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  • ONCOLOGY  (41)
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  • 1
    Keywords: CANCER ; EXPRESSION ; tumor ; carcinoma ; CELL ; Germany ; incidence ; GENE ; GENES ; HYBRIDIZATION ; microarray ; cell line ; DIFFERENTIATION ; TISSUE ; LINES ; ACTIVATION ; DNA ; FAMILY ; CELL-LINES ; MEMBER ; MEMBERS ; BREAST-CANCER ; cytokines ; IDENTIFICATION ; AMPLIFICATION ; COMPARATIVE GENOMIC HYBRIDIZATION ; microarrays ; NUMBER ; CHROMOSOMAL-ABERRATIONS ; CELL-LINE ; LINE ; PCR ; REGION ; REGIONS ; adenocarcinoma ; CANCER-RESEARCH ; FREQUENT ; REVEALS ; IMBALANCES ; OVEREXPRESSION ; cell lines ; pancreatic cancer ; pancreatic carcinoma ; GENOMIC HYBRIDIZATION ; HIGH-LEVEL ; CYTOKINE ; ONCOLOGY ; SUBSET ; RE ; PANCREATIC-CANCER ; FAMILIES ; AMPLIFICATIONS ; LEADS ; CANDIDATE GENES ; REAL-TIME ; EGFR ; MALT-LYMPHOMA
    Abstract: Genomic analyses aimed at the detection of high-level DNA amplifications were performed on 13 widely used pancreatic cancer cell lines and 6 pancreatic tumor specimens. For these analyses, array-based comparative genomic hybridization (Matrix-CGH) onto dedicated microarrays was used. In comparison with chromosomal CGH (eight amplifications), a 〉3-fold number of DNA amplifications was detected (n = 29). The most frequent amplifications mapped to 7p12.3 (three pancreatic cancer cell lines and three pancreatic tumor specimens), 8q24 (four pancreatic cancer cell lines and one pancreatic tumor specimen), 11q13 (three pancreatic cancer cell lines and three pancreatic tumor specimens), and 20q13 (four pancreatic cancer cell lines and three pancreatic tumor specimens). Genes contained in the consensus regions were MYC (8q24), EGFR (7p12.3), and FGF3 (11q13). In six of seven pancreatic cancer cell lines and pancreatic tumor specimens with 20q13 amplifications, the novel candidate gene NFAT C2, which plays a role in the activation of cytokines, was amplified. Other amplifications also affected genes for which a pathogenetic role in pancreatic carcinoma has not been described, such as BCL10 and BCL6, two members of the BCL family. A subset of amplified genes was checked for overexpression by means of real-time PCR, revealing the highest expression levels for BCL6 and BCL10. Thus, Matrix-CGH allows the detection of a high number of amplifications, resulting in the identification of novel candidate genes in pancreatic cancer
    Type of Publication: Journal article published
    PubMed ID: 15231651
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  • 2
    Keywords: APOPTOSIS ; CANCER ; CELLS ; EXPRESSION ; SURVIVAL ; CELL ; Germany ; GENE ; GENES ; PROTEIN ; SAMPLES ; cell cycle ; CELL-CYCLE ; DOWN-REGULATION ; TARGET ; DELETION ; LYMPHOMA ; MUTATION ; COMPONENT ; inactivation ; PATHOGENESIS ; MUTATIONS ; B-CELLS ; DEGRADATION ; POLYMERASE-CHAIN-REACTION ; point mutation ; REGULATOR ; TRANSCRIPTS ; ONCOLOGY ; TUMOR-SUPPRESSOR ; CLL ; ATM MUTATIONS ; POINT MUTATIONS ; LEVEL ; TARGET GENES ; analysis ; leukaemia ; ATM ; PP2A ; PHOSPHATASE ; CONFORMATION ; B-CELL ; apoptosis regulation ; B-cell chronic lymphocytic ; 11q22-q23 ; CUL5 ; NPAT ; PHOSPHATASE 2A ; PPP2R1B
