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PubMed2004

LCC15-MB cells are MDA-MB-435: a review of misidentified breast and prostate cell lines.

Current stocks of the LCC15-MB cell line, which we originally isolated from a human breast-bone metastasis, were found to be genetically matched to the MDA-MB-435 cell line from the Lombardi Cancer Center (MDA-MB-435-LCC) using comparative genomic hybridisation, DNA microsatellite analysis and chromosomal number. LCC15-MB stocks used for our previously published studies as well as the earliest available LCC15-MB cells also showed identity to MDA-MB-435-LCC cells. The original karyotype reported for LCC15-MB cells was considerably different to that of MDA-MB-435 cells, indicating that the original LCC15-MB cells were lost to contamination by MDA-MB-435-LCC cells. Chromosome number is the simplest test to distinguish original LCC15-MB cells (n approximately 75) from MDA-MB-435 (n approximately 52). Collectively, our results prove that LCC15-MB cells currently available are MDA-MB-435 cells and we suggest their re-designation as MDA-MB-435-LCC15 cells. We also review the known misclassification of breast and prostate cancer cell lines to date and have initiated a register maintained at http://www.svi.edu.au/cell_lines_registry.doc.

Breast Neoplasms↗
PubMed1999

LCC15-MB: a vimentin-positive human breast cancer cell line from a femoral bone metastasis.

The LCC15-MB cell line was established from a femoral bone metastasis that arose in a 29-year-old woman initially diagnosed with an infiltrating ductal mammary adenocarcinoma. The tumor had a relatively high (8%) S-phase fraction and 1/23 positive lymph nodes (LN). Both the primary tumor and LN metastasis were positive for estrogen receptor (ER) and progesterone receptor (PgR), but lacked erbB2 expression. Approximately one year later, the patient presented with a 0.8 cm comedo-type intraductal mammary adenocarcinoma in the left breast that was negative for ER and PgR, but positive for erbB2. Thirty-five months after the initial diagnosis she was treated for acute skeletal metastasis, and stabilized with a hip replacement. At this time, tumor cells were removed from surplus involved bone, inoculated into cell culture, and developed into the LCC 15-MB cell line. The bone metastasis was a poorly differentiated adenocarcinoma lacking ER, PgR, and erbB2, characteristics shared by the LCC15-MB cells, although ER can be re-expressed by treatment of the LCC15-MB cells for 5 days with 75 microM 5-aza-2'-deoxycytidine. The LCC15-MB cell line is tumorigenic when implanted subcutaneously in NCr nu/nu mice and produces long-bone metastases after intracardiac injection. Although the bone metastasis from which the LCC15-MB cell line was derived lacked vimentin (VIM) expression, the original primary tumor and lymph node metastasis were strongly VIM positive, as are LCC15-MB cells in vitro and in nude mice. The karyotype and isozyme profiles of LCC15-MB cells are consistent with its origin from a human female, with most chromosome counts in the hypertriploid range. Thirty-two marker chromosomes are present. These cells provide an in vitro/in vivo model in which to study the inter-relationships between ER, VIM, and bone metastasis in human breast cancer.

Adult↗
PubMed1979

Spontaneous course of ST-segment elevation in acute anterior myocardial infarction.

The spontaneous course of ST-segment elevation (sigmaST) in 24 patients with acute anterior myocardial infarction (AMI) was studied by precordial ST-segment mapping, which was recorded at 2-hour intervals during the first 48 hours after admission. Change of sigmaST between two registrations was expressed as mV/hr, and was compared with clinical and hemodynamic parameters, course of MB-CK curve, calculated infarct mass and arrhythmias. After an initial rapid increase, there was a decrease of sigmaST, which reaches a plateau-like curve approximately 12 hours after the onset of chest pain. A second new increase of sigmaST exceeding a value of 0.6 mV/hr correlates well with extension of necrosis, verified by re-elevation of MB-CK. During the first 2 days, extension of necrosis could be detected in 50% of our patients. As new ischemic episodes and extension of necrosis in AMI occur frequently and are promptly indicated by an increase of sigmaST, the physician should, while monitoring therapeutic interventions, concentrate on such a second increase rather than on a decrease of sigmaST (which may occur spontaneously), as has been suggested in most previous reports.

Adult↗
PubMed1997

Comparative Analysis of Coronary Surgery Risk Stratification Models.

