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  • 1
    Keywords: METASTASIS ; PROTEIN ; CANCER ; EXPRESSION ; cancer research ; BONE ; protein expression
    Type of Publication: Book chapter
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  • 2
    Keywords: CANCER ; CANCER CELLS ; CELLS ; EXPRESSION ; GROWTH ; proliferation ; TUMOR-CELLS ; CELL ; Germany ; human ; MODEL ; PROTEIN ; PROTEINS ; REDUCTION ; MR ; BREAST ; breast cancer ; BREAST-CANCER ; antibodies ; antibody ; GLYCOPROTEIN ; TARGET ; ASSAY ; METASTASIS ; PROSTATE-CANCER ; chemotherapy ; oligonucleotides ; CANCER-CELLS ; MIGRATION ; PROGNOSTIC VALUE ; GREECE ; GREEN FLUORESCENT PROTEIN ; ANTISENSE OLIGONUCLEOTIDES ; HUMAN BREAST ; GFP-MDA-MB-231,migration,metastasis,antisense oligonucleotides,osteopontin,bone sialoprotein ; HUMAN BREAST-CANCER ; SPARC
    Abstract: MDA-MB-231 human breast cancer cells transfected with GFP were used as model to determine the reduction in proliferation, colony formation, and migration in response to agents with anti-metastatic properties. These agents consisted of antisense oligonucleotides (ASOs) directed against osteopontin (OPN), bone sialoprotein II (BSP II), and osteonectin (ON), as well as an antibody directed against BSP II. A bisphosphonate derivative (ibandronate) and an alkylphosphocholine (erucylphospho-NNN-trimethylpropanolamine; ErPC3) were used as positive controls. The ASOs directed against OPN, BSP II and ON suppressed the expression of their respective target proteins by 81%, 74% and 69%, respectively. They were barely but significantly active in inhibiting the proliferation, but intermediately to highly active in inhibiting the colony formation and migration of GFP-MDA-MB-231 breast cancer cells. The antibody against human BSP II was significantly more active than all ASOs used and was equally active or even surpassed the activity of ibandronate and ErPC3 in all three assays. The results obtained suggest a specific anti-metastatic activity of this antibody as well as of the ASOs found effective in decreasing OPN and BSP II expression
    Type of Publication: Journal article published
    PubMed ID: 15067347
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  • 3
    Keywords: CANCER ; CELLS ; tumor ; carcinoma ; CELL ; evaluation ; Germany ; incidence ; liver ; SAMPLE ; SAMPLES ; PATIENT ; MESSENGER-RNA ; primary ; CONTRAST ; LYMPH-NODES ; MR ; SEQUENCE ; BONE-MARROW ; STAGE ; PATTERNS ; ASSAY ; MUTATION ; COLORECTAL-CANCER ; chemotherapy ; MARKERS ; WILD-TYPE ; COLON-CANCER ; MUTATIONS ; ONCOGENE ; EPITHELIAL-CELLS ; CANCER-PATIENTS ; CARCINOMAS ; COLORECTAL CARCINOMAS ; MICROMETASTASES ; POLYMERASE-CHAIN-REACTION ; PROGNOSTIC-SIGNIFICANCE ; RT-PCR ; GREECE ; CANCER PATIENTS ; PERIPHERAL-BLOOD ; NODES ; COLORECTAL-CARCINOMA ; disseminated tumor cells,circulating epithelial cells,K-ras,cytokeratin 20,guanylylcyclase C ; GUANYLYL CYCLASE-C
    Abstract: The aim of this prospective study was to relate the incidences of cytokeratin 20 (CK20) and guanylylcyclase C (GCC) in lymph node, liver, and bone marrow specimens of 245 colorectal cancer (CRC) patients with the K-ras oncogene status of the corresponding primary tumor. Qualitative RT-PCR detection of CK20 and GCC mRNA was used as marker of circulating epithelial cells (CEC). Samples were considered positive for CEC only when both markers were detected concomitantly. For the detection of K-ras mutations, a PCR-RFLP assay was used. In the group with K-ras mutated primary carcinomas (n=92), CEC were detected in 62% of lymph node-, 43% of liver-, and 2% of bone marrow samples. No statistical significance was found when comparing these results with those from patients with K-ras wild-type carcinoma (59%, 46%, and 0%, respectively). In contrast to this combined