Journal of cancer research and clinical oncology
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J. Cancer Res. Clin. Oncol. · Feb 2012
Enhanced ABL-inhibitor-induced MAPK-activation in T315I-BCR-ABL-expressing cells: a potential mechanism of altered leukemogenicity.
Targeted treatment of chronic myelogenous leukemia using imatinib has dramatically improved patient outcome. However, residual disease can be detected in the majority of patients treated with imatinib. Compensatory activation of MAP kinases (MAPK1/2) in response to BCR-ABL-inhibitors has been reported as a potential cytokine-dependent resistance mechanism leading to the rescue of leukemic progenitor cells. ⋯ Aberrant MAPK-activation triggered by ABL-inhibitors and positively regulated by BCR-ABL kinase mutation T315I might be an experimental explanation for the clinical observation that patients carrying high-resistance mutations show a highly aggressive course of their disease when tyrosine kinase inhibitor treatment is not discontinued in time.
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J. Cancer Res. Clin. Oncol. · Feb 2012
Nodal status--its impact on prognosis in advanced ovarian cancer.
Prognostic impact of nodal status or lymphadenectomy in advanced ovarian cancer is still unclear. Known best prognostic impact in advanced ovarian cancer has the residual tumor mass. The aim of this retrospective study is to examine the importance of nodal status in correlation with residual tumor mass. ⋯ Main intention of primary surgery is R0 resection with best prognosis in advanced stages. A systematic lymphadenectomy in cases with R0 resection or residual tumor <1 cm seems to be reasonable with positive impact on prognosis. Node status has impact on prognosis in patients with negative node after R0 resection with best PFS in FIGO III. Further prospective studies had to show whether systematic lymphadenectomy in suboptimally tumor-reduced patients can improve prognosis.
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J. Cancer Res. Clin. Oncol. · Feb 2012
The antitumor effect of mesenchymal stem cells transduced with a lentiviral vector expressing cytosine deaminase in a rat glioma model.
Mesenchymal stem cells (MSCs) have been recognized as promising delivery vehicles for gene therapy of gliomas. The purpose of this study was to evaluate the antitumor effect of cytosine deaminase (CD)-expressing MSCs in a rat C6 glioma model. ⋯ Genetically engineered MSCs have good therapeutic efficacy against experimental gliomas in rats.