Evidence map›Paper›PMID 40384196›Full record

ArticleRomanian journal of morphology and embryology = Revue roumaine de morphologie et embryologie

The role of CDX2, MUC5AC, and p53 in the evaluation of the progression of serrated lesions toward colorectal carcinoma.

Sergiu Marian Cazacu, Sevastiţa Iordache, Vlad Florin Iovănescu, Liliana Streba, Carmen Daniela Neagoe, Cristina Jana Busuioc, Dan Cârţu, Mirela Marinela Florescu

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Article in Romanian journal of morphology and embryology = Revue roumaine de morphologie et embryologie. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

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2citing papers in PubMed
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1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

8 authors.

Sergiu Marian CazacuDepartment of Gastroenterology, University of Medicine and Pharmacy of Craiova, Romania; iovanescu_vlad@yahoo.com; Department of Internal Medicine, University of Medicine and Pharmacy of Craiova, Romania; dananeagoe2014@gmail.com.
Sevastiţa Iordache
Vlad Florin Iovănescu
Liliana Streba
Carmen Daniela Neagoe
Cristina Jana Busuioc
Dan Cârţu
Mirela Marinela Florescu

Funding

University of Medicine and Pharmacy of Craiova 26/1121/1
6 · The paper itself

Abstract

backgroundSerrated colorectal lesions represent a potential precursor of 15-30% of colorectal carcinoma, although the exact mechanisms are not fully understood. The serrated pathway of colorectal carcinogenesis may be correlated with gastric-type metaplasia of the colon and modified expression of caudal type homeobox 2 (CDX2) and local mucins (MUCs). PATIENTS, MATERIALS AND

methodsWe performed a retrospective study of patients with resected polyps during 2014-2021. The prevalence of serrated lesions, risk factors associated with malignant polyps, and the role of gastric-type metaplasia associated with serrated pathway of carcinogenesis (CDX2, MUC5AC) and of p53 immunostaining in serrated lesions with dysplasia and carcinoma were assessed.

resultsFive hundred twenty two (522) patients had 1199 polyps removed. We noted a 12.8% prevalence of sessile serrated adenoma∕polyps (SSA∕P) and traditional serrated adenomas (TSA); 17.4% had hyperplastic polyps. The malignancy rate of resected polyps was higher in tubulovillous adenoma (TVA) and villous adenoma (12.3-20%) than in SSA∕P (8.3%) and TSA (4.8%). In TSA, no significant associations between malignancy and age, gender, size, location, or endoscopic appearance were noted. In SSA∕P, malignant polyps were much larger, especially for the right side lesions, but the macroscopic type was not correlated with malignancy risk. Immunohistochemistry (IHC) was performed in 26 polyps with dysplasia or carcinoma; all cases had CDX2 immunostaining in the tumor cell's nucleus, with an average percentage of 96.5%. MUC5AC immunostaining was identified in the tumor cells' cytoplasm, with an average percentage of 31.81%; the intensity reaction was variable (average score 4.5). The percentage, intensity, and score for CDX2 IHC were similar for TSA and TVA and were lower for SSA∕P with low-grade dysplasia (LGD), while for SSA∕P with high-grade dysplasia (HGD) or carcinoma in situ (CIS), the percentage, intensity, and score were similar to TSA and TVA. p53 immunostaining was also positive in all cases, with an average percentage of 50.95% in the tumor cells' nucleus. p53 and MUC5AC had increased percentage, intensity, and scores from LGD to HGD in SSA∕P and decreased mean percentage, intensity, and scores in TSA and TVA.

conclusionsThe risk of malignancy in serrated lesions seems lower than in conventional adenomas, however, sessile serrated lesions can be involved in the appearance of interval cancers because of flat and pale macroscopic aspects. Gastric-type intestinal metaplasia may be associated with the serrated pathway, but more studies are needed to clarify mechanisms associated with serrated carcinogenesis.

Indexed as

CDX2 Transcription FactorColorectal NeoplasmsMucin 5ACTumor Suppressor Protein p53AdultAgedDisease ProgressionFemaleHumansMaleMiddle AgedRetrospective StudiesCDX2 protein, humanCDX2 Transcription FactorMUC5AC protein, humanMucin 5ACTP53 protein, humanTumor Suppressor Protein p53CDX2malignant polypMUC5ACp53serrated lesion

Identifiers

PMID40384196
PMCPMC12236287

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.