Top PDF Methylation of the claudin 1 promoter is associated with loss of expression in estrogen receptor positive breast cancer.

Methylation of the claudin 1 promoter is associated with loss of expression in estrogen receptor positive breast cancer.

Methylation of the claudin 1 promoter is associated with loss of expression in estrogen receptor positive breast cancer.

We used the demethylating agents decitabine (DAC) and azacitidine (AZA) to further demonstrate that DNA methylation is responsible for claudin 1 silencing in the breast cancer cell lines MDA‑MB‑453, HCC1569 and BT‑474. Decitabine and azacitidine are distinct cytidine analogs that are used clinically for the treatment of patients with myelodysplastic syndromes and acute myeloid leukemia (AML) [33,34]. As a ribonucleoside, azacitidine is incorporated into both RNA and DNA, while decitabine, a deoxyribonucleoside, is incorporated solely into DNA) [35]. Both act to inhibit DNA methyltransferases [36,37], and to induce demethylation of DNA and re-expression of methylated and silenced genes [38]; however, decitabine shows equivalent activity at doses approximately 2-10 fold lower than azacitidine [18]. Cultured cells were treated daily for three days with decitabine (0.2 µM and 1µM) or azacitidine (1µM and 5µM). Decitabine caused re- expression of claudin 1 in MDA‑MB‑453, HCC1569 and BT‑474 cells; however, HCC1569 and BT‑474 cells achieved the higher level of expression, corresponding to approximately 40% of that of MCF 10A cells (Figure 3C). This represents a 2- fold increase for BT‑474 cells and a 6.6-fold increase for HCC1569 (P<0.0001). MDA‑MB‑453 cells had the lowest basal expression of claudin 1 among these cell lines, and although the gene was upregulated over 400 times by treatment with 1µM decitabine (P<0.0001), the overall level of expression remained lower than in the other two cell lines (Figure 3C). Treatment with azacitidine resulted in a similar upregulation of claudin 1 and was most effective in HCC1569 cells where it caused an 11.6-fold increase in expression (P<0.0001). Similarly to decitabine, azacitidine upregulated claudin 1 in MDA‑MB‑453 cells (up to 38.7-fold, P<0.0001) but the overall amount of
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Formal modeling and analysis of ER-α associated Biological Regulatory Network in breast cancer

Formal modeling and analysis of ER-α associated Biological Regulatory Network in breast cancer

Breast cancer (BC) is a heterogeneous disease which is one of the leading causes of cancer-related mortalities among females worldwide (DeSantis et al., 2014). Estimates indicate that out of 14.1 million new cancer cases globally (Ferlay et al., 2015), BC accounts for 25.2% of them (Hotes et al., 2004). The increasing incidence of BC is due to various genetic and environmental factors such as early menarche, late menopause, hormonal therapies, low breastfeeding, low parity and others (Madigan et al., 1995; McPherson, Steel & Dixon, 2000; Parkin & Fernandez, 2006). Increased expression of estrogen receptor- alpha (ER-α) is observed in 73–75% of diagnosed BC cases (Nadji et al., 2005; Rhodes et al., 2000) which leads to the disruption of various cellular processes (Seemayer et al., 2002). The mutations which increase ER-α expression can be caused by both genetic and environmental signals/conditions. There are two isoforms of ER, namely ER-α and ER-β (Fuqua et al., 1999; Saji et al., 2002). Approximately, there is 70% occurrence of ER-α positive and 30% of ER-α negative in the reported cases of BC (Hurvitz & Pietras, 2008; Madeira et al., 2013).
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Dissertation submitted to Faculdade de Ciências Médicas Universidade Nova de Lisboa for the degree of Doctor in Oncology - Breast Cancer SandraMargaridaCaldasAmaral

Dissertation submitted to Faculdade de Ciências Médicas Universidade Nova de Lisboa for the degree of Doctor in Oncology - Breast Cancer SandraMargaridaCaldasAmaral

