Fwd: Derivation and internal validation of a rule to predict hospital admission in prehospital patients.

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From: HubMed - cancer <rssfwd@rssfwd.com>
Date: Sat, Jun 28, 2008 at 4:00 PM
Subject: Derivation and internal validation of a rule to predict hospital admission in prehospital patients.
To: mesothelioma77@gmail.com


[1]Prehosp Emerg Care. 2008 Jul-Sep; 12(3): 314-9
Meisel ZF, Pollack CV, Mechem CC, Pines JM

Objective. To derive and internally validate a simple prediction rule, using routinely collected prehospital patient data, that discriminates between hospital admission and emergency department (ED) discharge for adult patients who arrive by ambulance. Methods. We performed a retrospective cohort study of consecutive adult nontrauma patients transported to two separate EDs over two months by a city-run emergency medical services (EMS) system. We tested whether specific prehospital variables could predict hospital admission using chi-square tests, logistic regression, and receiver-operating characteristic curves. We created a rule to predict the probabilities of hospital admission for individual patients. Results. Of 401 patients, the mean age was 47 years; 60% were black and 32% were white; 51% were female; and 33% were admitted to an inpatient service after evaluation in the ED. Independent predictors of admission were dyspnea (adjusted odds ratio [OR] 6.8; awarded 3 points), chest pain (OR 5.2; 3 points), and dizziness, weakness, or syncope (OR 3.5; 2 points). Also predictive were age >/=60 years (OR 5.5; 3 points) and the prehospital identification of a history of diabetes (OR 1.9; 1 point) or cancer (OR 3.9; 2 points). Patients who had a score of 5 or higher had a greater than 69% chance of being admitted to an inpatient unit. Conclusion. Routinely collected EMS patient information can help predict hospital admission for certain ED patients.



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Source: http://www.hubmed.org/display.cgi?uids=18584498
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Fwd: Prognostic Significance of HER2 Gene Amplification According to Stage of Breast Cancer.

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From: HubMed - breast cancer <rssfwd@rssfwd.com>
Date: Sat, Jun 28, 2008 at 4:00 PM
Subject: Prognostic Significance of HER2 Gene Amplification According to Stage of Breast Cancer.
To: mesothelioma77@gmail.com


[1]J Korean Med Sci. 2008 Jun; 23(3): 414-20
Kim YS, Won YS, Park KS, Song BJ, Kim JS, Oh SJ, Jeon HM, Jung SS, Park WC

It is well known that the amplification of the HER2 gene is closely associated with poor prognosis of breast cancer. However, there is controversy about the clinical significance of HER2 according to lymph node status in breast cancer. The aim of this study was to identify the differences in the prognostic significance of HER2 gene amplification according to the stages of breast cancer. We prepared a tissue array for fluorescence in situ hybridization (FISH) with breast cancer specimens from the surgery in 1994 to 1999. Total 338 cases of breast cancer were enrolled and the median follow-up period was 6.3 yr. The detection rates of HER2 gene amplification were as follows: 10.3% in stage I, 22.3% in stage II, and 43.8% in stage III. On survival analyses HER2-positive groups showed worse prognosis in stage III of breast cancer, but not in stage I or II. Multivariate analyses with a Cox-regression model also revealed that HER2 amplification was an independent prognostic factor only in stage III breast cancer. Regarding HER2 gene amplification as a prognostic factor of breast cancer, the clinical significance of the gene was found to be confined to advanced breast cancer.



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Source: http://www.hubmed.org/display.cgi?uids=18583876
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Fwd: Identification of Galectin-3 and mucin-type O-glycans in breast cancer and its metastasis to brain.