    Abstract: Deletion of 11q22-q23 is associated with an aggressive course of B-cell chronic lymphocytic leukaemia (B-CLL). Since only in a subset of these cases biallelic inactivation of ATM was observed, we sought to identify other disease-associated genes within 11q22-q23 by analysing NFAT (cell-cycle regulation), CUL5 (ubiquitin-dependent apoptosis regulation) and PPP2R1B (component of the cell-cycle and apoptosis regulating PP2A) for point mutations and their expression in B-CLL by single-strand conformation polymorphism/sequence analysis of the transcripts and real-time polymerase chain reaction. Though none of the genes were affected by deleterious mutations, we observed a significant down-regulation of NPAT in B-CLL versus CD19+ B cells and of CUL5 in 11q deletion versus non-deletion B-CLL samples and measured reduced PPP2R1B transcript levels in a subset of B-CLL cases. Alternative splicing of PPP2R1B transcripts (skipping of exons 2/3, 3, 9) was associated with a reduced activity of protein phosphatase 2A. Together, these results implicate deregulation of the cell-cycle and apoptosis regulators NPAT, CUL5 and PPP2R1B and a role for these genes in the pathogenesis of B-CLL. (C) 2007 Elsevier Ltd. All rights reserved
    Type of Publication: Journal article published
    PubMed ID: 17449237
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  • 3
    Keywords: APOPTOSIS ; EXPRESSION ; tumor ; CELL ; Germany ; human ; GENE ; GENES ; HYBRIDIZATION ; microarray ; PROTEIN ; SAMPLE ; SAMPLES ; transcription ; cell line ; RESOLUTION ; LINES ; NF-KAPPA-B ; ACTIVATION ; DNA ; primary ; BASE ; ANTIGEN ; CELL-LINES ; FREQUENCY ; FREQUENCIES ; AMPLIFICATION ; COMPARATIVE GENOMIC HYBRIDIZATION ; COPY NUMBER ; immunohistochemistry ; LYMPHOMA ; NUMBER ; CELL-LINE ; leukemia ; LINE ; REGION ; REGIONS ; LOCALIZATION ; leukocyte ; NF-kappa B ; DNA AMPLIFICATION ; CHROMOSOMAL LOCALIZATION ; cell lines ; GAINS ; non-hodgkin's lymphoma ; B-CELL LYMPHOMA ; HIGH-FREQUENCY ; MATRIX ; FEATURES ; ONCOLOGY ; HIGH-RESOLUTION ; CANDIDATE GENES ; DEFECTS ; ACTIVATOR ; analysis ; GENOTYPE ; LOSSES ; CANDIDATE ; HODGKIN LYMPHOMA ; genomic ; DEFECT ; B-CELL ; GENOMIC ALTERATIONS ; ARRAY CGH ; ARRAY-CGH ; POINT ; DNA-CHIP HYBRIDIZATION ; mediastinal B-cell lymphoma ; array-based comparative genomic hybridization ; NUCLEAR ACCUMULATION
    Abstract: Primary mediastinal B-cell lymphoma (PMBL) is an aggressive extranodal B-cell non-Hodgkin's lymphoma with specific clinical, histopathological and genomic features. To characterize further the genotype of PMBL, we analyzed 37 tumor samples and PMBL cell lines Med-B1 and Karpas1106P using array-based comparative genomic hybridization (matrix- or array-CGH) to a 2.8k genomic microarray. Due to a higher genomic resolution, we identified altered chromosomal regions in much higher frequencies compared with standard CGH: for example, +9p24 (68%), +2p15 (51%), +7q22 (32%), +9q34 (32%), +11q23 (18%), +12q (30%) and +18q21 (24%). Moreover, previously unknown small interstitial chromosomal low copy number alterations (for example, -6p21, -11q13.3) and a total of 19 DNA amplifications were identified by array-CGH. For 17 chromosomal localizations (10 gains and 7 losses), which were altered in more than 10% of the analyzed cases, we delineated minimal consensus regions based on genomic base pair positions. These regions and selected immunohistochemistries point to candidate genes that are discussed in the context of NF-kappa B transcription activation, human leukocyte antigen class I/II defects, impaired apoptosis and Janus kinase/signal transducer and activator of transcription (JAK/STAT) activation. Our data confirm the genomic uniqueness of this tumor and provide physically mapped genomic regions of interest for focused candidate gene analysis
    Type of Publication: Journal article published
    PubMed ID: 17728785
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  • 4
