Dietmar Siemann

Vascular targeting agents enhance chemotherapeutic agent activities in solid tumor therapy.

Preclinical evaluations of therapies combining the vascular targeting agent combretastatin A-4 disodium phosphate and conventional anticancer therapies in the treatment of Kaposi's sarcoma.

Enhancement of radiation therapy by the novel vascular targeting agent ZD6126.

Adeno-associated virus-mediated gene transfer of endostatin inhibits angiogenesis and tumor growth in vivo.

Antitumor efficacy of conventional anticancer drugs is enhanced by the vascular targeting agent ZD6126.

Enhancement of radiation therapy by vascular targeting agents.

Targeting the tumor blood vessel network to enhance the efficacy of radiation therapy.

Comparison of the EF-1 alpha and the CMV promoter for engineering stable tumor cell lines using recombinant adeno-associated virus.

Gene therapy delivery of endostatin enhances the treatment efficacy of radiation.

Postoperative radiation therapy for squamous cell carcinoma of the head and neck.

Simultaneous targeting of VEGF message and VEGF receptor signaling as a therapeutic anticancer approach.

Targeting the tumor vasculature: a strategy to improve radiation therapy.

Vascular-targeting therapies for treatment of malignant disease.

Therapeutic strategies that selectively target and disrupt established tumor vasculature.

Efficacy of combined antiangiogenic and vascular disrupting agents in treatment of solid tumors.

Utility of 19F MRS detection of the hypoxic cell marker EF5 to assess cellular hypoxia in solid tumors.

Differentiation and definition of vascular-targeted therapies.

The vascular disrupting agent ZD6126 shows increased antitumor efficacy and enhanced radiation response in large, advanced tumors.

Radiotherapy alone or combined with carbogen breathing for squamous cell carcinoma of the head and neck: a prospective, randomized trial.

Targeting the tumor vasculature: enhancing antitumor efficacy through combination treatment with ZD6126 and ZD6474.

Preclinical studies of the novel vascular disrupting agent MN-029.

Recombinant adeno-associated and adenoviral vectors for the transduction of pancreatic and colon carcinoma.

VEGF-associated tyrosine kinase inhibition increases the tumor response to single and fractionated dose radiotherapy.

Effect of the second-generation vascular disrupting agent OXi4503 on tumor vascularity.

Evaluations of vascular disrupting agents CA4P and OXi4503 in renal cell carcinoma (Caki-1) using a silicon based microvascular casting technique.

Augmented antitumor effects of radiation therapy by 4-1BB antibody (BMS-469492) treatment.

Impact of VEGF expression on the physiological characteristics of clonal cell lines.

Characterizing the tumor response to treatment with combretastatin A4 phosphate.

Monitoring the treatment efficacy of the vascular disrupting agent CA4P.

Oxidative stress regulates expression of VEGFR1 in myeloid cells: link to tumor-induced immune suppression in renal cell carcinoma.

Dual targeting of tumor vasculature: combining Avastin and vascular disrupting agents (CA4P or OXi4503).

Vascular targeted therapies in oncology.

Intrinsic radiosensitivity and repair of sublethal radiation-induced damage in canine osteosarcoma cell lines.

Development of an intramuscular xenograft model of canine osteosarcoma in mice for evaluation of the effects of radiation therapy.

The vascular endothelial growth factor receptor-2 tyrosine kinase inhibitor cediranib (Recentin; AZD2171) inhibits endothelial cell function and growth of human renal tumor xenografts.

A review and update of the current status of the vasculature-disabling agent combretastatin-A4 phosphate (CA4P).

X box-binding protein 1 regulates angiogenesis in human pancreatic adenocarcinomas.

Impact of tumor cell VEGF expression on the in vivo efficacy of vandetanib (ZACTIMA; ZD6474).

Bone marrow stem and progenitor cell contribution to neovasculogenesis is dependent on model system with SDF-1 as a permissive trigger.

In vivo functional differences in microvascular response of 4T1 and Caki-1 tumors after treatment with OXi4503.

Expression of pluripotent stem cell reprogramming factors by prostate tumor initiating cells.

Leukemia regression by vascular disruption and antiangiogenic therapy.

BMS-777607, a small-molecule met kinase inhibitor, suppresses hepatocyte growth factor-stimulated prostate cancer metastatic phenotype in vitro.

The unique characteristics of tumor vasculature and preclinical evidence for its selective disruption by Tumor-Vascular Disrupting Agents.

Temporal aspects of the action of ASA404 (vadimezan; DMXAA).

Support of a free radical mechanism for enhanced antitumor efficacy of the microtubule disruptor OXi4503.

Impact of hypoxia on the metastatic potential of human prostate cancer cells.

Development of optimized AAV3 serotype vectors: mechanism of high-efficiency transduction of human liver cancer cells.

Vascular effects of plinabulin (NPI-2358) and the influence on tumour response when given alone or combined with radiation.

Restraint of angiogenesis by zinc finger transcription factor CTCF-dependent chromatin insulation.

