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International Journal of Cancer

Cover image for International Journal of Cancer

1 May 2013

Volume 132, Issue 9

Pages 1971–2221

  1. Mini Reviews

    1. Top of page
    2. Mini Reviews
    3. Carcinogenesis
    4. Cancer Cell Biology
    5. Cancer Genetics
    6. Infectious Causes of Cancer
    7. Early Detection and Diagnosis
    8. Epidemiology
    9. Cancer Therapy
    10. Short Reports
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  2. Carcinogenesis

    1. Top of page
    2. Mini Reviews
    3. Carcinogenesis
    4. Cancer Cell Biology
    5. Cancer Genetics
    6. Infectious Causes of Cancer
    7. Early Detection and Diagnosis
    8. Epidemiology
    9. Cancer Therapy
    10. Short Reports
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      Circulating interleukin-6 level is a prognostic marker for survival in advanced nonsmall cell lung cancer patients treated with chemotherapy (pages 1977–1985)

      Chin Hao Chang, Chin Fu Hsiao, Yu Min Yeh, Gee Chen Chang, Ying Huang Tsai, Yuh Min Chen, Ming Shyan Huang, Hui Ling Chen, Yao Jen Li, Pan Chyr Yang, Chien Jen Chen, Chao A. Hsiung and Wu Chou Su

      Version of Record online: 29 OCT 2012 | DOI: 10.1002/ijc.27892

      What's new?

      IL-6 has been implicated in the development of drug resistance in tumors. In this study, the authors found that plasma levels of IL-6 from samples collected after chemotherapy provide a more accurate prediction of survival for patients with advanced non-small-cell lung cancer than samples collected before chemotherapy. In addition, patients with high plasma levels of IL-6 responded poorly to chemotherapy. Therefore, a high circulating IL-6 level is an independent prognostic marker for lung cancer-specific survival, especially for patients who have received chemotherapy.

  3. Cancer Cell Biology

    1. Top of page
    2. Mini Reviews
    3. Carcinogenesis
    4. Cancer Cell Biology
    5. Cancer Genetics
    6. Infectious Causes of Cancer
    7. Early Detection and Diagnosis
    8. Epidemiology
    9. Cancer Therapy
    10. Short Reports
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      Phosphorylated tubulin adaptor protein CRMP-2 as prognostic marker and candidate therapeutic target for NSCLC (pages 1986–1995)

      Erik Oliemuller, Rafael Peláez, Saray Garasa, María J. Pajares, Jackeline Agorreta, Rubén Pío, Luis M. Montuenga, Alvaro Teijeira, Susana Llanos and Ana Rouzaut

      Version of Record online: 20 OCT 2012 | DOI: 10.1002/ijc.27881

      What's new?

      Collapsin response mediator protein-2 (CRMP-2), when dephosphorylated, regulates the addition of tubulin to growing microtubules. Nuclear expression of phosphorylated CRMP-2 was linked here to poor prognosis in non-small cell lung cancer (NSCLC) and was found to interact with the mitotic spindle in a phosphorylation-dependent manner in NSCLC cells. Phosphodefective CRMP-2 induced aberrant cell division and led to increased p53 expression. The results indicate that phosphorylated CRMP-2 may be a prognostic marker and therapeutic target in NSCLC.

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      Isolation and characterization of calcium sensing receptor null cells: A highly malignant and drug resistant phenotype of colon cancer (pages 1996–2005)

      Navneet Singh, Guangming Liu and Subhas Chakrabarty

      Version of Record online: 2 NOV 2012 | DOI: 10.1002/ijc.27902

      What's new?

      Loss of calcium sensing receptor (CaSR) expression in the colon is linked to malignant transformation and progression. This study is the first to report the isolation and molecular profiling of the CaSR null colon cancer phenotype. The findings show that CaSR null cells present a greater propensity for growth and invasion, possess many of the molecular features that drive and sustain the malignant phenotype, and are highly drug resistant. The authors conclude that the development of therapeutic regimens that encompass the efficient killing of CaSR null cells could improve the treatment outcome for colon cancer.

