Cancer Research (CANCER RES)

Publisher: American Association for Cancer Research; International Cancer Research Foundation; William H. Donner Foundation, American Association for Cancer Research

Journal description

Cancer Research publishes significant, original studies in all areas of basic, clinical, translational, epidemiological, and prevention research devoted to the study of cancer and cancer-related biomedical sciences. Scientific topics include: biochemistry; chemical, physical, and viral carcinogenesis and mutagenesis; clinical investigations including clinical trials; endocrinology; epidemiology and prevention; experimental therapeutics; immunology and immunotherapy including biological therapy; molecular biology and genetics; radiobiology and radiation oncology; tumor biology; and virology. Thus its publication scope covers all subfields of cancer research. Papers are stringently reviewed and only those that report results of novel, timely, and significant research and meet high standards of scientific merit will be accepted for publication.

Current impact factor: 9.28

Impact Factor Rankings

2015 Impact Factor Available summer 2015
2013 / 2014 Impact Factor 9.284
2012 Impact Factor 8.65
2011 Impact Factor 7.856
2010 Impact Factor 8.234
2009 Impact Factor 7.543
2008 Impact Factor 7.514
2007 Impact Factor 7.672
2006 Impact Factor 7.656
2005 Impact Factor 7.616
2004 Impact Factor 7.69
2003 Impact Factor 8.649
2002 Impact Factor 8.318
2001 Impact Factor 8.302
2000 Impact Factor 8.46
1999 Impact Factor 8.614
1998 Impact Factor 8.37
1997 Impact Factor 8.426
1996 Impact Factor 8.958
1995 Impact Factor 8.206
1994 Impact Factor 6.822
1993 Impact Factor 6.011
1992 Impact Factor 5.156

Impact factor over time

Impact factor
Year

Additional details

5-year impact 8.58
Cited half-life 8.00
Immediacy index 1.54
Eigenfactor 0.30
Article influence 3.08
Website Cancer Research website
Other titles Cancer chemotherapy screening data., Cancer research (Chicago, Ill.), Cancer research
ISSN 0008-5472
OCLC 1553285
Material type Periodical, Internet resource
Document type Journal / Magazine / Newspaper, Internet Resource

Publisher details

American Association for Cancer Research

  • Pre-print
    • Archiving status unclear
  • Post-print
    • Author cannot archive a post-print version
  • Restrictions
    • 12 months embargo
  • Conditions
    • NIH authors may post authors' own version in PubMed Central for release 12 months after publication
    • HHMI, Wellcome Trust, Cancer Research UK and UK Medical Research Council authors may deposit authors own version in Europe PMC for release 6 months after publication
    • AACR will deposit on behalf of these authors, if required
    • Authors final version may be deposited on institutional website or institutional repository if required by institution
    • Published source must be acknowledged
    • Must link to the publisher PDF of article on journal website
  • Classification
    ​ white