The decision of endocrine breast cancer treatment relies on ERα IHC-based assessment. However, ER positivity does not predict response in all cases in part due to IHC methodological limitations. We investigated whether ESR1 and ESR2 gene expression and respective promoter methylation may be related to non-favorable outcome of a proportion of tamoxifen treated patients as well as to ER α and ERß loss. Formalin-fixed paraffin-embedded breast cancer samples from 211 patients diagnosed between 1988 and 2004 were submitted to IHC-based ER α and ERß protein determination. ESR1 whole mRNA and promoter C specific transcript levels, as well as ESR2_ß1, ESR2_ß2/cx, and ESR2_ß5 transcripts were assessed by real-time PCR. ESR1 promoters A and C, and ESR2 promoters 0N and 0K were investigated by CpG methylation analysis using bisulfite-PCR for restriction analysis, or methylation specific PCR. Due to the promising results related to ESR1 promoter methylation, we have used a quantification method by matrix- assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI- TOF MS) together with Epityper software to measure methylation at promoters A and C. mRNA stability was assessed in actinomycin D treated MCF-7 and MDA-MB-231 cells. ERα protein was quantified using transiently transfected breast cancer cells. Low ESR1_C transcript levels were associated with better overall survival (p = 0.017). High levels of ESR1_C transcript were associated with non-favorable response in tamoxifen treated patients (HR = 2.48; CI 95% 1.24-4.99), an effect that was more pronounced in patients with ERα/PgR double-positive tumors (HR = 3.41; CI 95% 1.45-8.04). The ESR1_C isoform had a prolonged mRNA half-life and a more relaxed 5’UTR structure compared to ESR1_A isoform. Western-blot analysis showed that at protein level, the promoter selectivity is undistinguishable. There was no correlation between levels of ESR2 isoforms or ESR2 promoter methylation and ERß protein staining. ESR1 promoter C CpG methylation and not promoter A was responsible for ER α loss. We propose ESR1_C levels as a putative novel marker for breast cancer prognosis and prediction of tamoxifen response.
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Prognostic and Clinicopathological Value of Programmed Death Ligand-1 in Breast Cancer: A Meta-Analysis.

Prognostic and Clinicopathological Value of Programmed Death Ligand-1 in Breast Cancer: A Meta-Analysis.

Recently, the interest in programmed death ligand-1 (PD-L1) as a prognostic marker in sev- eral types of malignant tumors has increased. In the present meta-analysis, we aimed to explore the prognostic and clinicopathological value of PD-L1 in breast cancer. We searched Medline/PubMed, Web of Science, EMBASE, the Cochrane Library databases, and grey literature from inception until January 20, 2016. Studies concerning breast cancer that focused on PD-L1 expression and studies reporting survival data were included; two authors independently performed the data extraction. The pooled risk ratio (RR) and 95% confidence interval (CI) were assessed to determine the association between the clinico- pathological parameters of patients and PD-L1 expression. Five studies involving 2061 patients were included in this meta-analysis. The results indicated that positive/higher PD- L1 expression was a negative predictor for breast cancer, with an RR of 1.64 (95% CI, 1.14–2.34) for the total mortality risk and an RR of 2.53 (95% CI, 1.78–3.59) for the mortality risk 10 years after surgery. Moreover, positive/higher PD-L1 expression was significantly associated with positive lymph node metastasis (RR, 1.33; 95% CI, 1.04–1.70), poor nuclear grade (RR, 1.24; 95% CI, 1.07–1.43), and negative estrogen receptor status (RR, 2.45; 95% CI, 1.31–4.60) in breast cancer patients. Our findings suggest that PD-L1 can serve as a significant biomarker for poor prognosis and the adverse clinicopathologic fea- tures of breast cancer and could facilitate the better management of individual patients.
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Loss of Expression of Reprimo, a p53-induced Cell Cycle Arrest Gene, Correlates with Invasive Stage of Tumor Progression and p73 Expression in Gastric Cancer.

Loss of Expression of Reprimo, a p53-induced Cell Cycle Arrest Gene, Correlates with Invasive Stage of Tumor Progression and p73 Expression in Gastric Cancer.

