The improved understanding of the molecular biology of @entity5 is helping to define the role of new targets and prognostic indices that can direct the most appropriate choice of treatment for @entity1442 . Many @entity1 @entity5 express high levels of growth factors and their receptors that can be used as potential therapeutical targets. @entity669 -kinase receptors, including many growth factor receptors such the receptors for @entity4179 ( @entity4179 ), @entity7 ( @entity7 ), and @entity1722 , have been found overexpressed in @entity5 . For many of these growth factor receptors, the degree of expression has been associated with the progression of @entity5 and a poor prognosis. Among the best studied growth factor receptors are the two members of @entity4179 receptor familiy @entity470 ( @entity470 ), and @entity1722 ( @entity1722 ). Several preclinical studies in @entity150 models, have confirmed that systemic administration of growth factor inhibitors inhibits the growth and @entity3 of @entity1 transitional cell @entity189 established in the bladder wall of athymic @entity19 . Additional studies indicate that therapy with @entity470 inhibitors enhances the activity of conventional cytoreductive chemotherapeutic agents, in part by inhibiting @entity5 cell proliferation, angiogenesis, and inducing apoptosis. Novel targeted therapy hold promise to improve the current results of @entity150 treatment. Based on the success seen with anti- @entity1722 monoclonal antibodies (Herceptin) and the promising results with @entity470 targeted agents (IMC-C225 Cetuximab, ZD1389 Iressa, @entity3866 Tarceva, GW 57016) in other @entity5 types, and based on the results obtained in preclinical models, there is a great interest in assessing these agents in @entity1 with @entity150 . Several trials are now ongoing testing these new agents alone or in combination with chemotherapy in @entity150 @entity1 . The integration of these newer biologic agents, probably to supplement rather than to supplant chemotherapeutic drugs, should be a primary direction of research with the objective to interfere with multiple aspects of @entity150 progression. However, the value of integration of biologically targeted agents into combined modality treatment for @entity1 with @entity150 has still to be proven.

Novel approaches with targeted therapies in XXXX . Therapy of @entity150 by blockade of the @entity4179 receptor family.

@entity1 :: ('9606', 'Species') :: ['human', 'patients'] @entity7 :: ('7422', 'Gene') :: ['vascular endothelial growth factor', 'VEGF'] @entity5 :: ('MESH:D009369', 'Disease') :: ['tumor', 'urothelial malignancies', 'cancer', 'urothelial tumors', 'tumors'] @entity470 :: ('1956', 'Gene') :: ['EGFr', 'ErbB-1', 'EGFR'] @entity19 :: ('10090', 'Species') :: ['nude mice'] @entity189 :: ('MESH:D002277', 'Disease') :: ['carcinoma'] @entity3866 :: ('MESH:C400278', 'Chemical') :: ['OSI-774'] @entity1442 :: ('MESH:D020178', 'Disease') :: ['advanced disease'] @entity4179 :: ('1950', 'Gene') :: ['epidermal growth factor', 'EGF'] @entity150 :: ('MESH:D001749', 'Disease') :: ['bladder cancer'] @entity3 :: ('MESH:D009362', 'Disease') :: ['metastasis'] @entity669 :: ('CHEBI:18186', 'Chemical') :: ['Tyrosine'] @entity1722 :: ('2064', 'Gene') :: ['ErbB-2', 'Her2/neu', 'HER2']
@entity150 :: (MESH:D001749,Disease) :: ['bladder cancer']