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      CD34+/CD38 acute myelogenous leukemia cells aberrantly express CD82 which regulates adhesion and survival of leukemia stem cells (pages 2006–2019)

      Chie Nishioka, Takayuki Ikezoe, Mutsuo Furihata, Jing Yang, Satoshi Serada, Tetsuji Naka, Atsuya Nobumoto, Sayo Kataoka, Masayuki Tsuda, Keiko Udaka and Akihito Yokoyama

      Version of Record online: 30 OCT 2012 | DOI: 10.1002/ijc.27904

      What's new?

      Acute myelogenous leukemia (AML) is maintained by a subset of self-renewing leukemia stem cells (LSCs). Thus, to effectively treat AML, treatments targeting LSCs are needed. AML cells expressing CD34 but not CD38 (CD34+/CD38-) contain abundant LSCs and were found in this study to express a greater amount of CD82 than CD34+/CD38+ AML cells. CD82 was further found to regulate the survival of CD34+/CD38- AML cells and their adhesion to the bone marrow microenvironment, suggesting that this glycoprotein could be an attractive target for LSC eradication.

  4. Cancer Genetics

    1. Top of page
    2. Mini Reviews
    3. Carcinogenesis
    4. Cancer Cell Biology
    5. Cancer Genetics
    6. Infectious Causes of Cancer
    7. Early Detection and Diagnosis
    8. Epidemiology
    9. Cancer Therapy
    10. Short Reports
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      Landscape of somatic allelic imbalances and copy number alterations in human lung carcinoma (pages 2020–2031)

      Johan Staaf, Sofi Isaksson, Anna Karlsson, Mats Jönsson, Leif Johansson, Per Jönsson, Johan Botling, Patrick Micke, Bo Baldetorp and Maria Planck

      Version of Record online: 20 OCT 2012 | DOI: 10.1002/ijc.27879

      What's new?

      Lung cancer is the worldwide leading cause of death from cancer and is a heterogeneous disease at the genomic level, with therapeutic implications. Here, the authors delineated copy number alterations and allelic imbalances in 2141 cases belonging to the four major lung cancer histotypes. The study provides a broad overview of the complex landscape of genomic alterations in lung cancer. It also identifies regions frequently subjected to copy number alterations in different histotypes harboring genes involved in tumor development and progression.

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      CEBP factors regulate telomerase reverse transcriptase promoter activity in whey acidic protein-T mice during mammary carcinogenesis (pages 2032–2043)

      Mukesh Kumar, Britta Witt, Uwe Knippschild, Sylvia Koch, Jitendra K. Meena, Christina Heinlein, Julia M. Weise, Frauke Krepulat, Florian Kuchenbauer, Sebastian Iben, Karl-Lenhard Rudolph, Wolfgang Deppert and Cagatay Günes

      Version of Record online: 25 OCT 2012 | DOI: 10.1002/ijc.27880

      What's new?

      Telomerase activity has been described in invasive breast cancer, but little is known about its regulation in this disease. In this study, telomerase activity and expression of the telomerase catalytic subunit TERT were found to be strongly induced in invasive but not non-invasive mammary carcinomas of mice. In addition, CEBP transcription factors were observed bound to the TERT promoter, suggesting that they are involved in TERT regulation and carcinogenesis. The findings could have implications for the treatment of breast cancer.

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      Germline variation in TP53 regulatory network genes associates with breast cancer survival and treatment outcome (pages 2044–2055)

      Maral Jamshidi, Marjanka K. Schmidt, Thilo Dörk, Montserrat Garcia-Closas, Tuomas Heikkinen, Sten Cornelissen, Alexandra J. van den Broek, Peter Schürmann, Andreas Meyer, Tjoung-Won Park-Simon, Jonine Figueroa, Mark Sherman, Jolanta Lissowska, Garrett Teoh Hor Keong, Astrid Irwanto, Marko Laakso, Sampsa Hautaniemi, Kristiina Aittomäki, Carl Blomqvist, Jianjun Liu and Heli Nevanlinna

      Version of Record online: 25 OCT 2012 | DOI: 10.1002/ijc.27884

      What's new?

      Single nucleotide polymorphisms (SNPs) that influence breast cancer survival could play a valuable role in assessing disease prognosis. Here, in an analysis of invasive breast cancer, improved survival was associated with either of two germ-line variations in PRKAG2 (rs4726050 and rs1029946). One of the variations was further associated with a SNP in MDM2, a negative regulator of the tumor promoter protein p53 (TP53). A variant in the gene PPP2R2B was found to be predictive of better survival after hormonal therapy.