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Chemotherapy-induced thrombocytopenia (CIT) can lead to chemotherapy treatment delays or dose reductions. The ability of romiplostim, a thrombopoietin (TPO) mimetic, to promote platelet recovery in a mouse model of multicycle chemotherapy/radiation therapy (CRT)-induced thrombocytopenia was examined. In humans, an inverse relationship between platelet counts and endogenous (e) TPO concentration exists. In a CRT mouse model, eTPO was not elevated during the first 5 days after CRT treatment (the "eTPO gap"), then increased to a peak 10 days after each CRT treatment in an inverse relationship to platelet counts, as seen in humans. To "bridge" the eTPO gap, mice were treated with 10-1000 μg/kg of romiplostim on day 0, 1, or 2 after CRT. In some mice, the romiplostim dose was approximately divided over 3 days. Platelet recovery occurred faster with romiplostim in most conditions tested. Romiplostim doses of >100 μg/kg given on day 0 significantly lessened the platelet nadir. Fractionating the dose over 3 days did not appear to confer a large advantage. These data may provide a rationale for clinical studies of romiplostim in CIT. Copyright © 2015 ISEH - International Society for Experimental Hematology. Published by Elsevier Inc. All rights reserved.
    Cancer Research 03/2015; 73(8 Supplement). DOI:10.1016/j.exphem.2015.02.004
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    ABSTRACT: Breast cancer is a heterogeneous disease characterized by varying response to therapeutic agents and significant differences in long-term survival. Thus there remains an unmet need for early diagnostic and prognostic tools and improved histological characterization for more accurate disease stratification and personalized therapeutic intervention. This study evaluated a comprehensive metabolic phenotyping method in breast cancer tissue that uses desorption electrospray ionization mass spectrometry imaging (DESI MSI), both as a novel diagnostic tool and as a method to further characterize metabolic changes in breast cancer tissue and the tumor microenvironment. In this prospective single centre study, 126 intra-operative tissue biopsies from tumor and tumor bed from 50 patients undergoing surgical resections were subject to DESI MSI. Global DESI MSI models were able to distinguish adipose, stromal and glandular tissue based on their metabolomic fingerprint. Tumor tissue and tumor-associated stroma showed evident changes in their fatty acid and phospholipid composition compared to normal glandular and stromal tissue. Diagnosis of breast cancer was achieved with an accuracy of 98.2% based on DESI MSI data (PPV 0.96, NVP 1, specificity 0.96, sensitivity 1). In the tumor group, correlation between metabolomic profile and tumor grade/hormone receptor status was found. Overall classification accuracy was 87.7% (PPV 0.92, NPV 0.9, specificity 0.9, sensitivity 0.92). These results demonstrate that DESI MSI may be a valuable tool in the improved diagnosis of breast cancer in the future. The identified tumor-associated metabolic changes support theories of de novo lipogenesis in tumor tissue and the role of stroma tissue in tumor growth and development and overall disease prognosis. Copyright © 2015, American Association for Cancer Research.
    Cancer Research 02/2015; DOI:10.1158/0008-5472.CAN-14-2258
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    ABSTRACT: TP53 is the most frequently altered gene in head and neck squamous cell carcinoma (HNSCC) with mutations occurring in over two third of cases, however, the predictive response of these mutations to cisplatin based therapy remains elusive. In the current study, we evaluate the ability of the Evolutionary Action score of TP53 coding variants (EAp53) to predict the impact of TP53 mutations on response to chemotherapy. The EAp53 approach clearly identifies a subset of high risk TP53 mutations associated with decreased sensitivity to cisplatin both in vitro and in vivo in pre-clinical models of HNSCC. Furthermore, EAp53 can predict response to treatment and more importantly a survival benefit for a subset of head and neck cancer patients treated with platinum based therapy. Prospective evaluation of this novel scoring system should enable more precise treatment selection for patients with HNSCC. Copyright © 2015, American Association for Cancer Research.
    Cancer Research 02/2015; DOI:10.1158/0008-5472.CAN-14-2729
