You have free access to this content

International Journal of Cancer

Cover image for Vol. 135 Issue 9

01 November 2014

Volume 135, Issue 9

Pages 1991–2233, E8–E10

  1. Mini Reviews

    1. Top of page
    2. Mini Reviews
    3. Carcinogenesis
    4. Cancer Cell Biology
    5. Cancer Genetics
    6. Tumor Immunology
    7. Epidemiology
    8. Cancer Therapy
    9. Letter to the Editor
    10. Errata
    1. You have free access to this content
    2. You have free access to this content
      STAT3 and metabolism: How many ways to use a single molecule? (pages 1997–2003)

      Marco Demaria, Annalisa Camporeale and Valeria Poli

      Version of Record online: 19 FEB 2014 | DOI: 10.1002/ijc.28767

  2. Carcinogenesis

    1. Top of page
    2. Mini Reviews
    3. Carcinogenesis
    4. Cancer Cell Biology
    5. Cancer Genetics
    6. Tumor Immunology
    7. Epidemiology
    8. Cancer Therapy
    9. Letter to the Editor
    10. Errata
    1. You have free access to this content
      Eicosapentaenoic acid free fatty acid prevents and suppresses colonic neoplasia in colitis-associated colorectal cancer acting on Notch signaling and gut microbiota (pages 2004–2013)

      Giulia Piazzi, Giuseppe D'Argenio, Anna Prossomariti, Vincenzo Lembo, Giovanna Mazzone, Marco Candela, Elena Biagi, Patrizia Brigidi, Paola Vitaglione, Vincenzo Fogliano, Leonarda D'Angelo, Chiara Fazio, Alessandra Munarini, Andrea Belluzzi, Claudio Ceccarelli, Pasquale Chieco, Tiziana Balbi, Paul M. Loadman, Mark A. Hull, Marco Romano, Franco Bazzoli and Luigi Ricciardiello

      Version of Record online: 28 MAR 2014 | DOI: 10.1002/ijc.28853

      What's new?

      Recent clinical data show that, as yet, there is no agent clearly protecting against colorectal cancer (CRC) development in long-standing inflammatory bowel diseases. This study tests the effect of dietary supplementation with eicosapentaenoic acid, as free fatty acid (EPA-FFA), in a mouse model of colitis-associated CRC. The results demonstrate for the first time that EPA-FFA is an effective chemopreventive agent during both initiation and promotion of colitis-associated colorectal cancer in mice, with changes in Notch1 signaling and gut microbiota composition. Early EPA-FFA supplementation could thus be a good strategy for CRC prevention in subjects affected by inflammatory bowel diseases.

    2. You have full text access to this OnlineOpen article
      Calcium-sensing receptor silencing in colorectal cancer is associated with promoter hypermethylation and loss of acetylation on histone 3 (pages 2014–2023)

      Irfete S. Fetahu, Julia Höbaus, Abhishek Aggarwal, Doris M. Hummel, Samawansha Tennakoon, Ildiko Mesteri, Sabina Baumgartner-Parzer and Enikő Kállay

      Version of Record online: 2 APR 2014 | DOI: 10.1002/ijc.28856

      What's new?

      Studies indicate that increased calcium intake may reduce the risk of colorectal cancer (CRC), and that the calcium-sensing receptor (CaSR) may play an important role in this process. CaSR expression is lost in colorectal cancer, but the mechanisms are not well understood. In this study, the authors found that hypermethylation of a CaSR promoter reduces CaSR expression during CRC tumorigenesis. Loss of histone acetylation has a similar effect. Strategies to upregulate CaSR expression, such as methylation inhibitors and histone deacetylase (HDAC) inhibitors, may thus be useful adjuncts to CRC therapy.

