Objective:To investigate the value of the clinical application of telom-erase activity by fine needle aspiration from breast masses for preoperative diagnosis of breast cancer in order to provide scientific basis for its practical clinical application. Methods: 85 patients with breast masses were aspirated by fine needles in the study. The samples obtained by aspiration were detected with telomerase activity by telomeric repeat amplification protocol (TRAP) assay and observed with cytomorphology by microscope respectively. The sensitivity, specificity and Youden's index of the two detective methods in diagnosis for breast cancer were compared respectively while postoperative paraffin slice pathologic results were considered as the final standard. Results:Compared with cytomorphology by microscope,preoperative telomerase activity detection's specificity which is 73.9% versus 82.6%(P

Objective:To explore the effects of lipoxygenase inhibitor NDGA on telomerase and bcl-2 of breast cancer MCF-7 cells.Methods:MCF-7 cells in the logarithmic growth state were selected and measured.Four cell groups (concentration:0,1,10,100?mol/L)were divided in the experiment.After 48h treatment of NDGA,the mRNA expression of telomerase was examined by RT-PCR and the expression of bcl-2 was measured by flow cytometry.Results:After 48h treatment of different concentration of NDGA,the expressions of hTERTmRNA and bcl-2 in NDGA groups were both significantly lower than the control group (P0.001).Conclusion:NDGA can prevent proliferation and induce apoptosis in MCF-7 cells by means of the down-regulated expressions of hTERTmRNA and bcl-2.

Pathological pain or clinical pain is caused by tissue and nerve injuries, and is usually chronic and mainly divided into inflammatory pain and neuropathic pain. Pathological pain is typically characterized by hyperalgesia (increased responsiveness to noxious stimuli) and allodynia (painful responses to normally innocuous stimuli). The mitogen-activated proteins kinases (MAPKs) are a family of evolutionally conserved molecules that play a critical role in cell signaling, consisting of extracellular signal regulated kinase (ERK), p38, and c-Jun N-terminal kinase (JNK), which play an important role in neural plasticity of pathological pain. Inhibition of MAPKs alleviates inflammatory pain and neuropathic pain in different animal models. It is very important to study the inhibition of MAPKs as a therapeutic approach to treat pathological pain.

Malignant tumors still threatens the human's health seriously. Metastasis and recurrence lead to the failure of treatment, and multidrug resistance adds the difficulty of therapy of to malignant tumors. But the mechanism is yet unclear. Nowadays, it is found that there's a small group of cells with selfrenewal and indefinite potency in the tumors, and they are the sources of metastasis and recurrence. This small group of cells is called cancer stem cells. Subsequently, the cancer stem ceils were separated and determined from hematological system tumor and solid tumor respectively. The cognitions for metastasis and recurrence and muhidrug resistance of malignant tumor have changed with proposal and verification of the cancer stem cell theory, which provides a new clue to the treatment of tumor and prevention for the metastasis and recurrence.

Objective To study the ER status in Adriamycin-sensitive and Adriamycin-resistant MCF-7 human breast cancer cell lines. MethodsThe status of ER of MCF-7/ADR and parental MCF-7 cells was detected by Western blot. The expression of ER mRNA was detected by RT-PCR .The growth and the sensitivity to Estrogen(E 2) and droloxifene(Dro) of cells were investigated by MTT assay, and the distribution of cell cycle was detected by flow cytometric assay. Results ER and ER mRNA were positive in MCF-7 cells, and negative in MCF-7/ADR cells. In comparison with MCF-7 cells, MCF-7/ADR cells showed lower growth rate, and the cell cycle was arrested at G 0/G 1 phase. E 2 at concentrations between 1?10 -12mol/L to 1?10 -7mol/L significantly stimulated the growth of MCF-7, but did not stimulate the growth of MCF-7/ADR.Dro at concentrations between 10*!?mol/L to 20*!?mol/L significantly inhabited the growth of MCF-7, and the inhibition was dose-dependent. Dro at concentrations below 20*!?mol/L did not inhibit the growth of MCF-7/ADR, dro inhabited the growth of MCF-7/ADR only at the concentration of 20*!?mol/L, and the inhibition was more effective than MCF-7. Conclusions ER was lost in MCF-7/ADR cells,probably at mRNA level. Compared with MCF-7, the growth rate of MCF-7/ADR decreased,MCF-7/ADR cells lost the dependence on estrogen and the sensitivity to endocrine therapy.