    Keywords: CANCER ; EXPRESSION ; CELL ; Germany ; IN-VIVO ; THERAPY ; DISEASE ; RISK ; GENE ; GENE-EXPRESSION ; GENES ; PATIENT ; ASSOCIATION ; DELETION ; COMPARATIVE GENOMIC HYBRIDIZATION ; gene expression ; DIFFERENCE ; NUMBER ; genetics ; leukemia ; DELETIONS ; REGION ; REGIONS ; HIGH-RISK ; CHILDREN ; CHRONIC MYELOGENOUS LEUKEMIA ; PROGNOSTIC FACTOR ; heredity ; ONCOLOGY ; CHILDHOOD ; THERAPIES ; PROGNOSTIC IMPACT ; CELL LYMPHOMA ; PROGNOSTIC-FACTOR ; USA ; LOSSES ; ARRAY-CGH ; PROFILE ; DERIVATIVE CHROMOSOME-9 ; EARLY TREATMENT RESPONSE ; INTRACHROMOSOMAL AMPLIFICATION ; TRANSLOCATION T(1/19)
    Abstract: In vivo response to initial therapy, as assessed by determination of minimal residual disease (MRD) after 5 and 12 weeks of treatment, has evolved as a strong prognostic factor in children with acute lymphoblastic leukemia (ALL) treated according to the BFM regime. Individual treatment response may be influenced by copy number alterations (CNA) leading to altered gene expression. We aimed to evaluate CNA using high-resolution array-comparative genomic hybridization (array-CGH) in different treatment-response groups. Leukemic genomic profiles of 25 standard risk (MRD-SR) and 25 high risk (MRD-HR) patients were compared. CNAs were found in 46/50 patients (92%). The most significant difference was a gain of 1q23-qter because of an unbalanced t(1; 19), found in 10/25 MRD-SR patients, but in none of the MRD-HR patients (P 〈 0.001). The most frequent Cl in the MRD-HR group were deletions of genomic regions harboring the immunoglobulin genes (1g), e.g., 2p11.2 in 60% of MRD-HR compared to 28% of MRD-SR (P = 0.045). Combining all 1g loci, significantly more MRD-HR than MRD-SR patients displayed deletions (17:8 patients, P = 0.02). Frequency of other CNAs, such as loss of 9p21 or gains of 21q, did not differ strongly between the two patient groups. This is the first study evaluating the clinical significance of CNA as detected by array-CGH in childhood ALL and the first to suggest that such analyses may provide clinically important data. This article contains Supplementary Material available at http://www.interscience.wiley.com/jpages/1045-2257/suppmat. (C) 2008 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 18311775
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  • 5
    Keywords: APOPTOSIS ; EXPRESSION ; GROWTH ; proliferation ; tumor ; carcinoma ; CELL ; FACTOR RECEPTOR ; Germany ; human ; KINASE ; PATHWAY ; PATHWAYS ; DISTINCT ; GENE ; GENE-EXPRESSION ; GENES ; microarray ; PROTEIN ; PROTEINS ; SAMPLE ; SAMPLES ; TISSUE ; ACTIVATION ; primary ; PROTEIN-KINASE ; ASSOCIATION ; MAP KINASE ; score ; STAGE ; NEOPLASIA ; immunohistochemistry ; gene expression ; metastases ; ABERRATIONS ; SIGNALING PATHWAY ; RELIABILITY ; HEAD ; squamous cell carcinoma ; GROWTH-FACTOR-BETA ; MICROARRAY ANALYSIS ; gene expression profiling ; CHRONIC LYMPHOCYTIC-LEUKEMIA ; protein expression ; EPIDERMAL-GROWTH-FACTOR ; NECK-CANCER ; signaling ; molecular ; CELL CARCINOMA ; ONCOLOGY ; INCREASE ; analysis ; CHIP ; USA ; lymph node metastases ; SQUAMOUS-CELL ; HUMAN HEPATOCELLULAR-CARCINOMA ; SET ; COLLECTION ; DETECT ; MAP-KINASE ; GENE-ONTOLOGY
    Abstract: In an attempt to further elucidate the pathomechanisms in oral squamous cell carcinoma (OSCC), gene expression profiling was performed using a whole-transcriptome chip that contains 35,035 gene-specific 70mere oligonucleotides (Human OligoSet 4.0; Operon, Cologne, Germany) to a set of 35 primary OSCCs. Altogether, 7390 genes were found differentially expressed between OSCC tumor samples and oral mucosa. To characterize the major biologic processes in this tumor collection, MAPPFinder, a component of GenMAPP version 2.1, was applied to this data set to generate a statistically ranked list of molecular signaling pathways. Among others, cancer-related pathways, such as mitogen-activated protein (MAP) kinase signaling (z score = 4.6, P 〈 .001), transforming growth factor-beta signaling (z score = 3.0, P = .015), and signaling pathways involved in apoptosis (z score = 2.1, P = .037), were found deregulated in the OSCC collection analyzed. Focusing on the MAP kinase signaling pathway, subsequent tissue microarray analyses by immunohistochemistry revealed an increase in protein expression of MAP kinase-related proteins ERK1 in 22.8% (48 of 209) and ERK5 in 27.4% (76 of 277), respectively. An association of high ERK5 but not of high ERK1 expression with advanced tumor stage and the presence of lymph node metastases was found (P = .008 and P = .016, respectively). Our analysis demonstrates the reliability of the combined approach of gene expression profiling, signaling pathway analyses, and tissue microarray analysis to detect novel distinct molecular aberrations in OSCC
    Type of Publication: Journal article published
    PubMed ID: 18472963
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  • 6
    Keywords: CANCER ; SURVIVAL ; Germany ; MODEL ; GENE ; GENES ; RNA ; CYCLE ; SUPPRESSION ; MOUSE ; REGION ; ONCOLOGY ; chronic lymphocytic leukemia ; GENOMIC ABERRATIONS ; B-CELL ; MIR-15A
    Abstract: miR-15a and miR-16-1 were the first microRNAs linked to cancer because their genes are commonly deleted in human chronic lymphocytic leukemia (CLL). In this issue of Cancer Cell, Klein and coworkers show that deleting a region with these genes in mouse provides a faithful model for human CLL
    Type of Publication: Journal article published
    PubMed ID: 20129242
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  • 7
    Keywords: brain ; tumor ; Germany ; MODEL ; MODELS ; ALGORITHM ; screening ; SYSTEM ; COHORT ; RISK ; HYBRIDIZATION ; TUMORS ; PATIENT ; ACTIVATION ; DNA ; MARKER ; IMPACT ; prognosis ; BIOLOGY ; DELETION ; IN-SITU ; AMPLIFICATION ; COMPARATIVE GENOMIC HYBRIDIZATION ; NUMBER ; ABERRATIONS ; MARKERS ; ONCOGENE ; beta-catenin ; PROGNOSTIC VALUE ; OUTCOMES ; CHILDREN ; ONCOLOGY ; ADULT ; ADULTS ; CHILDHOOD ; brain tumor ; GENOMIC ABERRATIONS ; DNA COPY NUMBER ; medulloblastoma ; methods ; PROGNOSTIC MARKER ; RISK STRATIFICATION ; LOCI ; MYC ; outcome ; TUMOR BIOLOGY ; Genetic ; NUCLEAR BETA-CATENIN ; clinical oncology ; STRATIFICATION
    Abstract: Purpose Medulloblastoma (MB) is the most common malignant brain tumor in children, whereas it rarely presents in adults. We aimed to identify genetic aberrations in 146 adult MBs to evaluate age-dependent differences in tumor biology and adapt age-specific risk stratification models. Methods As a screening set, we studied a cohort of 34 adult MBs by using array-based comparative genomic hybridization comparing molecular results with clinical data. DNA copy number aberrations identified as possible prognostic markers were validated in an independent cohort of 112 adult patients with MB by fluorescent in situ hybridization analysis. Results were compared with the data obtained from 404 pediatric patients with MB. Results CDK6 amplification, 10q loss, and 17q gain are the most powerful prognostic markers in adult MB. Whereas MYC/MYCN oncogene amplifications had a high prognostic value in pediatric MB, these aberrations were rarely observed in adult tumors. Surprisingly, adult MBs with 6q deletion and nuclear beta-catenin activation did not share the excellent prognosis with their pediatric counterparts. Conclusion Adult MB is distinct from pediatric MB in terms of genomic aberrations and their impact on clinical outcomes. Therefore, adult MBs require age-specific risk stratification models. We propose a molecular staging system involving three distinct risk groups based on DNA copy number status of 10q and 17q
    Type of Publication: Journal article published
    PubMed ID: 20479417
