Targeted cancer therapies attempt to stop the growth and spread of cancer by specifically targeting molecules that are involved in the progression of that cancer. A phase II clinical trial at the OSUCCC &ndash; James is working to help researchers develop better targeted therapies for patients whose cancer has spread to other parts of their body or contains mutations in its DNA sequence. Specifically this trial, supported by Pelotonia funds, will determine how well a drug called ponatinib works on patients with an alteration in a protein called fibroblast growth factor receptor (FGFR). &ldquo;Ponatinib hydrochloride may stop the growth of cancer cells by blocking some of the enzymes needed for cell growth,&rdquo; says principal investigator Sameek Roychowdhury, MD, PhD, a specialist in translational genomics and member of the Translational Therapeutics Program at the OSUCCC &ndash; James. &nbsp; The study&rsquo;s primary objective is to evaluate overall patient response to this drug and gain more insight into why some patients respond to therapy while others do not. Researchers are also interested in learning more about the cause of cancer resistance to targeted therapies. &ldquo;While we expect that patients with FGFR alterations will have disease regression, we also anticipate that patients will eventually acquire resistance to single-agent therapy with ponatinib and develop disease progression,&rdquo; the researchers state in their study application. &ldquo;Despite intensive study of FGFR in cancers, acquired resistance to FGF inhibition is unknown.&rdquo; The trial is open to patients 18 and older. Participants will orally receive ponatinib hydrochloride once daily for 28 days, and then repeat this course every 28 days in the absence of disease progression or adverse effects. Roychowdhury and co-investigator John Hays, MD, PhD, also of the Translational Therapeutics Program, will work together to study gene and protein alteration. To complete the clinical trial, Roychowdhury will collaborate with scientists at the University of Michigan. However, they hypothesize that acquired resistance is mediated through genomic or expressed alterations that provide a bypass for FGFR signaling. This study and its methods are designed to address their hypothesis.