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    ABSTRACT: Genetic alterations in the TGFβ signaling pathway in combination with oncogenic alterations lead to cancer development in the intestines. However, the mechanisms of TGFβ signaling suppression in malignant progression of intestinal tumors have not yet been fully understood. We have examined Apc(Δ716) Tgfbr2(ΔIEC) compound mutant mice that carry mutations in Apc and Tgfbr2 genes in the intestinal epithelial cells. We found inflammatory microenvironment only in the invasive intestinal adenocarcinomas but not in noninvasive benign polyps of the same mice. We thus treated simple Tgfbr2(ΔIEC) mice with dextran sodium sulfate (DSS) that causes ulcerative colitis. Importantly, these Tgfbr2(ΔIEC) mice developed invasive colon cancer associated with chronic inflammation. We also found that TGFβ signaling is suppressed in human colitis-associated colon cancer cells. In the mouse invasive tumors, macrophages infiltrated and expressed MT1-MMP, causing MMP2 activation. These results suggest that inflammatory microenvironment contributes to submucosal invasion of TGFβ signaling-repressed epithelial cells through activation of MMP2. We further found that regeneration was impaired in Tgfbr2(ΔIEC) mice for intestinal mucosa damaged by DSS treatment or X-ray irradiation, resulting in the expansion of undifferentiated epithelial cell population. Moreover, organoids of intestinal epithelial cells cultured from irradiated Tgfbr2(ΔIEC) mice formed "long crypts" in Matrigel, suggesting acquisition of an invasive phenotype into the extracellular matrix. These results, taken together, indicate that a simple genetic alteration in the TGFβ signaling pathway in the inflamed and regenerating intestinal mucosa can cause invasive intestinal tumors. Such a mechanism may play a role in the colon carcinogenesis associated with inflammatory bowel disease in humans. Cancer Res; 75(4); 766-76. ©2015 AACR. ©2015 American Association for Cancer Research.
    Cancer Research 02/2015; 75(4):766-76. DOI:10.1158/0008-5472.CAN-14-2036
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    ABSTRACT: Platinum and PARP inhibitor (PARPi) sensitivity commonly coexist in epithelial ovarian cancer (EOC) due to the high prevalence of alterations in the homologous recombination (HR) DNA repair pathway that confer sensitivity to both drugs. In this report, we describe a unique subset of EOC with alterations in another DNA repair pathway, the nucleotide excision repair (NER) pathway, which may exhibit a discordance in sensitivities to these drugs. Specifically, 8% of high-grade serous EOC from The Cancer Genome Atlas dataset exhibited NER alterations, including nonsynonymous or splice site mutations and homozygous deletions of NER genes. Tumors with NER alterations were associated with improved overall survival (OS) and progression-free survival (PFS), compared with patients without NER alterations or BRCA1/2 mutations. Furthermore, patients with tumors with NER alterations had similar OS and PFS as BRCA1/2-mutated patients, suggesting that NER pathway inactivation in EOC conferred enhanced platinum sensitivity, similar to BRCA1/2-mutated tumors. Moreover, two NER mutations (ERCC6-Q524* and ERCC4-A583T), identified in the two most platinum-sensitive tumors, were functionally associated with platinum sensitivity in vitro. Importantly, neither NER alteration affected HR or conferred sensitivity to PARPi or other double-strand break-inducing agents. Overall, our findings reveal a new mechanism of platinum sensitivity in EOC that, unlike defective HR, may lead to a discordance in sensitivity to platinum and PARPi, with potential implications for previously reported and ongoing PARPi trials in this disease. Cancer Res; 75(4); 1-7. ©2014 AACR. ©2014 American Association for Cancer Research.
    Cancer Research 02/2015; 75(4):628-634. DOI:10.1158/0008-5472.CAN-14-2593
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    ABSTRACT: The family of E2F transcription factors is the key downstream target of the retinoblastoma tumor suppressor protein (pRB), which is frequently inactivated in human cancer. E2F is best known for its role in cell-cycle regulation and triggering apoptosis. However, E2F binds to thousands of genes and, thus, could directly influence a number of biologic processes. Given the plethora of potential E2F targets, the major challenge in the field is to identify specific processes in which E2F plays a functional role and the contexts in which a particular subset of E2F targets dictates a biologic outcome. Recent studies implicated E2F in regulation of expression of mitochondria-associated genes. The loss of such regulation results in severe mitochondrial defects. The consequences become evident during irradiation-induced apoptosis, where E2F-deficient cells are insensitive to cell death despite induction of canonical apoptotic genes. Thus, this novel function of E2F may have a major impact on cell viability, and it is independent of induction of apoptotic genes. Here, we discuss the implications of these findings in cancer biology. Cancer Res; 75(4); 1-5. ©2014 AACR. ©2014 American Association for Cancer Research.
    Cancer Research 02/2015; 75(4):619-623. DOI:10.1158/0008-5472.CAN-14-2173
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    ABSTRACT: Chronic inflammation is a hallmark of many cancers, yet the pathogenic mechanisms that distinguish cancer-associated inflammation from benign persistent inflammation are still mainly unclear. Here, we report that the protein kinase ERK5 controls the expression of a specific subset of inflammatory mediators in the mouse epidermis, which triggers the recruitment of inflammatory cells needed to support skin carcinogenesis. Accordingly, inactivation of ERK5 in keratinocytes prevents inflammation-driven tumorigenesis in this model. In addition, we found that anti-ERK5 therapy cooperates synergistically with existing antimitotic regimens, enabling efficacy of subtherapeutic doses. Collectively, our findings identified ERK5 as a mediator of cancer-associated inflammation in the setting of epidermal carcinogenesis. Considering that ERK5 is expressed in almost all tumor types, our findings suggest that targeting tumor-associated inflammation via anti-ERK5 therapy may have broad implications for the treatment of human tumors. Cancer Res; 75(4); 1-12. ©2015 AACR. ©2015 American Association for Cancer Research.
