The mechanism and behavior of cesium adsorption from aqueous solutions onto carbonated cement slurry powder.

In this study, microstructural differences and changes in the adsorption capacity of cesium between cement and carbonated cement were investigated. Cement blocks were ground to powder for rapid carbonation, and microscopic variations were characterized by XRF, XRD, FT-IR, SEM, BET, and TGA. The characterization results show that the conversion of Ca(OH)2 and calcium silicate hydrate (C-S-H) gel to CaCO3 in cement after carbonation. And the component of Ca(OH)2 in the powder sample disappeared after three days of rapid carbonation. Batch experiments were used to investigate adsorption under the influence of time, initial cesium concentration, temperature, and ion coexistence. Pseudo-second-order kinetic and Langmuir isothermal model fitting could better describe the adsorption process and the results show that the maximum adsorption capacity of cement after carbonation surges from 29.6 µg‧g-1 to 1.58-5.89 mg‧g-1. (Different carbonating times lead to varying adsorption capacity.) The adsorption capacity decreases with increasing temperature. At temperatures of 293 K and 333 K, the calculated Gibbs free energy change values of cement with different carbonated degrees adsorbing cesium are -10.3 âˆ¼ -14.9 kJ‧mol-1 and -8.03 âˆ¼ -12.4 kJ‧mol-1. And the calculated values of enthalpy change and entropy change are -18.8 âˆ¼ -23.8 kJ‧mol-1 and -27.9 ∼ -37.1 J‧mol-1‧K-1. Combining the characterization and adsorption results, the huge increase in cesium adsorption capacity is closely related to the conversion of Ca(OH)2 to CaCO3, which will provide a new perspective on the adsorption mechanism of cesium in cement.

Fabrication and Supercritical Water Corrosion Resistance of TiN/TiNC/Al2O3 Multilayer Coating on Inconel 625 Alloy by CVD Method.

A TiN/TiNC/Al2O3 multilayer coating was deposited on an Inconel 625 alloy by the chemical vapor deposition method as a protective barrier to improve the corrosion resistance in supercritical water. The corrosion characteristics were evaluated in a reactor at 500 °C and 25 MPa for 72 h. The surface morphology of the coated samples was relatively dense with no obvious cracks or pores observed. The XRD analysis revealed that the coatings were composed of TiN, TiNC and α-Al2O3 phases. After exposure to supercritical water, the surface morphology of the coatings was still dense and kept integrity. The phase composition of the coatings was also not changed, with no obvious corrosion scales detected. This result demonstrates the effectiveness of TiN/TiNC/Al2O3 coatings as a protective coating under harsh supercritical water environments.

Sol-Gel-Derived Ni3Al Coating on Nickel Alloy for Oxidation Resistance in Supercritical Water Environments.

Although nickel-based alloys are widely used in industries due to their oxidation and corrosion resistance, the pursuit of better performance in harsh environments is still a great challenge. In this work, we developed a sol-gel method to synthesize Ni3Al coating on a nickel alloy, assisted by a post-annealing process, and investigated the oxidation-resistant performance. The coating thickness can be controlled by designing the deposition times, which keep the pure Ni3Al phase stable. In addition, the surface morphologies indicate that the coating is compact without obvious voids or cracks. Furthermore, the oxidation-resistant property of the coating was investigated by carrying out a supercritical water oxidation experiment. The crystalline structure and surface morphology of the samples before and after 72-h oxidation demonstrated the superior oxidation resistance of the coating. This work provides a convenient method to fabricate an oxidation-resistant coating on a nickel-based alloy, which would be significant for prolonging the service life of vessels under oxidation conditions, especially for supercritical water reactions.

Study on the uranium (U(⠥)) adsorption stability of high-dose γ-ray-irradiated clay.

The Alxa region (Inner Mongolia, China) is one of the areas preselected for use as a geological repository of high-level radioactive waste in China. Radioactive waste produces radioactive rays during long-term storage, and the cumulative absorbed dose in 1000 years can significantly exceed the maximum of 0.7 MGy, thereby challenging the long-term adsorption stability of clay. This study employed 60Co gamma (γ)-rays to irradiate clay in air under a dose rate of 10 kGy/h. The changes in the internal structure and mechanisms of clay under different gamma radiation doses (1, 2, and 3 MGy) were investigated. Additionally, the adsorption properties of irradiated clay for U(Ⅵ) were tested under different conditions. The clay samples underwent minimal structural changes following high-dose irradiation, and the interlayer spacing was altered due to the fractured framework, dehydroxylation, and radiolysis of water. After irradiation, the Fe (Ⅱ) content in clay was significantly increased, unlike Fe (Ⅲ) content. The adsorption mechanisms of clay before and after the experiments were verified, revealing that the adsorption capacity of irradiated clay to U(Ⅵ) is reduced.

