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International Journal of Cancer

Cover image for Vol. 134 Issue 6

15 March 2014

Volume 134, Issue 6

Pages 1257–1516

  1. Mini Review

    1. Top of page
    2. Mini Review
    3. Carcinogenesis
    4. Cancer Cell Biology
    5. Infectious Causes of Cancer
    6. Tumor Immunology
    7. Early Detection and Diagnosis
    8. Epidemiology
    9. Cancer Therapy
    10. Short Report
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    2. You have free access to this content
      Therapy-induced enrichment of putative lung cancer stem-like cells (pages 1270–1278)

      Daniela P. Freitas, Cristina A. Teixeira, Filipe Santos-Silva, M. Helena Vasconcelos and Gabriela M. Almeida

      Version of Record online: 21 OCT 2013 | DOI: 10.1002/ijc.28478

  2. Carcinogenesis

    1. Top of page
    2. Mini Review
    3. Carcinogenesis
    4. Cancer Cell Biology
    5. Infectious Causes of Cancer
    6. Tumor Immunology
    7. Early Detection and Diagnosis
    8. Epidemiology
    9. Cancer Therapy
    10. Short Report
    1. You have full text access to this OnlineOpen article
      Expulsion of micronuclei containing amplified genes contributes to a decrease in double minute chromosomes from malignant tumor cells (pages 1279–1288)

      Wei Ji, Zehua Bian, Yang Yu, Chao Yuan, Yang Liu, Lisa Yu, Chunxiang Li, Jing Zhu, Xueyuan Jia, Rongwei Guan, Chunyu Zhang, Xiangning Meng, Yan Jin, Jing Bai, Jingcui Yu, Ki-Young Lee, Wenjing Sun and Songbin Fu

      Version of Record online: 30 SEP 2013 | DOI: 10.1002/ijc.28467

      What's new?

      Double-minute chromosomes (DMs) are a hallmark of gene amplification and a major cytogenetic characteristic of malignant tumor cells. The function of DMs and DM-carried genes, however, remains to be clarified. Here, the authors identified amplification regions containing DM-carried genes that were themselves amplified and overexpressed in human malignant tumor cells. Knocking down the DM-carried amplified genes individually, they found that suppression of such oncogenes reduced the number of DMs, the amplification of these DM-carried genes, and cellular function. DNA damage and expulsion of micronuclei containing these DM-carried amplified genes may contribute to the decrease of DMs in tumor cells.

  3. Cancer Cell Biology

    1. Top of page
    2. Mini Review
    3. Carcinogenesis
    4. Cancer Cell Biology
    5. Infectious Causes of Cancer
    6. Tumor Immunology
    7. Early Detection and Diagnosis
    8. Epidemiology
    9. Cancer Therapy
    10. Short Report
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      HSP27 is required for invasion and metastasis triggered by hepatocyte growth factor (pages 1289–1299)

      Simona Pavan, Daniele Musiani, Erica Torchiaro, Giorgia Migliardi, Marta Gai, Ferdinando Di Cunto, Jessica Erriquez, Martina Olivero and Maria Flavia Di Renzo

      Version of Record online: 18 SEP 2013 | DOI: 10.1002/ijc.28464

      What's new?

      Hepatocyte growth factor, HGF, induces cancers to spread. Recently, researchers learned that it activates a small heat shock protein, HSP27, which is increased in advanced stage cancers, and associated with resistance to chemotherapy. In this paper, the authors showed that silencing HSP27 stopped ovarian cancer cells from metastasizing. Suppressing HSP27 also sensitized the tumors to Paclitaxel. The results show that HSP27 is important for metastasis and invasion, and could make a promising target for therapy.

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      Triacetin-based acetate supplementation as a chemotherapeutic adjuvant therapy in glioma (pages 1300–1310)

      Andrew R. Tsen, Patrick M. Long, Heather E. Driscoll, Matthew T. Davies, Benjamin A. Teasdale, Paul L. Penar, William W. Pendlebury, Jeffrey L. Spees, Sean E. Lawler, Mariano S. Viapiano and Diane M. Jaworski

      Version of Record online: 30 SEP 2013 | DOI: 10.1002/ijc.28465

      What's new?