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  • 8
    Keywords: ANGIOGENESIS ; CANCER ; CELLS ; GROWTH ; IN-VITRO ; proliferation ; tumor ; TUMOR-CELLS ; CELL ; ENDOTHELIAL GROWTH-FACTOR ; Germany ; IN-VIVO ; MICROSCOPY ; MODEL ; THERAPY ; VITRO ; VIVO ; POPULATION ; GENE-EXPRESSION ; DIFFERENTIATION ; cytokines ; ACID ; TARGET ; DESIGN ; resistance ; EFFICACY ; STEM-CELLS ; PPAR-GAMMA ; RETINOIC ACID ; PHASE-II ; chemoresistance ; TRANS-RETINOIC ACID ; CYTOKINE ; ONCOLOGY ; secretion ; GLIOMA ; GLIOMA-CELLS ; MALIGNANT GLIOMAS ; TUMORIGENICITY ; MOTILITY ; GLIOBLASTOMA ; STEM ; TUMOR-INITIATING CELLS ; MARKER CD133
    Abstract: Purpose: Stem-like tumor cells comprise a highly tumorigenic and therapy-resistant tumor subpopulation, which is believed to substantially influence tumor initiation and therapy resistance in glioma. Currently, therapeutic, drug-induced differentiation is considered as a promising approach to eradicate this tumor-driving cell population; retinoic acid is well known as a potent modulator of differentiation and proliferation in normal stem cells. In glioma, knowledge about the efficacy of retinoic acid-induced differentiation to target the stem-like tumor cell pool could have therapeutic implications. Experimental Design: Stem-like glioma cells (SLGC) were differentiated with all-trans retinoic acid-containing medium to study the effect of differentiation on angiogenesis, invasive growth, as well as radioresistance and chemoresistance of SLGCs. In vivo effects were studied using live microscopy in a cranial window model. Results: Our data suggest that in vitro differentiation of SLGCs induces therapy-sensitizing effects, impairs the secretion of angiogenic cytokines, and disrupts SLGCs motility. Further, ex vivo differentiation reduces tumorigenicity of SLGCs. Finally, we show that all-trans retinoic acid treatment alone can induce antitumor effects in vivo. Conclusions: Altogether, these results highlight the potential of differentiation treatment to target the stem-like cell population in glioblastoma. Clin Cancer Res; 16(10); 2715-28. (C) 2010 AACR
    Type of Publication: Journal article published
    PubMed ID: 20442299
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  • 9
    Keywords: brain ; APOPTOSIS ; CANCER ; CELLS ; EXPRESSION ; GROWTH ; GROWTH-FACTOR ; IN-VITRO ; INHIBITOR ; proliferation ; tumor ; CELL ; CELL-PROLIFERATION ; Germany ; INHIBITION ; MODEL ; PATHWAY ; PATHWAYS ; THERAPY ; VITRO ; EXPOSURE ; GENE ; microarray ; PROTEIN ; RNA ; DIFFERENTIATION ; MECHANISM ; INDUCTION ; mechanisms ; BIOLOGY ; ACID ; TARGET ; PROGRESSION ; AMPLIFICATION ; ASSAY ; PROMOTER ; genetics ; ONCOGENE ; STEM-CELLS ; PROGENITOR CELLS ; CANCER-THERAPY ; GLIOMAS ; RETINOIC ACID ; TRANS-RETINOIC ACID ; INHIBITORS ; signaling ; ONCOLOGY ; GLIOMA ; GLIOMA-CELLS ; MOLECULAR-MECHANISMS ; LOCUS ; GLIOBLASTOMA ; MicroRNAs ; MICRORNA ; CELL BIOLOGY ; TUMOR-INITIATING CELLS ; Genetic ; tumor grade ; Molecular mechanisms ; CTGF ; miR-17-92 ; NEURAL PRECURSORS ; spheroid culture
    Abstract: All-trans retinoic acid is a potent promoter of cellular differentiation processes, which is used in cancer therapy. Glioblastoma spheroid cultures are enriched in tumor-initiating cells, and provide a model to test new treatment options in vitro. We investigated the molecular mechanisms of response to exposure to differentiation-promoting conditions in such cultures. Microarray analyses of five independent cultures showed that after induction of differentiation, inhibitors of transforming growth factor beta/bone morphogenetic protein, Wnt/beta-catenin and IGF signaling were upregulated, whereas expression of several microRNAs