RPRM is a highly glycosylated protein localized predominantly in the cytoplasm and has been identified as a downstream effector of p53-induced cell cycle arrest at G2/M [10]. Reports suggest that RPRM expression is regulated by two mechanisms, one through DNA methylation at its promoter region [8] and the other by p53 pathway [10]. However, more recent studies have not been able to confirm these findings [6]. On the other hand, the clinical significance of RPRM has been poorly studied [11]. In the present study we evaluated the role of DNA methyl- ation in the regulation of RPRM expression, its clinical significance and its association with members of the p53 tumor suppressor protein family (i.e. p53 and p73). We found dense meth- ylation in the RPRM promoter region, which was associated with loss of expression in GC cell lines. In clinical cases, loss of expression was associated with the invasiveness stage of GC. Fur- thermore, we observed a positive association between expression of RPRM and p73, suggesting that other members of the p53 gene family might be novel candidates for the regulation of RPRM expression.
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Estrogen induces Vav1 expression in human breast cancer cells.

Estrogen induces Vav1 expression in human breast cancer cells.

Breast cancer is the most common death-causing cancer in females [1]. The persistent exposure to estrogen has been observed to closely correlate with the development of breast cancer [2–5]. The expression and responsiveness of estrogen receptor (ER) has been applied as one of the most important markers for the breast cancer classification and prognosis [6]. Two forms of estrogen receptors, ERa and ERb, have been identified [7]. ERa is the dominant form in the breast and uterus, whereas ERb has a wider distribution profile that expands in tissues such as prostate, ovary, lung, and spleen [8]. As a ligand, estrogen binds to ER, and induces its conformational change to activate it. The activated ER associates with the estrogen response element (ERE) at the promoter regions of a variety of genes [9], or complexes with other transcription factors, such as AP1 [10], SP1 [11], or E2F1 [12], modulating the expression of target genes that are involved in cell cycle checkpoint [12,13], cell proliferation [14,15], and apoptosis [16].
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Clinicopathologic Characteristics of Oestrogen Receptor-Positive/Progesterone Receptor-Negative/Her2-Negative Breast Cancer According to a Novel Definition of Negative Progesterone Receptor Status: A Large Population-Based Study from China.

Clinicopathologic Characteristics of Oestrogen Receptor-Positive/Progesterone Receptor-Negative/Her2-Negative Breast Cancer According to a Novel Definition of Negative Progesterone Receptor Status: A Large Population-Based Study from China.

Oestrogen and oestrogen receptors (ERs) play key roles in both normal breast development and breast cancer progression. ER expression is a prognostic factor and powerful indicator of endocrine responsiveness in the clinical management of breast cancer. Previous reports have shown that substantial progesterone receptor (PgR) positivity in tumours is commonly associ- ated with a better prognosis [1,2]. However, the ability of PgR expression to predict a benefit for endocrine therapy remains controversial. In 1975, researchers first hypothesised that PgR could predict the response to endocrine therapy [3]. Later, the PgR status was verified to signif- icantly improve outcome prediction over ER status alone for adjuvant endocrine therapy [4]. However, a few studies have suggested that the recurrence and death rate ratio is independent of PgR status in ER-positive (ER+) disease treated with adjuvant tamoxifen and that luminal A and B tumours similarly benefit from endocrine therapy regardless of PgR expression [5,6]. The absence of PgR expression indicates a higher risk of relapse [7] and is associated with poor survival outcome [8]. A previous study showed that ER+/PgR-negative (PgR-) tumours dis- played more aggressive characteristics than ER+/PgR-positive (PgR+) tumours [9]. Further- more, ER+/PgR- tumours expressed higher levels of HER1 and HER2 than ER+/PgR
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A common variant in the SIAH2 locus is associated with estrogen receptor-positive breast cancer in the Chinese Han population.

A common variant in the SIAH2 locus is associated with estrogen receptor-positive breast cancer in the Chinese Han population.

All 1203 breast cancer cases and 2525 healthy controls (female only) were enrolled based on physician referral through collabo- rations with multiple hospitals in provinces in central China. All breast cancer patients were diagnosed and categorized according to the tumor-node-metastasis (TNM) breast cancer classification. Clinical information was collected from the affected individuals through a full clinical examination by breast cancer specialists. Additional demographic information was collected from the cases via a structured questionnaire. The ER status of each case was evaluated by examination of breast tissue by biopsy or cytology and immunohistochemical analysis of ER positivity or negativity. These cases consisted of 807 estrogen receptor-positive individuals (67.1%) and 396 estrogen receptor-negative individuals (32.9%). Cases with one or more first-degree relatives with breast or ovarian cancer were considered to have a family history of breast cancer. All Chinese controls were clinically confirmed to be free of breast cancer, other neoplastic diseases, and systemic disorders. Addi- tionally, all controls lacked a family history of neoplastic diseases (including first-, second-, and third-degree relatives). All the cases and controls were female. The characteristics of the study population are presented in Table 1. All participants provided written informed consent. The study was approved by the Ethics Committee of Anhui Medical University and conducted according to the principles of the Declaration of Helsinki.
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Arq Bras Endocrinol Metab  vol.50 número4

