Matches in SemOpenAlex for { <https://semopenalex.org/work/W2029271749> ?p ?o ?g. }
- W2029271749 endingPage "7" @default.
- W2029271749 startingPage "1" @default.
- W2029271749 abstract "<i >Background</i>. The RAS-association domain family 1 A (RASSF1A) is a classical member of RAS effectors regulating cell proliferation and apoptosis. Loss of RASSF1A expression may shift the balance towards a growth-promoting effect without the necessity of activating K-ras mutations. Its potential association with K-ras mutations in colorectal cancer (CRC) is unclear. <i >Methods</i>. RASSF1A expression was examined in normal mucosa, adenoma, and tumor tissues of colon and rectum, respectively. We examined the association of RASSF1A expression, mutations of K-ras, and EGFR status in 76 primary CRCs. The relationship between clinicopathological characteristics and RASSF1A expression was also analyzed. <i >Results</i>. RASSF1A expression level decreased progressively in normal mucosa, adenoma and, tumor tissues, and the loss of RASSF1A expression occurred more frequently in tumor tissues. Of 76 primary CRCs, loss of RASSF1A expression and/or K-ras mutations were detected in 77% cases. Loss of RASSF1A expression was more frequent in K-ras wild-type than in mutation cases (63% versus 32%, <svg style=vertical-align:-0.1638pt;width:66.875px; id=M1 height=11.375 version=1.1 viewBox=0 0 66.875 11.375 width=66.875 xmlns:xlink=http://www.w3.org/1999/xlink xmlns=http://www.w3.org/2000/svg> <g transform=matrix(.017,-0,0,-.017,.062,11.112)><path id=x1D443 d=M619 482q0 -69 -40.5 -119t-96 -72.5t-118.5 -26.5h-44l-70 20l-31 -151q-14 -67 0.5 -83t89.5 -22l-5 -28h-287l8 28q65 7 81.5 22t29.5 83l79 398q12 56 0.5 70.5t-78.5 20.5l7 28h255q108 0 164 -43t56 -125zM524 478q0 141 -146 141q-25 0 -47 -8q-16 -6 -20.5 -13.5
t-10.5 -39.5l-43 -241q37 -13 83 -13q67 0 125.5 45t58.5 129z /></g><g transform=matrix(.017,-0,0,-.017,15.582,11.112)><path id=x3D d=M535 323h-483v50h483v-50zM535 138h-483v50h483v-50z /></g><g transform=matrix(.017,-0,0,-.017,30.286,11.112)><path id=x30 d=M241 635q53 0 94 -28.5t63.5 -76t33.5 -102.5t11 -116q0 -58 -11 -112.5t-34 -103.5t-63.5 -78.5t-94.5 -29.5t-95 28t-64.5 75t-34.5 102.5t-11 118.5q0 58 11.5 112.5t34.5 103t64.5 78t95.5 29.5zM238 602q-32 0 -55.5 -25t-35.5 -68t-17.5 -91t-5.5 -105
q0 -76 10 -138.5t37 -107.5t69 -45q32 0 55.5 25t35.5 68.5t17.5 91.5t5.5 105t-5.5 105.5t-18 92t-36 68t-56.5 24.5z /></g><g transform=matrix(.017,-0,0,-.017,38.446,11.112)><path id=x2E d=M113 -12q-24 0 -39.5 16t-15.5 42q0 24 16 40.5t40 16.5t40 -16.5t16 -40.5q0 -26 -16 -42t-41 -16z /></g><g transform=matrix(.017,-0,0,-.017,42.321,11.112)><use xlink:href=#x30/></g><g transform=matrix(.017,-0,0,-.017,50.481,11.112)><path id=x31 d=M384 0h-275v27q67 5 81.5 18.5t14.5 68.5v385q0 38 -7.5 47.5t-40.5 10.5l-48 2v24q85 15 178 52v-521q0 -55 14.5 -68.5t82.5 -18.5v-27z /></g><g transform=matrix(.017,-0,0,-.017,58.64,11.112)><use xlink:href=#x31/></g> </svg>). <i >Conclusions</i>. Our study indicates that loss of RASSF1A may be involved in pathogenesis of CRC, its expression was found predominantly in K-ras wild-type CRCs, suggesting that it may be another way of affecting RAS signaling, in addition to K-ras mutations." @default.
- W2029271749 created "2016-06-24" @default.
- W2029271749 creator A5004624217 @default.
- W2029271749 creator A5014465282 @default.
- W2029271749 creator A5026060144 @default.
- W2029271749 creator A5028809442 @default.
- W2029271749 creator A5042604761 @default.
- W2029271749 creator A5050405673 @default.
- W2029271749 creator A5051630281 @default.
- W2029271749 creator A5052964199 @default.
- W2029271749 creator A5067183622 @default.
- W2029271749 date "2013-01-01" @default.
- W2029271749 modified "2023-09-25" @default.