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      Genetic variants of p21 and p27 and hepatocellular cancer risk in a Chinese Han population: A case-control study (pages 2056–2064)

      Fei Liu, Yong-Gang Wei, Li-Mei Luo, Wen-Tao Wang, Lv-Nan Yan, Tian-Fu Wen, Ming-Qing Xu, Jia-Yin Yang and Bo Li

      Version of Record online: 25 OCT 2012 | DOI: 10.1002/ijc.27885

      What's new?

      Cell-cycle control proteins p21 and p27 can arrest cell proliferation, but alterations in these proteins could lead to cancer. In this study, the authors investigated whether individual variation in p21 and p27 contribute to risk of liver cancer in a Chinese population. By conducting a case-control study, they detected that certain p21 polymorphisms, either alone or in conjunction with p27 variants, can increase risk of hepatocellular carcinoma.

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      Oral benzo[a]pyrene in Cyp1a1/1b1(–/–) double-knockout mice: Microarray analysis during squamous cell carcinoma formation in preputial gland duct (pages 2065–2075)

      Marina Gálvez-Peralta, Zhanquan Shi, Jing Chen, Marian L. Miller and Daniel W. Nebert

      Version of Record online: 4 DEC 2012 | DOI: 10.1002/ijc.27897

      What's new?

      Polycyclic aromatic hydrocarbons such as BaP, present in cigarette smoke, among other places, are known to cause cancer. This study investigated the up- and down-regulation of various genes in response to oral BaP exposure in mice. The authors particularly looked at two enzymes, Cytochrome P450 1A1 and 1B1. Mice with both enzymes, and those missing 1B1, resist cancer when exposed to BaP, but mice lacking both CYP1A1 and CYP1B1 soon develop tumors of the preputial gland duct. What other genes are involved? Using microarray analysis, the authors identified a couple of dozen cancer-related genes that showed striking increases or decreases in expression with BaP treatment in the absence of Cyp1A1 and Cyp1B1. The gene encoding CYP3A59 emerged as the strongest candidate for cancer initiation.

  5. Infectious Causes of Cancer

    1. Top of page
    2. Mini Reviews
    3. Carcinogenesis
    4. Cancer Cell Biology
    5. Cancer Genetics
    6. Infectious Causes of Cancer
    7. Early Detection and Diagnosis
    8. Epidemiology
    9. Cancer Therapy
    10. Short Reports
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      Epstein–Barr virus-induced epigenetic alterations following transient infection (pages 2076–2086)

      Krista J. Queen, Mingxia Shi, Fangfang Zhang, Urska Cvek and Rona S. Scott

      Version of Record online: 2 NOV 2012 | DOI: 10.1002/ijc.27893

      What's new?

      In a transient Epstein-Barr virus (EBV) infection model, the authors provide a mechanistic framework for how a tumor virus hijacks the epigenetic machinery to induce heritable changes in host gene expression. Transient EBV infection resulted in epigenetic reprogramming with features of epithelial-to-mesenchymal transition, which were tracked as changes in DNA methylation and histone acetylation at the E-cadherin gene in transiently infected cells and in previously infected cells upon loss of viral infection. As epigenetic changes are amenable to therapeutic intervention, the authors propose that insight into virally induced epigenetic changes could inspire novel therapeutic strategies to EBV-associated malignancies.

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      Differential methylation of E2 binding sites in episomal and integrated HPV 16 genomes in preinvasive and invasive cervical lesions (pages 2087–2094)

      Arkom Chaiwongkot, Svetlana Vinokurova, Chamsai Pientong, Tipaya Ekalaksananan, Bunkerd Kongyingyoes, Pilaiwan Kleebkaow, Bandit Chumworathayi, Natcha Patarapadungkit, Miriam Reuschenbach and Magnus von Knebel Doeberitz

      Version of Record online: 26 NOV 2012 | DOI: 10.1002/ijc.27906

      What's new?