E-cadherin plasticity in prostate cancer stem cell invasion.

Another road leads to HIF-1 activation: implications for prostate cancer progression.

Impact of the SRC inhibitor dasatinib on the metastatic phenotype of human prostate cancer cells.

Impact of the small molecule Met inhibitor BMS-777607 on the metastatic process in a rodent tumor model with constitutive c-Met activation.

Inhibition of endothelial/smooth muscle cell contact loss by the investigational angiopoietin-2 antibody MEDI3617.

Src-signaling interference impairs the dissemination of blood-borne tumor cells.

Constitutively active c-Met kinase in PC-3 cells is autocrine-independent and can be blocked by the Met kinase inhibitor BMS-777607.

Vascular development in mouse lung metastases.

Cell-based selection provides novel molecular probes for cancer stem cells.

Transcriptional repression of VEGF by ZNF24: mechanistic studies and vascular consequences in vivo.

An update on the clinical development of drugs to disable tumor vasculature.

Adenomatous polyposis coli-mediated accumulation of abasic DNA lesions lead to cigarette smoke condensate-induced neoplastic transformation of normal breast epithelial cells.

Effect of bevacizumab on angiogenesis and growth of canine osteosarcoma cells xenografted in athymic mice.

Cathepsin L inhibition by the small molecule KGP94 suppresses tumor microenvironment enhanced metastasis associated cell functions of prostate and breast cancer cells.

Effects of exercise training on tumor hypoxia and vascular function in the rodent preclinical orthotopic prostate cancer model.

Effects of aurothiomalate treatment on canine osteosarcoma in a murine xenograft model.

MRI-based computational model of heterogeneous tracer transport following local infusion into a mouse hind limb tumor.

Modulation of blood flow, hypoxia, and vascular function in orthotopic prostate tumors during exercise.

In vivo spectral and fluorescence microscopy comparison of microvascular function after treatment with OXi4503, Sunitinib and their combination in Caki-2 tumors.

Limitations of the dorsal skinfold window chamber model in evaluating anti-angiogenic therapy during early phase of angiogenesis.

Targeting the Angiopoietin-2/Tie-2 axis in conjunction with VEGF signal interference.

Histone Methyltransferase hSETD1A Is a Novel Regulator of Metastasis in Breast Cancer.

VEGFR inhibitors upregulate CXCR4 in VEGF receptor-expressing glioblastoma in a TGFβR signaling-dependent manner.

Modulation of the tumor vasculature and oxygenation to improve therapy.

Cathepsin L targeting in cancer treatment.

Synthesis and biochemical evaluation of benzoylbenzophenone thiosemicarbazone analogues as potent and selective inhibitors of cathepsin L.

Cathepsin L inactivation leads to multimodal inhibition of prostate cancer cell dissemination in a preclinical bone metastasis model.

Chemosensitizing AML cells by targeting bone marrow endothelial cells.

Cathepsin L in tumor angiogenesis and its therapeutic intervention by the small molecule inhibitor KGP94.

Hypoxia regulates SOX2 expression to promote prostate cancer cell invasion and sphere formation.

Epithelial-to-mesenchymal transition confers pericyte properties on cancer cells.

Exercise and the Tumor Microenvironment: Potential Therapeutic Implications.

Have Clinical Trials Properly Assessed c-Met Inhibitors?

Tumor oxygenation and cancer therapy-then and now.

Treatment with Src inhibitor Dasatinib results in elevated metastatic potential in the 4T1 murine mammary carcinoma model.

Stromal cells in breast cancer as a potential therapeutic target.

Stability and Mobility of Magnetic Nanoparticles in Biological Environments Determined from Dynamic Magnetic Susceptibility Measurements.

Failures in preclinical and clinical trials of c-Met inhibitors: evaluation of pathway activity as a promising selection criterion.

Reliability of blood lactate as a measure of exercise intensity in different strains of mice during forced treadmill running.

Axl signaling is an important mediator of tumor angiogenesis.

Prostate cancer cell growth characteristics in serum and prostate-conditioned media from moderate-intensity exercise-trained healthy and tumor-bearing rats.

c-Src is required for hypoxia-induced metastasis-associated functions in prostate cancer cells.

Cathepsin L secretion by host and neoplastic cells potentiates invasion.

Gas6/Axl Signaling Pathway in the Tumor Immune Microenvironment.

Bioprinting on Live Tissue for Investigating Cancer Cell Dynamics.

Inhibition of the Axl pathway impairs breast and prostate cancer metastasis to the bones and bone remodeling.

Using a combination of gangliosides and cell surface vimentin as surface biomarkers for isolating osteosarcoma cells in microfluidic devices.

Normal tissue and tumor microenvironment adaptations to aerobic exercise enhance doxorubicin anti-tumor efficacy and ameliorate its cardiotoxicity in retired breeder mice.

Therapeutic Targeting of the Gas6/Axl Signaling Pathway in Cancer.