The change of myocatdial protein kinase C (PKC) activity during ische-mia and reperfusion was studied in isolated Langendorff perfused rat hearts. The enzymeactivity was determined by measuring the incorporation of ~(32)P from (r-~(32)P) ATP intohistone. The cytosolic PKC activity was similar in control, ischemic and reperfused hearts;however, there were significant increases in the membrane PKC activity during ischemia and reperfusion There were 1.68, 1.88, 2.18 and 1.34 fold increases of the membrane PKC activity at 15, 30, 45 and 60 minutes after ischemia respetively Following15 minutes of ischemia, repetfusion of heart only caused 1.37 fold increase in the mem-brane PKC activity, compared with that at 15 minutes after ischemta no siginificant differ-ence was found. These results suggested, that the signal transduction mediated by PKC wasimpaired during the development of ischemic and post-ischemic reperfusion injuty of theheart. Panaxadiol saponin decreased the enhanced membrane PKC avtivity induced by is-chemia by 62.5%.

Purpose:To evaluate the performance and feasibility of sentinel node biopsy (SNB) in breast cancer patients using 99mTc Sulphur colloid and gamma probe.Methods:At Cancer Hospital,from May 2000 30 patients with tumor less than 5 cm with clinically negative axilla underwent SNB, which is followed by standard axillary dissection. 99mTc sulphur colloid was injected around the breast tumor and gamma probe was used to detect the SLN during surgery. SNB is compared with standard axillary dissection for its ability to accurately reflect the final pathological status of the axillary nodes.Results:The sentinel node is successfully identified in 90% (27/30) of the patients. Number of sentinel nodes ranged from 1—3,average 1.5, nonsentinael nodes 5—20,average 13.3 per patient. Of the 27 patients 52%(14/27) were histologically positive. The sentinel node was falsely negative in 2 patients, yielding an accuracy of 92.6%. In T 1 tumors, SNB was more accurate than for T 2 tumors.Conclusions:Gamma probe guided method is technically feasible in detecting sentinel nodes in most cases and predicts the axillary status quite accurately, and appears to be more accurate for T 1 lesions than for larger lesions. This minimally invasive axillary staging procedure represents a major advance in the surgical treatment of breast cancer.

Objective To discuss the design of pedicled thoracodorsal artery perforator flap (TDAP flap),and to evaluate the aesthetic results and donor-site complications for immediate partial breast reconstruction (IPBR) after breast conserving surgery (BCS) for breast cancer patients.Method Clinical data of 13 breast cancer cases treated with BCS + IPBR using TDAP flap from November 2004 to November 2010 were retrospectively analyzed.Perforators were identified with Doppler preoperatively in all patients.Results All perforators originated within a median distance of 8.0 cm ( range,7.5 to 9.5 cm) from axillary plica at the posterior line of axilla.Median area of the flaps was 6.0 × 8.0 cm ( range,5.0 × 7.0 cm to 8.0 × 10.0 cm).One flap was muscle-sparing,while a small muscle strip was left embedding the perforators in other twelve flaps to increase the reliability of the vascular pedicle.Postoperatively patients were followedup from 4 to 71 months.Median follow-up time was 41 months.Flap necrosis and seroma in the donor-site were not found in all patients.Aesthetic results were graded as excellent or good in 9 patients,fair in 3,and poor in one.Conclusions TDAP flap is a good choice for IPBR after BCS for breast cancer patients whether lesions in outer quadrants or inner quadrants,especially for those patients with excisional biopsy.Preoperative mini-Doppler is helpful for determining the precise location of the main perforators,and decreasing the risk of vessels injury.

Objective To study the clinicopathologic characteristics of triple-negative breast cancer (TNBC) and its value in the prediction of prognosis. Method In this study,500 cases of female breast cancers were examined immunohistochcmically for the TNBC. The clinicopathologic characteristics of the 243 TNBC cases were inspected. Results TNBC accounted for 17.6% (88/500) of the 500 breast cancers. The histological types of the TNBC included mainly infihrative ductal carcinoma, metaplastic carcinoma and medullar carcinoma. Among those, histological grade Ⅲ accounted for 72.7% (64/88) of all the TNBC and was more common than that in hormone receptor positive breast cancers (HR+ group ) and Her-2 overexpression breast cancers (Her-2 group)(P=0.000). The positive rates of CK5/6 and EGFR in the TNBC were 30.7% (27/88) and 34.1% (30/88), respectively. The positive rates of ERCC1 and KIT in the TNBC were 28.4% (25/88) and 34.1% (30/88), respectively, Both of which were higher than those in the HR + group and Her-2 group, respectively (P=0.032 and P=0.026). 3-year survival rate of the TNBC was 71.5% and it was lower than that of HR group (P=0.021) and not significantly different from that of Her-2 group (P=0.474). Conclusions TNBC is the breast cancer with high aggressive pathologic futures and poor prognosis. EGFR and ERCC1 expression were positive in a portion of TNBC cases.