  3. Cancer Cell Biology

    1. Top of page
    2. Mini Reviews
    3. Carcinogenesis
    4. Cancer Cell Biology
    5. Cancer Genetics
    6. Tumor Immunology
    7. Epidemiology
    8. Cancer Therapy
    9. Letter to the Editor
    10. Errata
    1. You have free access to this content
      Cancer-associated fibroblast promote transmigration through endothelial brain cells in three-dimensional in vitro models (pages 2024–2033)

      Yoon Pyo Choi, Joo Hyun Lee, Ming-Qing Gao, Baek Gil Kim, Suki Kang, Se Hoon Kim and Nam Hoon Cho

      Version of Record online: 28 MAR 2014 | DOI: 10.1002/ijc.28848

      What's new?

      Metastasis of breast cancer cells through the blood-brain barrier (BBB) remains poorly understood. This study provides mechanistic insight for cancer-associated fibroblasts (CAFs)-directed breast cancer cell metastasis and colonization, based on integration of biological and physical properties of stromal cells using in vitro 3-D models and co-cultures mimicking brain metastasis. The results support the hypothesis that CAFs mediate BBB disruption and transmigration of breast cancer cells via enhanced vascular permeability, thus facilitating brain metastasis. Uncovering the changes of the BBB system during tumor cell invasion may lead to better understanding of the brain tumor microenvironment and development of novel therapeutic targets.

    2. You have free access to this content
      Pleiotropic antitumor effects of the pan-HDAC inhibitor ITF2357 against c-Myc-overexpressing human B-cell non-Hodgkin lymphomas (pages 2034–2045)

      Roberta Zappasodi, Alessandra Cavanè, Marilena V. Iorio, Monica Tortoreto, Carla Guarnotta, Giusi Ruggiero, Claudia Piovan, Michele Magni, Nadia Zaffaroni, Elda Tagliabue, Carlo M. Croce, Franco Zunino, Alessandro M. Gianni and Massimo Di Nicola

      Version of Record online: 26 MAR 2014 | DOI: 10.1002/ijc.28852

      What's new?

      c-Myc plays a critical role in aggressive B-cell non-Hodgkin lymphomas and multiple myelomas, and is associated with extremely poor prognosis. It hasn't been easy, though, to directly inhibit c-Myc. In this study, the authors found that a histone-deacetylase inhibitor (HDAC) called ITF2357 down-regulated c-Myc protein expression, and that microRNAs (miRNAs) may be involved. ITF2357 also significantly enhanced chemotherapy against human Burkitt's lymphoma in mice. These results suggest that indirectly interfering with c-Myc's oncogenic functions is a promising therapeutic strategy, and that ITF2357 may be a valuable addition to conventional treatments for c-Myc-overexpressing lymphomas.

      Corrected by:

      Erratum: Erratum

      Vol. 141, Issue 9, E6, Version of Record online: 4 SEP 2017

    3. You have free access to this content
      Inactivation of protein-phosphatase 2A causing hyperphosphorylation of autoantigenic paraprotein targets in MGUS/MM is due to an exchange of its regulatory subunits (pages 2046–2053)

      Klaus-Dieter Preuss, Natalie Fadle, Evi Regitz, Gerhard Held and Michael Pfreundschuh

      Version of Record online: 5 APR 2014 | DOI: 10.1002/ijc.28864

      What's new?

      Paraproteins are abnormal antibodies. People who carry a mutation that alters a protein called ‘paratarg-7’ (for ‘paraprotein target-7’) have an increased risk for several cancers, including monoclonal gammopathy of undetermined significance (MGUS) and multiple myeloma (MM). The altered form of paratarg-7 is hyperphosphorylated, due to loss of the enzyme protein-phosphatase 2A (PP2A). In this study, the authors identified the mechanism that inactivates PP2A. They also found that PP2A activity can be restored in vitro. This could eventually lead to a new therapeutic strategy for these cancers.

