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  • 1
    Language: English
    In: Oncology Letters, 6/2012, Vol.3(6), pp.1191-1194
    Description: The use of anticancer drugs in palliative settings is often limited by their severe toxic effects. In gastrointestinal carcinomas the 5-fluorouracil-based palliative regimen FOLFOX-4 is often preferred to the equally effective, but more convenient oral capecitabine-based regimen XELOX. This preference is mainly based on the fact that the highly effective oral agent capecitabine induces hand-foot syndrome (HFS). In this study, we investigated whether the continuous administration of skin prophylaxis (10% urea, panthenol, bisabolol, vitamin A, C and E) is capable of protecting against capecitabine-induced HFS and allowing a more convenient oral therapeutic option. In this retrospective analysis, the toxicity profiles, according to NCI CTCAE 3.0 criteria, of 54 patients with gastrointestinal cancer who received either XELOX (34 patients) or FOLFOX-4 (20 patients) were compared using Fisher tests. The treatment protocols that were compared, herein, did not differ significantly in the majority of the analyzed items, with the exception of increased nausea (XELOX-70), fatigue (XELOX-130) and tumor pain (XELOX-70 and XELOX-130). No significant differences were observed among the various groups with regard to emesis, diarrhea, mucositis, exanthema, alopecia, loss of weight and the incidence of infections. In particular, no significant differences in toxicity levels occurred in terms of dose, and HFS was limited if skin prophylaxis was performed continuously. XELOX-based palliative regimens provide an equally effective and comparably toxic therapeutic alternative to FOLFOX-4 if HFS prophylaxis is performed continuously. Since the oral administration of capecitabine is a more convenient method of application, it provides patients with a quality of life-preserving therapeutic alternative.
    Keywords: Capecitabine ; 5-Fluorouracil ; Hand-Foot Syndrome ; Gastrointestinal Carcinoma
    ISSN: 1792-1074
    E-ISSN: 1792-1082
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  • 2
    Language: English
    In: International Journal of Oncology, August 2011, Vol.39(2), pp.515-520
    Description: We performed this study in order to evaluate the impact of the chemokine CXCL12 and its single-nucleotide polymorphism (SNP) rs1801157 on clinicopathological parameters and survival in patients undergoing surgery for esophagogastric cancer. The expression pattern of CXCL12 and its polymorphisms were analyzed by RT-PCR and PCR-RFLP in 69 consecutive fresh-frozen samples of human esophagogastric junction and gastric adenocarcinomas and statistically analyzed. Expression of the CXCL12 (SNP rs1801157) polymorphisms GA/AA significantly correlated with distant metastasis (P=0.026), but not with prognosis. However, CXCL12 expression was not significantly associated with the tumor infiltration depth, lymphatic metastasis and grading. As CXCL12 polymorphisms mediate tumor cell dissemination in esophagogastric cancer, they could represent a marker indicating advanced disease. Antagonists targeting the CXCL12/ CXCR4 axis may be a novel therapeutic option in this entity.