      Cancer is associated with global decreases in acetylation and aerobic glycolysis, yet acetate supplementation as a therapeutic approach has not been studied extensively. This study shows that aspartoacylase, the enzyme that catabolizes N-acetyl-L-aspartate, the primary storage form of acetate in the brain, is reduced in glioma tumors. The food additive Triacetin (glyceryl triacetate) was found to induce growth arrest in oligodendroglioma- and glioblastoma-derived glioma stem-like cells and to potentiate the chemotherapeutic effects of temozolomide in orthotopic grafts. These preclinical data warrant further examination of Triacetin as a possible chemotherapeutic adjuvant in the treatment of glioma.

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      Epigenetic silencing of Aristaless-like homeobox-4, a potential tumor suppressor gene associated with lung cancer (pages 1311–1322)

      Wen-Bin Liu, Fei Han, Xing-Hua Du, Xiao Jiang, Yong-Hong Li, Yong Liu, Hong-Qiang Chen, Lin Ao, Zhi-Hong Cui, Jia Cao and Jin-Yi Liu

      Version of Record online: 11 NOV 2013 | DOI: 10.1002/ijc.28472

      What's new?

      ALX4 is a putative transcription factor involved in epithelial development. In this study, the authors examined whether the methylation status and function of ALX4 might play a role in lung cancer. They found that ALX4 was preferentially methylated in lung cancer, via CpG-island hypermethylation. This, in turn resulted in a loss of ALX4 expression. When ALX4 was restored, it induced apoptosis and suppressed tumorigenicity in mice. These findings indicate that ALX4 acts as a novel tumor suppressor in lung cancer, which may aid in early detection and provide a potential therapeutic target.

  4. Infectious Causes of Cancer

    1. Top of page
    2. Mini Review
    3. Carcinogenesis
    4. Cancer Cell Biology
    5. Infectious Causes of Cancer
    6. Tumor Immunology
    7. Early Detection and Diagnosis
    8. Epidemiology
    9. Cancer Therapy
    10. Short Report
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      The role of the antileukoprotease SLPI in smoking-induced human papillomavirus-independent head and neck squamous cell carcinomas (pages 1323–1334)

      Elgar Susanne Quabius, Paul Möller, Jochen Haag, Saskia Pfannenschmidt, Jürgen Hedderich, Tibor Görögh, Christoph Röcken and Markus Hoffmann

      Version of Record online: 23 SEP 2013 | DOI: 10.1002/ijc.28462

      What's new?

      With the incidence of human papillomavirus (HPV) head and neck squamous cell carcinoma (HNSCC) on the rise in non-smokers, a better understanding of the relationship between HPV infection, smoking, and oncogenesis is needed. This study demonstrates that smoking (in HNSCC and non-HNSCC patients) and nicotine incubation (ex vivo) increases expression of secretory leukocyte peptidase inhibitor (SLPI). Significant correlations between smoking and SLPI expression in tumors and mucosa of HNSCC and non-HNSCC patients were established. In addition, all HPV-positive patients showed no or low SLPI expression. The findings suggest that SLPI upregulation via smoking may protect against HPV infection.

  5. Tumor Immunology

    1. Top of page
    2. Mini Review
    3. Carcinogenesis
    4. Cancer Cell Biology
    5. Infectious Causes of Cancer
    6. Tumor Immunology
    7. Early Detection and Diagnosis
    8. Epidemiology
    9. Cancer Therapy
    10. Short Report
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      A transplantable TH-MYCN transgenic tumor model in C57Bl/6 mice for preclinical immunological studies in neuroblastoma (pages 1335–1345)

      Michiel Kroesen, Stefan Nierkens, Marleen Ansems, Melissa Wassink, Rimas J. Orentas, Louis Boon, Martijn H. den Brok, Peter M. Hoogerbrugge and Gosse J. Adema

      Version of Record online: 14 SEP 2013 | DOI: 10.1002/ijc.28463

      What's new?