Objective: To investigate the enhancing effect of ?-interferon on anticancer effect of tamoxifen against breast cancer cells in vitro. Methods: ER-positive MCF-7 and ER-negative MDA-MB-231 breast cancer cell lines were treated with tamoxifen alone, or in combination with ?-interferon or estrogen in vitro. Cell proliferation was evaluated by MTT assay; distribution of cell cycle was determined by flow cytometry( FCM) and cell apoptosis was determined by DNA gel electrophoresis and FCM. Results: Tamoxifen inhibited the growth of ER-negtive and-positive brest cancer cells, induced G0/G1 phase arrest and induced cell apoptosis. Tamoxifen at same concentration had stronger inhibitory effect on ER-positive cells than ER-negative ones. Promoting effect of estrogen on MCF-7 growth was blocked by TAM, but inhibition of MDA-MB-231 by TAM was not related to estrogen. Anticancer effect of TAM was enhanced when cells were pre-treated with ?-interferon for 24 h. Conclusion: TAM exerts its anti-cancer effect through inhibiting proliferation and inducing apoptosis of ER-positive/negative breast cancer cells in vitro, and ?-interferon can enhance this manticancer effect of TAM on breast cancer cells.

AIM To investigate the mechanism of apoptosis induced by oxymatrine on MCF 7 cell line METHODS Using light microscopy, electron microscopy, laser scanning confocal microscopy, flow cytometry (FCM) and DNA gel electrophoresis to demonstrate the presence of apoptosis RESULTS Morphological characteristics of apoptosis were observed on oxymatrine treated MCF 7 cells, such as condensation of nucleus, bubble of cytoplasm, fragment of nucleus, a ladder like pattern of DNA fragmentation in agarose gel eletrophoresis Laser scanning confocal microscopy showed decreasing of the content of DNA Sub G1 peak and increased S period ratio were analysed by FCM CONCLUSION Oxymatrine can induce the inhibition of cell growth by apoptosis and the mechanism of apoptosis is involved in blocking of S period cells

Objective To observe and assess the clinicopathological significance of smooth muscle differentiation in breast cancer stromal fibroblasts. Methods A monoclonal antibody recognizing ? smooth muscle actin was used to determine the smooth muscle differentiation of fibroblasts in 69 breast cancer(BC) tissues, compared with 8 breast tissues which were removed more than 5cm from the cancer margin comfirmed without cancer cells. The relationship between the smooth muscle differentiation and clinicopathological parameters including age, tumor size, lymph node metastatic status, histological grade and ER receptor status in invasive BC were analyzed. Results Stromal fibroblasts smooth muscle differentiation was defined in 55.0% of the invasive breast cancer tissues,whereas no immunostain was demonstrated in histological normal samples. Twenty eight of the 41 cases(68.3%) with matastatic lymph nodes showed stromal fibroblasts smooth muscle differentiation,which more than that of without lymphatic metastasis group (26.3%,P

Objective To study the arterial blood supply of nipple-areola and provide the anatomical basis for avoiding nipple-areola necrosis in breast operation. Methods The vascular structure of nipple-areola of 26 female breasts in 13 cadavers were studied. Results The nipple-areola mainly accepted arterial blood supply from branches of the lateral thoracic artery and the internal thoracic artery. The 2nd~4th intercostal ~perforating branches of the internal thoracic artery and branches of the lateral thoracic artery reach the base of nipple-areola from a superior,medial and upper lateral direction by passing between lobules of mammary gland, then ascend between the lacteal ducts to supply the nipple-areola; the perforators of the lateral thoracic artery and the superticial breast perforators of internal thoracic artery, formed extensive anastomoses ~subcutaneously , and particulatly under areola formed arterial rete, from which branches were given out to ~nipple-areola . The intercostal perforators and thoracoacromial perforators did not supply the nipple-areola. Conclusions When nipple-sparing mastectomy is performed, in order to avoid nipple-areola necrosis,it is necessary to protect the arterial rete under the areola, and thus, the thickness of areolar skin flap should not be less than 0.5cm; to ensure the blood supply of nipple-areola from the internal thoracic artery and the ~lateral thoracic artery in breast reduction, the superior-medial or superior-lateral breast pedicle should be used and the thickness of preserved posterior breast should not be less than 1.5cm.

Objective To explore the role of Bcl-2 and Caspase-3 in modulating apoptosis of ER-negative breast cancer cells induced by tamoxifen. Methods ER-negative breast cancer cell lines MDA-MB-231 were treated with 10.0?M tamoxifen for 12, 24, 36,48, 60 hours. The rate of cell apoptosis with or without caspase-3 inhibitor Ac-DEVD-CHO, and protein expression of Bcl-2,Bax were determined by flow cytometry, and the activity of Caspase-3 was examined with fluorophotometry. Results The expression of Bcl-2 was down-regulated, the activity of Caspase-3 and the rate of cell apoptosis were increased by TAM time-dependently, and the rate of apoptosis reached its peak at 48 hours. The expression of Bcl-2 was (negatively) correlated with activity of caspase-3. Tamoxifen, however, did not affect Bax protein expression. Ac-DEVD-CHO, a caspase-3 inhibitor, blocked the activation of caspase-3 and inhibited cell apoptosis (induced) by tamoxifen. Conclusions TAM could induce apoptosis in ER-negative breast cancer cells via (mitochondria) pathway by down-regulating Bcl-2 expression, and the activation of Caspase-3 might play an (important) role in the process of tamoxifen-induced apoptosis of ER-negative breast cancer cells.