    Keywords: Medicine;
    ISSN: 1019-6439
    E-ISSN: 17912423
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  • 3
    Language: English
    In: Gastroenterology, May 2013, Vol.144(5), pp.S-1088-S-1088
    Keywords: Medicine
    ISSN: 0016-5085
    E-ISSN: 1528-0012
    Source: ScienceDirect Journals (Elsevier)
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  • 4
    Language: English
    In: Molecular Medicine Reports, September-October 2010, Vol.3(5), pp.789-793
    Description: More than 80% of patients treated with cetuximab develop an acneiform follicular skin exanthema. Grade 3 exanthema develops in 9-19% of these cases, bearing the risk of cetuximab dose-reduction or cessation. We retrospectively analysed a cohort of 20 patients treated with cetuximab and an in-house reactive skin protocol upon development of an exanthema. The reactive skin protocol was built up as follows: grade 1 exanthema: topical cleansing syndet (Dermowas®) + topical metronidazole cream (Rosiced®); grade 2 exanthema: grade 1 treatment + oral minocycline 50 mg twice per day; grade 3 exanthema: grade 2 treatment + topical corticoid (Dermatop®) + topical nadifloxacin (Nadixa®). As soon as a grade 3 had improved to a grade less than or equal to 2, the application of the topical corticoid was ceased. During the initial 12 weeks of therapy with cetuximab, all patients developed a skin exanthema (20/20; 100%). Of these, 2 patients (10%) developed a grade 3 exanthema, 10 patients (50%) experienced a grade 2 and 8 patients (40%) a grade 1 exanthema. Time to onset ranged from 1 to 4 weeks, with the average time to onset being 2.8 weeks. Applying the reactive skin protocol after the first occurrence of an exanthema, the grade of exanthema was downgraded as follows: no patients (0%) had a persisting grade 3 exanthema, while only 2 patients (10%) experienced a persisting grade 2 exanthema and 8 patients (40%) a persisting grade 1 exanthema. In the majority of cases (10 patients; 50%), the reactive skin protocol completely controlled the exanthema (grade 0). The average time to exanthema reduction by one grade was 9.5 days. No dose reductions of cetuximab were necessary. Cetuximab-induced skin exanthema is effectively managed by applying our reactive protocol. The simple protocol is based on a topical cleansing syndet and topical metronidazole and is to be intensified by the addition of oral minocycline, a topical corticoid and topical nadifloxacine, in cases of high-grade exanthema. More comprehensive results are expected from a prospective study with higher patient numbers that is currently being planned.
    Keywords: Biology;
    ISSN: 1791-2997
    E-ISSN: 17913004
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  • 5
    Language: English
    In: Cancer Research, 04/15/2010, Vol.70(8 Supplement), pp.1741-1741
    ISSN: 0008-5472
    E-ISSN: 1538-7445
    Source: CrossRef
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  • 6
  • 7
    Language: English
    In: International Journal of Cancer, 01 September 2010, Vol.127(5), pp.1197-1208
    Description: The receptor tyrosine kinases (RTKs), epidermal growth factor receptor (EGFR) and vascular endothelial growth factor receptor 1‐3 (VEGFR1‐3), are frequently expressed in gastric cancer and are putative therapeutic targets in this disease. We have investigated the anti‐proliferative and chemosensitizing properties of the multitargeted small‐molecule RTK inhibitors sunitinib and vandetanib in a panel of 4 human gastric and esophageal cancer cell lines. In the 1st instance, the expression of potential targets of these small‐molecule inhibitors was examined by reverse transcriptase‐polymerase chain reaction, western blotting, and flow cytometry. EGFR mRNA and protein was detected in all cases, with VEGFR2 expression noted in all but 1 line. Both EGF and VEGF were shown to stimulate tumor cell growth, and both sunitinib and vandetanib were found to be associated with significant dose‐dependent inhibition of proliferation and an enhancement of apoptosis, as determined by MTT and propidium iodide/Annexin V labeling assays, respectively. The addition of sunitinib to VEGF‐stimulated NCI‐N87 cells was associated with a reduction in MAPK phosphorylation (pMAPK) but not Akt phosphorylation (pAkt), whereas the addition of vandetanib was associated with reductions in both VEGF‐ and EGF‐mediated VEGFR2 phosphorylation, pMAPK and pAkt. Co‐administration of sunitinib significantly enhanced the sensitivity of MKN‐45 cells to cisplatin and irinotecan. In addition, vandetanib synergistically enhanced the sunitinib‐associated inhibition of gastric cancer cell growth. In conclusion, these preliminary data confirm the importance of EGFR and VEGFR signaling in gastric cancer and suggest that the simultaneous inhibition of RTK‐pathways through sunitinib and vandetanib may provide therapeutic benefit in this disease.
    Keywords: Sunitinib ; Rtk ; Gastric Cancer ; Vandetanib ; Chemotherapy
    ISSN: 0020-7136
    E-ISSN: 1097-0215
    Source: John Wiley & Sons, Inc.