evaluation, separate analysis of K-ras codons 12 (n=75, 82%) and 13 (n=17, 18%) revealed significantly differing CEC incidences. Lymph node specimens from corresponding K-ras codon 13 mutated carcinomas showed a significantly higher CEC incidence (82%) than the groups with codon 12 mutation (57%, p〈0.05) or K-ras wild-type sequence (59%, p〈0.05). Unlike these findings in lymph nodes, liver biopsies from corresponding carcinomas with K-ras codon 12 mutation or wild-type sequence were significantly more often positive for CEC (31% and 29%) than specimens from K-ras codon 13 mutated primary CRC (12%, p〈0.04, respectively). In conclusion, colorectal carcinomas with K-ras codon 12 mutation showed the same pattern of tumor cell dissemination as their K-ras wild-type counterparts. Since K-ras codon 12 mutations prevailed 4-fold over codon 13 mutations, combined analysis of the two codons showed the same result. However, sub-analysis of patients with K-ras codon 13 mutation revealed that the respective CEC incidence was significantly increased in lymph nodes, but decreased in liver biopsies
    Type of Publication: Journal article published
    PubMed ID: 15138598
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  • 4
    Keywords: CANCER ; GROWTH ; SURVIVAL ; tumor ; COMBINATION ; Germany ; human ; LUNG ; THERAPY ; DIAGNOSIS ; DISEASE ; DRUG ; TUMORS ; LINES ; PATIENT ; colon ; CELL-LINES ; treatment ; TRIAL ; EXPERIENCE ; NUMBER ; metastases ; CELL-LINE ; chemotherapy ; leukemia ; LINE ; MELANOMA ; DERIVATIVES ; COLON-CANCER ; CANCER-PATIENTS ; SAFETY ; CANCER PATIENTS ; RANDOMIZED TRIAL ; cell lines ; DACARBAZINE ; RANDOMIZED-TRIAL ; FOTEMUSTINE ; INTERLEUKIN-2 ; CYTOTOXICITY ; STANDARD ; ONCOLOGY ; colon cancer ; TUMOR-GROWTH ; HUMAN CANCER ; IV ; CHINESE ; uveal melanoma ; MALARIA ; antimalarial ; artemisinin ; artesunate ; DIHYDROARTEMISININ ; HOLOTRANSFERRIN ; QINGHAOSU ; TOLERABILITY ; uvea
    Abstract: Artesunate (ART) is a derivative of artemisinin, the active principle of the Chinese herb Artemisia annua L. Artesunate is approved for the treatment of multidrug-resistant malaria and has an excellent safety profile. It has been shown that Artesunate, apart from its anti-malarial activity, has cytotoxic effects on a number of human cancer cell lines, including leukemia, colon cancer and melanoma. We report on the first long-term treatment of two cancer patients with ART in combination with standard chemotherapy. These patients with metastatic uveal melanoma were treated on a compassionate-use basis, after standard chemotherapy alone was ineffective in stopping tumor growth. The therapy-regimen was well tolerated with no additional side effects other than those caused by standard chemotherapy alone. One patient experienced a temporary response after the addition of ART to Fotemustine while the disease was progressing under therapy with Fotemustine alone. The second patient first experienced a stabilization of the disease after the addition of ART to Dacarbazine, followed by objective regressions of splenic and lung metastases. This patient is still alive 47 months after first diagnosis of stage IV uveal melanoma, a situation with a median survival of 2-5 months. Despite the small number of treated patients, ART might be a promising adjuvant drug for the treatment of melanoma and possibly other tumors in combination with standard chemotherapy. Its good tolerability and lack of serious side effects will facilitate prospective randomized trials in the near future
    Type of Publication: Journal article published
    PubMed ID: 16273263
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  • 5
