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International Journal of Cancer

Cover image for International Journal of Cancer

15 August 2013

Volume 133, Issue 4

Pages 779–1022

  1. Mini Reviews

    1. Top of page
    2. Mini Reviews
    3. Carcinogenesis
    4. Cancer Cell Biology
    5. Cancer Genetics
    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
  2. Carcinogenesis

    1. Top of page
    2. Mini Reviews
    3. Carcinogenesis
    4. Cancer Cell Biology
    5. Cancer Genetics
    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
      De novo-generated small palindromes are characteristic of amplicon boundary junction of double minutes (pages 797–806)

      Jing Zhu, Yang Yu, Xiangning Meng, Yihui Fan, Yu Zhang, Chunshui Zhou, Zhichao Yue, Yan Jin, Chunyu Zhang, Lisa Yu, Wei Ji, Xueyuan Jia, Rongwei Guan, Jie Wu, Jingcui Yu, Jing Bai, Xin-Yuan Guan, Mingrong Wang, Ki-Young Lee, Wenjing Sun and Songbin Fu

      Version of Record online: 9 MAR 2013 | DOI: 10.1002/ijc.28084

      What's new?

      Double minutes (DMs) are poorly understood hallmarks of gene amplification, a form of genomic aberration associated with tumor development. After cloning DMs from a human ovarian cancer cell line, the authors determined the precise breakpoints of two co-amplified amplicons and analyzed the complex DNA sequence joining them. They found that de novo creation of small palindromic sequences surrounding the breakpoints is a common characteristic of amplicon junction sequences in cancers. The palindromic sequences, which may be generated through non-homologous end joining in concert with a novel DNA repair machinery, may play a common role in amplicon rejoining and gene amplification.

  3. Cancer Cell Biology

    1. Top of page
    2. Mini Reviews
    3. Carcinogenesis
    4. Cancer Cell Biology
    5. Cancer Genetics
    6. Tumor Immunology
    7. Early Detection and Diagnosis
    8. Epidemiology
    9. Cancer Therapy
    10. Short Report
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      Nuclear expression of Glycogen synthase kinase-3β and lack of membranous β-catenin is correlated with poor survival in colon cancer (pages 807–815)

      Tavga Salim, Anita Sjölander and Janna Sand-Dejmek

      Version of Record online: 9 MAR 2013 | DOI: 10.1002/ijc.28074

      What's new?

      More than half of patients with stage III colorectal cancer will experience tumor recurrence. Currently there is no biomarker capable of distinguishing among patients with good or poor prognosis. In this study, nuclear expression of the Wnt signaling protein glycogen synthase kinase-3β (GSK-3β), combined with lack of membrane β-catenin, was found to be associated with poor prognosis. The findings emphasize the significance of deregulation of the Wnt/β-catenin signaling pathway as a hallmark of colon cancer and reveal a potential role for GSK-3β as a prognostic biomarker for the disease.

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      Identification of microRNAs specifically expressed in hepatitis C virus-associated hepatocellular carcinoma (pages 816–824)

      Giacomo Diaz, Marta Melis, Ashley Tice, David E. Kleiner, Lopa Mishra, Fausto Zamboni and Patrizia Farci

      Version of Record online: 16 MAR 2013 | DOI: 10.1002/ijc.28075

      What's new?

      Changes in microRNAs (miRNAs) have previously been associated with hepatocellular carcinoma but these changes were identified using the surrounding non-tumorous tissue as control, which is typically affected by cirrhosis or chronic hepatitis, and often associated with viral infection. The present study examines hepatocellular carcinomas associated with Hepatitis C Virus (HCV) infection and uses a unique series of specimens, including normal livers, as controls. The authors identify 18 miRNAs exclusively associated with HCV-related liver cancer that are characterized by high specificity and selectivity versus other liver diseases and connected in a regulatory network centered on the p53 tumor suppressor, the PTEN phosphatase and retinoic acid signaling. These miRNAs may represent new diagnostic and therapeutic tools that could advance the prospect of HCV-positive individuals afflicted with liver cancer.

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      Targeting the EP1 receptor reduces Fas ligand expression and increases the antitumor immune response in an in vivo model of colon cancer (pages 825–834)

      Grace O'Callaghan, Aideen Ryan, Peter Neary, Caitlin O'Mahony, Fergus Shanahan and Aileen Houston

      Version of Record online: 4 MAR 2013 | DOI: 10.1002/ijc.28076

      What's new?

