6 with benign tumor, and 9 were not found occupying lesion by sonography. Occupying lesions were found in 6 cases of nipple discharge by fiberoptic ductoscopy and were finally diagnosed by biopsy. CONCLUSION: Mammography and sonography are important methods in early discovering breast cancer. Early diagnosis rate of breast cancer can be elevated by signs of early breast cancer and combined examination of mammograply and sonography.

[Expressions of survivin and nm23 and the relationship among the expressions and the axillary lymph node metastasis in breast cancer].

OBJECTIVE: To investigate the expressions of Survivin protein and nm23 protein and the relationship among the expressions and axillary lymph node metastasis in breast cancer. METHODS: The expression of Survivin and nm23 in 80 cases of breast cancer tissues were detected by immunohistochemistry SP method, and their correlation with axillary lymph node metastasis and 5-year disease free survival (DFS) were analysed. RESULTS: Survivin protein positive expression rate was 68.75% (55/80) in breast cancer tissues, which had positive correlation with the axillary lymph nodes metastasis but negative correlation with 5 years FS (P < 0.05); nm23 protein expression had negative correlation with the axillary lymph nodes metastasis but positive to 5 years FS (P < 0.05). Survivin and nm23 proteins expression had no obvious correlation with the breast cancer pathology type, patient age and clinical stage (P > 0.05). CONCLUSION: The anti-apoptosis effect of Survivin protein and the anti-metastasis effect of nm23 protein may be important in the occurrence and advancement of breast cancer, suggesting that it may be a new indicator of prognostic and judgement in breast cancer.