      Natural killer (NK) cells may serve a role in immune defense against neuroblastoma, though limitations in existing models have prevented extensive study of the immunological characteristics of the disease. Here, to better understand the immunobiology of neuroblastoma, the TH-MYCN mouse model was adapted for immunological investigation. Tumor cells (9464D) derived from immunologically compatible C57Bl/6 TH-MYCN mice were found to express the tumor antigen GD2. In addition, depletion of NK cells was associated with tumor outgrowth in both wild-type and Rag1-/- C57Bl/6 mice, whereas immunotherapy targeted against GD2 decreased tumor growth.

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      CXCR2-mediated tumor-associated neutrophil recruitment is regulated by IFN-β (pages 1346–1358)

      J. Jablonska, C.-F. Wu, L. Andzinski, S. Leschner and S. Weiss

      Version of Record online: 31 OCT 2013 | DOI: 10.1002/ijc.28551

      What's new?

      Tumor-associated neutrophils (TANs) are known to support angiogenesis and thereby contribute to tumor growth. The present study examined the influence of IFN-β on TAN homing capacity, which involves chemokine receptors (CXCRs) and their ligands (CXCLs). The data indicates that IFN-β inhibits CXCR2-dependent neutrophil migration by down-regulating the expression of its ligands in tumors and disrupting chemokine gradients. Since neutrophil infiltration is indispensable for tumor vessel development and growth, the results suggest that IFN-β inhibition may interfere with tumor development.

  6. Early Detection and Diagnosis

    1. Top of page
    2. Mini Review
    3. Carcinogenesis
    4. Cancer Cell Biology
    5. Infectious Causes of Cancer
    6. Tumor Immunology
    7. Early Detection and Diagnosis
    8. Epidemiology
    9. Cancer Therapy
    10. Short Report
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      A four-miRNA signature identified from genome-wide serum miRNA profiling predicts survival in patients with nasopharyngeal carcinoma (pages 1359–1368)

      Na Liu, Rui-Xue Cui, Ying Sun, Rui Guo, Yan-Ping Mao, Ling-Long Tang, Wei Jiang, Xu Liu, Yi-Kan Cheng, Qing-Mei He, William C.S. Cho, Li-Zhi Liu, Li Li and Jun Ma

      Version of Record online: 30 SEP 2013 | DOI: 10.1002/ijc.28468

      What's new?

      Short non-coding RNA sequences, or microRNAs, that circulate in serum are easily accessible, promising biomarkers for incorporation into the tumor-node-metastasis (TNM) staging system. This study shows that a four-miRNA signature is able to predict survival in nasopharyngeal carcinoma, serving as an independent prognostic factor. When combined with TNM staging, the miRNA signature boosted the overall prognostic power, improving it over either approach alone. The results also suggest that serum miRNAs may play an important role in nasopharyngeal carcinoma development and progression, in addition to being potential prognostic biomarkers.

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      Decreased TIP30 expression predicts poor prognosis in pancreatic cancer patients (pages 1369–1378)

      Shiwei Guo, Wei Jing, Xiangui Hu, Xuyu Zhou, Lianjie Liu, Minhui Zhu, Fan Yin, Rui Chen, Jian Zhao and Yajun Guo

      Version of Record online: 3 OCT 2013 | DOI: 10.1002/ijc.28471

      What's new?

      Pancreatic ductal adenocarcinoma (PDAC) is known for its aggressive growth and poor prognosis. Novel biomarkers that could aid in predicting outcomes for PDAC patients would be extremely valuable. In this study, the authors examined the tumor suppressor TIP30 as a candidate biomarker. They found that decreased TIP30 expression in primary PDAC is an independent predictor for survival. TIP30 alone or combined evaluation of TIP30 and E-cadherin levels may thus provide new prognostic criteria for PDAC patients.