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From: HubMed - breast cancer <rssfwd@rssfwd.com>
Date: Sat, Jun 28, 2008 at 4:00 PM
Subject: Identification of Galectin-3 and mucin-type O-glycans in breast cancer and its metastasis to brain.
To: mesothelioma77@gmail.com


[1]Cancer Invest. 2008 Jul; 26(6): 615-23
Mayoral MA, Mayoral C, Meneses A, Villalvazo L, Guzman A, Espinosa B, Ochoa JL, Zenteno E, Guevara J

Galectin-3 has been implicated in tumor progression. We demonstrated immunohistochemically that Galectin-3 was negative in normal breast tissue, but it was highly increased in breast cancer and in metastatic tissues to brain. Similarly, histochemistry with mucin-specific lectins showed increased recognition in breast tumor and metastasis with Machaerocereus eruca agglutinin (Fualpha 1,2 (GalNAcalpha 1,3) Galss1,4 in complex mucin) but not for Amaranthus leucocarpus (Galss1,3-GalNAc-alpha 1,0-Ser/Thr) and Arachis hypogaea lectins (Galss1,3GalNAc/Galss1,4GlcNAc). Mucin-type glycans and Galectin-3 colocalized in breast cancer and metastasis, but not in normal tissue, suggesting upregulated biosynthesis of complex O-glycosidically linked glycans and Galectin-3 favor breast cancer progression and brain metastasis.



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Source: http://www.hubmed.org/display.cgi?uids=18584353
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Fwd: Expression of osteoprotegerin and receptor activator of nuclear factor-kappaB ligand (RANKL) in HCC70 breast cancer cells and effects of treatment with gonadotropin-releasing hormone on RANKL expression.

---------- Forwarded message ----------
From: HubMed - breast cancer <rssfwd@rssfwd.com>
Date: Sat, Jun 28, 2008 at 4:00 PM
Subject: Expression of osteoprotegerin and receptor activator of nuclear factor-kappaB ligand (RANKL) in HCC70 breast cancer cells and effects of treatment with gonadotropin-releasing hormone on RANKL expression.
To: mesothelioma77@gmail.com


[1]Gynecol Endocrinol. 2008 Jun; 24(6): 331-8
Schubert A, Schulz H, Emons G, Grundker C

Background. The majority of human breast cancers and in addition most breast-cancer cell lines express gonadotropin-releasing hormone (GnRH) receptors. Their proliferation and in addition their bone-directed invasion is time- and dose-dependently reduced by GnRH. Osteolytic metastases are characteristic for breast cancer-derived metastasis. Since the osteolytic activity depends on the receptor activator of nuclear factor-kappaB (NFkappaB) ligand (RANKL)/osteoprotegerin (OPG) ratio, we analyzed RANKL and OPG expression in different breast-cancer cell lines. Methods. Different human breast-cancer cell lines were tested for expression of GnRH receptor, OPG and RANKL. Using a co-culture system of breast-cancer cell lines and human primary osteoblasts (hOB), we analyzed the expression of OPG and RANKL in the GnRH receptor-positive breast-cancer cell line HCC70 co-cultured with or without hOB. In addition, we assessed the effects of GnRH analog treatment on OPG and RANKL mRNA and protein levels. Results. All tested breast-cancer cell lines were GnRH receptor-positive. The majority of these cell lines expressed OPG but not RANKL. The HCC70 breast-cancer cell line derived from an invasive ductal carcinoma with metastases was positive for both OPG and RANKL. The expression of RANKL by HCC70 cells was increased when co-cultured with hOB. Treatment with GnRH analogs reduced the expression of RANKL by HCC70 cells co-cultured with hOB. No effects were observed on breast cancer OPG expression. Conclusions. These data show that the majority of human breast-cancer cell lines express OPG but not RANKL. The HCC70 breast-cancer cell line is RANKL-positive. Co-culture of HCC70 breast cancer cells with hOB increases RANKL expression. Activation of tumor GnRH receptors reduces RANKL expression. These experiments demonstrate that HCC70 breast cancer cells are able to activate osteoclasts directly via RANKL. The interaction between HCC70 breast cancer cells and osteoblasts induces osteoclastogenesis through an increase of RANKL expression. GnRH seems to play an important role by modulating the RANKL expression in HCC70 breast cancer cells.



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Source: http://www.hubmed.org/display.cgi?uids=18584413
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Fwd: Stimulation of the human CTP: phosphoethanolamine cytidylyltransferase gene by early growth response protein 1.

