- MeSH
- Bacterial Load MeSH
- Staining and Labeling methods MeSH
- Escherichia coli MeSH
- Phenazines * MeSH
- Gentian Violet * MeSH
- Gram-Negative Bacterial Infections diagnosis MeSH
- Gram-Negative Bacteria isolation & purification MeSH
- Blood microbiology MeSH
- Blood Culture MeSH
- Sensitivity and Specificity MeSH
- Staphylococcus aureus MeSH
- Bacterial Typing Techniques methods MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
We studied 51 paired samples of tissue sections and cytosol extracts from patients with breast cancer. A very high affinity monoclonal antibody to human p53 protein, DO-1, and polyclonal serum CM-1 to p53 protein were used for two site ELISA assays and CM-1 was used for immunohistochemistry to detect p53 protein accumulation in breast cancer samples. Eighteen carcinomas were positive for p53 by tissue staining and ELISA assay. Nineteen tumours were negative by ELISA and immunohistochemistry, and 14 cases with low levels of positive staining by immunohistochemistry were negative by the ELISA assay. A statistically significant correlation has been found between the degree of staining and the amount of p53 protein measured by ELISA (Pearson's correlation coefficient r = 0.59, P < 0.00001). Our ELISA assay offers an alternative approach to evaluating the p53 status of breast biopsy material, using cytosol extracts routinely prepared for steroid hormone receptor assays. This assay should also be of general application to other situations where the level of p53 protein needs to be determined.
- MeSH
- Staining and Labeling methods MeSH
- Cytosol chemistry metabolism MeSH
- Enzyme-Linked Immunosorbent Assay * methods MeSH
- Immunohistochemistry * methods MeSH
- Humans MeSH
- Tumor Suppressor Protein p53 * analysis metabolism MeSH
- Breast Neoplasms * chemistry metabolism MeSH
- Check Tag
- Humans MeSH
- Female MeSH
- Publication type
- Research Support, Non-U.S. Gov't MeSH
- Comparative Study MeSH
- MeSH
- Staining and Labeling methods utilization MeSH
- Cell Wall MeSH
- Lignin analysis MeSH
- Publication type
- Meeting Abstract MeSH
PURPOSE: The basal-A subtype of triple-negative breast cancer is characterized by high levels of ΔNp63. Various functions have been proposed for p63 in breast cancer initiation and growth, and p63 mediates chemotherapeutic response in a subset of triple-negative breast cancers. We investigated the signaling pathways that are controlled by ΔNp63 in basal-A triple-negative breast cancer. METHODS: Human basal-A triple-negative breast cancer cell lines with ΔNp63α induction or inhibition were studied, along with primary human triple-negative breast cancer tissues. Proteomic, phospho-kinase array, mRNA measurements, and immunohistochemistry were employed. RESULTS: Global phosphoproteomics identified increased EGFR phosphorylation in MDA-MB-468 cells expressing ΔNp63α. ΔNp63α expression increased EGFR mRNA, total EGFR protein, and phospho-EGFR(Y1086), whereas silencing endogenous ΔNp63 in HCC1806 cells reduced both total and phospho-EGFR levels and inhibited the ability of EGF to activate EGFR. EGFR pathway gene expression analysis indicated that ΔNp63 alters EGFR-regulated genes involved in cell adhesion, migration, and angiogenesis. Addition of EGF or neutralizing EGFR antibodies demonstrated that EGFR activation is responsible for ΔNp63-mediated loss of cellular adhesion. Finally, immunohistochemical staining showed that p63-positive triple-negative breast cancers were more likely to express high levels of EGFR than p63-negative cancers, corroborated by in silico analysis of gene expression profiling data. CONCLUSIONS: These data identify EGFR as a major target for ΔNp63 regulation that influences cancer cell adhesion in basal-like triple-negative breast cancer.
