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The effects of focused ion beams (FIB) implanted into GaAs and similar materials, was studied to determine lateral spread of damage caused by the implantation and the cathodoluminescence intensity of the materials. Raman measurements were obtained for the crystallinity of the implanted structures, and spatial dependence, mobility and cathodoluminescence were measured.

Although various mechanisms involved in anticancer multidrug resistance (MDR) can be identified, it remains a major problem in oncology. Beyond that, the introduction of new “targeted” drugs have not solved the problem. On the contrary, it has been demonstrated that the “classical” MDR-associated mechanisms are similar or identical to those causing resistance to these novel agents. These mechanisms include the enhanced activity of drug pumps, i.e. ABC or alternative transporters; modulation of cellular death pathways; alteration and repair of target molecules; and various less common mechanisms. Together they build a complex network of cellular pathways and molecular mechanisms mediating an individual MDR phenotype. Although the application of new high throughput “-omics” technologies have identified multiple new gene-/protein expression signatures or factors associated with drug resistance, so far none of these findings has been useful for creating improved diagnostic assays, for prediction of individual therapy response, or for development of updated chemosensitizers. [ABSTRACT FROM AUTHOR]

Determination of oestrogen receptor alpha (ER) represents at present the most important predictive factor in breast cancers. Data of ours and of other authors suggest that promising predictive/prognostic factors may also include pS2, metallothionein (MT) and CD24. Present study aimed at determining prognostic and predictive value of immunohistochemical determination of ER, pS2, MT, and CD24 expression in sections originating from 104 patients with breast cancer. An univariate and multivariate analysis was performed. Both univariate and multivariate analyses demonstrated that cytoplasmic-membranous expression of CD24 (CD24c-m) represents a strong unfavourable prognostic factor in the entire group and in most of the subgroups of patients. In several subgroups of the patients also a prognostic value was demonstrated of elevated expression of pS2 and of membranous expression of CD24. Our studies demonstrated that all patients with good prognostic factors (higher ER and pS2 expressions, lower MT expression, CD24c-m negativity) survived total period of observation (103 months). The study documented that cytoplasmic-membranous expression of CD24 represented an extremely strong unfavourable prognostic factor in breast cancer. Examination of the entire panel of the studied proteins permitted to select a group of patients of an exceptionally good prognosis. [ABSTRACT FROM AUTHOR]

A monoclonal mouse antibody, Be-F4, was generated by means of immunization with a synthetic oligopeptide. In Western blots, this antibody recognizes an antigen with an apparent molecular mass of 62 kDa, termed p62. Immunohistochemical analysis of p62 in hepatocellular carcinoma (HCC) specimens (n=33) and in corresponding non-cancerous liver tissue was performed using monoclonal antibody Be-F4. All non-neoplastic hepatic cells showed, without exception, a moderate or strong staining intensity of the 62-kDa antigen, recognized by Be-F4. In contrast to the non-neoplastic hepatocytes, the cellular p62 content was unambiguously reduced in all malignant cells. The extent of decrease of p62 corresponded to the grade of histological differentiation of HCC cells (P<0.001). Using a semiquantitative scoring system, the median of p62 expression, which was 2.1 for normal hepatocytes, was significantly reduced to 1.2 for G1, 1.0 for G2, and 0.2 for G3 HCCs. These data suggest that neoplastic transformation is associated with a reduced p62 content. [ABSTRACT FROM AUTHOR]

Often, tumour cells acquire drug resistance phenotypes, which include the classical multidrug resistance (MDR) phenomenon accompanied by the synthesis of the P-glycoprotein (Pgp) and atypical MDR phenotypes mediated by different, in part unknown, mechanisms. To investigate the susceptibility of tumour cells exhibiting different kinds of MDR to treatment with heat, the hyperthermic survival of established human gastric and pancreatic carcinoma cell lines were studied and sublines exhibiting a classical and an atypical MDR phenotype were derived, respectively. Arrhenius analysis of this panel of gastrointestinal tumour cells revealed that both the classical and the atypical MDR variants exhibited no breaking points (T*) in contrast to the parent tumour cells. The activation enthalpies E[sub A] were about 40% lower at T > T* in comparison to the E[sub A] at lower temperatures. Classical MDR variants of both gastrointestinal tumour cell types exhibited a similar E[sub A] value, whereas the E[sub A] of atypical MDR gastric carcinoma cells was 1.6-fold higher than the E[sub A] of corresponding pancreatic carcinoma cells. In comparison to the parent lines, the drug resistant variants exhibited a 2.1-fold (gastric carcinoma, classical MDR), 2.7-fold (gastric carcinoma, atypical MDR) and 1.4-fold (pancreatic carcinoma, classical MDR) increase of activation enthalpies and a nearby unchanged E[sub A] in pancreatic carcinoma cells exhibiting an atypical MDR. [ABSTRACT FROM AUTHOR]