    Cancer Research 02/2015; 75(4). DOI:10.1158/0008-5472.CAN-13-3043
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    ABSTRACT: Asymmetric division is an evolutionarily conserved process that generates daughter cells with different fates through the unequal partitioning of fate determinants. While asymmetric division is critically important in generating diversity during development, its dysregulation can also promote oncogenesis. In particular, signals that shift the normal balance of symmetric and asymmetric division can lead to a differentiation arrest and trigger cancer progression. Here, we discuss the studies that have provided increasing support for this idea. Beginning with original work carried out in Drosophila, we trace more recent work in mammalian systems that suggest that the subversion of asymmetric division can contribute significantly to the development and progression of both hematologic malignancies and solid cancers. Cancer Res; 75(5); 1-6. ©2015 AACR. ©2015 American Association for Cancer Research.
    Cancer Research 02/2015; DOI:10.1158/0008-5472.CAN-14-2750
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    ABSTRACT: Preclinical cancer research would benefit from non-invasive imaging methods that allow tracking and visualization of early stage metastasis in vivo. While fluorescent proteins revolutionized intravital microscopy, two major challenges which still remain are tissue autofluorescence and hemoglobin absorption, which act to limit intravital optical techniques to large or subcutaneous tumors. Here we employ a time-domain technology for the effective separation of tissue autofluorescence from extrinsic fluorophores, based on their distinct fluorescence lifetimes. Additionally, we employ cancer cells labelled with near infra-red fluorescent proteins (iRFP) to allow deep-tissue imaging. Our results demonstrated that time-domain imaging allows the detection of metastasis in deep-seated organs of living mice with a more than 20-fold increase in sensitivity compared to conventional continuous wave techniques. Furthermore, the distinct fluorescence lifetimes of each iRFP enables lifetime multiplexing of three different tumors, each expressing unique iRFP labels in the same animal. Fluorescence tomographic reconstructions reveal 3D distributions of iRFP720-expressing cancer cells in lungs and brain of live mice, allowing ready longitudinal monitoring of cancer cell fate with greater sensitivity than otherwise currently possible. Copyright © 2015, American Association for Cancer Research.
    Cancer Research 02/2015; DOI:10.1158/0008-5472.CAN-14-3001
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    ABSTRACT: Genetically activated kinases have been attractive therapeutic targets in cancer due to the relative ease of developing tumor-specific treatment strategies for them. To discover novel putative oncogenic kinases, we identified 26 genes commonly amplified and overexpressed in breast cancer and subjected them to a lentiviral shRNA cell viability screen in a panel of breast cancer cell lines. Here we report that CLK2, a kinase that phosphorylates SR proteins involved in splicing, acts as an oncogene in breast cancer. Deregulated alternative splicing patterns are commonly observed in human cancers but the underlying mechanisms and functional relevance are still largely unknown. CLK2 is amplified and overexpressed in a significant fraction of breast tumors. Downregulation of CLK2 inhibits breast cancer growth in cell culture and in xenograft models and it enhances cell migration and invasion. Loss of CLK2 in luminal breast cancer cells leads to the upregulation of epithelial to mesenchymal transition (EMT) related genes and a switch to mesenchymal splice variants of several genes including ENAH (MENA). These results imply that therapeutic targeting of CLK2 may be used to modulate epithelial-mesenchymal splicing patterns and to inhibit breast tumor growth. Copyright © 2015, American Association for Cancer Research.
    Cancer Research 02/2015; DOI:10.1158/0008-5472.CAN-14-2443