    Keywords: RECEPTOR ; CANCER ; CELLS ; EXPRESSION ; GROWTH ; IN-VITRO ; SURVIVAL ; tumor ; TUMOR-CELLS ; carcinoma ; CELL LUNG-CANCER ; Germany ; VITRO ; DISEASE ; LINES ; PATIENT ; ACTIVATION ; RECEPTOR EXPRESSION ; prognosis ; CELL-LINES ; PROGRESSION ; ASSAY ; DESIGN ; NUMBER ; METASTASIS ; colorectal cancer ; COLORECTAL-CANCER ; LINE ; CANCER-CELLS ; MIGRATION ; RECEPTORS ; BEHAVIOR ; POOR-PROGNOSIS ; cell lines ; CELL-MIGRATION ; chemokine ; LOCATION ; ANTAGONIST ; intensity ; LYMPH-NODE METASTASIS ; CHEMOKINE RECEPTORS ; cell migration ; ASSAYS ; DISSEMINATION ; CELL-DERIVED FACTOR ; DISEASE PROGRESSION ; MATURE DENDRITIC CELLS
    Abstract: Purpose: The expression of chemokine receptors CXCR4 and CCR.7 has been associated with tumor dissemination and poor prognosis in a limited number of tumor entities. However, no data are currently available on the impact of chemokine receptor expression on disease progression and prognosis in human colorectal cancer. Experimental Design: The expression of CXCR4 and CCR7 was evaluated in 96 patients with histologically confirmed colorectal cancers and in four colorectal cancer cell lines by immunohistochemical staining. Furthermore, cell migration assays were done with SW480, SW620, and LS174T cancer cells to confirm the effect of the CXCR4 ligand stromal cell-derived factor 1alpha on migration. Results: Human colorectal cancer specimens and cell lines displayed a CXCR4 and CCR7 expression with variable intensities. Interestingly, strong expression of CXCR4, but not of CCR7, was significantly associated with higher Union International Contre Cancer stages 3/4 (P = 0.0017), lymph node metastasis (P = 0.00375), and distant metastasis (P = 0.00003) and further correlated with a reduced 3-year survival rate (P = 0.1). Strong CXCR4 and CCR7 expression positively correlated with the location of the primary tumor in the rectum (P 〈 0.01). Furthermore, activation of CXCR4-expressing cancer cells by stromal cell-derived factor 1alpha resulted in a significant increase of cell migration (P 〈 0.014). Conclusion: Strong expression of CXCR4 by colorectal cancer cells is significantly associated with lymphatic and distant dissemination in patients with colorectal cancer as well as with cancer cell migration in vitro
    Type of Publication: Journal article published
    PubMed ID: 15755995
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  • 6
    Keywords: CANCER ; EXPRESSION ; Germany ; GENE ; PROTEIN ; PROTEINS ; transcription ; TISSUE ; SURGERY ; LINES ; PATIENT ; COMPLEX ; DOMAIN ; tumour ; CELL-LINES ; SEQUENCE ; PROGRESSION ; ASSAY ; Drosophila ; colorectal cancer ; COLORECTAL-CANCER ; metastases ; LINE ; REGION ; MUTATIONS ; ADHESION ; MIGRATION ; cytoskeleton ; POLYMERASE-CHAIN-REACTION ; cell lines ; CELL-MIGRATION ; BINDS ; CELL POLARITY ; MAPS ; colon cancer ; TUMORIGENESIS ; cell adhesion ; cell migration ; ASSAYS ; SUPPRESSOR ; tumour suppressor ; APC ; 17P11.2 ; Hugl-1 ; II HEAVY-CHAIN ; LETHAL-GIANT-LARVAE ; lgl
    Abstract: The human gene, human giant larvae (Hugl-1/Llg1/Lgl1) has significant homology to the Drosophila tumour suppressor gene lethal( 2) giant larvae (lgl). The lgl gene codes for a cortical cytoskeleton protein, Lgl, that binds Myosin II and is involved in maintaining cell polarity and epithelial integrity. The human protein, Hugl-1 contains several conserved functional domains found in Lgl, suggesting that these proteins may have closely related functions. Whether loss of Hugl expression plays a role in human tumorigenesis has so far not been extensively investigated. Thus, we evaluated tumour tissues from 94 patients undergoing surgery for colorectal cancer (CRC) for loss of Hugl-1 transcription and compared our findings with the clinical data from each of these patients. We found that Hugl-1 was lost in 75% of tumour samples and these losses were associated with advanced stage and particularly with lymph node metastases. Reduced Hugl-1 expression during the adenoma-carcinoma sequence occurring as early as in colorectal adenomas was detected by both immunohistochemical and reverse transcription polymerase chain reaction analysis. Functional assays with ecdysone-inducible cell lines revealed that Hugl-1 expression increased cell adhesion and decreased cell migration. Our studies thus indicate that downregulation of Hugl-1 contributes to CRC progression