ECPC-ICP: A 6D Vehicle Pose Estimation Method by Fusing the Roadside Lidar Point Cloud and Road Feature.

In the vehicle pose estimation task based on roadside Lidar in cooperative perception, the measurement distance, angle, and laser resolution directly affect the quality of the target point cloud. For incomplete and sparse point clouds, current methods are either less accurate in correspondences solved by local descriptors or not robust enough due to the reduction of effective boundary points. In response to the above weakness, this paper proposed a registration algorithm Environment Constraint Principal Component-Iterative Closest Point (ECPC-ICP), which integrated road information constraints. The road normal feature was extracted, and the principal component of the vehicle point cloud matrix under the road normal constraint was calculated as the initial pose result. Then, an accurate 6D pose was obtained through point-to-point ICP registration. According to the measurement characteristics of the roadside Lidars, this paper defined the point cloud sparseness description. The existing algorithms were tested on point cloud data with different sparseness. The simulated experimental results showed that the positioning MAE of ECPC-ICP was about 0.5% of the vehicle scale, the orientation MAE was about 0.26°, and the average registration success rate was 95.5%, which demonstrated an improvement in accuracy and robustness compared with current methods. In the real test environment, the positioning MAE was about 2.6% of the vehicle scale, and the average time cost was 53.19 ms, proving the accuracy and effectiveness of ECPC-ICP in practical applications.

Mitochondrial pathway-mediated apoptosis is associated with erlotinib-induced cytotoxicity in hepatic cells.

For advanced non-small-cell lung cancer (NSCLC) with mutations to the epidermal growth factor receptor (EGFR), EGFR tyrosine kinase inhibitors, including erlotinib are indicated for the first-line treatment. Liver injury is one of the multiple adverse effects of erlotinib and may affect its safety. The present study investigated the mechanism of erlotinib-induced hepatotoxicity in vitro and provided experimental evidence for the screening of potential hepatoprotectors. Erlotinib induced dose-dependent cytotoxicity in human L-02 hepatic cells 72 h after treatment. In other experiments, L-02 cells were treated with erlotinib for 48 h and thereafter exhibited typical features of apoptosis. Erlotinib caused alterations to nuclear morphology, including chromatin condensation and karyopyknosis; it also increased the fraction of late apoptotic cells and regulated apoptotic protein levels, activating caspase-3 and cleaving of poly-ADP-ribose polymerase. Furthermore, 48 h exposure to erlotinib disturbed mitochondrial function by decreasing the ratio of B-cell lymphoma 2 (Bcl-2) to Bcl-associated X proteins and reducing mitochondrial membrane potential. The results of this in vitro study indicate that erlotinib-induced hepatotoxicity may occur through mitochondrial-pathway-mediated apoptosis.

Proteins associated with EGFR-TKIs resistance in patients with non-small cell lung cancer revealed by mass spectrometry.

The present study aimed to identify potential serum biomarkers for predicting the clinical outcomes of patients with advanced non-small cell lung cancer (NSCLC) treated with epidermal growth factor receptor tyrosine kinase inhibitors (EGFR­TKIs). A total of 61 samples were collected and analyzed using the integrated approach of magnetic bead­based weak cation exchange chromatography and matrix­assisted laser desorption/ionization­time of flight­mass spectrometry. The Zhejiang University Protein Chip Data Analysis system was used to identify the protein spectra of patients that are resistant and sensitive to EGFR­TKIs. Furthermore, a support vector machine was used to construct a predictive model with high accuracy. The model was trained using 46 samples and tested with the remaining 15 samples. In addition, the ExPASy Bioinformatics Resource Portal was used to search potential candidate proteins for peaks in the predictive model. Seven mass/charge (m/z) peaks at 3,264, 9,156, 9,172, 3,964, 9,451, 4,295 and 3,983 Da, were identified as significantly different peaks between the EGFR­TKIs sensitive and resistant groups. A predictive model was generated with three protein peaks at 3,264, 9,451 and 4,295 Da (m/z). This three­peak model was capable of distinguishing EGFR­TKIs resistant patients from sensitive patients with a specificity of 80% and a sensitivity of 80.77%. Furthermore, in a blind test, this model exhibited a high specificity (80%) and a high sensitivity (90%). Apelin, TYRO protein tyrosine kinase­binding protein and big endothelin­1 may be potential candidates for the proteins identified with an m/z of 3,264, 9,451 and 4,295 Da, respectively. The predictive model used in the present study may provide an improved understanding of the pathogenesis of NSCLC, and may provide insights for the development of TKI treatment plans tailored to specific patients.