---------- Forwarded message ----------
From: HubMed - breast cancer <rssfwd@rssfwd.com>
Date: Sat, Jun 28, 2008 at 4:00 PM
Subject: Stimulation of the human CTP: phosphoethanolamine cytidylyltransferase gene by early growth response protein 1.
To: mesothelioma77@gmail.com


[1]J Lipid Res. 2008 Jun 26;
Zhu L, Johnson C, Bakovic M

Change in phosphoethanolamine pool size in tumor tissues is an important indicator for tumor prognosis and drug therapy efficacy. Phosphoethanolamine is the substrate of the regulatory enzyme CTP:phosphoethanolamine cytidylyltransferase (ECT) in the de novo biosynthesis of phosphatidylethanolamine (PE). Metabolic labeling with 14C-ethanolamine revealed a reduced ECT activity in MCF-7 breast cancer cells, which led to an accumulation of phosphoethanolamine and a decrease in PE synthesis in comparison with MCF-10A mammary epithelial cells. The enhanced ECT activity in MCF-10A cells was due to significantly elevated CTP:phosphoethanolamine cytidylyltransferase gene (PCYT2) expression, at the level of promoter activity, mRNA and protein content. The early growth response protein 1 (EGR1) could account for most of the elevated ECT activity in MCF-10A cells relative to MCF-7 cells, as evidenced by promoter-luciferase reporter assays, gel-shift analyses and by alterations in the EGR1 gene expression. In MCF-7 cells EGR1 is present at lower levels and the basal PCYT2 promoter activity is maintained by proximal CAAT and GC regions and by elevated nuclear NFB activity. Together, these data demonstrate that EGR1 is an important transcriptional stimulator of the human PCYT2 and that conditions which modify EGR1 also affect the function of ECT and consequently PE synthesis.



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Source: http://www.hubmed.org/display.cgi?uids=18583706
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Fwd: Identification, and functional analysis of Ska2 interaction with the glucocorticoid receptor.

---------- Forwarded message ----------
From: HubMed - breast cancer <rssfwd@rssfwd.com>
Date: Sat, Jun 28, 2008 at 4:00 PM
Subject: Identification, and functional analysis of Ska2 interaction with the glucocorticoid receptor.
To: mesothelioma77@gmail.com


[1]J Endocrinol. 2008 Jun 26;
Ray D, Rice L, Waters C, Eccles J, Garside H, Sommer P, Kay P, Blackhall F, Zeef L, Telfer B, Stratford I, Clarke R, Singh D, White A, Stevens A

Glucocorticoid receptors (GR) have profound anti-survival effects on human small cell lung cancer (SCLC). To explore the basis of these effects, protein partners for GR were sought using a yeast two-hybrid screen. We discovered a novel gene, FAM33A, subsequently identified as a Ska1 partner and involved in mitosis, and so renamed Ska2. We produced an anti-peptide antibody which specifically recognized full-length, human Ska2 to measure expression in human cell lines, and tissues. There was wide variation in expression across multiple cell lines, but none detected in the liver cell line HepG2. A xenograft model of human SCLC had intense staining and archival tissue revealed Ska2 in several human lung, and breast tumours. Ska2 was found in the cytoplasm, where it co-localised with GR but nuclear expression of Ska 2 was seen in breast tumours. Ska2 overexpression increased glucocorticoid transactivation in HepG2 cells while Ska2 knockdown in A549 human lung epithelial cells decreased transactivation and prevented dexamethasone inhibition of proliferation. Glucocorticoid treatment decreased Ska2 protein levels in A549 cells, as did staurosporin, phorbol ester, and trichostatin A; all agents that inhibit cell proliferation. Overexpression of Ska2, potentiated the proliferative response to IGF-I exposure, and knockdown with shRNA caused cells to arrest in mitosis. Ska2 has recently been identified in HeLa S3 cells as part of a complex which is critical for spindle checkpoint silencing and exit from mitosis. Our new data show involvement in cell proliferation and glucocorticoid signaling; with implications for understanding how glucocorticoids impact on cell fate.



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Source: http://www.hubmed.org/display.cgi?uids=18583474
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