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Assessment of biomarkers in paired primary and recurrent colorectal adenocarcinomas

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dc.contributor.author김호근-
dc.date.accessioned2020-01-07T08:42:01Z-
dc.date.available2020-01-07T08:42:01Z-
dc.date.issued1999-
dc.identifier.issn0360-3016-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/173773-
dc.description.abstractPURPOSE: Recurrent colorectal cancers respond poorly to anticancer treatment including radiotherapy. To better understand the biological characteristics of the recurrent colorectal tumor, we investigated various biomarkers regulating cell proliferation and cell loss in paired primary and recurrent colorectal tumor specimens within each individual. METHODS AND MATERIALS: From a total of 11 colorectal adenocarcinoma patients, 22 specimens of paired primary and recurrent tumors were obtained for analysis. Apoptosis was evaluated by TUNEL labeling of apoptotic DNA fragmentation. Other biomarkers including proliferating cell nuclear antigen (PCNA), p53, WAF1, p34cdc2, and cyclins B1 and D1 were analyzed by immunohistochemical stains. RESULTS: PCNA index (PCNAI) showed an increase in 6 and a decrease in 5 recurrent tumors compared to primary tumors. Median PCNAI in primary and recurrent tumors were 33.5 and 48.3, respectively (p = 0.16). In contrast, the apoptotic index (AI) decreased in 9 of 11 recurrent tumors compared to primary tumors. Median AI decreased from 4.3 in primary tumors to 1.4 in recurrent tumors (p = 0.04). The p53 expression increased in more than half of recurrent tumors compared to primary tumors. Mean staining score increased from 0.7 in primary tumors to 1.2 in recurrent tumors (p = 0.059). WAF1 and cyclin B1 did not show significant change. In contrast, both cyclin D1 and p34cdc2 increased significantly in recurrent tumors. These two biomarkers showed increased expression in 8 (cyclin D1) and 7 (p34cdc2) recurrent tumors, respectively, compared to their primary counterparts. Mean staining scores of both biomarkers in recurrent tumors increased by more than twofold compared to those in primary tumors and these differences were statistically significant (cyclin D1, p = 0.007; p34cdc2, p = 0.008). CONCLUSION: This study showed significantly decreased apoptosis in recurrent colorectal tumors compared to their primary counterparts. The underlying regulatory mechanisms included increased expression of p53 and altered cell cycle regulators such as increased cyclin D1 and p34cdc2. With further study, it may be used for developing a new therapeutic strategy for the treatment of recurrent colorectal cancer.-
dc.description.statementOfResponsibilityrestriction-
dc.languageEnglish-
dc.publisherElsevier Science Inc.-
dc.relation.isPartOfInt J of Rad Oncol Physics-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.subject.MESHAdult-
dc.subject.MESHAged-
dc.subject.MESHApoptosis*/genetics-
dc.subject.MESHBiomarkers, Tumor/analysis*-
dc.subject.MESHCDC2 Protein Kinase/analysis-
dc.subject.MESHCell Division-
dc.subject.MESHColonic Neoplasms/chemistry*-
dc.subject.MESHColonic Neoplasms/drug therapy-
dc.subject.MESHColonic Neoplasms/pathology-
dc.subject.MESHCyclin B/analysis-
dc.subject.MESHCyclin B1-
dc.subject.MESHCyclin D1/analysis-
dc.subject.MESHCyclin-Dependent Kinase Inhibitor p21-
dc.subject.MESHCyclins/analysis-
dc.subject.MESHDNA Fragmentation-
dc.subject.MESHFemale-
dc.subject.MESHHumans-
dc.subject.MESHIn Situ Nick-End Labeling-
dc.subject.MESHMale-
dc.subject.MESHMiddle Aged-
dc.subject.MESHNeoplasm Recurrence, Local/chemistry*-
dc.subject.MESHNeoplasm Recurrence, Local/drug therapy-
dc.subject.MESHNeoplasm Recurrence, Local/pathology-
dc.subject.MESHProliferating Cell Nuclear Antigen/analysis-
dc.subject.MESHRectal Neoplasms/chemistry*-
dc.subject.MESHRectal Neoplasms/drug therapy-
dc.subject.MESHRectal Neoplasms/pathology-
dc.subject.MESHSigmoid Neoplasms/chemistry-
dc.subject.MESHSigmoid Neoplasms/drug therapy-
dc.subject.MESHSigmoid Neoplasms/pathology-
dc.subject.MESHTumor Suppressor Protein p53/analysis-
dc.titleAssessment of biomarkers in paired primary and recurrent colorectal adenocarcinomas-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Pathology (병리학교실)-
dc.contributor.googleauthorJinsil Seong-
dc.contributor.googleauthorEun Ji Chung-
dc.contributor.googleauthorHogeun Kim-
dc.contributor.googleauthorGwi Eon Kim-
dc.contributor.googleauthorNam Kyu Kim-
dc.contributor.googleauthorSeung Kuk Sohn-
dc.contributor.googleauthorJin Sik Min-
dc.contributor.googleauthorChang Ok Suh-
dc.identifier.doi10.1016/s0360-3016(99)00302-8-
dc.contributor.localIdA01183-
dc.relation.journalcodeJ01157-
dc.identifier.eissn1879-355X-
dc.identifier.pmid10613309-
dc.identifier.urlhttps://www.sciencedirect.com/science/article/pii/S0360301699003028-
dc.contributor.alternativeNameKim, Ho Keun-
dc.contributor.affiliatedAuthor김호근-
dc.citation.volume45-
dc.citation.number5-
dc.citation.startPage1167-
dc.citation.endPage1173-
dc.identifier.bibliographicCitationInt J of Rad Oncol Physics, Vol.45(5) : 1167-1173, 1999-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Pathology (병리학교실) > 1. Journal Papers

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