Arq Bras Endocrinol Metab vol.50 número4

receptors were described about four decades ago (1-3). For estrogens, there are two receptors, estrogen receptor alpha (ERα) and estrogen receptor β (ERβ). The two receptors are coded by different genes and their tissue expression varies across organs. ERα is pre- dominantly expressed in reproductive tissues (uterus, breast, ovaries) liver and central nervous system, whereas ERβ is expressed in other tissues such as bone, endothelium, lungs, urogenital tract, ovaries, central nervous system and prostate (4-10). Both ERs are formed by a single polypeptide chain with 565 aminoacids for the ERα and 530 for the ERβ (11). There are 6 homologous regions, A to F, with the ERβ lacking the carboxiterminal F domain (12). The domains of the estrogen receptors include sites for nuclear location, hormone binding, dimerization, DNA binding and transcription activation (12-16). Estrogens and SERMS activate estrogen genes by a series of events that occur after their binding to the ER. The interaction of the hormone with the naïve receptor induces conformational changes of the lig- and-receptor binding to nuclear proteins or adaptor proteins or corregulators (17,18) that induces the dis- sociation of heat-shock proteins associated with the inactive receptor. This results in receptor activation and and an interaction with DNA (19). This ligand- receptor complex binds to DNA response elements, called Estrogen-Response-Elements (ERE), located in the promoter region of the estrogen target genes, ini- tiating the transcription process and mRNA synthesis. The final result of the process, either inducing or inhibiting gene transcription by the ligand-ER dimer, depends on the type of cell and the presence of cor- regulator proteins and gene promoters. Rapid acting, non-genomic pathways are also activated by estrogens and SERMS such as those dependent upon NO (vasodilatation, ischemic myocardial damage, response to endothelial damage, coronary artery relaxation or vasodilation in hypertensive rats) (20-24). Figure 1
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Prostate Cancer: A State of The Heart

Prostate Cancer: A State of The Heart

men treated with CAB (LHRH agonist + anti- androgen) displayed massive bone metastasis perfusion associated with a lare, which does not occur with the GnRH antagonist (degarelix), indicating that CAB may not reduce tumour size. A comparison of ive studies in patients after orchiectomy was presented, which showed that LHRH agonists are associated with a breakthrough of testosterone levels, with 20% of patients unable to consistently drop their levels below 0.7 nmol/L (20 ng/dL). 11–13 Prof Klotz then went on to describe
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Calculating the uncertainty associated to the forecast of species dispersals: Stochastic Flow Connectivity

Calculating the uncertainty associated to the forecast of species dispersals: Stochastic Flow Connectivity

The optimization of  ( ) L can be properly achieved using genetic algorithms (GAs; Holland, 1975). GAs are powerful evolutionary models with wide potential applications in ecology and biology, such as optimization of protected areas (Parolo et al., 2009), optimal sampling (Ferrarini, 2012a; Ferrarini, 2012b), optimal detection of landscape units (Rossi et al., 2014) and networks control (Ferrarini, 2011; Ferrarini, 2013b; Ferrarini, 2013c; Ferrarini, 2013d; Ferrarini, 2013e; Ferrarini, 2014d).

