Metastatic breast cancer. Long-term monitoring is needed to determine whether these effects of perifosine in clinical improvement resulted. In a phase II trial with M Nnern with biochemically recurrent prostate cancer, 2-Methoxyestradiol 2-ME2 hormone-sensitive, perifosine administration Feedb Length led PSA 5/24 patients, but none of the patients met the predefined criteria for a true answer. A clinical phase II trial of celecoxib in patients with recurrent prostate cancer after radical prostatectomy or radiation therapy showed a significant inhibition of biochemical PSA doubling time. Three months after starting treatment, 90% of patients had a PSA doubling time of less than 11/40, a decrease in absolute PSA levels. However, a study with celecoxib compared with placebo in one Hnlichen patient population, no difference in PSA doubling time.
Has entered celecoxib in combination with docetaxel and estramustine in patients with CRPC Born a median survival time of 19.2 months, relative Similar TAX 327 and SWOG 99 16th Other tests, such as helping Stampede, the R The inhibition of COX-2 in the treatment of advanced prostate cancer OSI-930 c-Kit inhibitor and whether anti-tumor activity of t is due to its properties Aktinhibiting. Clinical investigation of mTOR inhibitors in oncology is a relatively new but promising study, which began in the last ten years. Rapamycin was originally con U as an immunosuppressant and is approved by the FDA in 1998 approved for this purpose. The pharmacokinetics of this drug is known for excellent absorption after oral administration and peak at about 1.5 hours of administration.
The incidence of severe toxic reactions were rare, and only mild side effects, including normal hyperlipidaemia Anemia, thrombocytopenia, leukopenia, diarrhea has been reported skin rash, pneumonia, and electrolyte abnormalities. There are also data on the rapid Elvitegravir Anh Ufung of pharmacological profiles Similar to rapamycin indicate that these analogues well tolerated Are possible and a minimal negative side effects. Effectiveness of mTOR inhibition has been demonstrated in early phase trials in a number of malignancies, and mTOR inhibitors are in clinical development in the building Rmutterkrebs, breast cancer, glioblastoma, lymphomas and sarcomas. ITC 779 was studied in a phase III trial in advanced renal cell carcinoma-high, and median overall survival was significantly increased compared to IFN Ht.
ITC 779 was subsequently Approved end of the FDA in 2007 for the treatment of advanced renal cell carcinoma. In prostate cancer, there are several ongoing Phase I and II trials of mTOR inhibitors. Some of these tests are stupid We in the neoadjuvant and / or adjuvant treatment. These tests on the analysis of the key factors in the mTOR signaling, and Ver its focus Changes in response to inhibition of mTOR. Certainly, the F Ability, to assess the molecular response to treatment is one of the advantages of central modifiers of cellular Ren signal transmission. Molecular stratification of patients with mTOR inhibitor therapy can help patients most likely to benefit from a treatment sparing patients who have not probable. The use of neoadjuvant mTOR-inhibiting k nnte Also an opportunity to target tumor cells before th