    Type of Publication: Journal article published
    PubMed ID: 15735678
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  • 7
    Keywords: CANCER ; CELLS ; GROWTH ; IN-VITRO ; proliferation ; tumor ; TUMOR-CELLS ; AGENTS ; CELL LUNG-CANCER ; COMBINATION ; Germany ; IN-VIVO ; INHIBITION ; MODEL ; VITRO ; EXPOSURE ; liver ; PATIENT ; RAT ; RATS ; SEQUENCE ; RAT-LIVER ; ASSAY ; METASTASIS ; colorectal cancer ; COLORECTAL-CANCER ; EFFICACY ; metastases ; chemotherapy ; arteries ; CANCER-CELLS ; COLON-CANCER ; LIVER METASTASES ; BOLUS ; AGENT ; GEMCITABINE ; colon cancer ; TUMOR-GROWTH ; END ; COLON ADENOCARCINOMA ; HEPATIC METASTASES ; PHASE-II TRIAL ; STARCH MICROSPHERES ; ANIMAL-MODEL ; liver metastasis ; PEMETREXED DISODIUM ; CC531-lac-Z ; chemoembolization ; chemoluminescence ; INTRAARTERIAL CHEMOTHERAPY ; MULTITARGETED ANTIFOLATE LY231514 ; SELECTIVE CHEMOEMBOLIZATION
    Abstract: Purpose: The aim of this study was to evaluate the combination effect of pemetrexed disodium (MTA; Alimta; LY 231514) and gemcitabine ( GEM) administered by hepatic artery and portal vein chemoembolization (HACE and PVCE) in a colorectal cancer rat liver metastasis model. Materials and methods: Proliferation studies on CC531-lac-Z rat colon cancer cells were performed using the MTT assay to obtain the optimal combination schedule of the two antineoplastic agents. To generate diffuse liver metastasis, 4 x 10(6) tumor cells were implanted into the portal vein of male WAG/Rij rats. MTA ( 30 mg/kg, 60 mg/kg, and 90 mg/kg) was administered locoregionally by portal vein chemoembolization ( PVCE) and compared with repeated systemic intravenous injection. GEM ( 50 mg/kg) was also given locoregionally by hepatic artery chemoembolization ( HACE) as well as systemically. All routes of administration were examined alone as well as in combination. Efficacy of treatment in terms of liver metastases burden was determined at the end of the experiment by measuring the beta-galactosidase activity of CC531-lac-Z cells with a chemoluminescence assay. Results: Combination experiments in vitro showed a more than additive tumor cell reduction after sequential exposure to MTA preceding GEM (observed/expected ratio [O/ E] = 0.73). Experiments with the reverse sequence ( GEM. MTA) resulted only in additive combination effects ( O/ E ratio = 1.08). Simultaneous drug exposure showed less than additive combination effects (O/ E ratios 〉= 1.25). In vivo, locoregional administration by HACE with GEM was significantly more effective than systemic intravenous bolus treatment (P = 0.03). Portal vein chemoembolization with MTA performed immediately after tumor cell inoculation was ineffective. Repeated systemic treatment with MTA yielded a slight reduction in tumor cell load that was significant versus control at the medium and high doses ( 60 mg/kg, P = 0.009; 90 mg/kg, P = 0.046) but not versus intraportal chemoembolization. The combination treatment of systemic ( 60 and 90 mg/kg) or locoregional ( 60 mg/kg) MTA with HACE using GEM ( 50 mg/kg) resulted in more than 80 % tumor growth inhibition; this antineoplastic combination effect was maximally additive. Conclusion: A regimen-dependent synergistic combination effect of both drugs was found in vitro. In animals, hepatic artery chemoembolization with GEM was superior to systemic intravenous bolus treatment. Portal vein chemoembolization with MTA was ineffective. The optimal in vitro regimen of MTA ( intravenous or PVCE) preceding GEM ( HACE) resulted in a maximally additive tumor growth inhibition. The results indicate that MTA and GEM can successfully be combined and favor further evaluation in patients
