Laboratory Investigation - Table of Contents alert Volume 96 Issue 3

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TABLE OF CONTENTS Volume 96, Issue 3 (March 2016) In this issue Inside the USCAP Journals 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 2016 96: 262-263; 10.1038/labinvest.2015.29 Full Text Research Articles Top BREAST, SKIN, SOFT TISSUE AND BONE Loss of antigenicity with tissue age in breast cancer Although archived tumor specimens provide a wealth of material for clinical investigation, such research generally relies on the assumption that the target biomarkers do not degrade with time. This paper demonstrates that there is a need for adjustment of tissue age when studying formalin-fixed paraffin embedded biospecimens. The rate of antigenicity loss is biomarker-specific and should be considered as an important variable for with studies using archived tissues. Susan E Combs, Gang Han, Nikita Mani, Susan Beruti, Michael Nerenberg and David L Rimm 2016 96: 264-269; advance online publication, November 16, 2015; 10.1038/labinvest.2015.138 Abstract | Full Text ENDOCRINE, VISUAL AND AUDITORY SYSTEMS Lymphatic endothelial lineage assemblage during corneal lymphangiogenesis Lymphangiogenesis plays an important role in the pathogenesis of inflammatory disease. Lineage tracing reveals that proliferating lymphatic endothelial cells assemble contiguously to comprise a subunit within a new lymphatic vessel in vivo. These findings raise fundamental questions regarding lymphatic endothelial precursor cell fate decisions and population dynamics during lymphangiogenesis. Alicia L Connor, Philip M Kelley and Richard M Tempero 2016 96: 270-282; advance online publication, December 14, 2015; 10.1038/labinvest.2015.147 Abstract | Full Text Diabetes enhances the efficacy of AAV2 vectors in the retina: therapeutic effect of AAV2 encoding vasoinhibin and soluble VEGF receptor 1 Adeno-associated virus type 2 (AAV2) vectors encoding vasoinhibin and soluble VEGF receptor 1 reverse blood-retinal barrier breakdown and reduce retinal microvascular abnormalities in diabetic rats. The diabetic state enhances the retinal transduction and efficacy of AAV2 vectors, possibly by elevating vector cell entry, supporting their utility as gene therapeutics to target diabetic retinopathy and macular edema. Nundehui Díaz-Lezama, Zhijian Wu, Elva Adán-Castro, Edith Arnold, Miguel Vázquez-Membrillo, David Arredondo-Zamarripa, Maria G Ledesma-Colunga, Bibiana Moreno-Carranza, Gonzalo Martinez de la Escalera, Peter Colosi and Carmen Clapp 2016 96: 283-295; advance online publication, November 16, 2015; 10.1038/labinvest.2015.135 Abstract | Full Text ORAL AND GASTROINTESTINAL SYSTEMS Tyrosine 397 phosphorylation is critical for FAK-promoted Rac1 activation and invasive properties in oral squamous cell carcinoma cells Focal adhesion kinase (FAK) is highly expressed in malignant tumors. This study examines the role of FAK phosphorylation at tyrosine 397 (pY397) in FAK-modulated oral squamous cell carcinoma (OSCC). The results show that the levels of FAK expression and pY397 are elevated in OSCC tumors. Furthermore, the pY397 is critical for FAK-promoted Rac1 GTPase activation and cell invasion. Ya-Wen Chiu, Li-Yin Liou, Pin-Ting Chen, Chieh-Ming Huang, Fuh-Jinn Luo, Yu-Kan Hsu and Ta-Chun Yuan 2016 96: 296-306; advance online publication, January 11, 2016; 10.1038/labinvest.2015.151 Abstract | Full Text Response of esophageal cancer cells to epigenetic inhibitors is mediated via altered thioredoxin activity Histone deacetylase inhibitor (HDACi) and 5-azacytidine (AZA) treatment selectively induce cell death of esophageal cancer cells. This study reveals that thioredoxin and reactive oxygen species are involved in cancer cell-selective responses to HDACi and AZA treatment in these cells. In situ and in vitro analyses disclose altered regulation of thioredoxin expression, localization and activity. Theresa D Ahrens, Sylvia Timme, Jenny Ostendorp, Lioudmilla Bogatyreva, Jens Hoeppner, Ulrich T Hopt, Dieter Hauschke, Martin Werner and Silke Lassmann 2016 96: 307-316; advance online