Embedded layer of Ag nanoparticles prepared by a combined PECVD/PVD process producing SiOxCy-Ag nanocomposite thin films.

Structural properties of SiO(x)C(y)-Ag nanocomposite thin films prepared by a dual process PVD-PECVD in the same reactor have been investigated. The experimental results have demonstrated the influence of a PECVD process carried out at room temperature for the growth of a dielectric matrix on the size and the distribution density of Ag nanoparticles (NPs) deposited beforehand by magnetron sputtering. The plasma during the growth of the encapsulation SiO(x)C(y) layer caused a diffusion of silver from NPs through the SiO(x)C(y) matrix associated with a decrease in the average size of nanoparticles and an increase of their distribution density. Silver diffusion is blocked at a barrier interface to form a buried layer of individual Ag NPs which, for instance, can find plasmonic applications. Silver also diffuses toward the outer surface inducing antibacterial properties. In both cases initial Ag NPs act as reservoirs for multifunctional properties of advanced nanostructured films.

Breast cancer associated with idiopathic thrombocytopenic purpura: a single center series of 10 cases.

The aim of this study was to define the characteristics of patients with idiopathic thrombocytopenic purpura (ITP) and breast cancer and discuss the relationship between these two diseases. Ten patients treated for breast cancer and presenting with ITP were screened for this study. The diagnosis of breast cancer was confirmed by biopsy or surgical sample. The diagnosis of ITP was defined by 1) platelet count less than 140.10(9)/l with normal or increased number of megakaryocytes on bone marrow aspirate, 2) after exclusion of thrombocytopenia-induced medication or disorders, and 3) absence of splenomegaly. ITP was diagnosed before breast cancer in three cases, concomitantly in three, and after the diagnosis of breast cancer in four cases. Platelet count and breast cancer showed an independent course in seven cases, and appeared to be correlated in the other three patients. No correlation was found between the development of ITP and tumor characteristics. In contrast, the median platelet count was 15.10(9)/l (range 3-26) for the 3 patients with a correlation between the course of ITP and breast cancer evolution and 70.10(9)/l (range 20-90) for the other cases (p = 0.05, Mann-Whitney U test). Breast cancers are associated with ITP, with a parallel course of the two diseases in one third of cases. This may suggest tumor-induced immunologic thrombocytopenia.

Proliferation markers predictive of the pathological response and disease outcome of patients with breast carcinomas treated by anthracycline-based preoperative chemotherapy.

The cell proliferation rate has been correlated to the response of breast carcinomas to preoperative chemotherapy (CT) and to disease outcome. However, this parameter is not yet used to select which tumours should be treated with preoperative CT. Furthermore, there is no consensus in the method used to evaluate cell proliferation. In poor prognosis breast carcinomas (PPBCs) treated by intensive preoperative CT, we compared the predictive value of S phase fraction (SPF), mitotic index (MI) and Ki67. We also evaluated the prognostic significance of the variation of the MI after CT. A series of 55 T2-T4N0N1M0 breast carcinomas were treated with 4 cycles of cyclophosphamide, 5-fluorouracil (5-FU) and doxorubicin. SPF was determined by flow cytometry on pre-therapeutic needle aspiration products. MI and Ki67 were evaluated on pre-therapeutic biopsy samples and on the tumours after CT. Fifteen patients (27%) had a pathological complete response (pCR), whereas 40 (73%) had residual disease. All three proliferative markers were found to have predictive value, but this value was higher for MI than for SPF (P = 0.04) and Ki67 (P = 0.03): the rate of pCR was 50% in cases with MI > 17/3.3 mm2, but was only 7% in cases with MI under this threshold (P = 0.0003). A significant decrease of MI (mean 10.97) was observed after CT (P = 0.001). Furthermore, we observed that even for patients with residual tumour, the variation of MI after CT was a prognostic parameter and overall survival. The sequential analysis of MI in breast cancers treated by preoperative CT thus provides a surrogate for predicting long-term outcome.

HER2 status in patients with breast carcinoma is not modified selectively by preoperative chemotherapy and is stable during the metastatic process.

BACKGROUND: The objective of this study was to determine whether HER2 expression levels in breast carcinomas were modified by chemotherapy or during the metastatic process. METHODS: HER2 expression was analyzed on sequential tissue specimens taken from the primary tumor before patients received preoperative chemotherapy (CT) and from post-CT residual breast tumor or at a metastatic site. The first group of patients included 59 women who presented with T2-T4,N1-N2 breast carcinoma and were treated by preoperative anthracycline-based CT and then underwent surgery. The second group included 44 patients with metastatic breast carcinoma localized to the lung (27 patients) or to the liver (17 patients). HER2 status was determined by immunohistochemistry using an anti-p185(HER/neu) monoclonal antibody and was classified as overexpressed or not overexpressed. RESULTS: Among the patients who received preoperative CT, HER2 overexpression was observed in 15 of 59 patients (25%). A complete pathologic response was observed in 2 of these 15 patients. HER2 still was overexpressed in 11 of 13 remaining residual tumors and was no longer detectable in 2 tumors. In addition, the 29 tumors with no HER2 overexpression before CT remained negative after treatment. In patients with metastatic breast carcinoma, HER2 was overexpressed in 11 of 44 primary tumors (25%). In 9 of these 11 tumors, HER2 overexpression was maintained in the metastases (9 pulmonary metastases and 4 hepatic metastases). In two patients who had low levels of HER2 overexpression in their primary tumors, no staining was observed in the secondary tumor (one pulmonary tumor and one liver tumor). There were no tumors in which the overexpression of HER2 was found only in the metastasis. CONCLUSIONS: The current study showed that, in most patients, HER2 overexpression was unchanged after CT and in metastatic sites. No HER2 negative primary tumors became HER2 positive after patients received CT or during the metastatic process. In a few patients, a diminution in the level of HER2 expression was observed after CT or in secondary tumors. This may have been due to a transitory state of altered tumor cells or to the selection of HER2 negative tumor cells clones.