- W2029271749 title "Loss of RASSF1A Expression in Colorectal Cancer and Its Association with K-ras Status" @default.
- W2029271749 cites W1679018437 @default.
- W2029271749 cites W1966598245 @default.
- W2029271749 cites W1992409084 @default.
- W2029271749 cites W2000246544 @default.
- W2029271749 cites W2001824694 @default.
- W2029271749 cites W2003673069 @default.
- W2029271749 cites W2023828454 @default.
- W2029271749 cites W2050395200 @default.
- W2029271749 cites W2052333525 @default.
- W2029271749 cites W2054614254 @default.
- W2029271749 cites W2064854706 @default.
- W2029271749 cites W2091234906 @default.
- W2029271749 cites W2098045211 @default.
- W2029271749 cites W2102378573 @default.
- W2029271749 cites W2107661773 @default.
- W2029271749 cites W2113459016 @default.
- W2029271749 cites W2114656575 @default.
- W2029271749 cites W2122321124 @default.
- W2029271749 cites W2123611321 @default.
- W2029271749 cites W2139526606 @default.
- W2029271749 cites W2146674564 @default.
- W2029271749 cites W2150741474 @default.
- W2029271749 cites W2154458783 @default.
- W2029271749 cites W2169124674 @default.
- W2029271749 doi "https://doi.org/10.1155/2013/976765" @default.
- W2029271749 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3705944" @default.
- W2029271749 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/23865079" @default.
- W2029271749 hasPublicationYear "2013" @default.
- W2029271749 type Work @default.
- W2029271749 sameAs 2029271749 @default.
- W2029271749 citedByCount "16" @default.
- W2029271749 countsByYear W20292717492014 @default.
- W2029271749 countsByYear W20292717492015 @default.
- W2029271749 countsByYear W20292717492016 @default.
- W2029271749 countsByYear W20292717492017 @default.
- W2029271749 countsByYear W20292717492018 @default.
- W2029271749 countsByYear W20292717492019 @default.
- W2029271749 countsByYear W20292717492020 @default.
- W2029271749 countsByYear W20292717492021 @default.
- W2029271749 crossrefType "journal-article" @default.
- W2029271749 hasAuthorship W2029271749A5004624217 @default.
- W2029271749 hasAuthorship W2029271749A5014465282 @default.
- W2029271749 hasAuthorship W2029271749A5026060144 @default.
- W2029271749 hasAuthorship W2029271749A5028809442 @default.
- W2029271749 hasAuthorship W2029271749A5042604761 @default.
- W2029271749 hasAuthorship W2029271749A5050405673 @default.
- W2029271749 hasAuthorship W2029271749A5051630281 @default.
- W2029271749 hasAuthorship W2029271749A5052964199 @default.
- W2029271749 hasAuthorship W2029271749A5067183622 @default.
- W2029271749 hasBestOaLocation W20292717491 @default.
- W2029271749 hasConcept C104317684 @default.
- W2029271749 hasConcept C121608353 @default.
- W2029271749 hasConcept C126322002 @default.
- W2029271749 hasConcept C203014093 @default.
- W2029271749 hasConcept C2777428134 @default.
- W2029271749 hasConcept C501734568 @default.
- W2029271749 hasConcept C502942594 @default.
- W2029271749 hasConcept C51785407 @default.
- W2029271749 hasConcept C526805850 @default.
- W2029271749 hasConcept C54355233 @default.
- W2029271749 hasConcept C62112901 @default.
- W2029271749 hasConcept C71924100 @default.
- W2029271749 hasConcept C86803240 @default.
- W2029271749 hasConceptScore W2029271749C104317684 @default.
- W2029271749 hasConceptScore W2029271749C121608353 @default.
- W2029271749 hasConceptScore W2029271749C126322002 @default.
- W2029271749 hasConceptScore W2029271749C203014093 @default.
- W2029271749 hasConceptScore W2029271749C2777428134 @default.
- W2029271749 hasConceptScore W2029271749C501734568 @default.
- W2029271749 hasConceptScore W2029271749C502942594 @default.
- W2029271749 hasConceptScore W2029271749C51785407 @default.
- W2029271749 hasConceptScore W2029271749C526805850 @default.
- W2029271749 hasConceptScore W2029271749C54355233 @default.
- W2029271749 hasConceptScore W2029271749C62112901 @default.
- W2029271749 hasConceptScore W2029271749C71924100 @default.
- W2029271749 hasConceptScore W2029271749C86803240 @default.
- W2029271749 hasFunder F4320321001 @default.
- W2029271749 hasLocation W20292717491 @default.
- W2029271749 hasLocation W20292717492 @default.
- W2029271749 hasLocation W20292717493 @default.
- W2029271749 hasLocation W20292717494 @default.
- W2029271749 hasLocation W20292717495 @default.
- W2029271749 hasOpenAccess W2029271749 @default.
- W2029271749 hasPrimaryLocation W20292717491 @default.