Search

Copyright of Canadian Diversity / Canadian Diversité is the property of Association for Canadian Studies and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The majority of penile squamous cell carcinomas is caused by transforming human papilloma virus (HPV) infection. The etiology of HPV-negative cancers is unclear, but TP53 mutations have been implicated. Archival tissues of 108 invasive squamous cell carcinoma from a single pathology institution in a low-incidence area were analyzed for HPV-DNA and p16ink4aoverexpression and for TP53 mutations by ion torrent next-generation sequencing. Library preparation failed in 32/108 squamous cell carcinomas. Institutional review board approval was obtained. Thirty of 76 squamous cell carcinomas (43%; average 63 years) were HPV-negative with 8/33 squamous cell carcinomas being TP53 wild-type (24%; average 63 years). Twenty-five of 33 squamous cell carcinomas (76%; average 65 years) showed 32 different somatic TP53 mutations (23 missense mutations in exons 5–8, 6 nonsense, 1 frameshift and 2 splice-site mutations). Several hotspot mutations were detected multiple times (R175H, R248, R282, and R273). Eighteen of 19 squamous cell carcinomas with TP53 expression in immunohistochemistry had TP53 mutations. Fifty percent of TP53-negative squamous cell carcinomas showed mostly truncating loss-of-function TP53 mutations. Patients without mutations had longer survival (5 years: 86% vs 61%; 10 years: 60% vs 22%), but valid clinically relevant conclusions cannot be drawn due to different tumor stages and heterogeneous treatment of the cases presented in this study. Somatic TP53 mutations are a common feature in HPV-negative penile squamous cell carcinomas and offer an explanation for HPV-independent penile carcinogenesis. About half of HPV-negative penile cancers are driven by oncogenic activation of TP53, while a quarter is induced by loss of TP53 tumor suppressor function. Detection of TP53 mutations should be carried out by sequencing, as immunohistochemical TP53 staining could not identify all squamous cell carcinomas with TP53 mutations.

The majority of penile squamous cell carcinomas is caused by transforming human papilloma virus (HPV) infection. The etiology of HPV-negative cancers is unclear, but TP53mutations have been implicated. Archival tissues of 108 invasive squamous cell carcinoma from a single pathology institution in a low-incidence area were analyzed for HPV-DNA and p16ink4aoverexpression and for TP53mutations by ion torrent next-generation sequencing. Library preparation failed in 32/108 squamous cell carcinomas. Institutional review board approval was obtained. Thirty of 76 squamous cell carcinomas (43%; average 63 years) were HPV-negative with 8/33 squamous cell carcinomas being TP53wild-type (24%; average 63 years). Twenty-five of 33 squamous cell carcinomas (76%; average 65 years) showed 32 different somatic TP53mutations (23 missense mutations in exons 5–8, 6 nonsense, 1 frameshift and 2 splice-site mutations). Several hotspot mutations were detected multiple times (R175H, R248, R282, and R273). Eighteen of 19 squamous cell carcinomas with TP53expression in immunohistochemistry had TP53mutations. Fifty percent of TP53-negative squamous cell carcinomas showed mostly truncating loss-of-function TP53mutations. Patients without mutations had longer survival (5 years: 86% vs61%; 10 years: 60% vs22%), but valid clinically relevant conclusions cannot be drawn due to different tumor stages and heterogeneous treatment of the cases presented in this study. Somatic TP53mutations are a common feature in HPV-negative penile squamous cell carcinomas and offer an explanation for HPV-independent penile carcinogenesis. About half of HPV-negative penile cancers are driven by oncogenic activation of TP53, while a quarter is induced by loss of TP53tumor suppressor function. Detection of TP53mutations should be carried out by sequencing, as immunohistochemical TP53staining could not identify all squamous cell carcinomas with TP53mutations.

In this paper, we construct a timeline to the arrival of 25,000 Syrian refugees in Canada in February 2016. We first provide some background information on the conflict in Syria. Correlating UNHCR data and major political interventions, we then draw a rough portrait of the refugee flows from Syria into the neighboring countries and Europe. Finally, we sketch out the situation that led to the acceptance of Syrian refugees in Canada and offer a preliminary portrait of those who arrived. [ABSTRACT FROM AUTHOR]

Copyright of Canadian Diversity / Canadian Diversité is the property of Association for Canadian Studies and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Usual ductal hyperplasia (UDH) of the breast is generally regarded as a nonneoplastic proliferation, albeit loss of heterozygosity has long been reported in a part of these lesions. To gain deeper insights into the molecular drivers of these lesions, an extended mutation profiling was performed. The coding regions of 409 cancer-related genes were investigated by next-generation sequencing in 16 cases of UDH, nine unassociated with neoplasia (classic) and seven arising within papillomas. Phosphatidylinositol 3-kinase/AKT/mammalian target of rapamycin (mTOR) activation was investigated by phosphorylated AKT, mTOR, and S6 immunohistochemistry. Of 16 lesions, 10 (63%) were mutated; 56% of classic lesions were unassociated with neoplasia, and 71% of lesions arose in papillomas. Fourteen missense mutations were detected: PIK3CA[6 (43%) of 14], AKT1[2 (14%) of 14], as well as GNAS, MTOR, PIK3R1, LPHN3, LRP1B, and IGF2R[each 1 (7%) of 14]. Phosphorylated mTOR was seen in 83% and phosphorylated S6 in 86% of evaluable lesions (phospho-AKT staining was technically uninterpretable). In conclusion, UDH displays mutations of the phosphatidylinositol 3-kinase/AKT/mTOR axis at different levels, with PIK3R1, MTOR, and GNASmutations not previously described. Specifically, oncogenic G-protein activation represents a yet unrecognized route to proliferation in UDH. On the basis of evidence of activating mutations, loss of heterozygosity, and a mass forming proliferation, we propose that UDH is most appropriately viewed as an early neoplastic intraductal proliferation.

