TABLE OF CONTENTS
| | | | Volume 97, Issue 2 (February 2017) | | In this issue Inside the USCAP Journals Pathobiology in Focus Mini Reviews Research Articles Corrigendum Also new AOP | | | | | Advertisement | | Join us at the USCAP Annual Meeting! We hope to see you at the Annual Meeting of the United States and Canadian Academy of Pathology (USCAP), taking place from March 4-10, 2017 in San Antonio, TX. Stop by the Springer Nature booth to speak with members of the Laboratory Investigation and Modern Pathology Editorial Teams. >>See the latest conference news | | | | | | Inside the USCAP Journals | Top | | Inside the USCAP Journals 2017 97: 116-117; 10.1038/labinvest.2016.144 Full Text | | Pathobiology in Focus | Top | | Lymphatic invasion and angiotropism in primary cutaneous melanoma Access of melanoma cells to the cutaneous vasculature either via lymphatic invasion or angiotropism is a proposed mechanism for metastasis. While lymphatic invasion and angiotropism are not currently part of routine melanoma reporting, the detection of these attributes using ancillary immunohistochemical stains may be useful in therapeutic planning for patients with melanoma. Andrea P Moy, Lyn M Duncan and Stefan Kraft 2017 97: 118-129; advance online publication, December 19, 2016; 10.1038/labinvest.2016.131 Abstract | Full Text | | | | Unexpected UVR and non-UVR mutation burden in some acral and cutaneous melanomas Whole genome sequencing data generated as part of the Australian Melanoma Genome Project identified 8.6% of acral melanomas with a predominant UVR mutation burden and 2.9% of cutaneous melanomas with a predominant non-UVR mutation burden. This study performs in depth clinicopathological correlation of these interesting cases with contradictory UVR signatures based on the anatomical site of the primary tumor. Robert V Rawson, Peter A Johansson, Nicholas K Hayward, Nicola Waddell, Ann-Marie Patch, Serigne Lo, John V Pearson, John F Thompson, Graham J Mann, Richard A Scolyer and James S Wilmott 2017 97: 130-145; advance online publication, January 9, 2017; 10.1038/labinvest.2016.143 Abstract | Full Text | | | | The NF1 gene in tumor syndromes and melanoma NF1 is a tumor suppressor mutated in neurofibromatosis type 1, a RASopathy characterized by neoplasms and pigment aberrations of the skin, eye, and nervous system. NF1 encodes neurofibromin 1, a RAS-GTPase-activating protein. Somatic mutations in NF1 are common in cancer including melanoma. NF1-mutant melanomas are associated with chronic sun-exposure, a high mutation rate, UV signature mutations, and histologic features of desmoplastic melanoma. Maija Kiuru and Klaus J Busam 2017 97: 146-157; advance online publication, January 9, 2017; 10.1038/labinvest.2016.142 Abstract | Full Text | | Mini Reviews | Top | | A review of kinase fusions in melanocytic tumors Translocations resulting in kinase fusions have been recently described in melanocytic neoplasms, particularly those with spitzoid morphology. Seen within approximately half of all spitzoid neoplasms and present within benign, atypical, and malignant lesions, kinase fusions likely represent an early oncogenic event. This review article focuses on kinase fusions described to date in spitzoid neoplasms and how subsequent studies have informed current melanoma research. Sara C Shalin 2017 97: 158-165; advance online publication, November 28, 2016; 10.1038/labinvest.2016.122 Abstract | Full Text | | | | Immunomodulating property of MAPK inhibitors: from translational knowledge to clinical implementation This review summarizes the off-target mechanisms of response to BRAF inhibitors and MEK inhibitors and the synergy between targeted therapy and immunotherapy as the biological source to open a window of strategic opportunities for the design of new exciting clinical trials. Mario Mandalà, Francesco De Logu, Barbara Merelli, Romina Nassini and Daniela Massi 2017 97: 166-175; advance online publication, December 19, 2016; 10.1038/labinvest.2016.132 Abstract | Full Text | | Research Articles | Top | | Targeting melanoma with front-line therapy does not abrogate Nodal-expressing tumor cells This study reveals that BRAF-inhibitor (BRAFi) therapy does not target nodal-expressing tumor