Sandbox Reserved 425: Difference between revisions

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==Introduction==

Potatinib was developed as a treatment option for chronic myeloid leukemia (CML) as other inhibitors in treatment have become ineffective. ~~Further mutations in~~ BCR-ABL, a kinase with a cancerous genetic mutation in chromosome 22 that leaves it always active, has left earlier ~~versions~~ of tyrosine kinases unable to bind in almost 30% of cases over a course of 5 years of treatment. The mutant BCR-ABL kinase’s ability to develop new ~~mutations~~ has pushed for newer developments in ~~inhibitiors like~~ Potatinib<ref name="seven">PMID: 21118377 </ref>.

Potatinib was developed as a treatment option for chronic myeloid leukemia (CML) as other inhibitors in treatment have become ineffective. BCR-ABL is a kinase with cancerous genetic mutation in chromosome 22 that leaves it always active. Further mutations in BCR-ABL has left earlier drugs of tyrosine kinases unable to bind in almost 30% of cases over a course of five years of treatment. The newer, mutant BCR-ABL kinase’s ability to develop new resistances has pushed for newer developments in inhibitors, such as Potatinib<ref name="seven">PMID: 21118377 </ref>.

Fibroblast growth factor (FGFR) signaling, the factor that normally activates the BCR-ABL kinase, is the protein behind both tissue development and repair. The activation happens through a series of cascading signals that induce proliferation and migration in cells. Though mutations in the regulation of the FGFR tyrosine kinase family can result in malignant tumor growth<ref name="two" />. The tyrosine kinase inhibitor Ponatinib has been used to

Fibroblast growth factor (FGFR) signaling is the factor that normally activates the BCR-ABL kinase. Also, it is the protein behind both tissue development and repair. The activation of BCR-ABL happens through a series of cascading signals that induce proliferation and migration in cells. Though mutations in the regulation of the FGFR tyrosine kinase family can result in malignant tumor growth<ref name="two" />. The tyrosine kinase inhibitor Ponatinib has been used to

<scene name='48/483882/Activation_loop/1'>bind</scene> to the mutant version of kinase BCR-ABL by the kinase's specific "DFG-out" conformation. The "DFG-out" conformation has the phenylalanine group of BCR-ABL flipped out of its hydrophobic binding site. Ponatinib is the first of its kind to be able to inhibit this specific mutation in BCR-ABL of the "DGF-out" combination<ref name="two" />.

Sandbox Reserved 425: Difference between revisions

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@@ Line 11: / Line 11: @@
 ==Introduction==
-Potatinib was developed as a treatment option for chronic myeloid leukemia (CML) as other inhibitors in treatment have become ineffective. Further mutations in BCR-ABL, a kinase with a cancerous genetic mutation in chromosome 22 that leaves it always active, has left earlier versions of tyrosine kinases unable to bind in almost 30% of cases over a course of 5 years of treatment. The mutant BCR-ABL kinase’s ability to develop new mutations has pushed for newer developments in inhibitiors like Potatinib<ref name="seven">PMID: 21118377 </ref>.
+Potatinib was developed as a treatment option for chronic myeloid leukemia (CML) as other inhibitors in treatment have become ineffective. BCR-ABL is a kinase with cancerous genetic mutation in chromosome 22 that leaves it always active. Further mutations in BCR-ABL has left earlier drugs of tyrosine kinases unable to bind in almost 30% of cases over a course of five years of treatment. The newer, mutant BCR-ABL kinase’s ability to develop new resistances has pushed for newer developments in inhibitors, such as Potatinib<ref name="seven">PMID: 21118377 </ref>.
-Fibroblast growth factor (FGFR) signaling, the factor that normally activates the BCR-ABL kinase, is the protein behind both tissue development and repair. The activation happens through a series of cascading signals that induce proliferation and migration in cells. Though mutations in the regulation of the FGFR tyrosine kinase family can result in malignant tumor growth<ref name="two" />. The tyrosine kinase inhibitor Ponatinib has been used to
+Fibroblast growth factor (FGFR) signaling is the factor that normally activates the BCR-ABL kinase. Also, it is the protein behind both tissue development and repair. The activation of BCR-ABL happens through a series of cascading signals that induce proliferation and migration in cells. Though mutations in the regulation of the FGFR tyrosine kinase family can result in malignant tumor growth<ref name="two" />. The tyrosine kinase inhibitor Ponatinib has been used to
 <scene name='48/483882/Activation_loop/1'>bind</scene> to the mutant version of kinase BCR-ABL by the kinase's specific "DFG-out" conformation. The "DFG-out" conformation has the phenylalanine group of BCR-ABL flipped out of its hydrophobic binding site. Ponatinib is the first of its kind to be able to inhibit this specific mutation in BCR-ABL of the "DGF-out" combination<ref name="two" />.