    4. You have free access to this content
      Opposing effects of HIF1α and HIF2α on chromaffin cell phenotypic features and tumor cell proliferation: Insights from MYC-associated factor X (pages 2054–2064)

      Nan Qin, Aguirre A. de Cubas, Ruben Garcia-Martin, Susan Richter, Mirko Peitzsch, Mario Menschikowski, Jacques W.M. Lenders, Henri J. L. M. Timmers, Massimo Mannelli, Giuseppe Opocher, Matina Economopoulou, Gabriele Siegert, Triantafyllos Chavakis, Karel Pacak, Mercedes Robledo and Graeme Eisenhofer

      Version of Record online: 7 APR 2014 | DOI: 10.1002/ijc.28868

      What's new?

      Chromaffin cell tumors can result from mutations in a number of different genes, and they show a variety of characteristics. In this study, the authors looked at patient samples to figure out how mutations in the Myc-associated factor X (MAX) gene influences gene expression patterns in the tumors. They also manipulated cell line models to see how the interactions of MAX, HIF1α, and HIF2α affect tumor characteristics. They found that tumors resulting from MAX mutations have a distinctive gene expression profile and phenotypic characteristics. HIF1α and HIF2α have opposing influences in the cell, they found, and the relative expression of these two can alter the characteristics of the tumor.

  4. Cancer Genetics

    1. Top of page
    2. Mini Reviews
    3. Carcinogenesis
    4. Cancer Cell Biology
    5. Cancer Genetics
    6. Tumor Immunology
    7. Epidemiology
    8. Cancer Therapy
    9. Letter to the Editor
    10. Errata
    1. You have free access to this content
      Genetic association of gastric cancer with miRNA clusters including the cancer-related genes MIR29, MIR25, MIR93 and MIR106: Results from the EPIC-EURGAST study (pages 2065–2076)

      Yolanda Espinosa-Parrilla, Xavier Muñoz, Catalina Bonet, Nadia Garcia, Adoración Venceslá, Nikos Yiannakouris, Alessio Naccarati, Sabina Sieri, Salvatore Panico, José M. Huerta, Aurelio Barricarte, Virginia Menéndez, Emilio Sánchez-Cantalejo, Miren Dorronsoro, Paul Brennan, Talita Duarte-Salles, H. B(as) Bueno-de-Mesquita, Elisabete Weiderpass, Eiliv Lund, Françoise Clavel-Chapelon, Marie-Christine Boutron-Ruault, Antoine Racine, Mattijs E. Numans, Rosario Tumino, Federico Canzian, Daniele Campa, Malin Sund, Mattias Johansson, Bodil Ohlsson, Björn Lindkvist, Kim Overvad, Anne Tjønneland, Domenico Palli, Ruth C. Travis, Kay-Tee Khaw, Nick Wareham, Heiner Boeing, Gabriella Nesi, Elio Riboli, Carlos A. Gonzalez and Núria Sala

      Version of Record online: 2 APR 2014 | DOI: 10.1002/ijc.28850

      What's New?

      Even though deregulation of miRNA expression has been associated with human cancers, the contribution of miRNAs to cancer genetic susceptibility is unclear. Here the authors designed a panel of 133 SNPs tagging 104 candidate miRNA genes and analysed their association with gastric cancer (GC). They describe an unreported significant genetic association of GC with miRNA clusters in chromosomes 7 and X including miR-29, miR-25, miR-93, and miR-106. These miRNAs have been previously involved in the pathophysiology of GC and have functionally validated target genes implicated in cancer-related processes. The data suggest these miRNAs as novel genetic susceptibility factors for GC.

    2. You have free access to this content
      A novel transcript, VNN1-AB, as a biomarker for colorectal cancer (pages 2077–2084)

      Marthe Løvf, Torfinn Nome, Jarle Bruun, Mette Eknæs, Anne C. Bakken, John P. Mpindi, Sami Kilpinen, Torleiv O. Rognum, Arild Nesbakken, Olli Kallioniemi, Ragnhild A. Lothe and Rolf I. Skotheim

      Version of Record online: 29 MAR 2014 | DOI: 10.1002/ijc.28855

      What's new?

