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  • American Association for Cancer Research (AACR)  (7)
  • 1
    Online Resource
    Online Resource
    Abstract B1: Heme oxygenase-1 transcription controlling GTn repeat polymorphism has contrary prognostic value in squamous cell carcinoma and adenocarcinoma of the esophagus
    American Association for Cancer Research (AACR) ; 2010
    In:  Clinical Cancer Research Vol. 16, No. 7_Supplement ( 2010-04-01), p. B1-B1
    Details
    In: Clinical Cancer Research, American Association for Cancer Research (AACR), Vol. 16, No. 7_Supplement ( 2010-04-01), p. B1-B1
    Abstract: Purpose: The regulation of basal transcription of heme oxygenase-1 (HO-1) is dependent upon a GTn repeat polymorphism (GTn) in the promoter of the heme oxygenase-1 gene (HMOX-1). Here, we evaluate the role of GTn in surgically resected esophageal cancer patients without neoadjuvant or adjuvant treatment. Patients and Methods: Genomic DNA was extracted from peripheral blood leucocytes of 297 patients. To determine the number of the GTn repeats DNA was amplified by RT-PCR and sequenced. The results were correlated with clinicopathological parameters, disseminated tumor cells (DTC) and clinical outcome. Results: Three genotypes (SS, SL and LL) were defined based on cut-off points for short allele (“S”) with GTn repeats & lt;25 and ≥25 as long allele (“L”). Throughout all analyses a contrary role of GTn was evident in squamous cell carcinoma (SCC) and adenocarcinoma (AC) patients. In SCC patients the SS genotype patients presented with less aggressive tumors in terms of tumor size, presence of regional and non-regional lymph node metastases, DTC and lower relapse rate compared to SL and LL genotype patients. In contrast, in AC patients the SS genotype patients displayed more aggressive tumor biology with bigger tumors, a higher rate of lymph node metastases, DTC as well as tumor recurrence compared to LL and SL genotype patients. The disease-free and overall survival in SCC patients was markedly reduced in LL genotypes compared to SL and SS genotypes. To the contrary, in AC the SS genotype patients displayed the worst disease-free and overall survival. Conclusion: GTn was identified as an independent prognostic factor with contrary prognostic value for tumor recurrence and death in the two subtypes of esophageal cancer, SCC and AC. Citation Information: Clin Cancer Res 2010;16(7 Suppl):B1
    Type of Medium: Online Resource
    ISSN: 1078-0432 , 1557-3265
    URL: Article
    DOI: 10.1158/1078-0432.TCME10-B1
    RVK:
    XA 36791
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2010
    detail.hit.zdb_id: 1225457-5
    detail.hit.zdb_id: 2036787-9
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  • 2
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    Online Resource
    Improved Risk Stratification by Circulating Tumor Cell Counts in Pancreatic Cancer
    American Association for Cancer Research (AACR) ; 2018
    In:  Clinical Cancer Research Vol. 24, No. 12 ( 2018-06-15), p. 2844-2850
    Details
    In: Clinical Cancer Research, American Association for Cancer Research (AACR), Vol. 24, No. 12 ( 2018-06-15), p. 2844-2850
    Abstract: Purpose: Pancreatic cancer is one of the most devastating diseases with a 5-year survival rate of 3% to 5%. Here, we investigated whether circulating tumor cells (CTC) may predict metastatic spread and survival in pancreatic cancer patients. Experimental Design: In a prospective study, we enrolled 69 pancreatic cancer patients. In peripheral blood, CTCs were identified by MACS enrichment (anti-cytokeratin/anti-EpCam) and subsequent automated analysis after combined anti-cytokeratin/anti-CD45/DAPI staining. CTC results were correlated to established clinicopathologic risk factors, detection of disseminated tumor cells (DTC) in bone marrow, and clinical outcome (follow-up time: 48 months). Results: Median patient survival was 11 months (0–48 months). Thirty-eight patients were male and 31 were female, and the majority received gemcitabine (58/69). CTCs were present in 23 of 69 patients (33.3%) ranging from 1 to 19 cells (17 with & gt;1 CTC). Although clinicopathologic parameters and DTC status did not correlate with CTC incidence, progression-free survival (PFS) and overall survival (OS) were significantly reduced in CTC-positive patients in univariate (P = 0.009, PFS; P = 0.030, OS, both log rank) and multivariate analysis [HR = 4.543; confidence interval (CI), 1.549–13.329; P = 0.006, PFS; HR = 2.093; CI, 1.081–4.050; P = 0.028, OS, both Cox regression). Also within patients receiving chemotherapy, PFS was significantly reduced in CTC-positive patients in univariate (P = 0.013) and multivariate (HR = 4.203; CI, 1.416–12.471; P = 0.010) analysis. Conclusions: CTCs affect the outcome of patients with pancreatic cancer independent from other risk factors, including patients receiving (adjuvant) cytotoxic therapy. CTC stratification may allow a better upfront identification of patients with a longer lifespan who might profit from new adjuvant therapies. Clin Cancer Res; 24(12); 2844–50. ©2018 AACR.
