6-Thioguanine Selectively Kills BRCA2-Defective Tumors and Overcomes PARP Inhibitor Resistance
نویسندگان
چکیده
منابع مشابه
6-thioguanine selectively kills BRCA2-defective tumors and overcomes PARP inhibitor resistance.
Familial breast and ovarian cancers are often defective in homologous recombination (HR) due to mutations in the BRCA1 or BRCA2 genes. Cisplatin chemotherapy or poly(ADP-ribose) polymerase (PARP) inhibitors were tested for these tumors in clinical trials. In a screen for novel drugs that selectively kill BRCA2-defective cells, we identified 6-thioguanine (6TG), which induces DNA double-strand b...
متن کاملPredicting PARP inhibitor sensitivity and resistance
A healthy diet rich in fruits and vegetables is an important part of a healthy lifestyle. Whereas epidemiological data sometimes fail to provide proof of this concept, molecular evidence is accumulating that clearly shows both preventive as well as therapeutic effects of compounds from natural origins. in the paper of Guido Kroemer's group about pro-autophagic polyphenols and their inhibitory e...
متن کاملRhodacyanine Derivative Selectively Targets Cancer Cells and Overcomes Tamoxifen Resistance
MKT-077, a rhodacyanine dye, was shown to produce cancer specific cell death. However, complications prevented the use of this compound beyond clinical trials. Here we describe YM-1, a derivative of MKT-077. We found that YM-1 was more cytotoxic and localized differently than MKT-077. YM-1 demonstrated this cytotoxicity across multiple cancer cell lines. This toxicity was limited to cancer cell...
متن کاملSelectively Kills Tumor Cells
nloaded 1 kinase activates multiple transcription factors and regulates the level of reactive oxygen species We have previously reported that ablation of TAK1 in keratinocytes causes hypersensitivity to ROSd cell apoptosis. It is known that some tumor cells produce ROS at higher levels compared with normal e used inducible epidermal-specific TAK1 knockout mice and examined whether ablation of T...
متن کاملThe CDK4/6 inhibitor LY2835219 overcomes vemurafenib resistance resulting from MAPK reactivation and cyclin D1 upregulation.
B-RAF selective inhibitors, including vemurafenib, were recently developed as effective therapies for melanoma patients with B-RAF V600E mutation. However, most patients treated with vemurafenib eventually develop resistance largely due to reactivation of MAPK signaling. Inhibitors of MAPK signaling, including MEK1/2 inhibitor trametinib, failed to show significant clinical benefit in patients ...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
ژورنال
عنوان ژورنال: Cancer Research
سال: 2010
ISSN: 0008-5472,1538-7445
DOI: 10.1158/0008-5472.can-09-3416