Phenformin Enhances the Efficacy of ERK Inhibition in NF1-Mutant Melanoma
نویسندگان
چکیده
منابع مشابه
Phenformin enhances the therapeutic benefit of BRAF inhibition in melanoma
Cutaneous Biology Research Center, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA 02129; Institute for Cancer Genetics and Departments of Dermatology and Pathology and Cell Biology, Columbia University Medical Center, New York, NY 10032; Department of Dermatology, Yale University School of Medicine, New Haven, CT 06520; Helen Diller Family Comprehensive Cancer Center...
متن کاملPhenformin enhances the therapeutic benefit of BRAF(V600E) inhibition in melanoma.
Biguanides, such as the diabetes therapeutics metformin and phenformin, have demonstrated antitumor activity both in vitro and in vivo. The energy-sensing AMP-activated protein kinase (AMPK) is known to be a major cellular target of biguanides. Based on our discovery of cross-talk between the AMPK and v-Raf murine sarcoma viral oncogene homolog B1 (BRAF) signaling pathways, we investigated the ...
متن کاملPLK1 inhibition enhances temozolomide efficacy in IDH1 mutant gliomas
Despite multimodal therapy with radiation and the DNA alkylating agent temozolomide (TMZ), malignant gliomas remain incurable. Up to 90% of grades II-III gliomas contain a single mutant isocitrate dehydrogenase 1 (IDH1) allele. IDH1 mutant-mediated transformation is associated with TMZ resistance; however, there is no clinically available means of sensitizing IDH1 mutant tumors to TMZ. In this ...
متن کاملTargeting Notch enhances the efficacy of ERK inhibitors in BRAF-V600E melanoma
The discovery of activating BRAF mutations in approximately 50% of melanomas has led to the development of MAPK pathway inhibitors, which have transformed melanoma therapy. However, not all BRAF-V600E melanomas respond to MAPK inhibition. Therefore, it is important to understand why tumors with the same oncogenic driver have variable responses to MAPK inhibitors. Here, we show that concurrent l...
متن کاملSustained MEK inhibition abrogates myeloproliferative disease in Nf1 mutant mice.
Children with neurofibromatosis type 1 (NF1) are predisposed to juvenile myelomonocytic leukemia (JMML), an aggressive myeloproliferative neoplasm (MPN) that is refractory to conventional chemotherapy. Conditional inactivation of the Nf1 tumor suppressor in hematopoietic cells of mice causes a progressive MPN that accurately models JMML and chronic myelomonocytic leukemia (CMML). We characteriz...
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: Journal of Investigative Dermatology
سال: 2017
ISSN: 0022-202X
DOI: 10.1016/j.jid.2017.01.013