publication, December 21, 2015; 10.1038/labinvest.2015.148 Abstract | Full Text microRNA-186 inhibits cell proliferation and induces apoptosis in human esophageal squamous cell carcinoma by targeting SKP2 Expression of miR-186 is down-regulated in esophageal squamous cell carcinoma (ESCC) in comparison with the adjacent normal tissue, and is significantly associated with differentiation level, TNM stage, and lymph node metastasis. Mechanistic experiments reveal that miR-186 plays a suppressive role in ESCC progression via the SKP2 ubiquitination/proteasomal degradation pathway and is therefore a potential therapeutic target for treatment ESCC. Wei He, Jianfang Feng, Yan Zhang, Yuanyuan Wang, Wenqiao Zang and Guoqiang Zhao 2016 96: 317-324; advance online publication, November 16, 2015; 10.1038/labinvest.2015.134 Abstract | Full Text Bile acids induce Delta-like 1 expression via Cdx2-dependent pathway in the development of Barrett’s esophagus Crosstalk between the notch signaling pathway and the transcription factor Cdx2 plays an important role in the development of Barrett's esophagus (BE). This study reveals a novel function for the notch ligand delta-like 1 (Dll1) in intestinal metaplasia: Dll1 primarily functions as an intracellular signaling molecule and not a notch agonistic ligand in the canonical pathway. Yuji Tamagawa, Norihisa Ishimura, Goichi Uno, Masahito Aimi, Naoki Oshima, Takafumi Yuki, Shuichi Sato, Shunji Ishihara and Yoshikazu Kinoshita 2016 96: 325-337; advance online publication, November 16, 2015; 10.1038/labinvest.2015.137 Abstract | Full Text GENITOURINARY AND REPRODUCTIVE SYSTEMS Fibroblasts prolong serum prostate-specific antigen decline after androgen deprivation therapy in prostate cancer Prolonged serum prostate-specific antigen (PSA) decline after androgen deprivation therapy (ADT) is strongly associated with favorable prognosis. Here the authors demonstrate that co-inoculation of fibroblasts with prostate cancer cells prolongs serum PSA decline and enhances the efficacy of ADT. This suggests the possibility of a role for fibroblasts in preserving the androgen-dependence of prostate cancer cells. Takeshi Sasaki, Kenichiro Ishii, Yoichi Iwamoto, Manabu Kato, Manabu Miki, Hideki Kanda, Kiminobu Arima, Taizo Shiraishi and Yoshiki Sugimura 2016 96: 338-349; advance online publication, December 7, 2015; 10.1038/labinvest.2015.136 Abstract | Full Text HEPATIC AND PANCREATIC SYSTEMS Inhibition of notch signaling pathway prevents cholestatic liver fibrosis by decreasing the differentiation of hepatic progenitor cells into cholangiocytes Cholestasis is associated with chronic liver disease, and inhibition of abnormal biliary epithelial cell activation and proliferation may reverse biliary fibrosis. In this study, the authors used a cholestatic liver fibrosis rat model to show that notch signaling is required for differentiation of hepatic progenitor cells into cholangiocytes. Inhibition of the notch signaling pathway may therefore offer a therapeutic approach for treatment of liver fibrosis. Xiao Zhang, Guangli Du, Ying Xu, Xuewei Li, Weiwei Fan, Jiamei Chen, Cheng Liu, Gaofeng Chen, Chenghai Liu, Mark A Zern, Yongping Mu and Ping Liu 2016 96: 350-360; advance online publication, December 21, 2015; 10.1038/labinvest.2015.149 Abstract | Full Text Versican: a novel modulator of hepatic fibrosis The large proteoglycan versican is dysregulated during liver fibrosis and reduces during recovery from liver injury. A reversible model of liver fibrosis indicates that during recovery, versican turnover occurs over time, corresponding with delayed changes in several proteolytic ADAMTS enzymes. Knockdown studies suggest that versican modulates hepatic stellate cell activation and hepatic fibrogenesis. Terence N Bukong, Sean B Maurice, Barinder Chahal, David F Schaeffer and Paul J Winwood 2016 96: 361-374; advance online publication, January 11, 2016; 10.1038/labinvest.2015.152 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. For other enquiries, please contact our customer feedback department. 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