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Differential Expression of ADAM23, CDKN2A (P16), MMP14 and VIM Associated with Giant Cell Tumor of Bone

Differential Expression of ADAM23, CDKN2A (P16), MMP14 and VIM Associated with Giant Cell Tumor of Bone

The VIM has shown an association in different types of cancer, including prostate cancer, breast cancer, gastric cancer and gallbladder cancer [80-83]. Studies of the ectopic overexpression of vimentin have shown the invasive behavior of epithelial carci- noma cells, which reveal the association of vimentin with tumor invasiveness and motility [84, 85]. One previous study found expression of VIM in mononu- clear cells of GCTB [86]. Our results show that the increased expression of vimentin in multinucleated giant cells, stromal cells and monocytic cells of GCTB is significantly associated with GCTB, and therefore, the increased expression of vimentin may act as a new indicator of this tumor. Zhao et al. [87] demonstrated that vimentin affects prostate cancer cell motility and invasion, and vimentin could be a predictive marker of tumors that might progress to metastatic disease. The MAP2K3 gene is translated into a mito- gen-activated protein kinase 3 and is involved in the signal transduction that controls proliferation and programmed cell death [88]. MAP2K3 protein is in- volved in the Ras-MKK3-p38-signaling cascade, the components of which may confer an invasive pheno- type to the cell [89]. Our study shows that the MAP2K3 gene is overexpressed in GCTB compared to normal tissue. The data support the hypothesis the MAP2K3 protein is implicated in tumor invasion and growth [90, 91].
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Detection of methylated CDO1 in plasma of colorectal cancer; a PCR study.

Detection of methylated CDO1 in plasma of colorectal cancer; a PCR study.

from 400 ml of CRC patients plasma. Half of the extracted DNA was applied to triplicate assays of both CDO1 and b-actin. Thus the plasma volume for each individual assay was 33.3 ml, which designated as 1 template volume. CDO1 methylation was detected in only 2 (10%) of the 20 CRC patients, while b-actin methylation was detected in all samples (Fig. 2). Fig. 2a shows a CDO1 positive cases; methylation of CDO1-3 was clearly detected, but that of CDO1-1 and CDO1-2 was marginal, because the signals were below threshold. However, this level of methylation may be valid, as PCR of 1/1000 dilution of the positive control exhibited a similar signal (Fig. 1d). In contrast, CDO1 negative cases never exhibited any signal at all of amplified CDO1 methylation (Fig. 2b). For these experiments, the amounts of DNA extracted from the initial 400 ml of plasma averaged 435 ng, ranging from 160 ng to 2000 ng. Therefore the amount of DNA applied to 1 PCR reaction corresponded to at least 16.7 (1/6) ng/reaction. This amount of DNA is thought to be sufficient for Q-MSP, if methylated alleles are included (see Fig. 1c). However, the Ct value for b-actin ranged from 34 to 38, which was totally different to that obtained when performing Q-PCR of cell lines, in which the usual Ct value of b-actin is around 28. This result suggested that detection of plasma DNA was less sensitive than that of DNA from cell lines, likely due to DNA degradation or other unknown reasons. Sufficient DNA for the PCR reaction was present only in 1 of 2 6 (64 fold) to 2 10 (1024 fold). This meant that the initial plasma volume used for DNA extraction should ideally be increased 100 to 1000 fold (i.e. to 4–40 ml plasma) for assay of plasma DNA using Q-MSP. Therefore, to obtain enough plasma DNA to detect minimal residual disease, more DNA than that used in this preliminary study would be needed. Thus our initial preliminary study had not used optimal conditions for detection of CDO1 methylation in plasma.
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Expression of claudin, paxillin and FRA-1 in non-nodular breast lesions in association with microcalcifications

Expression of claudin, paxillin and FRA-1 in non-nodular breast lesions in association with microcalcifications

In this regard, we found some imbalance of adhesion pro- tein expression even in the benign cases. Claudin-4 expression, for instance, was negative in 17 cases of non-malignant breast lesions, especially those harboring apocrine metaplasia and ade- nosis. Another important inding was that claudin-4 expression was maintained through the progression to atypical lesions and in situ carcinomas, thus resulting in a larger contingent of posi- tive samples in our series and therefore lacking correlation with morphological or radiological categories. Since the recent ind- ings of loss of claudin expression have mostly been linked to estrogen-negative and high-grade carcinomas 20 and/or aggres-
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The role of adhesion molecules as biomarkers for the aggressive prostate cancer phenotype.

The role of adhesion molecules as biomarkers for the aggressive prostate cancer phenotype.