Copyright of Canadian Diversity / Canadian Diversité is the property of Association for Canadian Studies and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

If migration studies in the 1990s were marked by the predominance of the “national models” approach, the early 2000s have seen an increasing rebuttal to this approach. This paper contributes to the debate by examining the politics of citizenship in Germany and Canada, two countries that are usually located at opposing poles of the “national models of immigration and citizenship continuum”. The paper combines inductive process tracing and discourse analysis to examine some of the most controversial citizenship legislation in both countries: Optionspflicht[the duty to choose] in Germany and the “first generation limitation” in Canada. Overall, the analysis presented agrees with recent critiques of the national models approach in migration studies. However, and in contrast to the latter, it maintains that national trajectories — rather than models — provide a cognitive matrix into which policy changes and their justifications need to be inserted.

Copyright of Canadian Diversity / Canadian Diversité is the property of Association for Canadian Studies and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

In this paper, we argue that the ideas of multiculturalism and interculturalism are not mutually exclusive. Rather, their difference and sometimes adversity must be situated within the context of two competing nation-building projects - a context in which Québécois interculturalism reveals traces of Canadian multiculturalism and multicultural Canada promotes intercultural dialogue without writing the latter on its forehead. [ABSTRACT FROM AUTHOR]

Diagnosis of cardiac allograft rejection is currently based on histologic exploration of endomyocardial biopsies. Moderate interobserver reproducibility in the estimation of number and distribution of inflammatory cells leads to disagreements in the assignment of rejection grades. Short-tandem repeat (STR) analysis is routinely used after hematopoietic stem-cell transplantation to determine the proportions of donor cells. We compared the amount of recipient-derived cells with the histopathologic grade of rejection in cardiac allografts to determine whether this method might be useful for the assessment of rejection episodes.

The role of β‐ketoacyl‐ACP synthases (condensing enzymes, KAS) in the regulation of the biosynthesis of medium‐chain fatty acids in Cuphea lanceolata seed(86.5% decanoic acid in oil) was investigated. KAS III catalyzes the first condensing step of fatty acid synthase (FAS) reaction between acetyl‐CoA and malonyl‐ACP. This condensing reaction was highly sensitive to inhibition by decanoyl‐ACP, as determined using FAS preparations from C. lanceolataseeds. These data provide strong evidences that KAS III is a target for feedback regulation of fatty acid biosynthesis. Studies on the elongation of octanoyl‐ and hexadecanoyl‐ACP by KAS I and KAS II, respectively, showed that the accumulation of β‐ketoacyl‐ACP, the direct product of condensing reaction, results in decarboxylation of malonyl‐ACP to acetyl‐ACP. The data demonstrate that condensing enzymes can modulate the levels of malonyl‐ACP inside the plastids during the fatty acid biosynthesis.

In order to identify regulatory steps in fatty acid biosynthesis, the influence of intermediate 3-oxoacyl-(acyl carrier proteins) (3-oxoacyl-ACPs) and end-product acyl-ACPs of the fatty acid synthase reaction on the condensation reaction was investigated in vitro, using total fatty acid synthase preparations and purified 3-oxoacyl-ACP synthases (KASs; EC 2.3.1.41) from Cuphea lanceolata seeds. KAS I and II in the fatty acid synthase preparations were assayed for the elongation of octanoyl- and hexadecanoyl-ACP respectively, and the accumulation of the corresponding condensation product 3-oxoacyl-ACP was studied by modulating the content of the reducing equivalents NADH and NADPH. Complete omission of reducing equivalents resulted with either KAS in the abnormal synthesis of acetyl-ACP from malonyl-ACP by a decarboxylation reaction. Supplementation with NADPH or NADH, separately or in combination with recombinant 3-oxoacyl-ACP reductase (EC 1.1.1.100), led to a decrease in the amount of acetyl-ACP and a simultaneous increase in elongation products. This demonstrates that the accumulation of 3-oxoacyl-ACP inhibits the condensation reaction on the one hand, and induces the decarboxylation of malonyl-ACP on the other. By carrying out similar experiments with purified enzymes, this decarboxylation was attributed to the action of KAS. Our data point to a regulatory mechanism for the degradation of malonyl-ACP in plants which is activated by the accumulation of the fatty acid synthase intermediate 3-oxoacyl-ACP.