      Upregulation of the E6 and E7 oncogenes in human papillomavirus (HPV) is known to promote tumor growth in the uterine cervix and has been hypothesized as being enhanced by the methylation of regulatory E2 binding sites (E2BSs). This analysis reveals a correlation between E2BSs methylation and viral integration state in invasive cervical cancers associated with the predominant high risk-HPV type, HPV16. Methylation levels varied according to whether HPV was only episomal and whether a single copy or multiple copies of HPV had been integrated into lesions. The data substantiate the crucial role of differential E2BS methylation in HPV-related neoplasms and could facilitate the development of novel treatments.

  6. Early Detection and Diagnosis

    1. Top of page
    2. Mini Reviews
    3. Carcinogenesis
    4. Cancer Cell Biology
    5. Cancer Genetics
    6. Infectious Causes of Cancer
    7. Early Detection and Diagnosis
    8. Epidemiology
    9. Cancer Therapy
    10. Short Reports
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      Exploiting FOXM1-orchestrated molecular network for early squamous cell carcinoma diagnosis and prognosis (pages 2095–2106)

      Muy-Teck Teh, Iain L. Hutchison, Daniela Elena Costea, Evelyn Neppelberg, Per Gunnar Liavaag, Karin Purdie, Catherine Harwood, Hong Wan, Edward W. Odell, Allan Hackshaw and Ahmad Waseem

      Version of Record online: 25 OCT 2012 | DOI: 10.1002/ijc.27886

      What's new?

      Early detection of pre-cancer lesions would greatly improve outcomes in head and neck squamous cell carcinoma (HSNCC), if it were possible to predict which lesions were likely to progress to cancer. Conventional histopathology is not up to the task, and this paper demonstrates a new molecular method for HSNCC detection. Using 14 genes associated with the FOXM1 oncogene, the authors created a diagnostic index capable of objectively stratifying cancer aggressiveness. They demonstrated a high detection rate and low false positive rate in classifying clinical tissue samples, making this system a practical diagnostic tool to improve patient outcomes.

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      Multifunctional nanobeacon for imaging Thomsen-Friedenreich antigen-associated colorectal cancer (pages 2107–2117)

      Hironori Kumagai, Wellington Pham, Makoto Kataoka, Ken-Ichiro Hiwatari, James McBride, Kevin J. Wilson, Hiroyuki Tachikawa, Ryoji Kimura, Kunio Nakamura, Eric H. Liu, John C. Gore and Shinji Sakuma

      Version of Record online: 30 OCT 2012 | DOI: 10.1002/ijc.27903

      What's new?

      Approximately half of the Western population will develop some form of colorectal tumor by age 70. Here the authors set to validate the potential suitability of a newly developed nanobeacon for imaging the Thomsen-Friedenreich (TF) antigen as a biomarker of colorectal cancer. They demonstrated that the probe specifically recognizes TF antigen-specific tumors in human tissues. When applied topically, the probe is also not absorbed by the mouse intestine, obviating systemic distribution-associated toxicity. The nanobeacon offers potential for colorectal cancer imaging via colonoscopy both for the early detection and prediction of the progression of colorectal cancer at the molecular level.

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      RAD51 overexpression is a negative prognostic marker for colorectal adenocarcinoma (pages 2118–2126)

      Pierre Tennstedt, Robert Fresow, Ronald Simon, Andreas Marx, Luigi Terracciano, Cordula Petersen, Guido Sauter, Ekkehard Dikomey and Kerstin Borgmann

      Version of Record online: 5 NOV 2012 | DOI: 10.1002/ijc.27907

      What's new

      RAD51 plays a central role in the repair of DNA double-strand breaks, and its overexpression has been associated with poor prognosis in several malignancies. In this analysis of 1,210 colorectal cancer biopsies, RAD51 overexpression was significantly correlated with poor prognosis. Its expression was further observed to be associated with that of other proteins, most importantly epidermal growth factor receptor. The results indicate the RAD51 may be an important prognostic marker and therapeutic target for colorectal cancer.