    Type of Publication: Journal article published
    PubMed ID: 15657768
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  • 8
    Keywords: CANCER ; CANCER CELLS ; CELLS ; EXPRESSION ; IN-VITRO ; proliferation ; carcinoma ; Germany ; VITRO ; LUNG-CANCER ; PROTEIN ; PATIENT ; RATS ; treatment ; BREAST ; breast cancer ; BREAST-CANCER ; antibodies ; LESIONS ; METASTASIS ; NUDE-MICE ; chemotherapy ; CANCER-CELLS ; MIGRATION ; INTEGRIN ALPHA(V)BETA(3) ; SERUM ; MATRIX ; MATRIX METALLOPROTEINASES ; anti-BSP antibody ; bone metastasis ; COLONY FORMATION ; MDA-MB-231 human breast cancer cell line ; nude rat model ; OSTEOPONTIN ; bone sialoprotein
    Abstract: The extracellular bone matrix protein bone sialoprotein (BSP) is considered to play an important role in the pathogenesis of lytic skeletal lesions which are associated with severe morbidity in breast, prostate or lung cancer patients. In addition to in vitro Studies, nude rats were implanted with 105 MDA-MB-231 cells transfected with GFP into a small branch of the femoral artery. Osteolytic lesions of the respective hind leg were detected by X-ray and CT analysis as well as by inimunohistochemistry. Exposure of MDA-MB-231(GFP) cells in vitro to an antibody against BSP (0-400 mu g/ml) decreased proliferation, colony formation and migration of these cells by up to 95, 83 and 89 T/C%, respectively. In nude rats, preincubation of MDA-MB-231GFP cells prior to inoculation (25-100 mu g/ml) reduced the mean osteolytic lesion size to 22 T/C% after 90 days of observation (p 〈 0.05). Treatment of overt lytic metastasis with the anti-BSP antibody (10 mg/kg) resulted in a significantly smaller mean lesion size of 57 T/C% at the end of the observation period (p 〈 0.05) as well as in new bone formation. Immunohistochemical analysis revealed the presence of BSP in MDA-MB-231(GFP) cells and in vessel endothelium cells during processes such as migration and invasion. In conclusion, an anti-BSP antibody decreased proliferation, colony formation and migration of MDA-MB-231(GFP) cells in vitro and reduced osteolysis besides inducing bone formation in a nude rat model
    Type of Publication: Journal article published
    PubMed ID: 16465361
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  • 9
    Keywords: APOPTOSIS ; CANCER ; CELLS ; GROWTH ; INHIBITOR ; proliferation ; CELL ; COMBINATION ; INHIBITION ; PATHWAY ; PATHWAYS ; TOXICITY ; transcription ; cell line ; LINES ; MICE ; TRANSDUCTION ; PATIENT ; NF-KAPPA-B ; ACTIVATION ; TRANSCRIPTION FACTOR ; REDUCTION ; CELL-LINES ; signal transduction ; SIGNAL ; ANTITUMOR-ACTIVITY ; BONE-MARROW ; culture ; LYMPHOMA ; GLUTATHIONE ; CHROMOSOMAL-ABERRATIONS ; EFFICACY ; SIGNAL-TRANSDUCTION ; CELL-LINE ; chemotherapy ; leukemia ; LINE ; ABERRATIONS ; NF-kappa B ; CISPLATIN ; curcumin ; FACTOR-I ; cell lines ; CANCER-THERAPY ; MULTIPLE-MYELOMA ; CYTOTOXICITY ; ARREST ; multiple myeloma ; INCREASE ; LEVEL ; ASSAYS ; CANCERS ; ENGLAND ; aberration ; antineoplasic effect ; antitumor activity ; bendamustine ; chemoprotection ; clastogenic effect ; GSH level ; myeloma ; ACAD
