Real or imagined women? Staff representations of international women postgraduate students

In Australia\u27s globalising universities many support staff and teaching staff now work with international women postgraduate students. But are they aware of the issues facing these women, and is their understanding of them adequate? Indeed, how do they represent them? In this paper we draw on a small-scale pilot study involving key university personnel. We argue that the ways in which such staff represent this group of students is problematic. Focusing primarily on academic issues and on the literature on learning styles, we analyse these staff members\u27 representations of international women postgraduate students from a postcolonial perspective. We explore the extent to which such representations, and the learning styles literature that reflects and informs them, are what Edward Said calls \u27Orientalist\u27. In so doing, we point to both the constitution of the international woman student as postcolonial female subject and show how this situates her in relation to the prevalent learning styles discourse. Further we argue that such representations of the students differ in crucial ways from the students\u27 self-representations, suggesting that in certain subtle ways such staff members are engaging with \u27imagined\u27 rather than \u27real\u27 women. <br /

Clusterin Mediated Apoptosis is Regulated by APC and is P21 Dependent but P53 Independent

Clusterin is a widely expressed glycoprotein that has been paradoxically observed to have both pro- and antiapoptotic functions. Recent reports suggest this apparent dichotomy of function may be related to two different isoforms, one secreted and cytoplasmic, the other nuclear. To clarify the functional role of clusterin in regulating apoptosis, we examined its expression in human colon cancer tissues and in human colon cancer cell lines. We additionally explored its expression and activity using models of adenomatous polyposis coli (APC)- and chemotherapy-induced apoptosis. Clusterin RNA and protein levels were decreased in colon cancer tissues largely devoid of wild-type APC when compared with matched normal tissue controls, suggesting a means for invasive cancers to avoid apoptosis. Conversely, induction of apoptosis by expression of wildtype APC or by treatment with chemotherapy led to increased clusterin RNA and protein levels localizing to apoptotic nuclei. We found that transient transfection of clusterin to colon cancer cell lines directly enhanced basal and chemotherapy-induced apoptosis. Clusterin-induced apoptosis was inhibited by antisense clusterin and was found to be highly dependent on p21 but not p53 expression, yet a deficit in p21 can be subverted by clusterin transfection. Collectively, these data support the hypothesis that nuclear clusterin function is proapoptotic when induced by APC or chemotherapy in the context of p21 expression. Absent of p21, clusterin in not induced, and apoptosis is significantly inhibited. These data support a potential therapeutic role for clusterin in enhancing chemotherapy-induced apoptosis and in promoting apoptosis in cells deficient in p21

Prognostic and Predictive Value of a Malignancy-Risk Gene Signature in Early-Stage Non-Small Cell Lung Cancer

Background The malignancy-risk gene signature is composed of numerous proliferative genes and has been applied to predict breast cancer risk. We hypothesized that the malignancy-risk gene signature has prognostic and predictive value for early-stage non-small cell lung cancer (NSCLC) patients. Methods The ability of the malignancy-risk gene signature to predict overall survival (OS) of early-stage NSCLC patients was tested using a large NSCLC microarray dataset from the Director's Challenge Consortium (n = 442) and two independent NSCLC microarray datasets (n = 117 and 133, for the GSE13213 and GSE14814 datasets, respectively). An overall malignancy-risk score was generated by principal component analysis to determine the prognostic and predictive value of the signature. An interaction model was used to investigate a statistically significant interaction between adjuvant chemotherapy (ACT) and the gene signature. All statistical tests were two-sided. Results The malignancy-risk gene signature was statistically significantly associated with OS (P < .001) of NSCLC patients. Validation with the two independent datasets demonstrated that the malignancy-risk score had prognostic and predictive values: Of patients who did not receive ACT, those with a low malignancy-risk score had increased OS compared with a high malignancy-risk score (P = .007 and .01 for the GSE13212 and GSE14814 datasets, respectively), indicating a prognostic value; and in the GSE14814 dataset, patients receiving ACT survived longer in the high malignancy-risk score group (P = .03), and a statistically significant interaction between ACT and the signature was observed (P = .02). Conclusions The malignancy-risk gene signature was associated with OS and was a prognostic and predictive indicator. The malignancy-risk gene signature could be useful to improve prediction of OS and to identify those NSCLC patients who will benefit from ACT

A Composite Gene Expression Signature Optimizes Prediction of Colorectal Cancer Metastasis and Outcome.