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      S100A7 overexpression is a predictive marker for high risk of malignant transformation in oral dysplasia (pages 1379–1388)

      Jatinder Kaur, Ajay Matta, Ipshita Kak, Gunjan Srivastava, Jasmeet Assi, Iona Leong, Ian Witterick, Terence J. Colgan, Christina MacMillan, K.W. Michael Siu, Paul G. Walfish and Ranju Ralhan

      Version of Record online: 8 OCT 2013 | DOI: 10.1002/ijc.28473

      What's new?

      Identification of oral lesions with dysplasia at high risk of malignant transformation remains a major clinical challenge, and is of utmost importance for identifying patients who would benefit from early intervention. Currently, there are no biomarkers that are being routinely used in clinics to predict high-risk lesions. Here, the authors evaluated the potential of five candidate protein biomarkers and correlated their expression with p16 and HPV 16/18 to identify oral lesions with dysplasia at high risk of cancer development. S100A7 overexpression demonstrated the potential to serve as a useful marker for estimating the risk of oral dysplasia progressing to cancer.

  7. Epidemiology

    1. Top of page
    2. Mini Review
    3. Carcinogenesis
    4. Cancer Cell Biology
    5. Infectious Causes of Cancer
    6. Tumor Immunology
    7. Early Detection and Diagnosis
    8. Epidemiology
    9. Cancer Therapy
    10. Short Report
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      Human papillomavirus prevalence and type distribution in invasive cervical cancer in sub-Saharan Africa (pages 1389–1398)

      Lynette Denny, Isaac Adewole, Rose Anorlu, Greta Dreyer, Manivasan Moodley, Trudy Smith, Leon Snyman, Edwin Wiredu, Anco Molijn, Wim Quint, Gunasekaran Ramakrishnan and Johannes Schmidt

      Version of Record online: 14 NOV 2013 | DOI: 10.1002/ijc.28425

      What's new?

      This was the first study conducted in sub-Saharan Africa using standardized and validated methods for human papillomavirus (HPV) detection and typing, and centralized pathology review for confirmation of the histological diagnosis. In women with invasive cervical cancer from Ghana, Nigeria, and South Africa, the HPV-positivity rate was 90.4%, HPV16, 18, 45, and 35 were the most common types, and the prevalence of single and multiple HPV infections seemed higher among HIV-positive than among HIV-negative women.

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      Germline variation in NCF4, an innate immunity gene, is associated with an increased risk of colorectal cancer (pages 1399–1407)

      Bríd M. Ryan, Krista A. Zanetti, Ana I. Robles, Aaron J. Schetter, Julie Goodman, Richard B. Hayes, Wen-Yi Huang, Mark J. Gunter, Meredith Yeager, Laurie Burdette, Sonja I. Berndt and Curtis C. Harris

      Version of Record online: 14 NOV 2013 | DOI: 10.1002/ijc.28457

      What's new?

      A single nucleotide polymorphism (SNP) known as rs5995355 in the gene NCF4, a member of the NADPH oxidase complex, is associated with increased risk of inflammatory bowel disease. The NADPH system functions in the elimination of invading microorganisms and has never previously been linked to colorectal cancer. As this screen for colorectal adenoma and cancer-related gene variants reveals, however, the NCF4 germline SNP may share a unique association with colon cancer. The analysis suggests that the variant disrupts the functionality of the NADPH complex, possibly impeding the ability of neutrophils to repel infectious agents.

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      Cytokine and cytokine receptor genes of the adaptive immune response are differentially associated with breast cancer risk in American women of African and European ancestry (pages 1408–1421)

      Lei Quan, Zhihong Gong, Song Yao, Elisa V. Bandera, Gary Zirpoli, Helena Hwang, Michelle Roberts, Gregory Ciupak, Warren Davis, Lara Sucheston, Karen Pawlish, Dana H. Bovbjerg, Lina Jandorf, Citadel Cabasag, Jean-Gabriel Coignet, Christine B. Ambrosone and Chi-Chen Hong

      Version of Record online: 8 OCT 2013 | DOI: 10.1002/ijc.28458

      What's new?

