Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q3V6T2 (ape)
 2,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The tracheo-bronchial mucosa of 27 surgical patients with esophageal cancer was examined by bronchofiberscope postoperatively, and the changes of the mucosa were divided into four grades, i.e., GI: no change or slight redness only (7 cases), GII: Severe redness or erosion (7 cases), GIII: Ulcer formation (11 cases) and GIV: Necrosis of the mucosa (2 cases). All the GI-III changes were reversible. However, GIV change was irreversible. The biopsy specimens were taken from the mucosa of the tracheal bifurcation on the 7th postoperative day, showing squamous metaplasia in 9 of 13 patients. Bilateral modified neck and upper mediastinal lymph node dissections were performed in 18 of 27 patients. The change of the mucosa was judged as GIII or IV in 12 of 18 patients (67%), whereas the change was less significant in the remaining 6 patients. Namely, the degree of mucosal change did not necessarily correspond with the extent of lymph node dissection. The changes of the mucosa were considered to be brought about not only by tracheo-bronchial ischemia but also by injurious effects on the pulmonary parenchyma following aggressive lymph node dissection. The assessment of the degree of the mucosal change might be a useful indicator for postoperative management of esophageal cancer patients.
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PMID:[A study on the changes in the tracheo-bronchial mucosa after esophagectomy for esophageal cancer; with special reference to the influence of neck and upper mediastinal lymph node dissections]. 260 15

The actin-binding protein Girdin is a hub protein that interacts with multiple proteins to regulate motility and Akt and trimeric G protein signaling in cancer cells. Girdin expression correlates with poor outcomes in multiple human cancers. However, those findings are not universal, as they depend on study conditions. Those data suggest that multiple aspects of Girdin function and its role in tumor cell responses to anticancer therapeutics must be reconsidered. In the present study, we found that Girdin is involved in DNA damage-induced cancer cell apoptosis. An esophageal cancer cell line that exhibited high Girdin expression showed a marked sensitivity to UV-mediated DNA damage compared to a line with low Girdin expression. When transcriptional activation of endogenous Girdin was mediated by an engineered CRISPR/Cas9 activation system, sensitivity to DNA damage increased in both stationary and migrating HeLa cancer cells. High Girdin expression was associated with dysregulated cell cycle progression and prolonged G1 and M phases. These features were accompanied by p53 activation, which conceivably increases cancer cell vulnerability to UV exposure. These data highlight the importance of understanding complex Girdin functions that influence cancer cell sensitivity to therapeutics.
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PMID:Complex roles of the actin-binding protein Girdin/GIV in DNA damage-induced apoptosis of cancer cells. 3287 99