      For colorectal cancer (CRC), prognosis is strongly associated with disease stage. Improved prognostic and predictive biomarkers would be extremely helpful. In this study, the authors used whole transcriptome sequencing of CRC and normal cells, followed by outlier-expression analysis from a large set of samples, to identify variant mRNA transcripts that might be useful as biomarkers of CRC. Real-time PCR showed that a novel transcript, VNN1-AB, had high sensitivity and 100% specificity for CRC. This transcript may thus be a valuable prognostic tool for stratifying CRC risk.

    3. You have full text access to this OnlineOpen article
      Differential DNA methylation analysis of breast cancer reveals the impact of immune signaling in radiation therapy (pages 2085–2095)

      Ann Rita Halvorsen, Åslaug Helland, Thomas Fleischer, Karen Marie Haug, Grethe Irene Grenaker Alnæs, Daniel Nebdal, Randi G. Syljuåsen, Nizar Touleimat, Florence Busato, Jörg Tost, Anna B. Sætersdal, Anne-Lise Børresen-Dale, Vessela Kristensen and Hege Edvardsen

      Version of Record online: 5 APR 2014 | DOI: 10.1002/ijc.28862

      What's new?

      Radiotherapy is a central treatment modality for breast cancer patients. This study set to investigate DNA methylation changes in tumors following radiotherapy and identify epigenetic markers predicting treatment outcome. Genome-wide methylation effects were studied by comparing breast cancer biopsies before and after irradiation. 82 differentially methylated genes enriched for immune regulation pathways were identified. Based on methylation levels before irradiation, a combination of 5 genes was significantly associated with response to radiotherapy. A dose dependency was seen for 2516 probes, mainly involved in immune response and apoptosis. This study sheds light on the genes and pathways involved in radiation response.

    4. You have free access to this content
      High coexpression of CCL2 and CX3CL1 is gender-specifically associated with good prognosis in soft tissue sarcoma patients (pages 2096–2106)

      Astrid Kehlen, Thomas Greither, Sven Wach, Elke Nolte, Matthias Kappler, Matthias Bache, Hans-Jürgen Holzhausen, Christine Lautenschläger, Steffen Göbel, Peter Würl, Uta-Dorothee Immel, Abbas Agaimy, Bernd Wullich and Helge Taubert

      Version of Record online: 4 APR 2014 | DOI: 10.1002/ijc.28867

      What's New?

      While chemokines are known to play key roles in both driving and preventing cancer progression, their expression and biological significance in soft tissue sarcoma (STS) remain unclear. This study shows that monocyte chemotactic protein-1 (MCP1/CCL2) and fractalkine (CX3CL1) affect the prognosis of STS patients. The high mRNA expression of both chemokines is correlated with a good outcome in STS patients, particularly in female STS patients. The study provides evidence supporting the hypothesis that CCL2 and CX3CL1 have a promoting effect on apoptosis induction in STS. A possible explanation for the gender difference is the gender-specific regulation of chemokines by hormones/receptors.

  5. Tumor Immunology

    1. Top of page
    2. Mini Reviews
    3. Carcinogenesis
    4. Cancer Cell Biology
    5. Cancer Genetics
    6. Tumor Immunology
    7. Epidemiology
    8. Cancer Therapy
    9. Letter to the Editor
    10. Errata
    1. You have free access to this content
      In vivo evidence that secretion of HLA-G by immunogenic tumor cells allows their evasion from immunosurveillance (pages 2107–2117)

      Laure Loumagne, Jeremy Baudhuin, Benoit Favier, Florent Montespan, Edgardo D. Carosella and Nathalie Rouas-Freiss

      Version of Record online: 7 APR 2014 | DOI: 10.1002/ijc.28845

      What's New?