      African American women are affected by aggressive and early-onset breast cancers more often than American women of European descent, though the reasons for this are not fully understood. Here, single nucleotide polymorphisms (SNPs) in genes involved in Th1 and Th2 immunity and in T regulatory cell-mediated immunosuppression were linked to breast cancer risk in African American women. Stratification according to estrogen-receptor status (ER positive or ER negative) revealed sets of risk-associated SNPs exclusive to African Americans. The findings suggest that host adaptive immunity plays a more prominent role in breast carcinogenesis among African Americans compared with European Americans.

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      Associations of dietary folate, Vitamins B6 and B12 and methionine intake with risk of breast cancer among African American and European American women (pages 1422–1435)

      Zhihong Gong, Christine B. Ambrosone, Susan E. McCann, Gary Zirpoli, Urmila Chandran, Chi-Chen Hong, Dana H. Bovbjerg, Lina Jandorf, Gregory Ciupak, Karen Pawlish, Quanjun Lu, Helena Hwang, Thaer Khoury, Bshara Wiam and Elisa V. Bandera

      Version of Record online: 30 SEP 2013 | DOI: 10.1002/ijc.28466

      What's new?

      Differences exist between African-American and European-American women when it comes to breast cancer. But while these differences may be explained in part by nutritional factors, such as intake of folate and other methyl-group nutrients, few studies have explored this possibility. Here, an inverse association was found between natural food folate intake and breast cancer risk in premenopausal and estrogen receptor (ER)-positive African Americans. By comparison, a positive association was found for synthetic folate intake in European Americans. Thus, race, menopausal and ER status, and folate source may influence a possible link between folate intake and breast cancer risk.

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      Circulating concentrations of insulin-like growth factor-I, insulin-like growth factor-binding protein-3, genetic polymorphisms and mammographic density in premenopausal Mexican women: Results from the ESMaestras cohort (pages 1436–1444)

      S. Rinaldi, C. Biessy, M. Hernandez, F. Lesueur, I. dos-Santos-Silva, M.S. Rice, M. Lajous, R. Lopez-Ridaura, G. Torres-Mejía and I. Romieu

      Version of Record online: 5 OCT 2013 | DOI: 10.1002/ijc.28469

      What's new?

      Genetic factors appear to play a significant role in mammographic density, which in turn is among the strongest predictors of breast cancer. High circulating levels of IGF-I have also been associated with increased breast cancer risk, and possibly with increased breast density. In this study, the authors evaluated the association between IGF-1 pathway SNPs, circulating concentrations of IGF-I and IGFBP-3, and mammographic density in Mexican premenopausal women. Their results do not support a strong association between circulating levels of growth hormones and mammographic density in this population.

      Corrected by:

      Erratum: Erratum

      Vol. 139, Issue 6, E10, Version of Record online: 9 JUL 2016

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      Cancer development based on chronic active gastritis and resulting gastric atrophy as assessed by serum levels of pepsinogen and Helicobacter pylori antibody titer (pages 1445–1457)

      Takeichi Yoshida, Jun Kato, Izumi Inoue, Noriko Yoshimura, Hisanobu Deguchi, Chizu Mukoubayashi, Masashi Oka, Mika Watanabe, Shotaro Enomoto, Toru Niwa, Takao Maekita, Mikitaka Iguchi, Hideyuki Tamai, Hirotoshi Utsunomiya, Nobutake Yamamichi, Mitsuhiro Fujishiro, Masataka Iwane, Tatsuya Takeshita, Toshikazu Ushijima and Masao Ichinose

      Version of Record online: 3 OCT 2013 | DOI: 10.1002/ijc.28470

      What's new?