The role of DNA topoisomerases (Topo) IIα and IIβ was investigated in various drug-resistant melanoma cells. Melanoma cells resistant to etoposide, exhibited an up to tenfold reduced Topo II activity corresponding to an increasing degree of drug resistance indicating that modulation of Topo II activity contribute to the drug-resistant phenotype. The reduction of Topo II activity was reflected by decreased nuclear amounts of both Topo II isoforms. [ABSTRACT FROM AUTHOR]

Background: Human cancer cell lines grown in the presence of the cytotoxic agent mitoxantrone frequently develop resistance associated with a reduction in intracellular drug accumulation without increased expression of the known drug resistance transporters P-glycoprotein and multidrug resistance protein (also known as multidrug resistance-associated protein). Breast cancer resistance protein (BCRP) is a recently described adenosine triphosphate-binding cassette transporter associated with resistance to mitoxantrone and anthracyclines. This study was undertaken to test the prevalence of BCRP overexpression in cell lines selected for growth in the presence of mitoxantrone.Methods: Total cellular RNA or poly A+ RNA and genomic DNA were isolated from parental and drug-selected cell lines. Expression of BCRP messenger RNA (mRNA) and amplification of the BCRP gene were analyzed by northern and Southern blot hybridization, respectively.Results: A variety of drug-resistant human cancer cell lines derived by selection with mitoxantrone markedly overexpressed BCRP mRNA; these cell lines included sublines of human breast carcinoma (MCF-7), colon carcinoma (S1 and HT29), gastric carcinoma (EPG85-257), fibrosarcoma (EPF86-079), and myeloma (8226) origins. Analysis of genomic DNA from BCRP-overexpressing MCF-7/MX cells demonstrated that the BCRP gene was also amplified in these cells.Conclusions: Overexpression of BCRP mRNA is frequently observed in multidrug-resistant cell lines selected with mitoxantrone, suggesting that BCRP is likely to be a major cellular defense mechanism elicited in response to exposure to this drug. It is likely that BCRP is the putative "mitoxantrone transporter" hypothesized to be present in these cell lines. [ABSTRACT FROM AUTHOR]

Measures the nonlinearity of the excitonic absorption in isolated indium arsenide quantum wells inserted in a gallium arsenide matrix. Observation of absorption changes; Determination of the saturation intensity; Calculation of the nonlinear absorption cross section.

Investigates the electroluminescence (EL) properties of resonantly coupled gallium arsenide/aluminum arsenide superlattices (SL). Use of superconductor SL for tunneling structures; Demonstration of higher subbands in SL by resonant tunneling; Insights on the light emitting mechanism of SL.

A novel unipolar transistor device has been realized starting from two-dimensional electron systems (2DES) in modulation-doped AlGaAs/GaAs heterostructures. A 600-nm-wide 1D channel is insulated laterally from 2DES regimes by 700-nm-wide deep mesa etched trenches. The conductivity in the quasi-one-dimensional channel can be tuned via the in-plane lateral field effect of the adjacent 2DES gates where the vacuum (or air) in the etched trenches serves as the dielectric. Room-temperature operation is demonstrated yielding a 17 μS transconductance corresponding to 170 mS/mm 2D transconductance. [ABSTRACT FROM AUTHOR]

Adhesion molecules such as integrins and extracellular matrix proteins like laminins have been identified to play an important role in cell proliferation, migration and invasion by regulating cell-extracellular matrix interaction in various cancers including oral squamous cell carcinoma (OSCC). In this study, the effect of estradiol (E2), and the E2 antagonists tamoxifen (TAM) and ICI 182,780 (ICI) on the expression of integrins and adhesion to laminin-1 in different OSCC in vitro models was analyzed. TAM and ICI inhibited growth in all OSCC cell lines. Dependent on estrogen receptor (ER) status E2 displayed a significant influence on growth after long-term administration. ICI reduced laminin-1 adhesion in all cell lines. beta1 Integrin transcription is reduced with TAM and E2 and alpha3 cell surface expression with TAM. This study shows that OSCC is estrogen and SERM sensitive and that these compounds can modulate cell-matrix interaction in part by modulating integrin expression and translation. The investigation also confirms that growth is significantly influenced by these adjuvant therapeutics. These data suggest that a greater understanding of basic biology and mechanisms of the ER and its ligands in oral squamous cells is needed to elucidate the use of specific pharmacological agents as therapeutics of anti-tumorigenic pathways. [ABSTRACT FROM AUTHOR]