Total protein was extracted using RIPA buffer (Sigma Aldrich, Dorset, UK). Thirty micrograms of protein was run on either 7.5% or 12% tris-glycine PAGE gels (Bio-Rad Laboratories, Hemel Hempstead, UK) depending on the size of the protein of interest. Proteins were transferred onto nitrocellulose membrane (Amersham Pharmacia Biotech, Amersham, UK). The mem- branes were blocked with 5% non fat dry milk in tween/TBS to inhibit non specific binding (all Sigma Aldrich, Dorset, UK) and incubated overnight at 4 uC using primary antibodies to, Occludin (1:83), ZO-1 (1:250), Claudin-1 (1:125), Claudin-7 (1:125) a- catenin (1:1000), b-catenin (1:1000) and E-cadherin (1:500). b- actin (1:1000) was used as a control for protein loading. Membranes were washed free of primary antibody and incubated with horseradish peroxidase conjugated secondary anti-mouse/ anti-rabbit antibodies (1:1000) for 1 hr at room temperature. Proteins were visualized using the Immun-Star WesternC chemiluminescene detection kit (Bio-Rad Laboratories, Hemel Hempstead, UK) and relative expression was quantified using densitometry and the Quantity One software programme (Bio- Rad Laboratories, Hemel Hempstead, UK). Western blots were performed in duplicate.
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The application of optical measurements for the determination of accuracy of gear wheels casts manufactured in the RT/RP process

The application of optical measurements for the determination of accuracy of gear wheels casts manufactured in the RT/RP process

Before taking the measurements, an anti-reflection coating was applied on the tested gear wheel. The thickness of the coating ranged from 0,8 µm do 1,2 µm. The measurements were taken at the Institute of Metrology and Measuring Systems, at Pozna ń University of Technology.

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SOCIAL ECONOMY – A FORM OF INCLUSION AND OF ''REACTIVATING'' OF LABOR IN THE CONTEXT OF THE CURRENT CRISIS

SOCIAL ECONOMY – A FORM OF INCLUSION AND OF ''REACTIVATING'' OF LABOR IN THE CONTEXT OF THE CURRENT CRISIS

)n the context of the cohesion policy, solidarity must represent a support for development . For that purpose, solidarity can be seen as a help for self‐help and its success depends a great deal on the capacity and the training of the people to whom the support of making maximum profit out of these addresses to. This support does not mean exclusively financial support, although it is necessary and important but, of all things, it means an exchange of experiences and cooperation, the development of capacity through training, open discussions with the interested factors and last but not least a critic, but a constructive dialogue between the various levels of government: European, national, regional, local. )n other words, a functional labor market should represent a catalyst for the general objective of the European Union – social and economical cohesion – because it has in view the connections with the different markets of the services and of the goods and generates the necessary income for supporting the participation of the individuals, bringing them together, placing them in collaborations. )n this context, the starting points for promoting the inclusion through the activities of social economy have in view: adapting the institutional environment, developing the public‐private partnership, developing the social dialogue between players, investments in the human capital and supporting the exchange of good practices within the European Union.
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Estrogen receptor status in relation to risk of contralateral breast cancer-a population-based cohort study.

Estrogen receptor status in relation to risk of contralateral breast cancer-a population-based cohort study.

As a sensitivity analysis we also calculated the SIRs restricted to patients with known ER-status (also of the second cancer, if present), with the aim of investigating the potential effect of missingness of ER-status. Further, we investigated whether the risk of CBC, as compared to the risk of breast cancer in the general population, differed depending on how long time had passed since the first breast cancer. In effect, the observed over expected ratio of CBC during the first five years from diagnosis of primary cancer was calculated, by counting the accumulated person time (which, by using the background rate for the general population, gave rise to the expected number of CBCs) and observed number of CBCs, during these first five years. Then, the number of observed CBCs occurring more than 5 years after the first breast cancer and the person time accumulated from the time point five years after first primary diagnosis and until the end of follow up was calculated, giving rise to an observed over expected ratio in this group. These two ratios could then be compared and whether they differ will answer the question of whether the risk of CBC, as compared to the risk of breast cancer in the general population, differ by time since the first breast cancer.
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Assessment Of Some Acceleration Schemes In The Solution Of Systems Of Linear Equations.

Assessment Of Some Acceleration Schemes In The Solution Of Systems Of Linear Equations.