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      Potential effect of the risk of ovarian cancer algorithm (ROCA) on the mortality outcome of the Prostate, Lung, Colorectal and Ovarian (PLCO) trial (pages 2127–2133)

      Paul F. Pinsky, Claire Zhu, Steve J. Skates, Amanda Black, Edward Partridge, Saundra S. Buys and Christine D. Berg

      Version of Record online: 5 NOV 2012 | DOI: 10.1002/ijc.27909

      What's new

      The Prostate, Lung, Colorectal and Ovarian (PLCO) trial found no mortality benefit for ovarian cancer screening using a single cutoff value for the biomarker CA125. PLCO, however, did not incorporate the potential impact of ROCA (Risk of Ovarian Cancer Algorithm), which evaluates serial CA125 values. Here, in a best-case scenario analysis, ROCA was found to have little impact on mortality in the context of PLCO. The findings do not rule out possible benefits from ROCA in the ongoing UK Collaborative Trial of Ovarian Cancer Screening.

  7. Epidemiology

    1. Top of page
    2. Mini Reviews
    3. Carcinogenesis
    4. Cancer Cell Biology
    5. Cancer Genetics
    6. Infectious Causes of Cancer
    7. Early Detection and Diagnosis
    8. Epidemiology
    9. Cancer Therapy
    10. Short Reports
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      Mortality audit of the Finnish cervical cancer screening program (pages 2134–2140)

      Stefan Lönnberg, Pekka Nieminen, Tapio Luostarinen and Ahti Anttila

      Version of Record online: 12 OCT 2012 | DOI: 10.1002/ijc.27844

      What's new?

      Cervical cancer screening may not be equally effective across targeted age groups. In this evaluation of the Finnish cervical cancer screening program, only a relatively small reduction in risk of death from the disease was observed in association with screening before age 40. Long-lasting risk reduction, however, was associated with screening at age 65, when mortality from cervical cancer increases. The findings suggest that an additional round of screening in older women could be beneficial.

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      The HPV test has similar sensitivity but more overdiagnosis than the Pap test—A randomised health services study on cervical cancer screening in Finland (pages 2141–2147)

      Nea Malila, Maarit Leinonen, Laura Kotaniemi-Talonen, Pekka Laurila, Jussi Tarkkanen and Matti Hakama

      Version of Record online: 12 OCT 2012 | DOI: 10.1002/ijc.27850

      What's new?

      Cervical cancer screeningresults in both benefit for preventing lesions from progressing to invasive cancer and harm for also detecting lesions that would never have led to invasive cancers. This randomised study compares the HPV test to the traditional Pap test in terms of sensitivity (detection of progressive lesions) and overdiagnosis (detection of non-progressive lesions).While the HPV test is known to detect a higher number of pre-invasive lesions, the authors found that sensitivity was high with both tests but overdiagnosis more common with the HPV test, suggesting the need to reconsider the implementation of HPV testing.

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      Soluble c-Met protein as a susceptible biomarker for gastric cancer risk: A nested case-control study within the Korean Multicenter Cancer Cohort (pages 2148–2156)

      Jae Jeong Yang, Ji Hyun Yang, Jungkon Kim, Seung Hyun Ma, Lisa Y. Cho, Kwang-Pil Ko, Aesun Shin, Bo Youl Choi, Hyun Ja Kim, Dong Soo Han, Chang Soo Eun, Kyu Sang Song, Yong Sung Kim, Soung-Hoon Chang, Hai-Rim Shin, Daehee Kang, Keun-Young Yoo and Sue K. Park

      Version of Record online: 25 OCT 2012 | DOI: 10.1002/ijc.27861

      What's new?

      Infection with Cag-A positive H. pylori is a major risk factor for gastric cancer. Certain genetic variants along the Cag-A signaling pathway influence this risk, and one of these genes is the c-Met protein. This protein also has a soluble form that can be easily measured in plasma. In this study, the authors investigated soluble c-Met as a biomarker for gastric cancer. They compared the plasma concentration c-Met between 290 sets of gastric cancer cases and matched controls. Protein levels were lower in cases than controls, and in fact, the levels decreased as the onset of cancer drew nearer, suggesting a protective effect conferred by the circulating c-Met.