BACKGROUND: Preoperative risk assessment models for coronary bypass surgery (CABG) have been proposed, but comparison of them using independent databases needs to be done. METHODS: Models of CABG hospital mortality were tested on a set of 3,443 patients who underwent CABG including a subset of 3,237 patients who had isolated CABG (no valve procedures), in our database since 1991. Four models previously described were designated as Parsonnet (PS), Cleveland (CL), and Society of Thoracic Surgeons version 1 (ST1) and version 2 (ST2). We developed our own Bayesian (BA) and logistic regression (LR) models and calibrated the PS and CL models on 2,842 patients operated on prior to 1991. Models were compared with respect to 1) mean predicted mortality, 2) correlation of predicted to observed mortality, 3) Brier mean probability score, 4) descriptive statistics, 4) the C-Index (area beneath the receiver operating characteristic curve), and 5) predictive efficiency. Since the ST1 and ST2 models were developed for use only with isolated CABG patients, these models were compared with the others using an isolated CABG subset. RESULTS: Observed mortality for all 3,443 CABG patients was 4.0%. For this group, the mean mortality predicted by PS, CL, BA, LR, was 9.0 +/- 8.0, 6.0 +/- 6.0, 7.6 +/- 15.6, and 5.1 +/- 7.7 (mean +/- standard deviation) respectively. C-Indexes were.80 +/-.02,.80 +/-.02,.83 +/-.02, and.80 +/-.02 (C-Index +/- standard error) respectively. Observed mortality for 3,237 isolated CABG patients was 3.7%. For this subgroup, the mean mortality predicted by PS, CL, BA, LR, ST1, and ST2 was 8.4 +/- 7.4, 5.7 +/- 5.9, 6.5 +/- 13.9, 4.5 +/- 6.5, 9.6 +/- 9.1, and 3.0 +/- 3.3 respectively. C-Indexes were.80 +/-.03,.80 +/-.03,.83 +/-.02,.79 +/-.03,.77 +/-.03, and.81 +/-.02 respectively. CONCLUSIONS: Existing CABG models can accurately discriminate outcome about 80 percent of the time. Models developed on a national database and those from non-local databases appear to have validity for our local data set. Predictions can vary widely between models and existing methods for comparing models appear to be inadequate. The methodology presented here is applicable for use with patients undergoing interventions in the cardiac catheterization laboratory.

Journal Article↗
PubMed2002

Developmental exposure to the pesticides paraquat and maneb and the Parkinson's disease phenotype.

Idiopathic Parkinson's disease (PD) is associated with advanced age, but it is still unclear whether dopaminergic neuronal death results from events initiated during development, adulthood, or represents a cumulative effect across the span of life. This study hypothesized that paraquat (PQ) and maneb (MB) exposure during critical periods of development could permanently change the nigrostriatal dopamine (DA) system and enhance its vulnerability to subsequent neurotoxicant challenges. C57BL/6 mice were treated daily with saline, 0.3 mg/kg PQ, 1 mg/kg MB or PQ + MB from post-natal (PN) days 5 to 19. At 6 weeks, a 20% decrease in activity was evident only in the PQ + MB group, with a further decline (40%) observed at 6 months. A subset of mice were re-challenged as adults with saline, 10 mg/kg PQ, 30 mg/kg MB, or PQ + MB 2 x a week for 3 weeks. Mice exposed developmentally to PQ + MB and rechallenged as adults were the most affected, showing a 70% reduction in motor activity 2 weeks following the last rechallenge dose. Striatal DA levels were reduced by 37% following developmental exposure to PQ + MB only, butfollowing adult re-challenge levels were reduced by 62%. A similar pattern of nigral dopaminergic cell loss was observed, with the PQ + MB treated group exhibiting the greatest reduction, with this loss being amplified by adult re-challenge. Developmental exposure to PQ or MB alone produced minimal changes. However, following adult re-challenge, significant decreases in DA and nigral cell counts were observed, suggesting that exposure to either neurotoxicant alone produced a state of silent toxicity that was unmasked following adult re-exposure. Taken together, these findings indicate that exposure to pesticides during the PN period can produce permanent and progressive lesions of the nigrostriatal DA system, and enhanced adult susceptibility to these pesticides, suggesting that developmental exposure to neurotoxicants may be involved in the induction of neurodegenerative disorders and/or alter the normal aging process.

Aging↗
PubMed1991

Hormonal regulation of cathepsin D following transfection of the estrogen or progesterone receptor into three sex steroid hormone resistant cancer cell lines.

The cathepsin D gene is differentially regulated by estrogens in hormone responsive breast cancer cells, by progestins in normal human endometrium and is highly expressed but not regulated by these steroids in estrogen (RE)- and progesterone receptor (RP)-negative breast cancer cells. We have stably transfected the RE-negative breast cancer cell line MDA-MB 231 and the Hela cell line with an expression vector for the human RE. The endogenous cathepsin D which is constitutively expressed was further stimulated by estradiol. However, the growth of both cell lines was not stimulated by estradiol and could not be inhibited by the antiestrogen ICI 164,384. By contrast, the cathepsin D gene in the estrogen responsive Ishikawa endometrial cancer cell line was unresponsive to estrogen or to progesterone even following stable transfection of expression vectors for the RP (both A and B isoforms). We conclude that the cathepsin D gene is potentially responsive to estrogens in MDA-MB 231 and Hela cells, which therefore express all of the transcriptional machinery (except the RE) necessary for this regulation. By contrast, cathepsin D remains unresponsive to estrogen and progesterone in Ishikawa cells. The cathepsin D gene is one of the first examples of an endogenous steroid responsive gene which can be controlled by steroids following stable transfection of a steroid receptor.

Breast Neoplasms↗
PubMed1984

Short answer questions in an undergraduate qualifying examination: a study of examiner variability.