      Tumors that express human leukocyte antigen-G (HLA-G) are associated with poor prognosis and resistance to immunotherapy in humans. Researchers have proposed that HLA-G secretion allows tumors to escape immunosurveillance, but direct evidence has been lacking. In this study, the authors found that when tumors are engineered to express HLA-G, they do indeed escape destruction by the immune system, via a number of different effects on T and B cells, and MDSC. Blocking HLA-G may therefore be a promising therapeutic strategy to enhance immunotherapy.

    2. You have free access to this content
      Effective immunotherapy of rat glioblastoma with prolonged intratumoral delivery of exogenous heat shock protein Hsp70 (pages 2118–2128)

      Maxim A. Shevtsov, Alexander V. Pozdnyakov, Anastasia L. Mikhrina, Ludmila Y. Yakovleva, Boris P. Nikolaev, Anatolii V. Dobrodumov, Elena Y. Komarova, Darya A. Meshalkina, Alexander M. Ischenko, Emil Pitkin, Irina V. Guzhova and Boris A. Margulis

      Version of Record online: 1 APR 2014 | DOI: 10.1002/ijc.28858

      What's New?

      Glioblastoma multiforme (GBM) is usually aggressive and notoriously difficult to treat. In this study, the authors examined whether heat-shock protein 70 (Hsp70) might affect GBM in rats. Hsp70 is believed to activate both NK cells and cytotoxic T cells, and has been studied for use in cancer vaccines. When GBM tumors were infused in vivo with Hsp70, tumor growth slowed and these rats lived almost twice as long as untreated rats. This suggests that Hsp70 may be a valuable addition to the therapeutic arsenal against GBM.

  6. Epidemiology

    1. Top of page
    2. Mini Reviews
    3. Carcinogenesis
    4. Cancer Cell Biology
    5. Cancer Genetics
    6. Tumor Immunology
    7. Epidemiology
    8. Cancer Therapy
    9. Letter to the Editor
    10. Errata
    1. You have free access to this content
      Childhood cancer survival in Finland (1953–2010): A nation-wide population-based study (pages 2129–2134)

      L.M. Madanat-Harjuoja, A. Pokhrel, S.M. Kivivuori and U.M. Saarinen-Pihkala

      Version of Record online: 2 APR 2014 | DOI: 10.1002/ijc.28844

      What's new?

      Survival rates for childhood cancers have greatly increased since 1953, but are they still improving? In this study, the authors analyzed survival rates after childhood cancers by decade from 1953 to 2010. They calculate that the largest improvement in 5-year survival came between the 1960s and the 1980s, followed by slight improvements in the 1990s, but very little improvement since 2000. This plateau in survival rates implies that new treatment strategies will be needed to effect any further increase in childhood cancer survival.

    2. You have free access to this content
      Estimated intake of vitamin D and its interaction with vitamin A on lung cancer risk among smokers (pages 2135–2145)

      Ting-Yuan David Cheng, Gary E. Goodman, Mark D. Thornquist, Matt J. Barnett, Shirley A.A. Beresford, Andrea Z. LaCroix, Yingye Zheng and Marian L. Neuhouser

      Version of Record online: 24 MAR 2014 | DOI: 10.1002/ijc.28846

      What's new?

      Data are limited on vitamin D and lung cancer prevention in high-risk populations. Vitamin A (retinol) plays important roles in cell growth, cell differentiation, and the vitamin D signaling axis, and it is unknown whether high-dose vitamin A assists or counteracts association of vitamin D with lung cancer among smokers. This study demonstrated inverse associations of estimated vitamin D intake with lung cancer risk among smokers ingesting higher levels of vitamin A or receiving high-dose retinol+β-carotene supplementation. This is the first study investigating the role of vitamin A in supraphysiologic dose in lung cancer prevention in relation to vitamin D.