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      Increasing prevalence of comorbidity in patients with colorectal cancer in the South of the Netherlands 1995–2010 (pages 2157–2163)

      N.J. van Leersum, M.L.G. Janssen-Heijnen, M.W.J.M. Wouters, H.J.T. Rutten, J.W. Coebergh, R.A.E.M. Tollenaar and V.E.P.P. Lemmens

      Version of Record online: 5 NOV 2012 | DOI: 10.1002/ijc.27871

      What's new

      Treating cancer in a patient who also has other diseases or conditions can be challenging, but is not unusual. In this study, the authors looked at comorbidity in patients with colorectal cancer over a period of 16 years, and found it increased over the time frame of the study, particularly hypertension and cardiovascular diseases. Patients with multiple conditions are less likely to respond well to treatment. These data underscore the importance of individualized treatment and awareness of other conditions that are increasingly present alongside the cancer.

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      Menstrual and reproductive factors in women, genetic variation in CYP17A1, and pancreatic cancer risk in the European prospective investigation into cancer and nutrition (EPIC) cohort (pages 2164–2175)

      Eric J. Duell, Noémie Travier, Leila Lujan-Barroso, Laure Dossus, Marie-Christine Boutron-Ruault, Françoise Clavel-Chapelon, Rosario Tumino, Giovanna Masala, Vittorio Krogh, Salvatore Panico, Fulvio Ricceri, Maria Luisa Redondo, Miren Dorronsoro, Esther Molina-Montes, José M. Huerta, Aurelio Barricarte, Kay-Tee Khaw, Nick J. Wareham, Naomi E. Allen, Ruth Travis, Peter D. Siersema, Petra H.M. Peeters, Antonia Trichopoulou, Eirini Fragogeorgi, Eleni Oikonomou, Heiner Boeing, Madlen Schuetze, Federico Canzian, Annekatrin Lukanova, Anne Tjønneland, Nina Roswall, Kim Overvad, Elisabete Weiderpass, Inger Torhild Gram, Eiliv Lund, Björn Lindkvist, Dorthe Johansen, Weimin Ye, Malin Sund, Veronika Fedirko, Mazda Jenab, Dominique S. Michaud, Elio Riboli and H. Bas Bueno-de-Mesquita

      Version of Record online: 30 OCT 2012 | DOI: 10.1002/ijc.27875

      What's new

      Because the incidence of pancreatic cancer is 30-50% higher in men than women, researchers have wondered whether exposure to estrogen might offer a protective effect. The answer thus far has been unclear, however. In this study, the authors examined menstrual and reproductive factors in women, as well as exogenous hormone use. They also examined variants of the CYP17A1 gene in both women and men, as this gene is essential for sex-steroid metabolism. Only early age of menarche showed any association with pancreatic cancer risk.

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      Alcohol consumption and PSA-detected prostate cancer risk—A case-control nested in the ProtecT study (pages 2176–2185)

      Luisa Zuccolo, Sarah J. Lewis, Jenny L. Donovan, Freddie C. Hamdy, David E. Neal and George Davey Smith

      Version of Record online: 25 OCT 2012 | DOI: 10.1002/ijc.27877

      What's new?

      Alcohol is not an established risk factor for prostate cancer; however, the current work suggests that heavy drinking could cause a small increase in risk of the more aggressive forms. If the results are confirmed to be causal, prostate cancer risk will be added to the many long-term health risks of heavy drinking, and public health strategies will then also reduce high-risk, poorer prognosis prostate cancer. The authors also found that heavy drinkers have lower PSA levels, suggesting that heavy alcohol consumption could be used as a marker to identify men in whom some cancers might be missed.

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      Type 2 diabetes mellitus, insulin-use and risk of bladder cancer in a large cohort study (pages 2186–2191)

      Christina C. Newton, Susan M. Gapstur, Peter T. Campbell and Eric J. Jacobs

      Version of Record online: 20 OCT 2012 | DOI: 10.1002/ijc.27878

      What's new?

      While type 2 diabetes mellitus (T2DM) has been associated with an increased risk of bladder cancer, some studies have reported no association. Few investigations, however, have assessed risk according to insulin use, duration of diabetes, or cancer stage. In this large prospective study, T2DM was not associated with overall bladder cancer risk, but long-term diabetes and insulin use were linked to a higher risk of invasive bladder cancer. The findings suggest that insulin use, or a correlate thereof, may contribute to bladder cancer progression.

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      The risk of Barrett's esophagus associated with abdominal obesity in males and females (pages 2192–2199)

      Bradley J. Kendall, Graeme A. Macdonald, Nicholas K. Hayward, Johannes B. Prins, Suzanne O'Brien, David C. Whiteman and for the Study of Digestive Health

      Version of Record online: 30 OCT 2012 | DOI: 10.1002/ijc.27887

      What's new?