Maintenance Therapy in Ovarian Cancer with Targeted Agents Improves PFS and OS: A Systematic Review and Meta-Analysis.

BACKGROUND: Maintenance therapy with targeted agents for prolonging remission for ovarian cancer patients remains controversial. As a result, a meta-analysis was conducted to assess the effectiveness and safety of using maintenance therapy with targeted agents for the treatment of ovarian cancer. METHODS: From inception to January 2015, we searched for randomized, controlled trials (RCTs) using the following databases: PubMed, ScienceDirect, the Cochrane Library, Clinicaltrials.gov and EBSCO. Eligible trials included RCTs that evaluated standard chemotherapy which was either followed or not followed by targeted maintenance in patients with ovarian cancer who had been previously receiving adjunctive treatments, such as cytoreductive surgery and standard chemotherapy. The outcome measures included progression-free survival (PFS), overall survival (OS) and incidence of adverse events. RESULTS: A total of 13 RCTs, which were published between 2006 and 2014, were found to be in accordance with our inclusion criteria. The primary meta-analysis indicated that both PFS and OS were statistically and significantly improved in the targeted maintenance therapy group as compared to the control group (PFS: HR = 0.84, 95%CI: 0.75 to 0.95, p = 0.001; OS: HR = 0.91, 95%CI: 0.84 to 0.98, p = 0.02). When taking safety into consideration, the use of targeted agents was significantly correlated with increased risks of fatigue, diarrhea, nausea, vomiting, and hypertension. However, no significant differences were found in incidence rates of abdominal pain, constipation or joint pain. CONCLUSIONS: Our results indicate that targeted maintenance therapy clearly improves the survival of ovarian cancer patients but may also increase the incidence of adverse events. Additional randomized, double-blind, placebo-controlled, multicenter investigations will be required on a larger cohort of patients to verify our findings.

Impact of ABCG2 polymorphisms on the clinical outcome of TKIs therapy in Chinese advanced non-small-cell lung cancer patients.

OBJECTIVE: The primary purpose of this study was to investigate the correlation between single nucleotide polymorphisms (SNPs) of ATP binding cassette superfamily G member 2 (ABCG2) and outcome of tyrosine kinase inhibitions (TKIs) therapy in Chinese advanced non-small-cell lung cancer (NSCLC) patients. The secondary objective was to identify biomarkers to evaluate the response to treatment and outcome of the targeted therapy. METHODS: SNP genotyping (34 G/A, 421 C/A, 1143 C/T and -15622 C/T) of ABCG2 gene in 100 patients was performed using matrix-assisted laser desorption/ionization time-of-flight mass spectrometry. The clinical characteristics of 100 patients were collected. A total of 70 patients were treated with TKIs (gefitinib, erlotinib and icotinib). The association between ABCG2 polymorphisms and clinical characteristics was evaluated. Kaplan-Meier survival curves were plotted for overall survival (OS) and analyzed with the log-rank test. RESULTS: The three polymorphisms of the ABCG2 34 G/A, 421 C/A and 1143 C/T occurred more frequently compared with -15622 C/T in Chinese advanced NSCLC patients. There was no association between ABCG2 polymorphisms and clinical characteristics (p > 0.05). The median OS of patients with GG genotype at position 34 of the ABCG2 gene was significantly shorter than those with GA or AA genotype (p < 0.05). No significant difference of OS was found in 421 C/A and 1143 C/T polymorphisms (p > 0.05). CONCLUSION: ABCG2 34 G/A may be a possible predictor of the clinical outcome of TKIs therapy in NSCLC patients.