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    ABSTRACT: Radiotherapy is a curative treatment option in prostate cancer. Nevertheless, patients with high-risk prostate cancer are prone to relapse. Identification of the predictive biomarkers and molecular mechanisms of radioresistance bears promise to improve cancer therapies. In this study, we show that aldehyde dehydrogenase (ALDH) activity is indicative of radioresistant prostate progenitor cells with an enhanced DNA repair capacity and activation of epithelial-mesenchymal transition (EMT). Gene expression profiling of prostate cancer cells, their radioresistant derivatives, ALDH+ and ALDH- cell populations revealed the mechanisms, which link tumor progenitors to radioresistance, including activation of WNT/β-catenin signaling pathway. We found that expression of ALDH1A1 gene is regulated by WNT signaling pathway and co-occurs with expression of β-catenin in prostate tumor specimens. Inhibition of WNT pathway led to a decrease in ALDH+ tumor progenitor population and to radiosensitization of cancer cells. Taken together, our results indicate that ALDH+ cells contribute to tumor radioresistance and their molecular targeting may enhance the effectiveness of radiotherapy.
    Cancer Research 02/2015; DOI:10.1158/0008-5472.CAN-14-1924
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    ABSTRACT: Excess production of the pro-inflammatory interleukin IL-6 has both local and systemic tumor-promoting activity in many cancers, including ovarian cancer. However, treatment of advanced ovarian cancer patients with a neutralizing IL-6 antibody yielded little efficacy in a previous Phase II clinical trial. Here we report results that may explain this outcome, based on the finding that neutralizing antibodies to IL-6 and STAT3 inhibition are sufficient to up-regulate the EGFR pathway in high-grade serous and other ovarian cancer cells. Cell treatment with the EGFR inhibitor gefitinib abolished upregulation of the EGFR pathway. Combining neutralizing IL-6 antibodies and gefitinib inhibited malignant cell growth in 2D and 3D culture. We found that ErbB-1 was localized predominantly in the nucleus of ovarian cancer cells examined, contrasting with plasma membrane localization in lung cancer cells. Treatment with anti-IL-6, gefitinib or their combination all led to partial restoration of ErbB-1 on the plasma membrane. In vivo experiments confirmed the effects of IL-6 inhibition on the EGFR pathway and the enhanced activity of a combination of anti-IL-6 antibodies and gefitinib on malignant cell growth. Taken together, our results offer a preclinical rationale to combine anti-IL-6 and gefitinib to treat patients with advanced stage ovarian cancer. Copyright © 2015, American Association for Cancer Research.
    Cancer Research 02/2015; DOI:10.1158/0008-5472.CAN-14-1801
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    ABSTRACT: Tumor protein phosphorylation analysis may provide insight into intracellular signaling networks underlying tumor behavior, revealing diagnostic, prognostic or therapeutic information. Human tumors collected by The Cancer Genome Atlas (TCGA) program potentially offer the opportunity to characterize activated networks driving tumor progression, in parallel with the genetic and transcriptional landscape already documented for these tumors. However, a critical question is whether cellular signaling networks can be reliably analyzed in surgical specimens, where freezing delays and spatial sampling disparities may potentially obscure physiological signaling. To quantify the extent of these effects, we analyzed the stability of phosphotyrosine (pTyr) sites in ovarian and colon tumors collected under conditions of controlled ischemia and in the context of defined intratumoral sampling. Cold-ischemia produced a rapid, unpredictable, and widespread impact on tumor pTyr networks within 5 minutes of resection, altering up to 50% of pTyr sites by more than 2-fold. Effects on adhesion and migration, inflammatory response, proliferation, and stress response pathways were recapitulated in both ovarian and colon tumors. Additionally, sampling of spatially distinct colon tumor biopsies revealed pTyr differences as dramatic as those associated with ischemic times, despite uniform protein expression profiles. Moreover, intra-tumoral spatial heterogeneity and pTyr dynamic response to ischemia varied dramatically between tumors collected from different patients. Overall, these findings reveal unforeseen phosphorylation complexity, thereby increasing the difficulty of extracting physiologically relevant pTyr signaling networks from archived tissue specimens. In light of this data, prospective tumor pTyr analysis will require appropriate sampling and collection protocols to preserve in vivo signaling features. Copyright © 2015, American Association for Cancer Research.
    Cancer Research 02/2015; DOI:10.1158/0008-5472.CAN-14-2309
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    ABSTRACT: Tumor-infiltrating lymphocytes are key mediators of tumor immune surveillance and are important prognostic indicators in cancer progression. Among the various lymphocyte subsets implicated in protection against cancer are γδ T lymphocytes, which can kill tumor cells and secrete potent antitumor cytokines. By contrast, recent reports have revealed an unexpected series of protumor functions of γδ T cells in mouse models and human patients. In particular, specific γδ T-cell subsets are capable of recruiting immunosuppressive myeloid populations, inhibiting antitumor responses, and enhancing angiogenesis, thus promoting cancer progression. A common mediator of such functions appears to be the cytokine IL17, whose pathogenic effects can override the antitumor immune response orchestrated by IFNγ. Here, we review these studies and discuss their implications for the manipulation of γδ T cells in cancer immunotherapy. Cancer Res; 75(5); 1-5. ©2014 AACR. ©2015 American Association for Cancer Research.