    3. You have free access to this content
      Lymphoid neoplasm incidence by WHO subtype in Australia 1982–2006 (pages 2146–2156)

      Marina T. van Leeuwen, Jennifer J. Turner, David J. Joske, Michael O. Falster, Preeyaporn Srasuebkul, Nicola S. Meagher, Andrew E. Grulich, Graham G. Giles and Claire M. Vajdic

      Version of Record online: 2 APR 2014 | DOI: 10.1002/ijc.28849

      What's New?

      Lymphoid neoplasms are a very heterogeneous group of cancers, but limited data exist on the incidence of specific lymphoma subtypes. The authors use population-based cancer registry data to systematically describe subtype-specific incidence patterns of lymphoid neoplasms in Australia. While the incidence rate of Non-Hodgkin lymphoma stabilized between 1997 and 2006, increases were observed for diffuse large B-cell, follicular, peripheral T-cell, plasmacytoma, and Hodgkin lymphoma. These observations may help answer questions related to etiology and public health burden associated with the individual lymphoid neoplasm subtypes.

    4. You have free access to this content
      Parental occupational pesticide exposure and the risk of childhood leukemia in the offspring: Findings from the childhood leukemia international consortium (pages 2157–2172)

      Helen D. Bailey, Lin Fritschi, Claire Infante-Rivard, Deborah C. Glass, Lucia Miligi, John D. Dockerty, Tracy Lightfoot, Jacqueline Clavel, Eve Roman, Logan G. Spector, Peter Kaatsch, Catherine Metayer, Corrado Magnani, Elizabeth Milne, Sophia Polychronopoulou, Jill Simpson, Jérémie Rudant, Vasiliki Sidi, Roberto Rondelli, Laurent Orsi, Alice Y. Kang, Eleni Petridou and Joachim Schüz

      Version of Record online: 4 APR 2014 | DOI: 10.1002/ijc.28854

      What's new?

      When parents are exposed to pesticides during pregnancy or conception, does this increase the risk of leukemia in their child? The answer is yes. Using pooled individual level occupational pesticide exposure data from 13 case-control studies the authors found an increased risk of acute myeloid leukemia with maternal exposure during pregnancy and a slightly increased risk of acute lymphoblastic leukemia with paternal exposure around conception. The next step is to get more detailed information on pesticide types and protective measures during application before conclusive recommendations for pesticide use in the workforce can be made.

    5. You have free access to this content
      Stage at breast cancer diagnosis and distance from diagnostic hospital in a periurban setting: A South African public hospital case series of over 1,000 women (pages 2173–2182)

      Caroline Dickens, Maureen Joffe, Judith Jacobson, Francois Venter, Joachim Schüz, Herbert Cubasch and Valerie McCormack

      Version of Record online: 7 APR 2014 | DOI: 10.1002/ijc.28861

      What's new?

      Later stage at diagnosis is known to be associated with poor breast cancer survival and is a particular problem in Sub-Saharan Africa. This study sought to quantify the effect of the distance from the hospital on breast cancer stage at diagnosis in a peri-urban public South African population. They found that living beyond just 20 km away increased the likelihood of a late-stage at diagnosis, a shorter distance than previously thought. This effect was more noticeable in an underrepresented population of women over the age of 70. Targeting efforts for early diagnosis of breast cancer in these women could help reduce the number of lives taken by breast cancer in these settings.

    6. You have free access to this content
      Hormone replacement therapy and oral contraceptives and risk of oesophageal adenocarcinoma: A systematic review and meta-analysis (pages 2183–2190)

      Katarina Lagergren, Jesper Lagergren and Nele Brusselaers

      Version of Record online: 10 APR 2014 | DOI: 10.1002/ijc.28869

      What's New?

      Because men are more often afflicted with cancer of the esophagus, estrogens may be protective for this type of cancer. In this meta-analysis, the authors investigated whether the use of hormone replacement therapy and oral contraceptives modified the risk to develop esophageal adenocarcinoma. Hormone replacement therapy significantly decreased the risk of esophageal adenocarcinoma, and the same trend was observed with oral contraceptives. These findings might prompt future research into the potential use of hormonal therapy in selected risk groups of esophageal cancer.