KIT and BRAF heterogeneous mutations in gastrointestinal stromal tumors after secondary imatinib resistance.

BACKGROUND AND AIMS: Gastrointestinal stromal tumors (GISTs) are the most common mesenchymal tumor of the digestive tract and characterized by expression of KIT protein. Imatinib is the frontline therapy for metastatic and unresectable GIST patients showing clinical responses in 80 % of cases. Despite the often long-lasting clinical benefit seen in most patients treated with imatinib, many will eventually suffer disease progression. The most frequent mechanism of imatinib resistance in GIST is the acquisition of secondary mutations in either KIT or PDGFRA. There are also some imatinib-resistant GIST patients lacking an identifiable mechanism of treatment failure. Recently, activating BRAF mutation was detected in a small percentage of GISTs. In this study, we report a case of GIST with acquired resistance to imatinib during therapy. METHODS: Histological, immunohistochemical, Western blot and mutational analyses were performed on GIST tissues before and after imatinib resistance. RESULTS: The imatinib-resistant tumor showed not only heterogeneous mutations of KIT and BRAF besides the primary mutation, but also transdifferentiation into a rhabdomyosarcoma phenotype. According to Western blot analysis, in imatinib-resistant GIST with both KIT V559D and BRAF V600E mutations, the inhibition of KIT V559D by imatinib caused a strong decrease of AKT phosphorylation, while ERK1/2 phosphorylation was not affected. CONCLUSIONS: This finding, in combination with the loss of KIT expression, suggests the possibility of activation of RAS-RAF-MEK-ERK pathways driven by a KIT-independent oncogenic mechanism. Understanding the genetic aberrations beyond KIT and PDGFRA may lead to the identification of additional therapeutic targets for GISTs.

Rechallenge with gefitinib following severe drug-induced hepatotoxicity in a patient with advanced non-small cell lung cancer: A case report and literature review.

Gefitinib has come to be the most widely used epidermal growth factor receptor-tyrosine kinase inhibitor in the treatment of advanced non-small cell lung cancer (NSCLC) in Asian patients. Common side effects include mild to moderate skin rash and diarrhea, however, drug-induced liver injury of varying severity is overlooked in long-term gefitinib administration and rarely reported. The current case report presents a female Chinese NSCLC patient who developed severe gefitinib-induced hepatotoxicity and was rechallenged with gefitinib following a 3-month break. The patient achieved partial clinical remission but developed drug-induced grade 4 hepatotoxicity following gefitinib administration for 14 months. As an alternative, 4 cycles of chemotherapy were administered to control tumor progression. Following restoration of the patient's liver function, gefitinib was rechallenged together with active hepatoprotective therapy. The patient presented good disease control and maintained normal liver function for >6 months. Thus, sequential chemotherapy and gefitinib rechallenge with hepatoprotective therapy may be a potential new treatment strategy for gefitinib-induced hepatotoxicity.

Mechanism of kidney injury caused by bevacizumab in rats.

OBJECTIVE: We investigate kidney injury caused by high dose bevacizumab to uncover the possible mechanisms involving in this process. METHODS: Forty rats were divided into four groups: cisplation group (treated with 1 mg/kg cisplation), Bev-high group (treated with 5 mg/kg bevacizumab); Bev-low group (treated with 2.5 mg/kg bevacizumab) and control group (treated with saline). The urine microalbumin, serum cystatin C, blood urea nitrogen and serum creatinine were detected in the four group rats, respectively. The immunoglobulin of IgG, IgA and IgM and protein of VEGF (vascular endothelial growth factor) and nephrin were detected by immunohistochemical methods. RESULTS: All the levels of microalbumin, cystatin C, serum creatinine and blood urea nitrogen in Bev-high group were significantly higher than those in normal control group (P < 0.05). The cystatin C was much more increased in kidney Bev-high group than cisplatin and Bev-low groups (P < 0.05). The light microscope showed a normal glomerular morphology in the four groups, while the electronic microscopy showed the podocytes were extensively fused in cisplatin group and Bev-high group. The two groups were found IgG and IgM deposition as well. The VEGF in kidney amples were down regulated in high dose bevacizumab group, whereas the nephrin and IgA showed no significant expression changes at all. CONCLUSION: Bevacizumab increases the risk of injury in glomerular filtration barrier in a dose dependent model. The injury may not only associate with the rising level of proteinuria but also with podocyte-dependent membrane structures.