    Cancer Research 02/2015; DOI:10.1158/0008-5472.CAN-14-3228
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    ABSTRACT: Pregnancy at early, but not late age, has a strong and life-long protective effect against breast cancer. The expected overall increase in breast cancer incidence demands the development of a pharmaceutical mimicry of early-age pregnancy-mediated protection. Recently, converging results from rodent models and women on molecular and cellular mechanisms underlying the protective effect of early-age pregnancy have opened the door for translational studies on pharmacologic prevention against breast cancer. In particular, alterations in Wnt and TGFβ signaling in mammary stem/progenitor cells reveal new potential targets for preventive interventions, and thus might help to significantly reduce the incidence of breast cancer in the future. Cancer Res; 1-5. ©2014 AACR. ©2015 American Association for Cancer Research.
    Cancer Research 02/2015; DOI:10.1158/0008-5472.CAN-14-2717
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    ABSTRACT: miRNAs are important regulatory elements for gene expression that are involved in diverse physiologic and pathologic processes. Canonical miRNA biogenesis consists of a two-step processing, from primary transcripts (pri-miRNA) to precursor miRNAs (pre-miRNA) mediated by Drosha in the nucleus and from pre-miRNAs to mature miRNAs mediated by Dicer in the cytoplasm. Various routes of miRNA maturation that are tightly regulated by signaling cascades and specific to an individual or a subclass of miRNAs have been recently identified. Here, we review the current findings in signaling-mediated miRNA processing as well as their potential clinical relevance in cancer. Cancer Res; 75(5); 1-9. ©2014 AACR. ©2015 American Association for Cancer Research.
    Cancer Research 02/2015; DOI:10.1158/0008-5472.CAN-14-2568
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    ABSTRACT: Breast cancer stem cells (BCSC) are resistant to conventional chemotherapy and radiation, which may destroy tumor masses but not all BCSC that can mediate relapses. In the present study, we showed that the level of Wnt/β-catenin signaling in BCSC is relatively higher than in bulk tumor cells, contributing to a relatively higher level of therapeutic resistance. We designed a highly potent small molecule inhibitor, CWP232228, which antagonizes binding of β-catenin to TCF in the nucleus. Notably, although CWP232228 inhibited the growth of both BCSC and bulk tumor cells by inhibiting β-catenin-mediated transcription, BCSC exhibited greater growth inhibition than bulk tumor cells. We also documented evidence of greater insulin-like growth factor-I (IGF-I) expression by BCSC than by bulk tumor cells, and that CWP232228 attenuated IGF-I mediated BCSC functions. These results suggested that the inhibitory effect of CWP232228 on BCSC growth might achieved through the disruption of IGF-I activity. Taken together, our findings indicate that CWP232228 offers a candidate therapeutic agent for breast cancer that preferentially targets BCSC as well as bulk tumor cells. Copyright © 2015, American Association for Cancer Research.
    Cancer Research 02/2015; DOI:10.1158/0008-5472.CAN-14-2041
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    ABSTRACT: The ability of chemotherapeutic agents to induce apoptosis, predominantly via the mitochondrial (intrinsic) apoptotic pathway, is thought to be a major determinant of the sensitivity of a given cancer to treatment. Intrinsic apoptosis, regulated by the BCL-2 family, integrates diverse apoptotic signals to determine cell death commitment and then activates the nodal effector protein BAK to initiate the apoptotic cascade. In this study, we identified the tyrosine kinase BMX as a direct negative regulator of BAK function. BMX associates with BAK in viable cells and is the first kinase to phosphorylate the key tyrosine residue needed to maintain BAK in an inactive conformation. Importantly, elevated BMX expression prevents BAK activation in tumor cells treated with chemotherapeutic agents and is associated with increased resistance to apoptosis and decreased patient survival. Accordingly, BMX expression was elevated in prostate, breast and colon cancers compared to normal tissue, including in aggressive triple-negative breast cancers where BMX over-expression may be a novel biomarker. Furthermore, BMX silencing potentiated BAK activation rendering tumor cells hypersensitive to otherwise sublethal doses of clinically relevant chemotherapeutic agents. Our finding that BMX directly inhibits a core component of the intrinsic apoptosis machinery opens opportunities to improve the efficacy of existing chemotherapy by potentiating BAK-driven cell death in cancer cells. Copyright © 2015, American Association for Cancer Research.
    Cancer Research 02/2015; DOI:10.1158/0008-5472.CAN-14-1340