Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C1658953 (tumor vasculature)
 2,390 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cardiac toxicity of chemotherapeutic agents is a rapidly evolving area of increasing significance because of the increasing pool of long-term cancer survivors. The spectrum of cardiotoxicity with chemotherapeutic agents includes hypertension, QTc prolongation, acute cardiomyopathy, and bradyarrhythmias. The most common issue to arise has been cardiomyopathy with anthracyclines. Preventative strategies that have met with some success have included the use of less cardiotoxic analogs such as epirubicin and liposomal anthracycline preparations. The cardioprotectant agent dexrazoxane reduces cardiomyopathy but there are significant toxicity issues. Therefore, the main strategy for preventing cardiotoxicity remains careful monitoring with radionuclide angiography or echocardiography. The role of investigational markers of myocardial injury, such as troponin T or brain natriuretic peptide, remains of great interest. Management is according to conventional management of congestive heart failure. Trastuzumab is an antibody therapy directed against the human epidermal growth factor receptor-2 (HER2) receptor, which increases survival in patients with metastatic breast cancer and is under evaluation in the adjuvant setting. It also causes a decrease in left ventricular ejection fraction (LVEF) in a minority of patients. Incidence is increased if trastuzumab is given in conjunction with paclitaxel or anthracyclines. It differs from anthracycline cardiotoxicity in that it is not cumulative dose-dependent and often improves after withdrawal of treatment. Re-treatment with trastuzumab is often possible. Novel agents under development offer a different spectrum of toxicity to existing anticancer drugs and it appears likely that cardiovascular toxicity will be an important issue for many of these drugs, particularly those that target the tumor vasculature.
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PMID:The prevention and management of cardiovascular complications of chemotherapy in patients with cancer. 1598 6

The identification of a specific biomarker involves the development of new clinical diagnostic tools, and an in-depth understanding of the disease at the molecular level. When new blood vessels form in tumor cells, endothelial cell production is induced, a process that plays a key role in disease progression and metastasis to distinct organs for solid tumor types. The present study reports on the identification of a new biomarker on primary cultured mouse tumor endothelial cells (mTECs) using our recently developed high-affinity DNA aptamer AraHH001 (Kd = 43 nmol/L) assisted proteomics approach. We applied a strategy involving aptamer-facilitated biomarker discovery. Biotin-tagged AraHH001 was incubated with lysates of mTECs and the aptamer-proteins were then conjugated with streptavidin magnetic beads. Finally, the bound proteins were separated by sodiumdodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) with silver staining. We identified troponin T via matrix assisted laser desorption ionization-time of flight (MALDI-TOF) mass spectrometry, the molecular target of aptamer AraHH001, and its presence was confirmed by measuring mRNA, protein levels, western blot, immunostaining, a gel shift assay of AraHH001 with troponin T. We first report here on the discovery of troponin T on mTECs, a promising and interesting diagnostic tool in the development of antiangiogenic therapy techniques the involves the targeting of the tumor vasculature.
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PMID:Identification and expression of troponin T, a new marker on the surface of cultured tumor endothelial cells by aptamer ligand. 2481 Aug 1