red blood cells are the part of gi tract that absorbs iron.
what part of gi tract is iron absorbed?
red blood cells
the symptoms of meitl are generally non-specific. the diagnosis depends on endoscopic findings in the gi tract, histological findings on biopsied specimens from involved areas of the gi tract, evidence of disease involvement outside of the gi tract, and the differentiation of meitl from other gi tract lymphomas and benign lymphoproliferative diseases. endoscopy typically shows multiple raised and/or ulcerated lesions involving the jejunum or ileum, and less commonly, the duodenum, stomach, or colon. these lesions may occur at multiple sites or spread throughout large areas of the gi tract. biopsied tissues show abnormally broad intestinal villi caused by the infiltration of sheets of uniformly-sized lymphocytes. these lymphocytes may also infiltrate and disrupt the architecture of nearby intestinal crypts and the epithelial lining. unlike celiac disease-associated eatl, the lesions usually have little evidence of inflammatory cells (particularly lymphoplasmacytoid cells, i.e. cells showing a mixture of b cell and plasma cell morphological features) or of infiltration of the epithelium lining by the types of lymphocytes seen in celiac disease. the lymphocytes in these lesions are t cells expressing the marker molecules and genetic abnormalities given in the above pathophysiology section. ct scans commonly reveal involvement of mesenteric lymph nodes. advanced cases have involvement of the bone marrow and/or dissemination into other organs.
monomorphic epitheliotropic intestinal t cell lymphoma
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