[Establishment and pathologic analysis of imatinib-resistant gastrointestinal stromal tumor xenografts].

OBJECTIVE: To establish and characterize imatinib-resistant gastrointestinal stromal tumor (GIST) xenografts. Further provided an ideal experimental platform through the imatinib-resistant GIST xenografts to investigate the mechanism of resistance to imatinib. METHODS: Imatinib-resistant GIST cells were injected under the skin of athymic nude mice to establish animal models of human imatinib-resistant GIST. The molecular and histopathologic features of GIST xenografts were also analysed and compared with their counterpart of cell lines. RESULTS: The xenograft tumor models had been established by subcutaneously injection of GIST cells into nude mice. Immunohistochemistry results showed CD117 expression was positive in GIST-PR2 xenograft tumor, but negative in GIST-R. In GIST-PR1, tumor areas showing rhabdomyoblastic differentiation were presented next to areas with classic GIST morphology. The rhabdomyoblastic component demonstrated consistently positivity for desmin and myogenin, whereas CD117 was completely negative. The mutation profiles of these xenograft tumors were the same as their counterpart of cell lines. CONCLUSIONS: Human GIST xenografts with mutation in c-kit have been established from imatinib-resistant GIST lines. Those models will enable further studies on mechanisms of resistance, combination therapies and allow testing of novel targeted therapies.

Gene mutations and prognostic factors analysis in extragastrointestinal stromal tumor of a Chinese three-center study.

BACKGROUND: Most gastrointestinal stromal tumors (GISTs) have gain-of-function mutation of the c-kit gene, and some have mutation of the platelet-derived growth factor receptor-α (PDGFR-α) gene. Extragastrointestinal stromal tumors (EGISTs) are mesenchymal tumors that occur outside the digestive tract. But the clinicopathologic characteristics of EGISTs are still poorly understood. METHODS: Paraffin-embedded tissues from 25 cases of EGIST were analyzed for CD117, CD34, Ki-67, S-100, smooth muscle actin, and desmin expression by immunohistochemical method. These cases of EGISTs were also evaluated for the presence of c-kit exons 9, 11, 13, and 17 mutations and PDGFR-α exons 12 and 18 mutations. Survival analysis was used to evaluate the prognostic factors. RESULTS: c-kit mutations were detected in 44% of EGIST patients and all were exon 11 mutations. PDGFR-α mutations were found in 12% of the 25 cases and all were exon 18 mutations. Survival analysis indicated that mitotic count and Ki-67 labeling index (Ki-67 LI) were significant predictors of survival. CONCLUSION: The pattern of c-kit and PDGFR-α mutation in EGISTs was essentially similar to that in GISTs. From the molecular genetics aspect, EGISTs may be a special subtype of GISTs. The results also show that the combination of mitotic counts and Ki-67 LI may be useful for predicting the prognosis of EGISTs.

Survival and prognostic factors analysis in surgically resected gastrointestinal stromal tumor patients.

BACKGROUND/AIMS: Gastrointestinal stromal tumor (GIST) is the most common mesenchymal tumor of the digestive tract and predicting the clinical behavior and prognosis of GISTs has still been problem for both pathologists and clinicians. The aim of this study was to investigate the survival and prognostic factors of gastrointestinal stromal tumors after surgery. METHODOLOGY: Hematoxylin and eosin (H&E) stained histopathological slides of tumors from patients with GISTs were reviewed. Immunohistochemical staining was performed to demonstrate CD117, CD34, platelet -derived growth factor receptor (PDGFR-alpha) and Ki-67 protein expression. Clinicopathologic features (age, sex, tumor location and size, cell type, mitotic count, risk category, necrosis, surgical method, expression of CD117, CD34, PDGFR-alpha and Ki-67 protein) were evaluated by univariate and multivariate analyses in 135 patients with resected primary GISTs to identify independent prognostic factors. RESULTS: The overall disease-specific survival of 135 patients was 94.1% at 1 year, 76.3% at 3 years and 65.9% at 5 years. Multivariate analyses indicated that the tumor size, primary location, mitotic count, risk category, necrosis and Ki-67 index were independent significant predictors of survival (p < 0.05). Ki-67 index was strong poor predictors of survival as tumor size and mitotic count. CONCLUSIONS: Fletcher's biological behavior ranking method was a good approach to predict prognosis of GIST patients and had significant clinical value. It's better to combine other factors such as Ki-67 index and tumor primary location et al to predict prognosis accurately. Accurate prognostic prediction could provide evidence for postoperative adjuvant targeted therapy.

