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The brand name for ponatinib is Iclusig. Iclusig received an accelerated approval grant through the Food and Drug Administration. It was mainly prescribed to patients suffering from Chronic Myeloid Leukemia or Acute Lymphoblastic Leukemia who did not make any progress with the first and second generation TKIs. However, the clinical trials data displayed a spike in adverse effects. These consequences include heart failure, stroke, coronary artery disease, loss of blood flow to body parts leading to amputation amongst other narrowing of blood vessels<ref>FDA Drug Safety Communication: FDA investigating leukemia drug Iclusig (ponatinib) after increased reports of serious blood clots in arteries and veins; Drug Safety and Availability; United States Food and Drug Administration (2013). Web. [http://www.fda.gov/Drugs/DrugSafety/ucm370945.htm]</ref>.  
The brand name for ponatinib is Iclusig. Iclusig received an accelerated approval grant through the Food and Drug Administration. It was mainly prescribed to patients suffering from Chronic Myeloid Leukemia or Acute Lymphoblastic Leukemia who did not make any progress with the first and second generation TKIs. However, the clinical trials data displayed a spike in adverse effects. These consequences include heart failure, stroke, coronary artery disease, loss of blood flow to body parts leading to amputation amongst other narrowing of blood vessels<ref>FDA Drug Safety Communication: FDA investigating leukemia drug Iclusig (ponatinib) after increased reports of serious blood clots in arteries and veins; Drug Safety and Availability; United States Food and Drug Administration (2013). Web. [http://www.fda.gov/Drugs/DrugSafety/ucm370945.htm]</ref>.  


FGFR-4 is abundantly present in human prostate cancer observed in vitro and in mouse model simulations<ref name="nine">PMID: 22573348</ref>. A <scene name='48/483882/Variant/9'>variant</scene> of FGFR-4 with Arg388 replacing Gly388 is implicated with increased human prostate cancer. This variation causes increased receptor stability and activation<ref name="ten">PMID:18670643</ref>. A study revealed that the inhibition of FGFR-4 signaling completely curtailed prostate cancer cell lines that were responsible for tumor growth<ref name="nine">PMID: 22573348</ref>. Due to the significant results of diminished cell growth in treated tumors, targeting fibroblast growth factor signaling appears to provide a promising step towards combating aggressive prostate cancer.  
FGFR-4 is abundantly present in human prostate cancer observed in vitro and in mouse model simulations<ref name="nine">PMID: 22573348</ref>. A <scene name='48/483882/Variant/9'>variant</scene> of FGFR-4 with Arg388 replacing Gly388 is implicated with increased human prostate cancer. This variation causes increased receptor stability and activation<ref name="ten">PMID:18670643</ref>. A study revealed that the <scene name='48/483882/Inhibition/1'>inhibition</scene> of FGFR-4 signaling completely curtailed prostate cancer cell lines that were responsible for tumor growth<ref name="nine">PMID: 22573348</ref>. Due to the significant results of diminished cell growth in treated tumors, targeting fibroblast growth factor signaling appears to provide a promising step towards combating aggressive prostate cancer.  




Proteopedia Page Contributors and Editors (what is this?)Proteopedia Page Contributors and Editors (what is this?)

OCA, Lynmarie K Thompson, Student