decreased, particularly that of the miR-17-92 cluster. In primary astrocytic gliomas (n = 82), expression of several members of miR-17-92 was significantly higher relative to those of normal brain (n = 8) and significantly increased with tumor grade progression (P 〈 0.05). A high-level amplification of the miR-17-92 locus was detected in one glioblastoma specimen. Transfection of inhibitors of miR-17-92 induced increased apoptosis and decreased cell proliferation in glioblastoma spheroids. Mir-17-92 inhibition was also associated with increased messenger RNA (mRNA) and/or protein expression of CDKN1A, E2F1, PTEN and CTGF. The CTGF gene was shown to be a target of miR-17-92 in glioblastoma spheroids by luciferase reporter assays. Our results suggest that miR-17-92 and its target CTGF mediate effects of differentiation-promoting treatment on glioblastoma cells through multiple regulatory pathways. Oncogene (2010) 29, 3411-3422; doi:10.1038/onc.2010.83; published online 22 March 2010
    Type of Publication: Journal article published
    PubMed ID: 20305691
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  • 10
    Keywords: CANCER ; EXPRESSION ; SURVIVAL ; tumor ; BLOOD ; Germany ; THERAPY ; GENE ; GENE-EXPRESSION ; GENES ; microarray ; TISSUE ; SURGERY ; PATIENT ; COMPLEX ; COMPLEXES ; MARKER ; LYMPH-NODES ; CYCLE ; treatment ; BREAST ; breast cancer ; BREAST-CANCER ; TRIAL ; IDENTIFICATION ; gene expression ; chemotherapy ; PCR ; SAFETY ; CYCLOPHOSPHAMIDE ; gene expression profiling ; PHASE-II ; PREOPERATIVE CHEMOTHERAPY ; SERUM ; ONCOLOGY ; analysis ; methods ; PHASE ; SIGNATURE ; USA ; docetaxel ; PREDICTOR ; SET ; gene expression signature ; pathologic complete response ; primary breast cancer ; response prediction ; GENE-EXPRESSION SIGNATURE ; prediction of response and resistance ; translational research
    Abstract: Background: Microarray gene expression profiling has indicated that complex molecular gene expression signatures might be predictive of outcome after systemic treatment for early breast cancer. Neoadjuvant systemic therapy (NST) with its assessment of pathologic complete response (pCR), so far the best surrogate parameter for cure, provides a unique opportunity to rapidly identify such molecular predictors. Patients and Methods: Currently, an International, randomized phase II study of 2 sequential regimens as NST is being conducted in patients with primary invasive breast cancer T2-4a-c N0-2 MO. Patients receive 4 cycles of doxorubicin/pemetrexed, followed by 4 cycles of docetaxel (AP-Doc) or 4 cycles of doxorubicin/cyclophosphamide, followed by 4 cycles of docetaxel (AC-Doc). Tumor, tissue, blood, and serum are collected at baseline and, if available, after 4 cycles of chemotherapy, and at surgery. The clinical objectives are to assess pCR rate, tumor response, rate of histologically negative axillary lymph nodes, disease-free survival, and safety after NST with AP-Doc or AC-Doc. Translational research objectives include the identification of differentially expressed genes predictive for the achievement of pCR after either treatment regimen. Results: As of January 2007, 178 of the 256 patients planned for this study had been enrolled at 12 European centers. The recommendation after a planned interim safety and efficacy analysis was to continue with the trial as planned. Conclusion: We anticipate this study will provide a better understanding of the treatment options with pemetrexed in primary breast cancer and give insight into the practical robustness of the new marker sets in response prediction
    Type of Publication: Journal article published
    PubMed ID: 17509164
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