Breast cancer is a hormone-dependent malignant carcinoma. Many well-established studies have shown estrogen receptor , especially estrogen receptor alpha (ERα), play an important role in the development of breast cancer. Recently, increasing evidences have shown that another subtype of estrogen receptor,estrogen receptor beta (ER β), may play an important role in the development of breast cancer. In contrast to the function of ERa, ER β played an anti-proliferation role in cell model and animal experiments of breast cancer. We review the recent articles on the relationship between ERB and invasion and metastasis of breast cancer, the coexpression and interaction among ERβ , ERα and PR.

Fourteen cases of pheochromocytoma diagnosed by B-tnode ultrasound were reported. All of them the diagnoses were confirmed by operation and pathology. Three tumors crose in right and 5 in left and 4 in bilateral adrenal glands; two were extraadrenal. The ultrasonographic features of pheochromocytoma and its differential diagnosis were discussed. The ultrasonic diagnosis of extra-adrenal pheochromocytoma is objectively assessed; it has significant importance especially in the surgical resection of the tumor.

As an increasing threat to women's health worldwide, breast cancer has many well-established risk factors, including genetic suscebility, high concentration of serum estrogen, early-age menarche, late-age menopause and postmenopansal obesity. However, these risk factors only account for about half of the in-cidence of breast cancer. Recent studies provided some clues that three primary hormone responsive virues-human papilloma virus (HPV), mouse mammary tumor virus (MMTV) and Epstein Barr virus (EBV)may act play roles in pathogenesis of human breast cancer. This review aims to have a close look at advances on the potential role, probable mechanism and relating hypothesis of Human papillomavirus in human breast cancer.

Leptin,a 16 kD protein encoded by ob gene,has been shown to play a pivotal role in satiaty control and adipose metabolism.However,numemus recent studies indicme that leptin may also take part in mammary cells transformation,proliferation and angiogensis.Those evidences suggest that leptin has an important role in the mammary cell tumorigenesis and progession,but the undedine mechanism needs further exploration.Our aim is to review the current andvances on leptin's role in tumourigenesis and progression of breast cancer from perspectives of in vitro,aniamal model and breast cancer biopsy studies.

Since Bence-Jones protein was discovered and used in multiple myeloma, many tumor markers have been used in diagnosis and treatment monitoring of various cancers. However the lack of specificity and sensitivity of most tumor markers is always limiting their application in research and clinical diagnosis currently. It is predicted that the future development of tumor marker research may mainly focus on the innovation of research strategies, such as combined detection of a set of related tumors marker and comprehensive interpretation of testing results.

Triple negative breast cancer (TNBC) is characterized by lack of expression of the estrogen (ER)and progesterone receptors (PRs) and the human epidermal growth factor receptor (HER-2) that are commonly observed in other breast cancer subtypes.Treatment options are limited since the hormonal receptor and HER-2 antagonists are ineffective for TNBC.In contrast to non-TNBC,TNBC is more aggressive with higher recurrence,metastatic,and mortality rates.Besides further studies on cytotoxic drugs and chemotherapy regimens,More studies on potential targeted molecular treatment of TNBC should be strengthened.For the moment,potential targeted molecular treatment of TNBC including antiangiogenic agents,epidermal growth factor receptor (EGFR) inhibitors and poly (adenosine diphosphate ribose) polymerase (PARP).In contrast to their surprising anti-tumor effectivness in basic experiments,these targeted molecular agents show no promising results in clinical trials by now.This article aims to review advancements of targeted molecular treatment of TNBC in recent years.