      Infection with the bacteria H. pylori is the most common risk factor for developing gastric cancer. The infection causes chronic inflammation leading to a sequence of gastritis, atrophy, metaplasia, dysplasia, cancer. This study follows up a cohort of 6,000 men after 16 years and showed that cancer risk increased with the progression of inflammation and atrophy, which can be measured by serum tests. These tests, the authors suggest, would be useful in assessing risk among people infected with H. pylori.

  8. Cancer Therapy

    1. Top of page
    2. Mini Review
    3. Carcinogenesis
    4. Cancer Cell Biology
    5. Infectious Causes of Cancer
    6. Tumor Immunology
    7. Early Detection and Diagnosis
    8. Epidemiology
    9. Cancer Therapy
    10. Short Report
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      Complete regression of glioblastoma by mesenchymal stem cells mediated prodrug gene therapy simulating clinical therapeutic scenario (pages 1458–1465)

      Cestmir Altaner, Veronika Altanerova, Marina Cihova, Katarina Ondicova, Boris Rychly, Ladislav Baciak and Boris Mravec

      Version of Record online: 13 SEP 2013 | DOI: 10.1002/ijc.28455

      What's new?

      One reason that glioblastomas are so difficult to treat is the persistence of chemo-and radio-resistant cancer stem cells. If suicide genes could be delivered directly to these cells, combination therapy might be more effective. In this study, the authors used non-maligant stem cells, called mesenchymal stem cells (MSCs), to treat glioblastomas in rats. The MSCs were engineered to express the suicide gene cytosine deaminase::uracil phosphoribosyltransferase (CDy::UPRT), then injected into the brain with 5–fluorocytosine. This resulted in strong inhibition of tumor growth, and a significant number of animals appeared to be completely cured.

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      Anti-CD73 therapy impairs tumor angiogenesis (pages 1466–1473)

      Bertrand Allard, Martin Turcotte, Kathleen Spring, Sandra Pommey, Isabelle Royal and John Stagg

      Version of Record online: 18 SEP 2013 | DOI: 10.1002/ijc.28456

      What's new?

      The pro-tumorigenic nucleotidase CD73, a potential therapeutic target, plays a key role in the generation of the extracellular immunosuppressor adenosine. While its pro-tumorigenic effects have thus far been attributed to adenosine-mediated immunosuppression, this study shows that CD73 also promotes tumor angiogenesis via enzymatic and non-enzymatic functions. Tumor levels of vascular endothelial growth factor (VEGF) were reduced and tumor angiogenesis suppressed in a breast cancer mouse model following treatment with a monoclonal antibody targeted against CD73. The findings highlight a previously unknown mechanism of action for anti-CD73 therapy and further support its clinical development for cancer treatment.

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      The anticancer effect of PQ1 in the MMTV-PyVT mouse model (pages 1474–1483)

      Stephanie N. Shishido, Adélaïde Delahaye, Amanda Beck and Thu Annelise Nguyen

      Version of Record online: 19 SEP 2013 | DOI: 10.1002/ijc.28461

      What's new?

      Cancer cells commonly turn off intercellular communication via gap junctions. Thus, targeting gap junctions may help focus cancer therapies on the disease cells only, without disturbing healthy cells. This study tested a compound, PQ1, that targets cancer cells by homing in on gap junctions and reactivating them. In a mouse mammary tumor model, the authors showed that treatment with PQ1 at any stage of development significantly reduced tumor growth.

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      Increased oral availability and brain accumulation of the ALK inhibitor crizotinib by coadministration of the P-glycoprotein (ABCB1) and breast cancer resistance protein (ABCG2) inhibitor elacridar (pages 1484–1494)

      Seng Chuan Tang, Luan N. Nguyen, Rolf W. Sparidans, Els Wagenaar, Jos H. Beijnen and Alfred H. Schinkel

      Version of Record online: 3 OCT 2013 | DOI: 10.1002/ijc.28475

      What's new?