    Type of Medium: Online Resource
    ISSN: 1078-0432 , 1557-3265
    URL: Article
    DOI: 10.1158/1078-0432.CCR-18-0120
    RVK:
    XA 36791
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2018
    detail.hit.zdb_id: 1225457-5
    detail.hit.zdb_id: 2036787-9
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  • 3
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    Online Resource
    Abstract 4547: Clinical relevance of circulating tumor cells in esophageal cancer
    American Association for Cancer Research (AACR) ; 2012
    In:  Cancer Research Vol. 72, No. 8_Supplement ( 2012-04-15), p. 4547-4547
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 72, No. 8_Supplement ( 2012-04-15), p. 4547-4547
    Abstract: Background: Current modalities to predict tumor recurrence and survival in esophageal cancer are insufficient. Locoregional and distant relapse is even common in lymph node-negative patients and more precise staging methods are therefore needed. Little is known about the utility of circulating tumor cells (CTC) as staging tool in esophageal cancer. Methods: In a prospective study we identified CTC in peripheral blood of esophageal cancer patients by two separate methods. We enrolled 85 consecutive esophageal cancer patients (03/2010-10/2011) who were surgically resected (R0) and patients received neither neoadjuvant nor adjuvant therapy. Peripheral blood was taken at the time of primary surgery and CTC were detected by either manual MACS enrichment (anti-cytokeratin plus anti-EpCam) with subsequent anti-cytokeratin staining or the automated CellSearch system (cleared by the FDA for CTC detection in metastatic breast, colon and prostate cancer) in parallel. CTC detection rates and correlation with clinicopathologic parameters were evaluated. The median clinical follow-up time is 11 months ranging from 1 to 19 months. Results: So far, 67 patients have been analysed of which 21 (31.3%) had CTCs using MACS, and 10 (14.9%) using CellSearch. CTCs detected with MACS significantly correlated with tumor size (p=0.040) and aggressive tumor biology as indicated by presence of regional lymph node (p=0.040) and distant metastases (p=0.019). CTCs detected with CellSearch correlated significantly with lymph node (p=0.044) and distant metastases (p=0.045), while no correlation was observed for tumor size or grading. CTC-positive patients had a worse overall survival than CTC-negative patients when tested with the CellSearch system (p=0.009). Conclusion: The presence of CTCs in patients with resectable esophageal cancer correlates with clinicopathologic risk factors.and predicts an unfavorable prognosis. Thus, our pilot study suggests that CTC detection may contribute to an improved staging in esophageal cancer. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 4547. doi:1538-7445.AM2012-4547
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2012-4547
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2012
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 4
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    Online Resource
    Differential Gene Expression in Metastasizing Cells Shed from Kidney Tumors
    American Association for Cancer Research (AACR) ; 2004
    In:  Cancer Research Vol. 64, No. 7 ( 2004-04-01), p. 2469-2473
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 64, No. 7 ( 2004-04-01), p. 2469-2473
    Abstract: We developed a novel orthotopic mouse tumor model of renal cell carcinoma to collect and characterize cells spontaneously shed from SN12C (renal cell carcinoma) and SN12L1 (high metastatic variant of SN12C) tumors grown in kidneys of severe combined immunodeficient mice. Viability of the shed cell population was greater for SN12L1 tumors (25%) compared with SN12C tumors (11%, P & lt; 0.05). Gene array analysis of 23 genes involved in metastasis showed that CD44, α3 integrin, and caveolin were down-regulated in the shed tumor cells compared with their primary counterparts, and blocking α3 integrin or CD44 function inhibited attachment and migration of both cell lines. These results suggest that cohesion of the cells within the primary tumor mediated by CD44 and α3 integrins hinders metastasis and that shedding is a passive process not necessarily mediated by cell migration in these tumors. Furthermore, resistance to apoptosis may enhance metastasis in the higher metastatic tumor.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/0008-5472.CAN-03-0256
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2004
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 5
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    Online Resource