    7. You have free access to this content
      Plasma folate concentrations and colorectal cancer risk: A case-control study nested within the Shanghai Men's Health Study (pages 2191–2198)

      Yumie Takata, Martha J. Shrubsole, Honglan Li, Qiuyin Cai, Jing Gao, Conrad Wagner, Jie Wu, Wei Zheng, Yong-Bing Xiang and Xiao-Ou Shu

      Version of Record online: 11 APR 2014 | DOI: 10.1002/ijc.28871

      What's new?

      Epidemiological studies of folate and colorectal cancer (CRC) have yielded inconsistent results. In this large, prospective study, the authors investigated whether pre-diagnostic plasma folate levels are linked to CRC, in a population where food is not routinely fortified with folic acid and people rarely use supplements. The study found that folate levels were positively associated with CRC risk among men who may have had pre-neoplastic lesions. These findings highlight the need to consider the timing of folate assessment and pre-existing colorectal conditions when investigating folate and CRC.

  7. Cancer Therapy

    1. Top of page
    2. Mini Reviews
    3. Carcinogenesis
    4. Cancer Cell Biology
    5. Cancer Genetics
    6. Tumor Immunology
    7. Epidemiology
    8. Cancer Therapy
    9. Letter to the Editor
    10. Errata
    1. You have free access to this content
      Key role for myeloid cells: Phase II results of anti-GD2 antibody 3F8 plus granulocyte-macrophage colony-stimulating factor for chemoresistant osteomedullary neuroblastoma (pages 2199–2205)

      Nai-Kong V. Cheung, Irene Y. Cheung, Kim Kramer, Shakeel Modak, Deborah Kuk, Neeta Pandit-Taskar, Elizabeth Chamberlain, Irina Ostrovnaya and Brian H. Kushner

      Version of Record online: 3 APR 2014 | DOI: 10.1002/ijc.28851

      What's New?

      In high-risk neuroblastoma, persistence of osteomedullary metastases forebodes poor outcome. Here, in a phase II trial, anti-GD2 murine antibody 3F8 plus subcutaneously-administered granulocyte-macrophage colony-stimulating factor (GM-CSF) was used against primary refractory neuroblastoma in metastatic osteomedullary sites. The experience documents activity against histologically and/or radiologically-visible chemoresistant neuroblastoma. Large study size and lengthy follow-up allow use of prognostic variables (minimal residual disease, MYCN, Fcγ receptors, KIR genotypes of natural killer cells) in a multivariate analysis not described with other anti-GD2 antibodies. Correlative studies highlight the anti-neoplastic potency of myeloid effectors rather than lymphocytes, usually the focus in the immunotherapy of solid tumors.

    2. You have free access to this content
      Aberrantly activated claudin 6 and 18.2 as potential therapy targets in non-small-cell lung cancer (pages 2206–2214)

      Patrick Micke, Johanna Sofia Margareta Mattsson, Karolina Edlund, Miriam Lohr, Karin Jirström, Anders Berglund, Johan Botling, Jörg Rahnenfuehrer, Millaray Marincevic, Fredrik Pontén, Simon Ekman, Jan Hengstler, Stefan Wöll, Ugur Sahin and Özlem Türeci

      Version of Record online: 8 APR 2014 | DOI: 10.1002/ijc.28857

      What's new?

      Non-small-cell lung cancer (NSCLC) is a heterogeneous disease with a high unmet need for new treatments. This study aimed to determine the prevalence of CLDN6 and CLDN18.2 in NSCLC in order to decide whether the ongoing clinical development, in other tumor types, of the respective therapeutic antibodies, IMAB027 and IMAB362, could be extended to lung cancer. The findings show expression of CLDN6 and CLDN18.2 in NSCLC samples and thus suggest both CLDN6 and CLDN18.2 as drug targets, as well as markers for the dynamics of the disease. This study provides a rationale for clinical testing of both antibodies in NSCLC.

