Laboratory Investigation - Table of Contents alert Volume 94 Issue 1

TABLE OF CONTENTS Volume 94, Issue 1 (January 2014) In this issue Inside the USCAP Journals Pathobiology in Focus Mini Review Research Articles Also new AOP Sign up for e-alerts Recommend to your library Web feed Subscribe Inside the USCAP Journals Top Inside the USCAP Journals 2014 94: 2-3; 10.1038/labinvest.2013.144 Full Text Pathobiology in Focus Top Pathophysiologic mechanisms in septic shock Sepsis continues to be an extensive clinical problem with significant mortality and economic burden. This brief review provides an overview of the immunopathologic and coagulopathic alterations that occur in sepsis, soluble inflammatory mediators as potential diagnostic and prognostic biomarkers, and management of the septic patient. Elizabeth G King, Gustavo J Bauzá, Juan R Mella and Daniel G Remick 2014 94: 4-12; advance online publication, September 23, 2013; 10.1038/labinvest.2013.110 Abstract | Full Text Melanoma stem cells and metastasis: mimicking hematopoietic cell trafficking? This review evaluates the state of malignant melanoma-initiating cell (MMIC) biology and proposes the intriguing possibility that MMICs hijack hematopoietic trafficking mechanisms in completion of the metastatic cascade to target tissues. These newly hypothesized mediators of MMIC homing may prove useful as biomarkers for improved melanoma staging and prognosis. Nayoung Lee, Steven R Barthel and Tobias Schatton 2014 94: 13-30; advance online publication, October 14, 2013; 10.1038/labinvest.2013.116 Abstract | Full Text Matrikine and matricellular regulators of EGF receptor signaling on cancer cell migration and invasion Cancer invasion is a complex process requiring, among other events, extensive remodeling of the extracellular matrix including deposition of pro-migratory and pro-proliferative moieties. This review summarizes findings which indicate that matricellular proteins that can induce both integrin and growth factor signaling and are being deposited at the invasive tumor fronts, enabling cancer cell migrational plasticity and promoting invasion. Jelena Grahovac and Alan Wells 2014 94: 31-40; advance online publication, November 18, 2013; 10.1038/labinvest.2013.132 Abstract | Full Text Mini Review Top CD151 in cancer progression and metastasis: a complex scenario The tetraspanin CD151 promotes tumor neovascularization. The molecular mechanism of CD151 in cancer is based on its ability to organize distribution and function of interacting proteins, i.e., laminin-binding integrins, receptors for growth factors, and matrix metalloproteinases. These findings indicate the importance of CD151 as a diagnostic and prognostic marker and as a potential target of anti-cancer therapy. Rafal Sadej, Alicja Grudowska, Lukasz Turczyk, Radzislaw Kordek and Hanna M Romanska 2014 94: 41-51; advance online publication, November 18, 2013; 10.1038/labinvest.2013.136 Abstract | Full Text Research Articles Top HEPATIC AND PANCREATIC SYSTEMS Deregulation of the NLRP3 inflammasome in hepatic parenchymal cells during liver cancer progression This study provides a comprehensive investigation of the multiprotein nucleotide-binding domain, leucine-rich family pyrin-containing-3 (NLRP3) inflammasome platform in the parenchymal cells of hepatocellular carcinoma (HCC) tissue. This study reveals a dynamic expression pattern of NLRP3 inflammasome components in the development of HCC and demonstrates that a deficiency of this molecular platform is involved in HCC progression. Qing Wei, Kun Mu, Tao Li, Ying Zhang, Zhaowen Yang, Xiaoqing Jia, Wei Zhao, Wanwan Huai, Pengbo Guo and Lihui Han 2014 94: 52-62; advance online publication, October 28, 2013; 10.1038/labinvest.2013.126 Abstract | Full Text PSCs and GLP-1R: occurrence in normal pancreas, acute/chronic pancreatitis and effect of their activation by a GLP-1R agonist Increased glucagon-like peptide-1 receptor (GLP-1R) expression in pancreatic stellate cells (PSCs) occurs during acute/chronic pancreatitis. This paper shows that liraglutide, a drug used to treat type 2 diabetes, induces GLP-1R activation in PSCs. This