      Crizotinib is an oral tyrosine kinase inhibitor approved for treating non-small cell lung cancer (NSCLC) patients with anaplastic lymphoma kinase rearrangements. While NSCLC patients are likely to develop brain metastases, brain accumulation of crizotinib is limited. This study investigates the consequences of crizotinib transport by murine Abcb1 and Abcg2 and ways to counter them. Crizotinib oral availability and brain accumulation were restricted by Abcb1 at a non-saturating dose, and co-administration of the dual ABCB1/ABCG2 inhibitor elacridar drastically increased oral availability and brain delivery. This principle might be used to enhance therapeutic efficacy of crizotinib against brain metastases in NSCLC patients.

  9. Short Report

    1. Top of page
    2. Mini Review
    3. Carcinogenesis
    4. Cancer Cell Biology
    5. Infectious Causes of Cancer
    6. Tumor Immunology
    7. Early Detection and Diagnosis
    8. Epidemiology
    9. Cancer Therapy
    10. Short Report
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      XPF protein levels determine sensitivity of malignant melanoma cells to oxaliplatin chemotherapy: Suitability as a biomarker for patient selection (pages 1495–1503)

      Stephanie B. Hatch, Lonnie P. Swift, Simona Caporali, Rebecca Carter, Esme J. Hill, Thomas P. MacGregor, Stefania D'Atri, Mark R. Middleton, Peter J. McHugh and Ricky A. Sharma

      Version of Record online: 14 NOV 2013 | DOI: 10.1002/ijc.28454

      What's new?

      With options for systemic treatment of malignant melanoma (MM) on the rise, there is an increasing need to develop biomarkers for patient selection. To that end, this study explored the possibility of a biomarker to improve objective response rates to the drug oxaliplatin. The study reveals a mechanism by which mammalian cells are rendered hypersensitive to oxaliplatin that centers around the loss of endonuclease XPF-ERCC1. Sensitivity to oxaliplatin was directly related to XPF and ERCC1 protein levels. The findings indicate that XPF may be a suitable biomarker for MM patient selection for oxaliplatin therapy.

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      Alcohol consumption and breast cancer risk among women from five ethnic groups with light to moderate intakes: The Multiethnic Cohort Study (pages 1504–1510)

      Song-Yi Park, Laurence N. Kolonel, Unhee Lim, Kami K. White, Brian E. Henderson and Lynne R. Wilkens

      Version of Record online: 9 OCT 2013 | DOI: 10.1002/ijc.28476

      What's new?

      Alcohol is a well-established risk factor for breast cancer in white women, but its impact in women of other ethnicities is largely unknown. Here, the authors conducted a prospective study of light to moderate alcohol-drinking postmenopausal women within the Multiethnic Cohort of Hawaii and California. In addition to whites, an increased risk of breast cancer with higher alcohol intake was found in African Americans, Japanese Americans, and Latinas, but not in Native Hawaiians, who showed the highest incidence of breast cancer in this cohort. The findings point to the existence of unique factors contributing to breast cancer in Native Hawaiians. They further underscore that alcohol restriction, even among light drinkers, could make a meaningful contribution to breast cancer prevention in most ethnic groups.

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      Loss of stromal JUNB does not affect tumor growth and angiogenesis (pages 1511–1516)

      Jennifer Braun, Karin Strittmatter, Tobias Nübel, Dorde Komljenovic, Melanie Sator-Schmitt, Tobias Bäuerle, Peter Angel and Marina Schorpp-Kistner

      Version of Record online: 9 OCT 2013 | DOI: 10.1002/ijc.28477

      What's new?

      JUNB is a subunit of the AP-1 transcription factor and a critical activator of Vegfa, the master regulator of angiogenesis. Here, the authors used conditional Junb knockout mice to define the role of stromal JUNB on tumor growth and angiogenesis. Surprisingly, although tumor-derived JUNB is known to critically regulate these properties, stromal, host-derived JUNB is dispensable for these processes. The study indicates that loss of stromal JUNB is well compensated by the tumor itself as well as infiltrating immune cells that provide pro-angiogenic factors and matrix metalloproteinases otherwise induced by JUNB expression in the tumor microenvironment.

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