PURPOSE: We previously found that an epithelial-to-mesenchymal transition (EMT)-based gene expression signature was highly correlated with the first principal component (PC1) of 326 colorectal cancer tumors and was prognostic. This study was designed to improve these signatures for better prediction of metastasis and outcome. EXPERIMENTAL DESIGN: A total of 468 colorectal cancer tumors including all stages (I-IV) and metastatic lesions were used to develop a new prognostic score (ΔPC1.EMT) by subtracting the EMT signature score from its correlated PC1 signature score. The score was validated on six other independent datasets with a total of 3,697 tumors. RESULTS: ΔPC1.EMT was found to be far more predictive of metastasis and outcome than its parent scores. It performed well in stages I to III, among microsatellite instability subtypes, and across multiple mutation-based subclasses, demonstrating a refined capacity to predict distant metastatic potential even in tumors with a "good" prognosis. For example, in the PETACC-3 clinical trial dataset, it predicted worse overall survival in an adjusted multivariable model for stage III patients (HR standardized by interquartile range [IQR] = 1.50; 95% confidence interval, 1.25-1.81; P = 0.000016, N = 644). The improved performance of ΔPC1.EMT was related to its propensity to identify epithelial-like subpopulations as well as mesenchymal-like subpopulations. Biologically, the signature was correlated positively with RAS signaling but negatively with mitochondrial metabolism. ΔPC1.EMT was a "best of assessed" prognostic score when compared with 10 other known prognostic signatures. CONCLUSIONS: The study developed a prognostic signature score with a propensity to detect non-EMT features, including epithelial cancer stem cell-related properties, thereby improving its potential to predict metastasis and poorer outcome in stage I-III patients

Adenomatous polyposis coli (APC) regulates miR17-92 cluster through \u3b2-catenin pathway in colorectal cancer

Adenomatous polyposis coli (APC) mutation is the most common genetic change in sporadic colorectal cancer (CRC). Although deregulations of miRNAs have been frequently reported in this malignancy, APC-regulated miRNAs have not been extensively documented. Here, by using an APC-inducible cell line and array analysis, we identified a total of 26 deregulated miRNAs. Among them, members of miR-17-92 cluster were dramatically inhibited by APC and induced by enforced expression of \u3b2-catenin. Furthermore, we demonstrate that activated \u3b2-catenin resulted from APC loss binds to and activates the miR-17-92 promoter. Notably, enforced expression of miR-19a overrides APC tumor suppressor activity, and knockdown of miR-19a in cancer cells with compromised APC function reduced their aggressive features in vitro. Finally, we observed that expression of miR-19a significantly correlates with \u3b2-catenin levels in colorectal cancer specimens, and it is associated to the aggressive stage of tumor progression. Thus, our study reveals that miR-17-92 cluster is directly regulated by APC/\u3b2-catenin pathway and could be a potential therapeutic target in colon cancers with aberrant APC/\u3b2-catenin signaling.Oncogene advance online publication, 25 January 2016; doi:10.1038/onc.2015.522

Review of Jean‐Jacques Rosa, The Second Twentieth Century

Abstract The book reviewed here contends that production techniques – and in particular today, techniques embodying modern information technology – determine political attitudes and, hence, the structure and role of the state. The book's author, Jean‐Jacques Rosa, is not successful in making a compelling case for this thesis. He does, though, offer a host of fascinating observations along the way.Computer, Information Technology, Decentralization, Role of the State, Ideology, D23, D72, D83, H10,

p8 is critical for tumour development induced by ras(V12) mutated protein and E1A oncogene

The p8 protein is involved in the cellular stress response of many tissues. Because p8 is overexpressed in many cancers, we investigated whether its expression was required for tumour development. Mouse embryo fibroblasts (MEFs) from p8(+/+) and p8(–/–) animals were transformed with the pBabe-ras(V12)/E1A retroviral vector, which expresses both the ras(V12) mutated protein and the E1A oncogene. As expected, transformed p8(+/+) MEFs could form colonies in soft agar. However, transformed p8(–/–) MEFs could not. In addition, subcutaneous or intraperitoneal injections of transformed p8(+/+) MEFs always led to tumour formation in nude mice, but, again, no tumour was observed with transformed p8(–/–) MEFs. However, restoring p8 expression in transformed p8(–/–) MEFs before injection led to tumour formation. In the tumours, p8 expression was induced during tumour development. It was concluded that p8 expression in transformed MEFs is necessary for tumour formation, suggesting that the stress-response mechanisms governed by p8 are required for tumour establishment