      Inhibition of the inflammatory mediator prostaglandin E2 (PGE2) through blockade of cycloxygenase enzyme activity slows tumor growth but also causes severe side effects, a problem that may be bypassed with the identification of alternative anti-inflammatory drug targets. One such target may be the PGE2 receptor EP1, reported here. Dietary administration and direct injection of the EP1 antagonist ONO-8713 was found to slow tumor growth in a colon cancer mouse model. Targeting of the EP1 receptor was associated with reduced FasL expression, reduced regulatory T-cell infiltration, and an improved anti-tumor immune response.

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      High male chimerism in the female breast shows quantitative links with cancer (pages 835–842)

      Eugen Dhimolea, Viktoria Denes, Monika Lakk, Sana Al-Bazzaz, Sonya Aziz-Zaman, Monika Pilichowska and Peter Geck

      Version of Record online: 4 MAR 2013 | DOI: 10.1002/ijc.28077

      What's new?

      During pregnancy, allogeneic stem/progenitor cells from the fetus integrate into adult niches in the mother, but their biology and the niches are not well known. The current study shows that a potential niche for long-term integration in the mother is the mammary gland. Using a new Y-chromosome assay the authors show that most healthy women carry male cells in their breasts, but both under- and overrepresentation correlate with breast cancer. At levels linked with tissue integrity chimeric cells share densities with mammary progenitors, pointing to novel chimeric/host stem-cell interactions that may serve to protect from cancer development.

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      Vacuolar H+ ATPase expression and activity is required for Rab27B-dependent invasive growth and metastasis of breast cancer (pages 843–854)

      An Hendrix, Raija Sormunen, Wendy Westbroek, Kathleen Lambein, Hannelore Denys, Gwen Sys, Geert Braems, Rudy Van den Broecke, Veronique Cocquyt, Christian Gespach, Marc Bracke and Olivier De Wever

      Version of Record online: 7 MAR 2013 | DOI: 10.1002/ijc.28079

      What's new?

      Regulated exocytosis has emerged as a new mechanism that may offer cancer cells a selective advantage for invasive growth. This study examines the molecular mechanisms of how Rab27B-regulated vesicles in tumor cells deliver pro-invasive cellular regulators to the extracellular environment. The study utilized mass spectrometry of Rab27B-positive vesicles and identified VATPase, a multi-subunit ATP-dependent proton pump as a critical mediator of Rab27B-mediated vesicle release in estrogen receptor-α-positive breast cancer. The authors point to V-ATPase as a promising therapeutic target to prevent the release of pro-invasive growth regulators and thus inhibit Rab27B-dependent invasive growth of ERα-positive breast tumors.

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      EpCAM-associated claudin-7 supports lymphatic spread and drug resistance in rat pancreatic cancer (pages 855–866)

      Florian Thuma and Margot Zöller

      Version of Record online: 9 MAR 2013 | DOI: 10.1002/ijc.28085

      What's new?

      EpCAM, a cancer-initiating cell marker, frequently associates with claudin-7 in gastrointestinal tumors, an interaction that has been implicated in facilitating the progression of disease. Here, independent knockdown of EpCAM or claudin-7 in rat pancreatic adenocarcinoma cells was found to reduce cell motility, though the effect was most pronounced in cells lacking claudin-7. Loss of EpCAM or claudin-7 also led to an increase in apoptosis. However, increased Pten expression, which augments apoptosis and drug susceptibility, was observed only in claudin-7 knockdowns. The findings suggest that claudin-7, rather than EpCAM, may be a driving force behind progression and therefore a key biomarker for metastasis.

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      MicroRNA-138 suppresses ovarian cancer cell invasion and metastasis by targeting SOX4 and HIF-1α (pages 867–878)

      Yu-Ming Yeh, Chi-Mu Chuang, Kuan-Chong Chao and Lu-Hai Wang

      Version of Record online: 9 MAR 2013 | DOI: 10.1002/ijc.28086

      What's new?

      A microRNA (miRNA) called miR-138 is known to be down-regulated in several types of cancer. In this study, the authors found that miR-138 suppresses ovarian cancer (OvCa) metastasis in mice, by targeting two transcriptional factors, SOX4 and HIF-1α. They also found that OvCa cells with low levels of miR-138 and high SOX4 levels were associated with a highly malignant phenotype. These results identify novel signaling pathways and potential biomarkers in OvCa that may provide new therapeutic targets, as well as useful prognostic information.