Gefitinib-induced hair alterations.

Human epidermal growth factor receptor (EGFR) is an attractive target for anticancer therapy. EGFR tyrosine kinase inhibitors are generally well tolerated and do not have the severe systemic side-effects usually seen with cytotoxic drugs. A specific adverse effect common to this class of agent is a papulopustular rash, usually on the face and upper torso. During prolonged treatment with EGFR inhibitors, changes of the hairs can be noticed. This report describes a rare case of a non-small-cell lung cancer with hair changes after several months of treatment with the EGFR inhibitor gefitinib. The patient's scalp hair grew more slowly and adopted a finer, more brittle and curly aspect. However, the eyelashes, eyebrows and hair of other parts of the face did not display similar changes. Little is known about the aetiology of this kind of hair alteration, and there are no clear evidence-based management recommendations. Histological data indicate that the hair alteration may be caused by EGFR inhibition in skin, although this has not been confirmed. Further studies are needed to investigate the reason for this phenomenon.

Secondary C-kit mutation is a cause of acquired resistance to imatinib in gastrointestinal stromal tumor.

C-kit gene gain of function mutations are important in the pathogenesis of gastrointestinal stromal tumors (GISTs). Imatinib is a selective tyrosine kinase inhibitor of KIT and achieves a partial response or stable disease in most patients with metastatic GIST, but there is increasing evidence of acquired resistance. We report a case of GIST with acquired resistance to imatinib during therapy and secondary c-kit mutation besides the primary mutation.

[Influence of microencapsulated ovary cells modified with maspin gene on the microvessel density and lung metastasis of breast carcinoma].

OBJECTIVE: To observe the inhibition of maspin on the angiogenesis in tumor and lung metastasis of breast carcinoma and the feasibility of treatment of tumor by microencapsulated transgene cells in vivo. METHODS: Microencapsulated Chinese hamster ovarian epithelial cells (CHO) modified with maspin gene, CHO/pcDNA3.1/maspin cells, were prepared. Twenty BALB/C nude rats underwent subcutaneous injection of breast carcinoma cells of the line Bcap37 to establish tumor-loaded animal models and then randomly divided into 2 groups: maspin group, undergoing subcutaneous injection of CHO/pcDNA3.1/maspin cells next to the transplanted tumor, and control group undergoing subcutaneous injection of microencapsulated CHO/pcDNA3.1 cells. One month later, the rats were killed and the size and microvessel density (MVD) of the transplanted tumor and metastatic tumor in lung were observed. RESULTS: The MVD of the transplanted tumor of the maspin group was 26 +/- 9, significantly lower than that of the control group (60 +/- 16, P < 0.05). The lung metastatic rate of the maspin group was 15%, significantly lower than that of the control group (55%, P < 0.05). CONCLUSION: Maspin may inhibit the MVD in tumor and the occurrence of metastatic tumor in lung. It is feasible to use microencapsulated transgene cells as tumor-killer.

[Effects of microencapsulated CHO cells modified with maspin gene on the motility and adhesiveness of breast carcinoma cells Bcap37].

OBJECTIVE: To investigate the effects of microencapsulated Chinese hamster ovary (CHO) cells modified with maspin gene on the motility and adhesiveness of breast carcinoma cells Bcap37 and to explore the possibility and feasibility of its clinical application in treatment of malignant tumors. METHODS: After the Bcap37 cells were co-cultured with the microencapsulated CHO cells modified with maspin gene, their motility and adhesion to vascular endothelial cells (ECV304), changes in CD44v6 and E-cadherin expression were examined. RESULTS: After the treatment, the motility of Bcap37 cells, their adhesion to vascular endothelial cells ECV304 and the CD44v6 expression were significantly reduced. The adhesiveness of Bcap37 cells and their E-cadherin expression were significantly enhanced. CONCLUSION: The microencapsulated CHO cells modified with maspin gene decrease motility and adhesiveness of breast carcinoma cells Bcap37, which help explain the anti-metastatic effects of maspin.