absorption is a major function of the gi tract and is accomplished by active transport, facilitated diffusion.
absorption is a major function of the gi tract and is accomplished by active transport, facilitated diffusion.
absorption is a major function of the gi tract. how is absorption accomplished in the gi tract?
active transport , facilitated diffusion
Na
Na
activating mutations in pdgfra are also involved in the development of 2–15% of the most common mesenchymal neoplasm of the gastrointestinal tract (gi tract), viz., gastrointestinal stromal tumors or (gists). gist tumors are sarcomas derived from the gi tract's connective tissue whereas most gi tract tumors are adenocarcinomas derived from the tract's epithelium cells. gist tumors occur throughout the gi tract but most (66%) occur in the stomach and when developing there have a lower malignant potential than gist tumors found elsewhere in the gi tract. the most common pdgfra mutations found in gist tumors occur in exon 18 and are thought to stabilize pdgfra's tyrosine kinase in an activated conformation. a single mutation, d842v, in this exon accounts for 70% of gist tumors. the next most common gist tumor mutation occurs in exon 18, accounts for <1% of gists tumors, and is a deletion of codons 842 to 845. exon 12 is the second most commonly mutated pdgfra exon in gist, being found in ~1% of gist tumors. mutations in pdgfra's exon 14 are found in <1% of gist tumors. while some "pdgfra" mutation-induced gist tumors are sensitive to the tyrosine kinase inhibitor, imatinib, the most common mutation, d842v, as well as some very rare mutations are resistant to this drug: median overall survival is reported to be only 12.8 months in patients whose tumors bear the d842v mutation compared to 48–60 months in large series of imatinib-treated patients with other types of gist mutations. consequently, it is critical to define the exact nature of "pdgfr"-induced mutant gist tumors in order to select appropriate therapy particularly because a novel pdgfra selective kinase inhibitor, crenolanib, is under investigation for treating d842v-induced and other imatinib-resistant gist tumors. a randomized trial testing the efficacy of crenolanib in patients with gist tumors bearing the d842v mutation is under recruitment.
pdgfra