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The discovery of a new therapeutic target site on the STAT3 oncoprotein – a protein that interferes with chemotherapy by halting deaths of cancerous cells – could cut down on acute myeloid leukemia (AML) relapse in chemoresistant patients, according to research published in Angewandte Chemie.
The STAT3 protein – which stands for “signal transducer and activator of transcription 3” – is a suspected factor in the relapse of nearly 40% of children with AML. A team of researchers from Rice University, working with colleagues at Baylor College of Medicine and the University of Texas MD Anderson Cancer Center, all in Houston, developed a proximity-driven rhodium (II) catalyst known as MM-206, which blocks STAT3 function by identifying the STAT3 coiled-coil domain as a novel ligand-binding site and delivering a naphthalene sulfonamide inhibitor, thus halting the disease promoting effects of STAT3.
The effects were replicated in tumor growth models and testing in a leukemia mouse model suggest this approach can be used to shut down STAT3 activity in AML patients, according to coauthor Dr. Zachary Ball of the department of chemistry at Rice.
Read the full article here: Angew Chem Int Ed Engl. 2015 Sep 7. doi: 10.1002/anie.201506889.
The discovery of a new therapeutic target site on the STAT3 oncoprotein – a protein that interferes with chemotherapy by halting deaths of cancerous cells – could cut down on acute myeloid leukemia (AML) relapse in chemoresistant patients, according to research published in Angewandte Chemie.
The STAT3 protein – which stands for “signal transducer and activator of transcription 3” – is a suspected factor in the relapse of nearly 40% of children with AML. A team of researchers from Rice University, working with colleagues at Baylor College of Medicine and the University of Texas MD Anderson Cancer Center, all in Houston, developed a proximity-driven rhodium (II) catalyst known as MM-206, which blocks STAT3 function by identifying the STAT3 coiled-coil domain as a novel ligand-binding site and delivering a naphthalene sulfonamide inhibitor, thus halting the disease promoting effects of STAT3.
The effects were replicated in tumor growth models and testing in a leukemia mouse model suggest this approach can be used to shut down STAT3 activity in AML patients, according to coauthor Dr. Zachary Ball of the department of chemistry at Rice.
Read the full article here: Angew Chem Int Ed Engl. 2015 Sep 7. doi: 10.1002/anie.201506889.
The discovery of a new therapeutic target site on the STAT3 oncoprotein – a protein that interferes with chemotherapy by halting deaths of cancerous cells – could cut down on acute myeloid leukemia (AML) relapse in chemoresistant patients, according to research published in Angewandte Chemie.
The STAT3 protein – which stands for “signal transducer and activator of transcription 3” – is a suspected factor in the relapse of nearly 40% of children with AML. A team of researchers from Rice University, working with colleagues at Baylor College of Medicine and the University of Texas MD Anderson Cancer Center, all in Houston, developed a proximity-driven rhodium (II) catalyst known as MM-206, which blocks STAT3 function by identifying the STAT3 coiled-coil domain as a novel ligand-binding site and delivering a naphthalene sulfonamide inhibitor, thus halting the disease promoting effects of STAT3.
The effects were replicated in tumor growth models and testing in a leukemia mouse model suggest this approach can be used to shut down STAT3 activity in AML patients, according to coauthor Dr. Zachary Ball of the department of chemistry at Rice.
Read the full article here: Angew Chem Int Ed Engl. 2015 Sep 7. doi: 10.1002/anie.201506889.
FROM ANGEWANDTE CHEMIE