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  • 8
    Language: English
    In: Journal of Cancer Research and Clinical Oncology, 2011, Vol.137(7), pp.1139-1145
    Description: Byline: Carl C. Schimanski (1), Markus Moehler (1), Ines Gockel (2), Tim Zimmermann (1), Hauke Lang (2), Peter R. Galle (1), Martin R. Berger (3) Keywords: CCR5; Chemokine receptor; Colorectal cancer; Liver metastases; Molecular metastases; Micrometastases; Tumor cells Abstract: Background Molecular metastases are precursors of postoperative recurrence, detected by molecular-biological tools. Chemokines and their receptors contribute to dissemination and local immune recognition. A strong expression of the chemokine receptor CCR5 is associated with non-metastatic colorectal cancer and increased CD8+ T-cell infiltration. The aim of this study was to analyze whether CCR5 expression correlates with the presence of hepatic molecular metastases (MM). Methods Ninety-three patients undergoing elective surgery for colorectal cancer were assessed. The K-ras mutation status was defined by PCR--RFLP, and the CCR5 expression status was analyzed by CCR5-specific reverse transcription (RT-PCR) analysis. Liver biopsy samples had been intra-operatively taken to screen for MM. MM were detected by K-ras-specific PCR--RFLP and nested CK20/GCC RT-PCR. Prevalence of MM was correlated with CCR5 expression status. Results Human colorectal cancer harboured K-ras mutations in 53% (codon 12: 47% codon 13: 6%) of cases. Among K-ras mutants, MM were detected in 27--53% of patients, dependent on the technique applied (K-ras-specific PCR--RFLP assay vs. nested CK20/GCC RT-PCR approach (P = 0.004)). CCR5 expression of K-ras mutants ranged from absent (23/49: 47%), weak (17/49: 35%), intermediate (4/49: 8%) to strong (5/49: 10%). MM were found in 30% of CCR5 negative and in 23% of CCR5 positive cancer patients by the K-ras-specific PCR--RFLP assay. The nested CK20/GCC RT-PCR assay detected MM in 87% of CCR5 negative and in 27% of CCR5 positive colorectal cancer patients (P = 0.00002). Conclusion Thus, CCR5 expression of the primary cancer might be a valuable biomarker indicating the absence of hepatic molecular metastases. Author Affiliation: (1) Department of Internal Medicine, Johannes Gutenberg University of Mainz, Langenbeckstrasse 1, 55101, Mainz, Germany (2) Department of general and abdominal surgery, Johannes Gutenberg University of Mainz, Langenbeckstrasse 1, 55101, Mainz, Germany (3) German Cancer Research Center, INF 280, 69120, Heidelberg, Germany Article History: Registration Date: 22/03/2011 Received Date: 24/08/2010 Accepted Date: 22/03/2011 Online Date: 06/04/2011 Article note: Electronic supplementary material The online version of this article (doi: 10.1007/s00432-011-0980-6) contains supplementary material, which is available to authorized users.
    Keywords: CCR5 ; Chemokine receptor ; Colorectal cancer ; Liver metastases ; Molecular metastases ; Micrometastases ; Tumor cells
    ISSN: 0171-5216
    E-ISSN: 1432-1335
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  • 9
    Language: English
    In: Expert Review of Gastroenterology & Hepatology, 01 June 2011, Vol.5(3), pp.371-384
    Description: Objectives: Endoscopic local procedures are increasingly applied in patients with superficial esophageal cancer as an alternative to radical oncologic resection. The objective of this article is to determine the risk of nodal metastases in submucosal (sm) esophageal cancer, comparing the two predominating histologic tumor types, squamous cell cancer (SCC) and adenocarcinoma (ADC). Methods: A query of PubMed, MEDLINE, Embase and Cochrane Library (1980-2009) using predetermined search terms revealed 675 abstracts, of which 485 full-text articles were reviewed. A total of 105 articles met the selection criteria. A review of article references and consultation with experts revealed additional articles for inclusion. Studies that enrolled patients with submucosal esophageal cancer and provided adequate extractable data were included. Results: The pooled outcomes of 7645 patients with esophageal cancer involving the sm level of infiltration were included in the analysis. Overall, the percentage of lymph node metastasis in submucosal cancer was 37%. Lymph node (N), lymphatic (L) and vascular (V) invasion in sm1 esophageal cancers was 27, 46 and 22%, respectively. Within sm2 lesions, N, L and V invasion were involved in 38, 63 and 38% of patients, respectively. Finally, N, L and V involvement in patients with sm3 lesions was 54, 69 and 47%, respectively. The rates of lymph node metastasis for sm1 and sm2 were higher in SCC compared with ADC, whereas the lymph node metastasis for sm3 was comparable, with 〉50% involvement in both histologic subtypes. SCC revealed an overall more aggressive behavior compared with ADC (N+: 45 vs 26%; L+: 57 vs 37%; V+: 40 vs 18%). Discussion: While endoscopic therapy may be adequate in selected patients with 'low-risk' sm1 ADC, submucosal SCC necessitates esophageal resection and systematic lymphadenectomy because of its aggressive nature and tendency for early metastasis.