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      The abrogation of the HOXB7/PBX2 complex induces apoptosis in melanoma through the miR-221&222-c-FOS pathway (pages 879–892)

      M. Cristina Errico, Federica Felicetti, Lisabianca Bottero, Gianfranco Mattia, Alessandra Boe, Nadia Felli, Marina Petrini, Maria Bellenghi, Hardev S. Pandha, Marco Calvaruso, Claudio Tripodo, Mario P. Colombo, Richard Morgan and Alessandra Carè

      Version of Record online: 13 MAR 2013 | DOI: 10.1002/ijc.28097

      What's new?

      Cutaneous melanoma is the fastest increasing cancer worldwide. Although several molecular abnormalities have been associated with melanoma progression, the underlying mechanisms are still largely unknown. Here the authors show that the HOXB7/PBX2 complex is a new transcriptional activator of the oncogenic microRNA-221 and 222 in melanoma inducing tumor malignancy. The authors also identified c-FOS as a direct target of miR-221&222 whose repression causes reduced apoptosis. The abrogation of HOXB7 and/or miR-221&222 or the disruption of HOXB7/PBX2 dimers by the peptide HXR9 might thus represent novel molecular approaches for advanced melanoma, an aggressive neoplasm refractory to traditional therapies.

  4. Cancer Genetics

    1. Top of page
    2. Mini Reviews
    3. Carcinogenesis
    4. Cancer Cell Biology
    5. Cancer Genetics
    6. Tumor Immunology
    7. Early Detection and Diagnosis
    8. Epidemiology
    9. Cancer Therapy
    10. Short Report
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      ABO blood group and nasopharyngeal carcinoma risk in a population of Southeast China (pages 893–897)

      Liming Sheng, Xiaojiang Sun, Lizhen Zhang and Dan Su

      Version of Record online: 9 MAR 2013 | DOI: 10.1002/ijc.28087

      What's new?

      The ABO blood group has been reported to alter individual susceptibility to a number of malignancies, but whether such an association exists between the ABO blood group and nasopharyngeal carcinoma (NPC) remains unknown. In a large-scale case-control study carried out in China, the authors observed a statistically significant increased risk for NPC among patients with blood group A or AB, compared with those with blood group O. Blood type A was also associated with more advanced NPC in male patients. The results suggest that ABO blood group antigens may play an important role in the carcinogenesis of nasopharyngeal cancer.

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      Determining the profiles and parameters for gene amplification testing of growth factor receptors in lung cancer (pages 898–907)

      Eva Pros, Sylvie Lantuejoul, Lydia Sanchez-Verde, Sandra D Castillo, Ester Bonastre, Ana Suarez-Gauthier, Esther Conde, Juan C Cigudosa, Fernando Lopez-Rios, Juan Torres-Lanzas, Josep Castellví, Santiago Ramon y Cajal, Elisabeth Brambilla and Montse Sanchez-Cespedes

      Version of Record online: 9 MAR 2013 | DOI: 10.1002/ijc.28090

      What's new?

      Targeting growth factor receptors is a good way to treat cancer, in the right patients. Therefore, it's important to be able to identify patients with alterations in relevant GFRs. One way they get activated is by gene amplification, but it can be tricky to establish whether amplification has taken place. This study provides the first comprehensive analysis of gene copy number and gene expression alteration in non-small cell lung carcinoma (NSCLC). By combining the analyses of alterations at the DNA, mRNA, and protein levels for certain growth factors in a panel of 300 NSCLC, the authors were able to identify those tumors that carry gene amplifications. These new results establish parameters for gene amplification that will be useful for routine screening.

  5. Tumor Immunology

    1. Top of page
    2. Mini Reviews
    3. Carcinogenesis
    4. Cancer Cell Biology
    5. Cancer Genetics
    6. Tumor Immunology
    7. Early Detection and Diagnosis
    8. Epidemiology
    9. Cancer Therapy
    10. Short Report
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      Expression of NTRK1/TrkA affects immunogenicity of neuroblastoma cells (pages 908–919)

      Kristian W. Pajtler, Vera Rebmann, Monika Lindemann, Johannes H. Schulte, Stefanie Schulte, Michael Stauder, Ivo Leuschner, Kurt-Werner Schmid, Ulrike Köhl, Alexander Schramm and Angelika Eggert

      Version of Record online: 16 MAR 2013 | DOI: 10.1002/ijc.28096

      What's new?