Many practical problems can be reduced to systems of linear equations Ax = b, where A, b are known matrices and x is a vector of unknowns. Systems of linear equations play a prominent role in economics, engineering, physics, chemistry, computer science and other fields of Pure and Applied Sciences [2]. A solution to a system of linear equations is a set of numerical values ….. that satisfies all the equations in a system [1]. There are two classes of iterative methods [3]: linear stationary and linear nonstationary. The stationary iterative methods are the Jacobi, Gauss-Seidel and SOR and Nonstationary include Krylov subspace methods: Conjugate Gradient, Minimal Residual, Quasi-Minimal Residual, Generalizes Minimal Residual and Biconjugate gradient methods. The choice of a method for solving linear systems will often depend on the structure of the matrix A. According to [8] ideally, iterative methods should have the property that for any starting vector , it converges to a solution Ax = b. [5] is of the view that examination of the Jacobi iterative method shows that in general one must save all the components of the vector while computing the components of the vector for an iterative method. According to Hadjidimos [6], the first step in the construction of solution of stationary iterative methods usually begins with splitting of matrix A. Thus, A = M – N where det M and M is easily invertible so that A = b is equivalent to = T + C , where T = and C = giving the iterative scheme = T + C , (k = 0,1,2……). [2] noted that for systems of linear equation A the splitting matrix may be chosen in a different way; that is, one can split matrix A as A = D L U where D is the diagonal matrix, L and U are strictly lower and strictly upper triangular matrices respectively. In solving the systems of linear equations Ax = b, therefore, we consider any convergent method which produces a sequence of iterates { [7] .Quite often the convergence is too slow and it has to be accelerated. According to [9] to improve the convergence rate of the basic iterative methods, one may transform the original system A = b into the preconditioned form PA = Pb, where � is called the preconditioned or a preconditioning matrix. Convergent numerical sequences occur quite often in natural Science and Engineering. Some of such sequences converge very slowly and their limits are not available without suitable convergent acceleration method. Some known acceleration schemes are: Chebyshev Extrapolation scheme [4] and residual Smoothing.
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J. Bras. Patol. Med. Lab.  vol.51 número5

J. Bras. Patol. Med. Lab. vol.51 número5

Introdução: O carcinoma ductal invasivo de tipo histológico não especial (CDINE) caracteriza-se por grande heterogeneidade morfológica, sendo responsável por cerca de 70%-80% dos tumores malignos de mama. Os principais fatores prognósticos são o tamanho tumoral, o grau de diferenciação e o status dos linfonodos axilares. O CDINE corresponde a 15%-18% das metástases no sistema nervoso central (MSNC) e, geralmente, sua resposta aos tratamentos sistêmicos/quimioterápicos é pouco satisfatória. Objetivo: Estimar a relação entre achados clínicos e anatomopatológicos do CDINE com a presença de MSNC. Método: Foram avaliadas as informações clínicas de 171 espécimes de setorectomia/mastectomia com esvaziamento axilar por CDINE, sendo determinadas as seguintes variáveis anatomopatológicas: tamanho tumoral, grau histológico, status nodal, expressão dos receptores de estrogênio (RE) e progesterona (RP) e de oncoproteína HER-2/neu/receptor do fator de crescimento epidérmico humano (c-erb-B2) e presença de MSNC. Os casos de MSNC em CDINE foram submetidos a ressecção e comprovação do sítio primário pela técnica de imuno-histoquímica. Resultados: A prevalência de MSNC foi igual a 9,4% (n = 16) e apresentou correlação com faixa etária (p = 0,01) e expressão dos RP (p = 0,004). Embora os casos de CDINE com MSNC estivessem relacionados com maior tamanho tumoral, maior grau histológico e metástases nodais, não foi encontrada associação estatística (p = 0,221, p = 0,224 e p = 0,99, respectivamente). A expressão de RE e c-erb-B2 não foi significativa entre os dois grupos (p = 0,072 e p = 0,31, respectivamente). Conclusão: O presente estudo mostrou que as pacientes mais jovens e a expressão dos RP relacionam-se com a presença de MSNC. A avaliação de achados anatomopatológicos específicos no CDINE pode ajudar a estabelecer fatores de risco e/ou parâmetros clínicos associados ao desenvolvimento de MSNC.
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