    Keywords: Risk of Lymph Node Metastasis ; Sm1 ; Sm2 ; Sm3 ; Submucosal Depth of Tumor Infiltration ; Submucosal Esophageal Cancer ; Surgically Resected Specimens ; Medicine
    ISSN: 1747-4124
    E-ISSN: 1747-4132
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  • 10
    Language: English
    In: Cancer Chemotherapy and Pharmacology, 2012, Vol.69(6), pp.1601-1615
    Description: Byline: Annett Mueller (1), Erika Bachmann (1), Monika Linnig (1), Katrin Khillimberger (1), Carl Christoph Schimanski (1), Peter R. Galle (1), Markus Moehler (1) Keywords: Inhibition; PI3K; Cancer cell lines; Chemotherapy; Wild type Abstract: Purpose New targeted agents like antibodies or small molecules against tyrosine and lipid kinases clearly expand the standard therapy options in oncology. However, tumour resistance is still a challenge, often induced by mutations in growth-related signalling cascades. Twenty and ten percentage of all patients with colorectal and gastric cancers, respectively, carry phosphatidyl-3-kinase (PI3K) mutations and do not respond to receptor-blocking therapies. Recently, selective kinase inhibitors have been generated, which block the PI3K signalling pathway in tumour cells. So far, their therapeutic role for the treatment of mutated versus wild-type human gastrointestinal cancers has not been clarified in detail. Methods To define the inhibitory and pro-apoptotic effects of the two PI3K inhibitors BEZ235 and BKM120 in three human colon cancer (HT-29, HCT-116 and DLD-1) and three gastric cancer (NCI-n87, AGS and MKN-45), cell lines with different PIK3CA gene mutation status were used. Firstly, viability, apoptosis and caspase assays were performed during incubation with either the inhibitors alone or combined with different cytotoxic agents. Secondly, the molecular consequences for the cell cycle and signalling pathways were analysed by defining the protein levels by FACS and Western blot analysis. Results Both the PI3K inhibitors BEZ235 and BKM120 induced a clear concentration-dependent reduction in cell viability and an increase in apoptotic cell death, with the mutated cells being more sensitive to treatment. However, single-agent BEZ235 caused a G1 arrest in tumour cells, whilst BKM120 induced a G2 shift in a half of the gastrointestinal cancer cell lines. There was a clear downregulation in the protein levels of the PI3K--AKT pathway at the concentrations of 100nM for both agents and for BEZ235 the additional inhibition of the mTOR pathway. Furthermore, BEZ235 caused synergistic induction of apoptosis when combined with irinotecan in colon cancer cell lines. Human gastric cancer cells were less sensitive to both BEZ235 and BKM120. Conclusions BEZ235 and BKM120 induced pro-apoptotic effects in all cell lines and especially with an increased response in the PI3KCA mutated cells. Our data support the clinical development of these PI3K inhibitors for patients with wild-type or mutated colon cancers. Author Affiliation: (1) First Department of Internal Medicine, University Medical Centre of the Johannes Gutenberg University Mainz, Langenbeckstrasse 1, 55101, Mainz, Germany Article History: Registration Date: 13/04/2012 Received Date: 02/11/2011 Accepted Date: 12/04/2012 Online Date: 29/04/2012 Article note: Electronic supplementary material The online version of this article (doi: 10.1007/s00280-012-1869-z) contains supplementary material, which is available to authorized users.
    Keywords: Inhibition ; PI3K ; Cancer cell lines ; Chemotherapy ; Wild type
    ISSN: 0344-5704
    E-ISSN: 1432-0843
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