Scripts of a short answer Final MB examination paper were re-marked by the original examiner and three colleagues. While individual question marks varied considerably, most examiners agreed quite well as to the overall rank order of candidates--although not about absolute total marks--but a few disagreed considerably. Examiners exhibited remarkably consistent idiosyncratic behaviour in terms of the distribution of marks awarded. These factors led to haphazard pass/fail and pass/distinction decisions on this particular component of the examination. Recommendations are put forward to improve the marking consistency and use of short answer question papers.

Education, Medical, Undergraduate↗
PubMed2000

Task-specific effects of orientation information: neuropsychological evidence.

The deficits underlying orientation agnosia in a patient (MB) with a right fronto-temporo-parietal lesion were examined. Like similar patients in the literature, MB was impaired at discriminating whether objects were upright or not and, in copying, she tended to re-represent stimuli as upright. In addition, MB failed to show the normal effects of rotation on object identification; her naming of objects rotated 45 degrees from upright was no slower than her naming of upright items. Effects of the degree of rotation did emerge, however, when she had to perform a matching task that required mental rotation. The evidence suggests that orientation may be coded in several ways (e.g. separately between objects and relative to the viewer), and that brain-damage can selectively affect the use of some but not all types of orientation information.

Agnosia↗
PubMed2005

Deep EEG recordings of the mammillary body in epilepsy patients.

PURPOSE: To our knowledge, the epileptic and nonepileptic electroencephalographic (EEG) discharges recorded within the human mammillary body (MB) and mammillothalamic tract (MTT) areas have never been published. Herein, we present the EEG recordings from these structures in patients with refractory epilepsy (RE). METHODS: Three men (ages 41-43 years) were enrolled in a clinical trial for deep brain stimulation (DBS) of MB-MTT in RE. Previous evaluations had demonstrated a low likelihood of successful response to medication or resective surgery. DBS macroelectrodes were bilaterally implanted within the MB-MTT under general anesthesia and their location checked by magnetic resonance imaging (MRI). We obtained a surface-depth EEG for a 2- to 4-day period, including monitoring of the cardiorespiratory and mnemonic functions. RESULTS: The background pattern of EEG recorded from MB-MTT was low-amplitude (usually <25 microv for MB and <20 microv for MTT) waves with a variable combination of theta-beta rhythms. In two patients, pseudoperiodic slow spikes were unilaterally recorded with or without clinical signs. For one patient, several focal ictal discharges were recorded in the right MB without scalp EEG changes. CONCLUSIONS: The analysis of our depth EEG revealed that the theta-beta pattern represents the predominant physiologic profile of MB. Paroxysmal epileptiform discharges can be observed in human MB. These data supplement those available from animal observations.

Adult↗
PubMed2002

DNA methylation dominates transcriptional silencing of Pax5 in terminally differentiated B cell lines.

Pax5 plays a key role in the progression of B cell development. Its expression is observed in a wide range of cell types from early lineage-committed precursors up to mature B cells, but is silenced in terminal differentiated plasma cells. In this report, we show that DNA methylation is involved in the silencing of Pax5. In the Pax5-expressing cell lines 38B9 (pre-B) and 2PK-3 (mature B), all CpG sites in TATA-containing upstream promoter were unmethylated, whereas these sites were completely methylated in myeloma cell lines FO and Sp-2/0, which do not express Pax5. Demethylation of FO and Sp-2/0 with 5-aza-2'-deoxycytidine (5-aza-dC) resulted in Pax5 re-expression with the concomitant expression of CD19 and mb-1 genes, which are known to be the target genes of Pax5. Re-expression of Pax5 was also induced by trichostatin A (TSA), which was a specific inhibitor of histone deacetylase. This re-expression was, however, transcribed only from the TATA-less downstream promoter. Taken together, we concluded that the upstream promoter was predominantly inactivated by DNA methylation, while the downstream promoter was repressed by the histone deacetylation. This synergetic inactivation of two promoters results in the final silencing of Pax5 expression in terminally differentiated B cell lines.

Animals↗
PubMed2004

Re-expression of estrogen receptor alpha using a tetracycline-regulated gene expression system induced estrogen-mediated growth inhibition of the MDA-MB-231 breast cancer cell line.

Estrogen receptor (ER)-negative breast carcinomas are often difficult to treat with antiestrogens. This work was performed to determine if the re-expression of the human ER alpha could restore the hormone response of these cells. We have transfected the human wild-type ER alpha to an ER-negative breast cancer cell line (MDA-MB-231) using a tetracycline-regulated gene expression system. We obtained a new cell line, MDA-A4-5/2. Cell count and flow cytometry "S" phase cell fraction showed that 17-beta-estradiol induced an inhibition on the proliferation of these cells; on the contrary, the antiestrogens ICI 182 780, and tamoxifen blocked this effect. Finally, we demonstrated an induction of the endogenous progesterone receptor gene when ER alpha was present. These results suggest that the re-expression of ER alpha in ER-negative breast cancer cells recreate, at least partially, a hormone-responsive phenotype and may be useful as a therapeutic approach to control this pathology.

Breast Neoplasms↗