      Elevated expression of neurotrophic tyrosine kinase type 1 receptor (NTRK1, or TrkA) previously was found to be associated with favorable prognosis in neuroblastoma. That effect may be the result of TrkA-induced enhancement of the immune response toward neuroblastoma cells, as reported here. The findings suggest that TrkA-associated immune activity might partly explain spontaneous regression of low-stage neuroblastomas. They also have novel translational implications, among them the possibility for the development of T cell-based immunotherapy approaches.

  6. Early Detection and Diagnosis

    1. Top of page
    2. Mini Reviews
    3. Carcinogenesis
    4. Cancer Cell Biology
    5. Cancer Genetics
    6. Tumor Immunology
    7. Early Detection and Diagnosis
    8. Epidemiology
    9. Cancer Therapy
    10. Short Report
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      MALDI mass spectrometric imaging based identification of clinically relevant signals in prostate cancer using large-scale tissue microarrays (pages 920–928)

      Stefan Steurer, Carina Borkowski, Sinje Odinga, Malte Buchholz, Christina Koop, Hartwig Huland, Michael Becker, Matthias Witt, Dennis Trede, Maryam Omidi, Olga Kraus, Ahmad S. Bahar, A. Shoaib Seddiqi, Julius M. Singer, Marcel Kwiatkowski, Maria Trusch, Ronald Simon, Marcus Wurlitzer, Sarah Minner, Thorsten Schlomm, Guido Sauter and Hartmut Schlüter

      Version of Record online: 4 MAR 2013 | DOI: 10.1002/ijc.28080

      What's new?

      Matrix-assisted laser desorption/ionization (MALDI) mass spectrometry is a powerful tool with the potential to measure biomolecular features of cancer that may be of investigative, diagnostic, or prognostic significance. In this study, MALDI was found to be capable of identifying mass-per-charge signals associated with TMPRSS2-ERG gene fusion in a prostate cancer tissue microarray based on patient samples. The findings suggest that the approach could be used to characterize clinically relevant molecular signals of malignant disease and therefore could be of value for clinical screening.

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      A prospective evaluation of a breast cancer prognosis signature in the observational RASTER study (pages 929–936)

      C.A. Drukker, J.M. Bueno-de-Mesquita, V.P. Retèl, W.H. van Harten, H. van Tinteren, J. Wesseling, R.M.H. Roumen, M. Knauer, L.J. van 't Veer, G.S. Sonke, E.J.T. Rutgers, M.J. van de Vijver and S.C. Linn

      Version of Record online: 4 MAR 2013 | DOI: 10.1002/ijc.28082

      What's new?

      The “MammaPrint” is a 70-gene signature developed to predict the risk of breast cancer metastases. This study, the RASTER study, provides the first prospective data looking at this 70-gene signature to evaluate it's performance. For 427 patients, treatment decisions were based on standard guidelines, the 70-gene signature, and doctors' and patients' preferences. Here, 124 patients were categorized as “low-risk” by the 70-gene signature, but high-risk by other measures, such as age, tumor size, nodal status, and other clinicopathological factors. Of these, 76% did not receive adjuvant chemotherapy, and 98% survived 5 years with no recurrence of disease. Thus, withholding chemotherapy based on the low-risk gene signature result, and in accordance with doctors' and patients' preferences, did not negatively impact recurrence rate, confirming the prognostic value of this new tool.

  7. Epidemiology

    1. Top of page
    2. Mini Reviews
    3. Carcinogenesis
    4. Cancer Cell Biology
    5. Cancer Genetics
    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
      Fatherhood status and risk of prostate cancer: Nationwide, population-based case–control study (pages 937–943)

      Sara M. Wirén, Linda I. Drevin, Sigrid V. Carlsson, Olof Akre, Erik C. Holmberg, David E. Robinson, Hans G. Garmo and Pär E. Stattin

      Version of Record online: 8 MAR 2013 | DOI: 10.1002/ijc.28057

      What's new?

      Previous studies have indicated that childless men may have a decreased risk of prostate cancer compared with men who are fathers, possibly because childless men may be infertile and therefore have reduced androgen levels that would otherwise predispose them to disease. This population-based case-control study supports the finding that childless men have a decreased risk of prostate cancer, but adjustment for socioeconomic factors substantially weakened an association for low-risk cancers. The results indicate that the relationship between fatherhood status and prostate cancer may be due largely to socioeconomic factors that influence health-care seeking behavior and hence testing of prostate specific antigen levels.