- MeSH
- Cell Adhesion genetics MeSH
- Epidermal Growth Factor genetics metabolism MeSH
- ErbB Receptors genetics MeSH
- Neoplasm Invasiveness genetics MeSH
- Humans MeSH
- Membrane Proteins genetics MeSH
- Neoplasm Metastasis MeSH
- Cell Line, Tumor MeSH
- Cell Proliferation genetics MeSH
- Proteomics MeSH
- Gene Expression Regulation, Neoplastic MeSH
- Signal Transduction MeSH
- Triple Negative Breast Neoplasms drug therapy genetics pathology MeSH
- Check Tag
- Humans MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
The antioxidant properties of black and green teas are well known. It is also possible to determine their antioxidant capacity by using a chemiluminscent method. This method is based on the measurement of the delay in the emission of light from the luminol reaction in the presence of the antioxidant. Bloodstains which are invisible to the naked eye can also be detected by luminol. Three common methods (detection using the Grodsky or Weber formulations and by Bluestar® Forensic latent bloodstain reagent) are based on the luminol chemiluminescence reaction. The bloodstains can be masked by drinks and/or foods containing antioxidants. The aim of this work was to compare the ability of black and green teas containing antioxidants to cause false negative results during chemiluminescent bloodstain detection.
- MeSH
- Antioxidants analysis chemistry MeSH
- Tea chemistry MeSH
- False Negative Reactions MeSH
- Blood Stains MeSH
- Humans MeSH
- Luminescence MeSH
- Luminescent Agents MeSH
- Luminescent Measurements instrumentation MeSH
- Luminol MeSH
- Beverages MeSH
- Check Tag
- Humans MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
Triple-negative breast cancers are defined by a lack of expression of oestrogen, progesterone, and ERBB2 receptors. This subgroup accounts for 15% of all types of breast cancer and for a higher percentage of breast cancer arising in African and African-American women who are premenopausal. Because of the absence of specific treatment guidelines for this subgroup, triple-negative breast cancers are managed with standard treatment; however, such treatment leaves them associated with a high rate of local and systemic relapse. Histologically, such cancers are poorly differentiated, and most fall into the basal subgroup of breast cancers, characterised by staining for basal markers (ie, cytokeratin 5/6). Analyses of microarray gene-expression profiling data show that they form a homogeneous group (or so-called cluster) in transcriptional terms and, increasingly, research studies are identifying basal cancers on the basis of exhibiting this distinctive transcriptional profile. Histologically and transcriptionally, triple-negative breast cancers have many similarities to BRCA1-associated breast cancers, which suggests that dysfunction in BRCA1 or related pathways occurs in this subset of sporadic cancers. In this review, we discuss the molecular features of triple-negative breast cancers and consider how the use of existing cytotoxic agents can be optimised for this patient group. We discuss the implications of a possible underlying BRCA1-pathway dysfunction in this subgroup in terms of treatment and we also investigate the predominant proliferative signals and the on-going research addressing the suitability of these signals as therapeutic targets.
Progrese buněčného cyklu z fáze Gl do fáze S je řízena cyklin-dependentními kinázami (CDK), na které působí aktivátory a inhibitory. Protein p27kip1 je inhibitorem CDK, který ovládá přechod z fáze Gl do fáze S. Tento protein však může mít také pozitivní regulační vliv. V nenádorových tkáních a ve většině zkoumaných tumorů je mezi imunohístochemickou pozitivitou p27kip1 a proliferačním indexem nepřímo úměrný vztah. Výjimku z této závislosti mezi B-lymfomy představují lymfom z plášťových buněk, leukémie z vlasatých buněk a imunoblastický typ difuzního velkobuněčného B-lymfomu s pozitivitou latentního membránového proteinu viru Epsteina-Barrové u pacientů s AIDS. Ztráta exprese p27kip1 je negativním prognostickým faktorem u mnoha nádorů, včetně většiny B-lymfomů.
Cell cycle progression is governed by cyclin dependent kinases (CDK) that are activated by cyclin binding and inhibited by CDK inhibitors. Protein p27kip1 functions as a CDK inhibitor, which controls the progression from Gl to S phase. Further, p27kip1 may have a positive regidative influence. In nonneoplastic tissiies and in the majority of tumors investigated so far, the immunohistochemical positivity of p27kip1 showed an inversely proportional relationship to the proliferation index. Among B-cell non-Hodgkin lymphomas, the exceptions to this rule are represented by mantle cell lymphoma, hairy cell leukemia, and the immunoblastic Epstein-Barr virus latent membrane antigen positive diffuse large B-cell lymphoma in AIDS patients. The loss of p27kip1 expression is a negative prognostic factor in numerous tumors, including the majority of B-cell lymphomas.
