{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,17]],"date-time":"2026-08-17T14:44:07Z","timestamp":1786977847181,"version":"build-2736575974"},"reference-count":50,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2011,4,1]],"date-time":"2011-04-01T00:00:00Z","timestamp":1301616000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Intl Journal of Cancer"],"published-print":{"date-parts":[[2011,10,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    To understand the importance of frequent deletion of chromosomal 11q23.3\u201024.3 region in cervical carcinogenesis, alterations (deletion\/methylation\/mutation\/expression) of the candidate genes\n                    <jats:italic>LOH11CR2A, EI24<\/jats:italic>\n                    and\n                    <jats:italic>CHEK1<\/jats:italic>\n                    located in the region were analyzed in 29 cervical intraepithelial neoplasia (CIN), 112 cervical carcinoma (CACX) samples and two CACX cell lines. The deletion frequency of these genes was low in CIN than in CACX [CIN:\n                    <jats:italic>CHEK1<\/jats:italic>\n                    : 28%,\n                    <jats:italic>EI24<\/jats:italic>\n                    : 21%,\n                    <jats:italic>LOH11CR2A<\/jats:italic>\n                    : 15% and CACX:\n                    <jats:italic>CHEK1<\/jats:italic>\n                    : 51%,\n                    <jats:italic>EI24<\/jats:italic>\n                    : 41%,\n                    <jats:italic>LOH11CR2A<\/jats:italic>\n                    : 36%]. Similar trend was seen in promoter methylation of these genes [CIN:\n                    <jats:italic>CHEK1<\/jats:italic>\n                    : 10%,\n                    <jats:italic>EI24<\/jats:italic>\n                    : 3%,\n                    <jats:italic>LOH11CR2A<\/jats:italic>\n                    : 3% and CACX:\n                    <jats:italic>CHEK1<\/jats:italic>\n                    : 55%,\n                    <jats:italic>EI24<\/jats:italic>\n                    : 31%,\n                    <jats:italic>LOH11CR2A<\/jats:italic>\n                    : 14%]. Mutations of the genes are a rare event. Overall alterations (deletion and methylation) of\n                    <jats:italic>CHEK1<\/jats:italic>\n                    and\n                    <jats:italic>EI24<\/jats:italic>\n                    were associated with progression of CACX. Quantitative mRNA expression analysis showed reduced expression of the three genes in concordance to their molecular alterations. A shorter isoform of\n                    <jats:italic>CHEK1<\/jats:italic>\n                    lacking exon 8, hence impaired in substrate binding capacity, was found in two samples. Immunohistochemical analysis showed nuclear expression of Chek1, p\u2010Chek1 and Ei24 in tumor tissues, whereas the cell lines exhibited both nuclear and cytoplasmic expression of Chek1 and Ei24, as is also evident from Western blot analysis suggesting differential localization of the proteins. Alterations of\n                    <jats:italic>CHEK1<\/jats:italic>\n                    and\n                    <jats:italic>EI24<\/jats:italic>\n                    coupled with tumor stage and early sexual debut (\u226419 years) predicted worst prognosis. Thus, our data suggest that inactivation of\n                    <jats:italic>EI24<\/jats:italic>\n                    and\n                    <jats:italic>CHEK1<\/jats:italic>\n                    through two independent mechanisms contributes to the development of CACX.\n                  <\/jats:p>","DOI":"10.1002\/ijc.25849","type":"journal-article","created":{"date-parts":[[2010,12,10]],"date-time":"2010-12-10T10:37:52Z","timestamp":1291977472000},"page":"1859-1871","source":"Crossref","is-referenced-by-count":32,"title":["Inactivation of\n                    <i>CHEK1<\/i>\n                    and\n                    <i>EI24<\/i>\n                    is associated with the development of invasive cervical carcinoma: Clinical and prognostic implications"],"prefix":"10.1002","volume":"129","author":[{"given":"Dipanjana","family":"Mazumder 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