    Abstract: Curcumin is the pigment of turmeric and has been reported as a signal transduction modulator and inhibitor of transcription factors, for example, NF-kappa B. In our article we found a concentration-dependent cytotoxic activity of curcumin in a panel of eight leukemic cell lines (SKW-3, CEM, U-937, HL-60, HL-60/Dox, K-562, LAMA-84, and AR-230). Additive to synergistic interactions was recorded for combinations with bendamustine and idarubicine in SKW-3 and LAMA-84 cells. Noteworthy, in multiple myeloma cells (RPMI-8226 and U-266) a potentiation of the efficacy of bendamustine by curcumin application was found. Moreover, curcumin increased the bendamustine cytotoxicity in cultures of cells isolated from the bone marrow of a patient with non-Hodgkin's lymphoma (NHL). The increased bendamustine efficacy could be explained by NF-kappa B inhibition, because this factor is activated in many cancers, especially leukemia and multiple myeloma. Curcumin is characterized by low toxicity and was described to have a chemoprotective activity. Therefore, the level of reduced glutathione (GSH) was measured and a concentration-dependent increase of GSH levels was recorded in AR-230 and SKW-3 cells (concentration range 5-25 mu M). Experiments with mice showed significant protection against cisplatin-induced chromosomal aberrations (clastogenic effect) and inhibition of mitoses in bone marrow cells. Curcumin alone caused reduction of the mitotic index. In combination with cisplatin, however, this parameter was increased when compared to cisplatin alone. Our data indicate that curcumin has pleiotropic effects on signal transduction by inhibiting transcription thus exerting antitumor activity. In addition, curcumin has protective and anticlastogenic activity by enhancing the scavenging of free radicals
    Type of Publication: Journal article published
    PubMed ID: 17404048
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  • 10
    Keywords: CANCER ; Germany ; THERAPY ; INFORMATION ; DISEASE ; RISK ; validation ; BREAST ; breast cancer ; BREAST-CANCER ; NO ; hormone ; HEALTH ; DESIGN ; NUMBER ; AGE ; HORMONE REPLACEMENT THERAPY ; cancer risk ; REGION ; REGIONS ; RELIABILITY ; case-control studies ; BREAST-CANCER RISK ; POSTMENOPAUSAL WOMEN ; breast neoplasms ; case control study ; case-control study ; RE ; DETERMINANTS ; THERAPIES ; RECALL ; ESTROGEN ; case control studies ; INTERVAL ; RANDOMIZED CONTROLLED-TRIAL ; REPLACEMENT THERAPY ; correlation ; population-based ; CANCER-RISK ; AGREEMENT ; case control ; postmenopausal ; comparison ; validation studies ; prescription ; ESTROGEN REPLACEMENT THERAPY ; postmenopause ; RECORDS
    Abstract: Objective: In a population-based case-control study examining the effects of postmenopausal hormone therapy (HT) on breast cancer risk, the authors conducted a validation study comparing prescription data from gynecologists with self-reports. Study Design and Setting: The study was conducted in the Rhein-Neckar and Hamburg regions of Germany from 2002 to 2005. A total of 224 cases and 225 controls, stratified by region, age, and hormone use were randomly selected for the validation study. Results: For ever/never use 88.2% agreement was seen, and agreement for ever/never use by type of HT was 80.6%, 80.3%, and 90.5% for mono-estrogen, cyclical combined, and continuous combined therapy, respectively. The intraclass correlation coefficient (ICC) for duration of use was high, 0.82 (95% confidence interval [CI]: 0.77, 0.85), as were the ICCs for age at first and last use, 0.88 (95% CI: 0.85, 0.91) and 0.98 (95% CI: 0.97, 0.98). Despite the exceptionally high number of different HT prescriptions available in Germany, comparison of exact brand name resulted in perfect agreement for 50.2% of participants, partial agreement for 29.3%, and no agreement for 20.7%. In general, agreement was not differential by disease status. Conclusion: Overall, the self-reported HT of the study participants corresponded well with physicians' reports. (C) 2007 Elsevier Inc. All rights reserved
    Type of Publication: Journal article published
    PubMed ID: 17998083
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