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      Latitude gradients for lymphoid neoplasm subtypes in Australia support an association with ultraviolet radiation exposure (pages 944–951)

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

      Version of Record online: 4 MAR 2013 | DOI: 10.1002/ijc.28081

      What's new?

      Studies examining the relationship between exposure to ultraviolet radiation (UVR) and risk of lymphoid neoplasms have produced conflicting results, with UVR implicated as both causative and preventative. This investigation of incidence by residential latitude band in Australia lends support to the idea that UVR exposure is protective, but specifically for certain subtypes of non-Hodgkin and Hodgkin lymphoma. The incidence of those subtypes, among which were several mature B-cell and T-cell neoplasms, was found to increase with increasing distance from the equator. The protective effect of UVR may be mediated through vitamin D-related immune modulation.

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      Soy isoflavone intake and breast cancer risk in Japan: From the Takayama study (pages 952–960)

      Keiko Wada, Kozue Nakamura, Yuya Tamai, Michiko Tsuji, Toshiaki Kawachi, Akihiro Hori, Naoharu Takeyama, Shinobu Tanabashi, Shogen Matsushita, Naoki Tokimitsu and Chisato Nagata

      Version of Record online: 9 MAR 2013 | DOI: 10.1002/ijc.28088

      What's new?

      Previous reports have suggested that high intake of isoflavone-rich soy foods may be modestly associated with a reduced risk of breast cancer in Asian populations. Here, soy and isoflavone intake at both high and moderate levels was found to be associated with reduced postmenopausal but not premenopausal breast cancer risk in Japanese women. The inverse association between soy intake and postmenopausal disease risk was discovered to be nonlinear, suggesting a threshold effect.

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      2-Amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP)-DNA adducts in benign prostate and subsequent risk for prostate cancer (pages 961–971)

      Deliang Tang, Oleksandr N. Kryvenko, Yun Wang, Sheri Trudeau, Andrew Rundle, Satoru Takahashi, Tomoyuki Shirai and Benjamin A. Rybicki

      Version of Record online: 9 MAR 2013 | DOI: 10.1002/ijc.28092

      What's new?

      While exposure to high levels of PhIP (2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine)—a heterocyclic amine found in cooked meat—is associated with the development of prostate malignancies in animals, it is unclear whether this same risk exists in humans. Here, risk of prostate cancer in men was found to be increased only in the presence of both glandular inflammation and elevated levels of PhIP-DNA adducts, based on analysis of benign prostate specimens. However, certain subgroups of White males, who had higher PhIP-DNA adduct levels than African Americans, may be at greater risk for the disease. Given the putative role of inflammation in cancer, targeted prevention strategies in men with known high PhIP exposure levels may lead to beneficial health outcomes.

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      Does removal of out-of-pocket costs for cervical and breast cancer screening work? A quasi-experimental study to evaluate the impact on attendance, attendance inequality and average cost per uptake of a Japanese government intervention (pages 972–983)

      Takahiro Tabuchi, Takahiro Hoshino, Tomio Nakayama, Yuri Ito, Akiko Ioka, Isao Miyashiro and Hideaki Tsukuma

      Version of Record online: 13 MAR 2013 | DOI: 10.1002/ijc.28095

      What's new?

      Out-of-pocket costs may be a barrier to cancer screening, though their removal in some countries has met with mixed results. Here, analysis of uptake, government expenditure, and socioeconomic inequalities associated with a cost-free breast and cervical cancer screening program introduced in Japan in 2009 indicates that while attendance increased for both types of screening, overall spending for the program was considerable. Furthermore, while inequalities in attendance decreased for breast cancer screening, they increased for cervical cancer screening.

  8. Cancer Therapy

    1. Top of page
    2. Mini Reviews
    3. Carcinogenesis
    4. Cancer Cell Biology
    5. Cancer Genetics
    6. Tumor Immunology
    7. Early Detection and Diagnosis
    8. Epidemiology
    9. Cancer Therapy
    10. Short Report
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      Coexistent mutations of KRAS and PIK3CA affect the efficacy of NVP-BEZ235, a dual PI3K/MTOR inhibitor, in regulating the PI3K/MTOR pathway in colorectal cancer (pages 984–996)

      Areumnuri Kim, Jung-Eun Lee, Seung-Sook Lee, Cherin Kim, Sun-Joo Lee, Won-Suk Jang and Sunhoo Park

      Version of Record online: 8 MAR 2013 | DOI: 10.1002/ijc.28073

      What's new?