cells in matched unresectable stage III and IV melanoma patient samples (that preceded eventual death). Accompanying experiments showed the advantage of using combinatorial treatment with BRAFi plus anti-Nodal mAb to suppress tumor growth and metastasis, a significant improvement over monotherapy. Mary JC Hendrix, Irawati Kandela, Andrew P Mazar, Elisabeth A Seftor, Richard EB Seftor, Naira V Margaryan, Luigi Strizzi, George F Murphy, Georgina V Long and Richard A Scolyer 2017 97: 176-186; advance online publication, October 24, 2016; 10.1038/labinvest.2016.107 Abstract | Full Text | | | | The influence of tumor regression, solar elastosis, and patient age on pathologists’ interpretation of melanocytic skin lesions The authors surveyed 207 U.S. pathologists to determine whether patient age and tumor characteristics influenced the direction of their diagnosis when interpreting melanocytic skin lesions. The majority (54.6%) reported influence toward a less severe diagnosis by patient age <30, and toward a more severe diagnosis by patient age >70 (58.6%), tumor regression (71.0%), and solar elastosis (57.0%). Linda Titus, Raymond L Barnhill, Jason P Lott, Michael W Piepkorn, David E Elder, Paul D Frederick, Heidi D Nelson, Patricia A Carney, Stevan R Knezevich, Martin A Weinstock and Joann G Elmore 2017 97: 187-193; advance online publication, November 28, 2016; 10.1038/labinvest.2016.120 Abstract | Full Text | | | | Effects of fatty acid synthase inhibitors on lymphatic vessels: an in vitro and in vivo study in a melanoma model Fatty acid synthase (FASN) has shown to be overexpressed in melanomas and associated with poor prognosis. FASN inhibitiors decrease the viability, proliferation, migration, filopodia-like extensions of human lymphatic endothelial cells, and the volume of metastases in experimental melanomas. The anti-metastatic properties of these compounds may result from their effects on both lymphatic endothelium and melanoma cells. Débora C Bastos, Jenny Paupert, Catherine Maillard, Fabiana Seguin, Marco A Carvalho, Michelle Agostini, Ricardo D Coletta, Agnès Noël and Edgard Graner 2017 97: 194-206; advance online publication, December 5, 2016; 10.1038/labinvest.2016.125 Abstract | Full Text | | | | Gene expression profiling of anti-CTLA4-treated metastatic melanoma in patients with treatment-induced autoimmunity Although ipilimumab therapy in metastatic melanoma improves survival, after initial responses disease progression generally ensues. The authors identify targetable genes that are significantly altered by interaction between a highly activated, ipilimumab -treated immune system and melanoma cells. This study provide insight into how melanomas may evolve to resist checkpoint blockade therapy in spite of systemic evidence of an activated cytotoxic immune response in the form of autoimmunity. Scott C Bresler, Le Min, Scott J Rodig, Andrew C Walls, Shuyun Xu, Songmei Geng, F Stephen Hodi, George F Murphy and Christine G Lian 2017 97: 207-216; advance online publication, December 5, 2016; 10.1038/labinvest.2016.126 Abstract | Full Text | | | | Vemurafenib and trametinib reduce expression of CTGF and IL-8 in V600EBRAF melanoma cells The authors explored effects of vemurafenib and trametinib on V600EBRAF-mutated melanoma cell populations. Despite diverse characteristics, all populations responded with reduced expression of IL-8 and CTGF, diminished NF-κB activity and increased percentage of cells with high expression of CD271 and low expression of Ki-67. CTGF inhibition was ERK1/2-dependent but not NF-κB-dependent. Mariusz L Hartman, Michal Rozanski, Marta Osrodek, Izabela Zalesna and Malgorzata Czyz 2017 97: 217-227; advance online publication, January 9, 2017; 10.1038/labinvest.2016.140 Abstract | Full Text | | Corrigendum | Top | | Selective deletion of adipocytes, but not preadipocytes, by TNF-α through C/EBP- and PPARγ-mediated suppression of NF-κB Minori Tamai, Tsuyoshi Shimada, Nobuhiko Hiramatsu, Kunihiro Hayakawa, Maro Okamura, Yasuhiro Tagawa, Shuhei Takahashi, Shotaro Nakajima, Jian Yao and Masanori Kitamura 2017 97: 228; 10.1038/labinvest.2016.124 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. 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