Patients are randomized to sorafenib or placebo capecitabine. Sorafenib 600 mg / day is the average t Possible dose w While eff ective SOLTI 0701 was manageable. The dose may be escalated to 2500 mg/m2 and 800 mg / day or decreased the toxicity Manage t. Re dose increase after reduction is only allowed for the sorafenib / placebo. Prophylactic therapy and guidelines detailed symptomatic HFSR / HFS. Radiological evaluation is every 6 weeks for 36 weeks, then every 9 weeks. The LY2228820 prime Re endpoint was progression-free survival. Secondary Re objectives include overall survival, time to progression, overall response rate, and duration of response. Registration began in November 2010 and has 519 patients. Conclusion RESILIENCE offer nitive challenge PFS data for sorafenib capecitabine as fi rst-line or second-line therapy in HER2-negative BC tip and better characterize the profi t of risk benefits of this plan. Luminal breast cancer Her2 positive and negative long been successfully treated with anti- Estrogen therapy, aligned the Year fi anti-cancer agents in breast cancer.
Recently, molecular Ans PageSever profiling have improved identifi cation of a subgroup of Andarine poor prognosis, but the biological mechanisms that contribute to this Ph Genotype currently unclear. Related to the projection defi nition, it is clear that the proliferation markers. Clearly ER/HER2 breast separate into at least two prognostic groups Immunohistochemistry with Ki67 levels of proteins and genes prognostic signatures as MammaPrint � Score of 21 genes offense that ratio Ratio of two genes and genomic quality t While quantitative Ma Took proliferative activity t. However, a big e not exist biologically relevant section. Defi nitionen molecular subtype with the PAM50 gene expression or other classifications based toren not provide more consistent and reproducible definition luminal A or B Defi. Improve the defi nition and clinical management of luminal subtypes come from a better amplifier Ndnis the molecular factors of Ph Genotype.
Recently, mutations in PIK3CA and AKT1 proven with a good prognosis luminal A Ph Associated genotype, w While FGFR1 and ZNF703 amplification Rkern cations for about 25% of the luminal Ph Genotype B. It is hoped that new technologies as sequencing Next generation ages insight st ERpositive new biology of breast cancer. Recent studies by sequential lacing adorns the new generation have identified mutations in MAP3K1 and MYST3 ATR 10% of all F lle Breast cancer that ER may be associated with de novo resistance hormone. It is shown that oncogenic driver can shed new light on the biology of breast cancer and endocrine responsive shed inspire new therapeutic strategies. After all, the recent results suggest the BOLERO-2 trial that metastases k Can be eff ective with the addition of an inhibitor of mTORC1 treated RE, suggesting that for many patients with acquired resistance to endocrine therapy, Activation of the mTOR signaling pathway plays an r German cant in the biology of the tumor. Breast cancer is the luminal almost all ER positive and as such is about 75 to 80% of the disease.