Isplatin alone. Data on overall survival
is yet to come, and if it does not reach their prime Ren endpoint verst Strengths the results the idea that, the anti-EGFR agents have r Important role in TNBC. Has entered Adding cetuximab to irinotecan and carboplatin Born a Erh hung ORR ABT-751 E7010 subset of TNBC O Shaughnessy, s Phase II study performed in patients with metastatic disease. A disadvantage, however, that the main toxicity t Combination of irinotecan carboplatin in patients who verst again RKT was U cetuximab. Preferences INDICATIVE results of a clinical phase I and II of cetuximab in combination with paclitaxel or docetaxel showed a response to be sick. The toxicity observed t Cumulative toxicity of this combination was t of the individual agents expected.
Patients can suffer, the temperatures between reactions to the infusion of cetuximab, a chim Monoclonal Bodies with panitumumab, Bicalutamide a completely Constantly human Antique EGFR monoclonal anti body to be treated. This new agent is currently under clinical investigation in the context of metastatic triple-negative. Anti-EGFR tyrosine kinase inhibitors ITC has promise tt prior to clinical trials, hormonrefrakt efficacy in treating breast cancer Rem shown. Theoretically, these drugs have proven very effective in TNBC, given the proliferation of these tumors seems dependent His ngig EGFR. But clinical trials have the best hypothesis CONFIRMS, only the TKI studies not impressive in the Bev POPULATION heavily pretreated metastatic or treated in the ER Bev POPULATION, EGFR overexpression.
Instead, the TKI is to be more effective in the emergency room seemed, patients resistant to tamoxifen, tomoderate although the expression of EGFR in tumor rather low. But as cetuximab, the key to effective use of TKI probably lies in the combination treatment. Gefitinib in combination with carboplatin and docetaxel has been shown to improve the response of the synergistic and TNBC cells. ADAM inhibitors k Can be potential partners for TKI treatment in TNBC. Studies test Gefitinib with TMI, see no zus Tzlichen benefit when both drugs were administered simultaneously, the treatment administered gefitinib hours after ADAM inhibitor, however, was more effective, although the difference was not statistically significant. Inhibitor unnamed both Adam and Adam was found to reduce cell growth forward in clinical trials and has shown that TNBC, s migratory capacity decrease t.
Several tyrosine kinase inhibitors dasatinib and sunitinib have been tested mainly in populations of patients who were heavily pretreated. A Phase II study of dasatinib monotherapy in patients with anthracycline and, locally advanced or metastatic TNBC taxane or found only m Owned activity t. Genomic markers for selection of candidates were identified dasatinib therapy in patients with breast cancer and is tested for clinical utility. Sunitinib has been found a TKI targeting VEGF associated traditional knowledge in order to receive a response in TNBC patients. A Phase II study in patients with metastatic disease previously treated with an anthracycline and taxane showed a response rate of under-TNBC. But as bevacizumab, is this medicine increasingly seen as ineffective in breast cancer .