    Notch Signaling Activated by Replication Stress–Induced Expression of Midkine Drives Epithelial–Mesenchymal Transition and Chemoresistance in Pancreatic Cancer
    American Association for Cancer Research (AACR) ; 2011
    In:  Cancer Research Vol. 71, No. 14 ( 2011-07-15), p. 5009-5019
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 71, No. 14 ( 2011-07-15), p. 5009-5019
    Abstract: The incidence of pancreatic ductal adenocarcinoma (PDAC) nearly equals its mortality rate, partly because most PDACs are intrinsically chemoresistant and thus largely untreatable. It was found recently that chemoresistant PDAC cells overexpress the Notch-2 receptor and have undergone epithelial–mesenchymal transition (EMT). In this study, we show that these two phenotypes are interrelated by expression of Midkine (MK), a heparin-binding growth factor that is widely overexpressed in chemoresistant PDAC. Gemcitabine, the front-line chemotherapy used in PDAC treatment, induced MK expression in a dose-dependent manner, and its RNAi-mediated depletion was associated with sensitization to gemcitabine treatment. We identified an interaction between the Notch-2 receptor and MK in PDAC cells. MK–Notch-2 interaction activated Notch signaling, induced EMT, upregulated NF-κB, and increased chemoresistance. Taken together, our findings define an important pathway of chemoresistance in PDAC and suggest novel strategies for its clinical attack. Cancer Res; 71(14); 5009–19. ©2011 AACR.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/0008-5472.CAN-11-0036
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2011
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 6
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    The Multifunctional Growth Factor Midkine Promotes Proliferation and Migration in Pancreatic Cancer
    American Association for Cancer Research (AACR) ; 2014
    In:  Molecular Cancer Research Vol. 12, No. 5 ( 2014-05-01), p. 670-680
    Details
    In: Molecular Cancer Research, American Association for Cancer Research (AACR), Vol. 12, No. 5 ( 2014-05-01), p. 670-680
    Abstract: Pancreatic ductal adenocarcinoma (PDAC) has a devastating prognosis among solid tumors and despite increased knowledge of the molecular mechanisms contributing to progression and metastasis, minimal progress has been done in establishing new targeted therapies for this deadly disease. The expression of the multifunctional growth/differentiation factor midkine (MK) promotes a variety of cellular functions leading to increased angiogenesis, proliferation, migration, and survival. Moreover, MK is intensively discussed as a potential new-therapy target and as biomarker for cancer progression and chemotherapeutic resistance in multiple cancers. Therefore, the present study investigated the molecular role of MK in pancreatic cancer. It was found that MK is elevated in PDAC and differentially expressed in other histologic subtypes of pancreatic cancer, whereas normal pancreatic cells did not express MK, thus making it an attractive candidate for targeted therapies. As a secreted growth/differentiation factor, MK was investigated as a biomarker in clinical serum specimens using ELISA. In addition, knockdown studies of MK revealed a link to proliferation and migration status in vitro. Finally, upstream signaling pathways were analyzed, with TNF-α and EGF being the main inductors of MK expression in PDAC. Implications: This study presents novel MK functions and new upstream signaling effectors that induce its expression to promote PDAC and therefore defines an attractive new therapeutic target in pancreatic cancer. Mol Cancer Res; 12(5); 670–80. ©2014 AACR.
    Type of Medium: Online Resource
    ISSN: 1541-7786 , 1557-3125
    URL: Article
    DOI: 10.1158/1541-7786.MCR-13-0467
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2014
    detail.hit.zdb_id: 2097884-4
    SSG: 12
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  • 7
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    ABO Blood Group IgM Isoagglutinins Interact with Tumor-Associated O-Glycan Structures in Pancreatic Cancer
    American Association for Cancer Research (AACR) ; 2014
    In:  Clinical Cancer Research Vol. 20, No. 23 ( 2014-12-01), p. 6117-6126
    Details
    In: Clinical Cancer Research, American Association for Cancer Research (AACR), Vol. 20, No. 23 ( 2014-12-01), p. 6117-6126
    Type of Medium: Online Resource
    ISSN: 1078-0432 , 1557-3265
    URL: Article
    DOI: 10.1158/1078-0432.CCR-14-0716
    RVK:
    XA 36791
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2014
    detail.hit.zdb_id: 1225457-5
    detail.hit.zdb_id: 2036787-9
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