      Barrett's esophagus (BE), a condition in which the lining of the esophagus is damaged by stomach acid, leads to esophageal cancer. It's suspected that obesity leads to BE, which occurs more often in males than females. This paper reports the results of a case-control study, which show that abdominal obesity does strongly associate with BE in males, but not females, independent of gastroesophageal reflux.

  8. Cancer Therapy

    1. Top of page
    2. Mini Reviews
    3. Carcinogenesis
    4. Cancer Cell Biology
    5. Cancer Genetics
    6. Infectious Causes of Cancer
    7. Early Detection and Diagnosis
    8. Epidemiology
    9. Cancer Therapy
    10. Short Reports
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      HDAC11 is a novel drug target in carcinomas (pages 2200–2208)

      Hedwig E. Deubzer, Marie C. Schier, Ina Oehme, Marco Lodrini, Bernard Haendler, Anette Sommer and Olaf Witt

      Version of Record online: 25 OCT 2012 | DOI: 10.1002/ijc.27876

      What's new?

      Histone deacetylase (HDAC) enzymes influence the regulation of numerous cellular processes, and their inhibition by small molecules has been shown to provide benefits against multiple cancer types. Here, HDAC11, a recently identified member of the HDAC family, was found to play an important role in the control of proliferation and survival pathways in several carcinoma cell lines. The high incidence of the tumors represented suggests that HDAC11 could be a valuable drug target in oncology.

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      Methylation and microsatellite status and recurrence following adjuvant FOLFOX in colorectal cancer (pages 2209–2216)

      Sae-Won Han, Hyun-Jung Lee, Jeong Mo Bae, Nam-Yun Cho, Kyung-Hun Lee, Tae-Yong Kim, Do-Youn Oh, Seock-Ah Im, Yung-Jue Bang, Seung-Yong Jeong, Kyu Joo Park, Jae-Gahb Park, Gyeong Hoon Kang and Tae-You Kim

      Version of Record online: 29 OCT 2012 | DOI: 10.1002/ijc.27888

      What's new?

      Colorectal cancer is characterized by a number of molecular subtypes, the impact of which on the outcome of leucovorin, 5-fluorouracil, and oxaliplatin (FOLFOX) therapy is not fully understood. In this report, the colorectal cancer CpG island methylator phenotype (CIMP), which is associated with microsatellite instability, was not linked to disease-free survival. High disease recurrence, however, was associated with methylation of the CpG loci NEUROG1 and CDKN2A (p16), suggesting that these loci may be valuable prognostic markers.

  9. Short Reports

    1. Top of page
    2. Mini Reviews
    3. Carcinogenesis
    4. Cancer Cell Biology
    5. Cancer Genetics
    6. Infectious Causes of Cancer
    7. Early Detection and Diagnosis
    8. Epidemiology
    9. Cancer Therapy
    10. Short Reports
    1. You have free access to this content
      Recurrent inactivating mutations of ARID2 in non-small cell lung carcinoma (pages 2217–2221)

      Gilles Manceau, Eric Letouzé, Cécile Guichard, Audrey Didelot, Aurelie Cazes, Hélène Corté, Elizabeth Fabre, Karine Pallier, Sandrine Imbeaud, Françoise Le Pimpec-Barthes, Jessica Zucman-Rossi, Pierre Laurent-Puig and Hélène Blons

      Version of Record online: 20 NOV 2012 | DOI: 10.1002/ijc.27900

      What's new?

      Chromatin plays a key role in tissue-specific gene expression during development and differentiation and is often corrupted in cancer cells. The authors focused on the identification of mutations in chromatin-remodeling genes in non-small cell lung carcinoma, the most frequent type of lung cancer. They identified several inactivating mutations of ARID2, a subunit of the SWI/SNF chromatin-remodeling complex. With a loss-of-function mutation rate of 5%, ARID2 is one of the most frequently mutated genes in this cancer type, after TP53, KRAS, EGFR, CDKN2A and STK11. These results underscore the central role of chromatin in curbing cancer and implicate ARID2 as a new tumor suppressor in lung cancer development.

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