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Invited Commentary (invited + commentary)
Selected AbstractsInvited Commentary: Introduction of An Opcab Program Aimed at Total Arterial Grafting In A Multidisciplinary Setting: Feasible and Safe?JOURNAL OF CARDIAC SURGERY, Issue 2 2007F.A.C.S., F.R.C.S.C., M.Sc., Richard J. Novick M.D. No abstract is available for this article. [source] The role of the RNA-binding protein Sam68 in mammary tumourigenesis,THE JOURNAL OF PATHOLOGY, Issue 3 2010David J Elliott Abstract The RNA binding protein Sam68 (Src- associated in mitosis 68 kD) is implicated in cell signalling, transcriptional regulation, pre-mRNA splicing, and is overexpressed and/or hyperphosphorylated in breast, prostate, and renal cancers. Sam68 has roles in normal breast development; however, a study by Song et al published in this issue of The Journal of Pathology reports overexpression of nuclear and cytoplasmic Sam68 protein in a large cohort of clinical breast tumours, implicating Sam68 as a potential prognostic indicator and target for therapy. In breast cancer cells, nuclear Sam68 protein might affect the expression of cancer-relevant genes and/or modulate exon splicing patterns in a dose-dependent manner. Sam68-regulated expression of alternative transcripts may help drive mammary tumourigenesis. The high levels of cytoplasmic Sam68 protein observed in breast cancer cells could also impact on cellular signalling pathways important for mammary tumour cell biology. Copyright © 2010 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd. Invited Commentary for Song L et al. Sam68 up-regulation correlates with, and its down-regulation inhibits, proliferation and tumourigenicity of breast cancer cells. Journal of Pathology, http://dx.doi.org/10.1002/path.2751 [source] ,-Catenin dysregulation in cancer: interactions with E-cadherin and beyond,THE JOURNAL OF PATHOLOGY, Issue 2 2010Qun Lu Abstract Stable E-cadherin-based adherens junctions are pivotal in maintaining epithelial tissue integrity and are the major barrier for epithelial cancer metastasis. Proteins of the p120ctn subfamily have emerged recently as critical players for supporting this stability. The identification of the unique juxtamembrane domain (JMD) in E-cadherin that binds directly to ,-catenin/NPRAP/neurojungin (CTNND2) and p120ctn (CTNND1) provides a common motif for their interactions. Recently, crystallographic resolution of the JMD of p120ctn further highlighted possibilities of intervening between interactions of p120ctn subfamily proteins and E-cadherin for designing anti-cancer therapeutics. For most epithelial cancers, studies have demonstrated a reduction of p120ctn expression or alteration of its subcellular distribution. On the other hand, ,-catenin, a primarily neural-enriched protein in the brain of healthy individuals, is up-regulated in all cancer types that have been studied to date. Two research articles in the September 2010 issue of The Journal of Pathology increase our understanding of the involvement of these proteins in lung cancer. One reports the identification of rare p120ctn (CTNND1) gene amplification in lung cancer. One mechanism by which ,-catenin and p120ctn may play a role in carcinogenesis is their competitive binding to E-cadherin through the JMD. The other presents the first vigorous characterization of ,-catenin overexpression in lung cancer. Unexpectedly, the authors observed that ,-catenin promotes malignant phenotypes of non-small cell lung cancer by non-competitive binding to E-cadherin with p120ctn in the cytoplasm. Looking towards the future, the understanding of ,-catenin and p120ctn with and beyond their localization at the cell,cell junction should provide further insight into their roles in cancer pathogenesis. Copyright © 2010 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd. Invited Commentary for Castillo et al. Gene amplification of the transcription factor DP1 and CTNND1 in human lung cancer, Journal of Pathology, 2010; 222: 89,98. And for Zhang et al. ,-Catenin promotes malignant phenotype of non-small cell lung cancer by non-competative binding to E-cadherin with p120ctn in cytoplasm. Journal of Pathology, 2010; 222: 76,88. [source] You can win by losing: p53 mutations in rhabdomyosarcomas,THE JOURNAL OF PATHOLOGY, Issue 2 2010Sean M Post Abstract Rhabdomyosarcomas are soft tissue sarcomas of mesenchymal origin. Unlike rhabdomyosarcomas observed in paediatric patients which typically respond well to chemotherapeutic treatment, adults generally present with pleomorphic rhabdomyosarcomas that are typically associated with poor prognosis. Therefore, understanding the molecular biology that gives rise to pleomorphic rhabdomyosarcomas is critical. In this issue of The Journal of Pathology, Doyle and colleagues have generated elegant tissue-specific Cre/loxP-dependent mouse models that mimic pleomorphic rhabdomyosarcoma development in humans. In this report, the authors employed KRasG12V -expressing mouse models that concomitantly either express mutant p53 (p53R172H) or have deleted the p53 gene. Mice that express mutant p53 have decreased survival with development of aggressive metastases as compared to mice that have simply lost wild-type p53. The data presented herein provide the first in vivo evidence that in rhabdomyosarcomas, expression of mutant p53 results in a more aggressive p53R172H-dependent gain-of-function phenotype. Copyright © 2010 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd. Invited Commentary for Doyle B et al.p53 mutation and loss have different effects on tumourigenesis in a novel mouse model of pleomorphic rhabdomyosarcoma. Journal of Pathology, 2010; 222: 129,137. [source] Invited commentary on the case series by J. Krishnan and W. Morrison: Airway pressure release ventilation: A Pediatric Case Series.PEDIATRIC PULMONOLOGY, Issue 1 2007Ped Pulmon 2007;42:8 No abstract is available for this article. [source] A Reason for Optimism in Rural Mental Health Care: Emerging Solutions and Models of Service DeliveryCLINICAL PSYCHOLOGY: SCIENCE AND PRACTICE, Issue 3 2007Myra Elder Psychology Service This invited commentary responds to Jameson and Blank's literature review (2007) and utilizes different source materials, such as personal communications among clinicians and policymakers, Internet-based information, and direct professional experience. An update is provided regarding new graduate programs training clinicians for rural service. In addition, perceived barriers to treatment are challenged, because they are drawn from research results that could be interpreted in different ways, given the cultural heritage of southern and central Appalachian people. Lastly, the efforts of the Veterans Affairs Health Care System to reach rural citizens for mental health treatment are summarized. Some of these federal processes could be replicated at the state level, if sociopolitical and economic factors were more directly addressed. The commentary concludes, from the perspective of a professional providing clinical services in a rural setting, that a more optimistic outlook on the state of rural mental health care may be warranted. [source] | ||||||||||