result indicates that chronic treatment with GLP-1R agonists could lead to proliferation/chronic activation of PSCs, with serious side effects. Taichi Nakamura, Tetsuhide Ito, Masahiko Uchida, Masayuki Hijioka, Hisato Igarashi, Takamasa Oono, Masaki Kato, Kazuhiko Nakamura, Koichi Suzuki, Robert T Jensen and Ryoichi Takayanagi 2014 94: 63-78; advance online publication, November 11, 2013; 10.1038/labinvest.2013.133 Abstract | Full Text BLOOD, LYMPHATICS, IMMUNE SYSTEM AND STEM CELLS Characterization of subpopulation lacking both B-cell and plasma cell markers in Waldenstrom macroglobulinemia cell line Cancer cells with tumorigenic potential are limited to a small population known as cancer-initiating cells (CICs). CICs may be a major cause of tumor recurrence because they efficiently escape apoptosis. To date, CICs have not been identified in non-Hodgkin's lymphomas. This paper reveals a candidate for CICs in an indolent non-Hodgkin's lymphoma, Waldenstrom macroglobulinemia: CD20- CD138- cells. Naoki Wada, Maosheng Zhan, Yumiko Hori, Keiichiro Honma, Jun-ichiro Ikeda and Eiichi Morii 2014 94: 79-88; advance online publication, November 4, 2013; 10.1038/labinvest.2013.129 Abstract | Full Text GENITOURINARY AND REPRODUCTIVE SYSTEMS CCAAT-enhancer binding protein delta (C/EBPδ) attenuates tubular injury and tubulointerstitial fibrogenesis during chronic obstructive nephropathy CCAAT-enhancer-binding protein delta (C/EBPδ) deficiency results in a more profound fibrotic response upon unilateral ureteral obstruction that does not depend on an altered proliferation/apoptosis balance or on a differential inflammatory response in the obstructed kidney. Modulating C/EBPδ expression could consequently be a potential anti-fibrotic strategy in patients with chronic kidney disease. JanWillem Duitman, Keren S Borensztajn, Willem PC Pulskens, Jaklien C Leemans, Sandrine Florquin and C Arnold Spek 2014 94: 89-97; advance online publication, November 18, 2013; 10.1038/labinvest.2013.127 Abstract | Full Text MODELS AND TECHNIQUES Quantitative assessment Ki-67 score for prediction of response to neoadjuvant chemotherapy in breast cancer This study describes the objective measurement of Ki-67, a marker of cell proliferation, by quantitative immunofluorescence to determine the optimal approach to predict outcome for neoadjuvant chemotherapy. Assessment of the average of all fields of view, as well as the score from the highest field of view, are valuable for predicting pathological complete response. Jason R Brown, Michael P DiGiovanna, Brigid Killelea, Donald R Lannin and David L Rimm 2014 94: 98-106; advance online publication, November 4, 2013; 10.1038/labinvest.2013.128 Abstract | Full Text Programmed death ligand-1 expression in non-small cell lung cancer Programmed death ligand-1 (PDL1) is a key mechanism of immune evasion in human cancers, and PD-L1 expression on cancer cells may predict response to anti-PD1 therapy. This paper describes a reproducible method of measuring PD-L1 protein and mRNA in formalin-fixed paraffin-embedded samples and demonstrates the prognostic relevance of these biomarkers in non-small cell lung cancer. Vamsidhar Velcheti, Kurt A Schalper, Daniel E Carvajal, Valsamo K Anagnostou, Konstantinos N Syrigos, Mario Sznol, Roy S Herbst, Scott N Gettinger, Lieping Chen and David L Rimm 2014 94: 107-116; advance online publication, November 11, 2013; 10.1038/labinvest.2013.130 Abstract | Full Text Please note that you need to be a subscriber or site-licence holder to enjoy full-text access to Laboratory Investigation. In order to do so, please purchase a subscription. You have been sent this Table of Contents Alert because you have opted in to receive it. You can change or discontinue your e-mail alerts at any time, by modifying your preferences on your nature.com account at: www.nature.com/nams/svc/myaccount (You will need to log in to be recognised as a nature.com registrant). For further technical assistance, please contact our registration department. For print subscription enquiries, please contact our subscription department. 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