Objective To investigate inhibition effect of leptin on apoptosis of MCF-7 cells and its potential mechanism.Methods MCF-7 cells were cultured and devided into 5 groups:control group,tamoxifen (10-5 mol/L) group,tamoxifen(10-5 mol/L)-leptin(102 ng/mL)group,tamoxifen (10-5 mol/L)-leptin(103 ng/mL) group,tamoxifen(10-5 mol/L)-leptin(104 ng/mL)group.Fourty-eight hours after being treated with corresponding concentration of leptin and tamoxifen respectively,all groups of cells were quantatively tested for apoptosis by ELISA and were semi-quantatively detected for survivin,Bcl-2,Bax mRNA change by real-time PCR.Results Tamoxifen induced MCF-7 apoptosis were inhibited by leptin at a serial concentration of 103 ng/mL,104 ng/mL.Meanwhile,leptin largely enhanced survivin mRNA expression in MCF-7 cells,compared with control group.However,no significant increase of BCL-2,BAX mRNA in MCF-7 cells was observed after leptin treatment in either group.Conclusions Leptin could effectively inhibit tamoxifen induced MCF-7 apoptosis in a dose dependent manner.The potential mechanisrn of leptin' apoptosis inbition in MCF-7 cells may involve upregulation of survivin mRNA.

Objective To find out the correlation between MMP-13 and clinicopathological parameters of breast cancer and identify clinical significance of MMP-13 overexpression on overall survival of breast cancer.Methods Immunohistochemistry was performed on paraffin-embedded tissue microarray containing 159 tissue dots from breast cancer patients.The intensity and the extent of IHC were scored by pathologists blind to clinicopathological parameters of the specimens.Different expression profiles of MMP-13 in breat cancer tissues and paraneoplastic tissues,and correlation between MMP-13 and breast cancer clinicopathological parameters were analyzed for statistical significance respectively.The impact of MMP-13 overexpression on overall survival of breast cancer.Results MMP13 expression were significantly higher in breast cancer tissues(54.4％) than in their corresponding paraneoplastic tissues(27.5％)(P =0.003).Expression of MMP-13 in breast cancer positively correlated with lymphma node metastasis(r =0.257,P =0.006),clinical TNM classification (r =0.310,P =0.001),HER2 expression (r =0.192,P =0.041).However,no significant correlation were oberserved between MMP-13 expression and tumor size,MMP-13 expression and tumor grade,MMP-13 expression and ER expression,MMP-13 expression and PR expression respectively.Conclusions Overexpress of MMP-13 is more common in breast cancer tissues than in their corresponding paraneoplastic tissues,and is an independent prognosis indicator of breast cancer.

ObjectiveTo investigate the inhibitory effect of lentivirusly-mediated ObR-siRNA on transplanted MCF-7 human breast cancer cells by intratumoral injection.MethodsA model of subcutaneous implanted tumor was generated through injecting MCF-7 human breast cancer cells into the nude mice.Thirty established mice with MCF-7 breast cancer cells xenograft were divided into 3 groups randomly,and mice in the experimental group were intratumorally injected with ObR-siRNA lentivirus,while the negative control group and blank control group mice were injected with the same dose of negative lentivirus and normal saline.All mice were subcutaneously injected with recombinant human leptin around the tumor site once a day.Tumor size was blindly measured every other day and the mRNA expression and protein expression levels of ObR in each group were determined.ResultsKnockdown of ObR-treated xenografted nude mice with a high leptin microenvironment was successfully established.Local injection of ObR-siRNA lentivirus significantly suppressed the established tumor growth in nude mice(P ＜ 0.01,P ＜0.01 ).Real time-PCR and Western blotting showed that the mRNA and protein expression of ObR was decreased in the ObR-siRNA lentivirus group( P ＜ 0.01,P ＜ 0.01 ).ConclusionsIntratumoral injection of recomhinant ObR-siRNA lentivirus inhibits the growth of MCF-7 cells xenografts in the nude mice,suggesting that ObR might represent a therapeutic target in the genotherapies of human breast cancer.

Objective To explore the correlation between the expression of somatostatin (SS), gastrin (GAS), apoptosis index (AI),and p53 gene in colonic carcinoma. Methods The expression of GAS, SS, p53 and apoptosis cell were detected by immunohistochemistry (streptavidin-biotin-pero xidase complex, SABC) and in situ apoptosis detecting technic (TUNEL) . Results AI is higher in SS high and middle expression cases than in low expression cases(q=5.06,q=3.95,P