    3. You have free access to this content
      Changes in mutational status during third-line treatment for metastatic colorectal cancer—Results of consecutive measurement of cell free DNA, KRAS and BRAF in the plasma (pages 2215–2222)

      Karen-Lise Garm Spindler, Niels Pallisgaard, Rikke Fredslund Andersen and Anders Jakobsen

      Version of Record online: 17 APR 2014 | DOI: 10.1002/ijc.28863

      What's new?

      Mutations in the genes KRAS and BRAF contribute to chemotherapy resistance, but people whose primary tumors lack those mutations also develop resistance. Could there be a way to determine when resistance sets in, to avoid continuing an ineffective treatment? In this study, the authors sampled circulating free DNA, looking for mutations before and during treatment. They detected KRAS mutations popping up in patients who had wild-type tumors, and these mutations heralded a turn for the worse in disease progression. Similarly, some patients had tumors that contained the mutation, but wild-type KRAS in their plasma, and these patients responded better to treatment. Thus, circulating DNA might provide a useful indicator for how well the treatment is working.

    4. You have free access to this content
      SGI-110 and entinostat therapy reduces lung tumor burden and reprograms the epigenome (pages 2223–2231)

      Carmen S. Tellez, Marcie J. Grimes, Maria A. Picchi, Yushi Liu, Thomas H. March, Matthew D. Reed, Aram Oganesian, Pietro Taverna and Steven A. Belinsky

      Version of Record online: 5 APR 2014 | DOI: 10.1002/ijc.28865

      What's new?

      While DNA demethylating agents are now approved for the treatment of myelodysplastic syndrome, a barrier to full efficacy in solid tumors is the deamination of these drugs by cytidine deaminase.  Here, the authors developed an orthotopic lung cancer model to evaluate the efficacy of SGI-110, a second-generation DNA methyltransferase inhibitor. They report improved plasma half-life of the drug that resulted in reduced tumor burden, specifically in synergy with entinostat, a histone deacetylase inhibitor. These results reinforce the potential of epigenetic reprogramming as a strategy for lung cancer treatment.

  8. Letter to the Editor

    1. Top of page
    2. Mini Reviews
    3. Carcinogenesis
    4. Cancer Cell Biology
    5. Cancer Genetics
    6. Tumor Immunology
    7. Epidemiology
    8. Cancer Therapy
    9. Letter to the Editor
    10. Errata
    1. You have free access to this content
      Evaluating the evidence for the relationship between passive smoking and lung cancer (pages 2232–2233)

      Claire H. Kim, Lina Mu, Ming Wu, Jin-Kou Zhao and Zuo-Feng Zhang

      Version of Record online: 7 APR 2014 | DOI: 10.1002/ijc.28860

  9. Errata

    1. Top of page
    2. Mini Reviews
    3. Carcinogenesis
    4. Cancer Cell Biology
    5. Cancer Genetics
    6. Tumor Immunology
    7. Epidemiology
    8. Cancer Therapy
    9. Letter to the Editor
    10. Errata
    1. You have free access to this content
      Erratum (page E8)

      Version of Record online: 14 AUG 2014 | DOI: 10.1002/ijc.28914

      This article corrects:

      Absence of TERT promoter mutations in esophageal adenocarcinoma

      Vol. 134, Issue 8, 2014–2015, Version of Record online: 12 NOV 2013

    2. You have free access to this content
      Erratum (page E9)

      Version of Record online: 14 AUG 2014 | DOI: 10.1002/ijc.28916

      This article corrects:
    3. You have free access to this content
      Erratum (page E10)

      Version of Record online: 14 AUG 2014 | DOI: 10.1002/ijc.28918

      This article corrects:

SEARCH

SEARCH BY CITATION