      Two of the mutations frequently seen in colorectal cancer are KRAS and PI3KCA, which boost the PI3K/AKT/MTOR signal transduction pathways that stimulate cell proliferation and inhibit apoptosis. Patients with both these mutations tend to have poor prognosis. In this study, the authors investigated how mutations in KRAS or PI3KCA affect sensitivity to a new antiproliferative agent, BEZ235. BEZ235 inhibits PI3K and MTOR, sensitizing the cell to apoptosis. The authors looked at KRAS mutant cell lines with or without mutations in PI3KCA to see how well BEZ235 could halt their growth. Dual mutations in these two genes, which step up the activity of the PI3K/MTOR signaling pathway, do allow the cell to sidestep the effects of BEZ235, they found.

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      A dose-finding study of temsirolimus and liposomal doxorubicin for patients with recurrent and refractory bone and soft tissue sarcoma (pages 997–1005)

      K.A. Thornton, A.R. Chen, M.M. Trucco, P. Shah, B.A. Wilky, N. Gul, M.A. Carrera-Haro, M. Fogle Ferreira, U. Shafique, J.D. Powell, C.F. Meyer and D.M. Loeb

      Version of Record online: 4 MAR 2013 | DOI: 10.1002/ijc.28083

      What's new?

      Despite promising evidence from in vitro experiments, inhibition of mammalian target of rapamycin (mTOR) has been largely ineffective at preventing the recurrence of sarcoma in patients following cytotoxic chemotherapy. The results of a Phase I/II clinical trial reported here, however, reveal that concurrent administration of the mTOR inhibitor temsirolimus with liposomal doxorubicin may result in increased tumor exposure to the active temsirolimus metabolite, sirolimus. The combination of drugs appeared to be relatively safe for heavily pretreated sarcoma patients. The approach could change existing treatment strategies for certain types of sarcoma.

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      Neoadjuvant epirubicin, gemcitabine and docetaxel for primary breast cancer: Long-term survival data and major prognostic factors based on two consecutive neoadjuvant phase I/II trials (pages 1006–1015)

      Frederik Marmé, Julia Aigner, Justo Lorenzo Bermejo, Peter Sinn, Christof Sohn, Dirk Jäger and Andreas Schneeweiss

      Version of Record online: 16 MAR 2013 | DOI: 10.1002/ijc.28094

      What's new?

      Pathologic complete response (pCR) after neoadjuvant chemotherapy is an important prognostic factor for primary breast cancer and is considered an endpoint for accelerated drug approval. In this long-term follow-up of two consecutive phase I/II trials we demonstrate that molecular features of the tumour and pre-treatment clinical stage play an important prognostic role beyond pCR. Our data suggest a clinical utility for prognostic scoring systems tailored to specific subtypes rather than pCR as a single prognostic factor.

  9. Short Report

    1. Top of page
    2. Mini Reviews
    3. Carcinogenesis
    4. Cancer Cell Biology
    5. Cancer Genetics
    6. Tumor Immunology
    7. Early Detection and Diagnosis
    8. Epidemiology
    9. Cancer Therapy
    10. Short Report
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      Prognostic factors in gemcitabine–cisplatin polychemotherapy regimens in pancreatic cancer: XPD-Lys751Gln polymorphism strikes back (pages 1016–1022)

      Amir Avan, Paola Pacetti, Michele Reni, Michele Milella, Enrico Vasile, Andrea Mambrini, Vanja Vaccaro, Sara Caponi, Stefano Cereda, Godefridus J. Peters, Maurizio Cantore and Elisa Giovannetti

      Version of Record online: 4 MAR 2013 | DOI: 10.1002/ijc.28078

      What's new?

      Recent advances in treatments of pancreatic cancer include a novel combination therapy of cisplatin-gemcitabine-based polychemotherapeutic regimens. However, this treatment shows increased hematologic or extra-hematologic side effects calling for the identification of biomarkers that predict treatment outcome. In this study, the XPD-Lys751Gln gene polymorphism was identified as the most significant independent predictor for death and progression-risk in pancreatic cancer patients who underwent such treatment. Determined by a simple blood test, the polymorphism offers an innovative tool for optimizing palliative chemotherapy in advanced pancreatic cancers. The authors call for prospective trials to validate their findings, which may ultimately lead to a more individualized treatment in selected pancreatic cancer patients.

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