Objective: To investigate the effect of cinobufacini on proliferation, celly cycle distribution, invasion capability of MDA-MB-231 breast cancer cell line in vitro and possible mechanism. Methods: The effect of cinobufacini on cell growth was measured by CCK-8 reagent kit. Cell cycle distribution was determined by flow cytometry. The invasion capability in vitro was detected by Transwell chamber assay. The mRNA expressions of cell cycle related factors (cyclin) and p21 were tested by RT-PCR. Results: Cinobufacini inhibited proliferation of MDA-MB-231 cells. The half inhibition concentration (IC50) was 0.31 mg/mL. The inhibitory effect was timE-dependent (P<0.05). Cinobufacini significantly decreased invasion capability of MDA-MB-231 cells in vitro compared with control group (P<0.05). Cinobufacini induced S-phase arrest of MDA-MB-231 cells in a concentration-dependent manner (P<0.000 1). Cinobufacini down-regulated the expression levels of cyclin A1, cyclin D1, and cyclin E1, while up-regulated that of p21 in MDA-MB-231 cell line. However, there was no marked change in the expression of cyclin B1. Conclusion: Cinobufacini inhibits cell proliferation and influences the cell cycle distribution in vitro by regulating the expression of cyclin A1, cyclin D1, cyclin E1 and p21 in breast can-cer cells.

Objective To explore the influencing factors for postoperative adjuvant chemotherapy effects in elderly patients with breast cancer. Methods Five hundred and ninety female patients aged 65 years or older with invasive breast cancer were treated in our hospital, and the influencing factors for postoperative adjuvant chemotherapy effects were analyzed by chi-square test and logistic regression. Results Two hundred and thirty-one (39.2%) patients received postoperative adjuvant chemotherapy. The results showed that diabetes, age, patterns of operation and pathological characteristics of tumor had significant influences on postoperative adjuvant chemotherapy effects (χ2=4.49,88. 27,23.49 and 9.40, all P<0.05). Logistic regression analysis showed that age, tumor size, lymph node status(pN) and estrogen receptor (ER) status were related to postoperative adjuvant chemotherapy effects(χ2=68.857,15. 284,43. 540 and 7.009 ,all P<0.01). Forty-four patients (66.7%) with pN(+)/ER(-) received adjuvant chemotherapy. Conclusions Age, tumor size, lymph node status and ER status were independent predictive factors for postoperative adjuvant chemotherapy effects in elderly patients with breast cancer.

OBJECTIVETo evaluate the accuracy of sentinel lymph node biopsy (SLNB) to predict the axillary lymph node status in breast cancer patients and its clinical significance.

METHODSSeventy patients with clinical TNM status T(1 - 2)N(0)M(0) underwent sentinel lymph node biopsy using Tc-99m sulfur colloid radiotracer and gamma probe, which was followed by standard axillary dissection. SLNB was compared with standard axillary dissection for its ability to reflect the final pathological status of the axillary nodes. The SLNs that were tumor negative in conventional HE staining were further evaluated using immunohistochemical stains for CK8, CK19 and KP-1 antibodies.

RESULTSThe sentinel lymph node (SLN) was successfully identified in 67 (95.7%) out of 70 patients. The number of sentinel nodes harvested ranged from 1 to 5 (average 1.6). The nonsentinel nodes ranged from 5 to 20 (average 12.3). Of the 67 patients, 29 (43.3%) had histologically positive axillary lymph nodes. SLN was positive in 24 patients with metastasis (35.8%), and in 7 patients without metastasis (10.4%). In 5 patients, SLN was negative for tumor with positive nodes. The accuracy of sentinel lymph node biopsy to predict the axillary lymph node status was 92.5% and the false negative rate was 7.5%. For tumors with diameter less than or equal to 2 cm, the accuracy was 100%. 65 SLNs that were negative for HE stain were also non-reactive to immunostain for CK8 and CK19 antibody.

CONCLUSIONSSLNB can accurately predict the axillary lymph node status in most of breast cancer patients. The accuracy is about 100% in patients with T(1) lesions. Immunohistochemical staining at the same level of HE stain can not increase the detection of lymph node micrometastasis.

Adult ; Aged ; Aged, 80 and over ; Axilla ; Breast Neoplasms ; pathology ; Female ; Humans ; Lymph Nodes ; pathology ; Lymphatic Metastasis ; Middle Aged ; Sentinel Lymph Node Biopsy

Development of ovarian cancer involves the co-evolution of neoplastic cells together with the adjacent microenvironment. Steps of malignant progression including primary tumor outgrowth, therapeutic resistance, and distant metastasis are not determined solely by genetic alterations in ovarian cancer cells, but considerably shaped by the fitness advantage conferred by benign components in the ovarian stroma. As the dynamic cancer topography varies drastically during disease progression, heterologous cell types within the tumor microenvironment (TME) can actively determine the pathological track of ovarian cancer. Resembling many other solid tumor types, ovarian malignancy is nurtured by a TME whose dark side may have been overlooked, rather than overestimated. Further, harnessing breakthrough and targeting cures in human ovarian cancer requires insightful understanding of the merits and drawbacks of current treatment modalities, which mainly target transformed cells. Thus, designing novel and precise strategies that both eliminate cancer cells and manipulate the TME is increasingly recognized as a rational avenue to improve therapeutic outcome and prevent disease deterioration of ovarian cancer patients.
Animals ; Antineoplastic Agents ; pharmacology ; therapeutic use ; Female ; Humans ; Ovarian Neoplasms ; drug therapy ; pathology ; Tumor Microenvironment ; drug effects