Protein expression of Fragile Histidine Triad and cyclooxgenase-2 in serrated neoplasia of the colorectum

Tamoto, Akihiro; Yashima, Kazuo; Hosoda, Kohei; Yamamoto, Sohei; Kawata, Soichiro; Ikebuchi, Yuichiro; Matsumoto, Kazuya; Kawaguchi, Koichiro; Harada, Kiyoshi; Murawaki, Yoshikazu; Isomoto, Hajime

doi:10.3892/ol.2017.6634

Cited by 3 publications

(5 citation statements)

References 34 publications

(47 reference statements)

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“…It can be observed that out of the seven studies on SSPND (i.e. SSA/P without dysplasia) (11,47,48,50,51,53,54), only one reported p53 immunoreactivity (50). However, the immunoreactivity in that report was described and illustrated as low and diffuse, affecting the cells of the lower third of the crypts (base) (50).…”

Section: Discussionmentioning

confidence: 95%

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Sessile Serrated Polyps Without Dysplasia Thrives With Asymmetric Relocation of Cell Proliferation-domains

Rubio

Schmidt

2020

Anticancer Res

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Background/Aim: Sessile serrated polyps without dysplasia (SSPND) are characterized by crypts with serrated epithelium, albeit with irregular, corrupted shapes (CCS). Patients and Methods: Cell proliferation was explored in the CCS from 60 SSPND and in the crypts from 12 normal colons. Sections were immuno-stained with the Ki-67 proliferation-cell (PC) marker, and with the p53 tumoursuppressor gene. Results: Three predominant PC-phenotypes were found in the CCS from the 60 SSPND: 44 (73.3%) exhibited ectopic, asymmetric, randomly distributed PCclusters, 12 (20.0%), continuous PC in one or in both slopes of the crypts, and in the remaining 4 (6.7%), single, randomly distributed PC were recorded. In contrast, the scrutiny of more than 200,000 normal colon crypts (controls) showed symmetrically aligned PC, restricted to the lower third of the crypts. p53-up-regulation in CCS was recorded in 11(18.3%) of the 60 NDSSP, but in none of the normal crypts in the 12 controls. Conclusion: The non-dysplastic epithelium that lines CCS in SSPND coexists with an asymmetric relocation of the PC-domains. In addition, the CCS in nearly one-fifth of the SSPND exhibited p53-upregulated cells. Taken together, the non-dysplastic CCS epithelium in SSPND thrives with somatic mutations. The accretion of putative mutated non-dysplastic CCS might be a crucial event in the evolution of colonic SSPND towards sessile serrated adenomas.

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Section: Discussionmentioning

confidence: 95%

“…Several reports deal with the expression of p53 in SSP without dysplasia and in SSA/P (11,(45)(46)(47)(48)(49)(50)(51)(52)(53)(54). The results of those studies are condensed in Table II.…”

Section: Discussionmentioning

confidence: 99%

Sessile Serrated Polyps Without Dysplasia Thrives With Asymmetric Relocation of Cell Proliferation-domains

Rubio

Schmidt

2020

Anticancer Res

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“…p16 gene is a multi-tumor suppressor gene that acts primarily on the cell cycle anti-oncogene (15). The study demonstrated that p16 protein mainly competes with cyclin D1 for binding to CDK4/CDK6 and promotes cell arrest in G1 phase, which ultimately plays a negative regulatory role in cell proliferation (16,17).…”

Section: Discussionmentioning

confidence: 99%

Effect of interventional embolotherapy on FHIT and p16 expression in hepatocellular carcinoma patients

Wang

et al. 2018

Oncol Lett

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Effects of interventional embolotherapy on the expression of fragile histidine triad (FHIT) and p16 in hepatocellular carcinoma (HCC) patients were investigated. Patients with primary HCC who were definitely diagnosed and treated in the Department of Gastroenterology in Qingdao Central Hospital from March 2014 to March 2016 were selected, and they underwent interventional embolotherapy. HCC and cancer-adjacent tissues of the patients were harvested for immunohistochemical staining. The correlation between the expression levels of FHIT and p16 was analyzed at the gene and protein level. Clinical data were collected, and whether they were correlated with the expression of FHIT and p16 was investigated. The expression levels of FHIT and p16 in primary HCC tissues were remarkably lower than that in cancer-adjacent tissues (P<0.05). In HCC tissues, FHIT expression was obviously positively correlated with p16 expression (Spearman's correlation coefficient, r=0.308; P=0.025). FHIT was related to HCC tumor-node-metastasis (TNM) staging, the differentiation degree in Edmondson-Steiner grading, lymph node metastasis and portal vein thrombosis (P<0.05 in all comparisons), whereas, p16 was associated with tumor size and the differentiation degree in Edmondson-Steiner grading (P<0.05 in all comparisons). The expression of FHIT and p16 genes and proteins in HCC tissues were obviously lower than those in cancer-adjacent tissues (P<0.05 in all comparisons). FHIT and p16 genes, as tumor suppressor genes, inhibit the proliferation of HCC, and there is a positive correlation between them. The proteins of the FHIT and p16 can be used as new indicators for clinical detection, thus providing a new method for clinical diagnosis.

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“…As described in our previous study on fragile histidine triad and cyclooxygenase-2 expression in serrated neoplasia (19) (5). The 20 HPs were subdivided into ten microvesicular HPs (MVHPs) and ten goblet cell HPs (GCHPs).…”

Section: Methodsmentioning

confidence: 99%

“…All other tumorous lesions in the colon were termed polypoid lesions. The clinical characteristics of the patients are reported in our previous study (19). All cases were de-identified prior to analysis, and written informed consent was obtained from all patients.…”

Section: Methodsmentioning

confidence: 99%

Expression of doublecortin and CaM kinase‑like‑1 protein in serrated neoplasia of the colorectum

et al. 2017

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Abstract. The adenoma-carcinoma sequence (ACS) and the serrated pathway are two distinct developmental routes leading to the formation of colorectal carcinoma. Recently, the doublecortin and CaM kinase-like-1 protein (DCLK1) has been reported to serve as an intestinal cancer stem cell marker and has been demonstrated to be overexpressed through the ACS; however, there is a lack of reports on the role of DCLK1 in the serrated pathway. To clarify the correlation between DCLK1 protein expression and clinicopathological characteristics of the serrated tumorigenic pathway, the present study used immunohistochemistry to examine the expression of DCLK1 in endoscopically resected samples of 62 serrated polyps [20 hyperplastic polyps (HPs), 16 traditional serrated adenomas (TSAs) and 26 sessile serrated adenoma-polyps (SSA/Ps)], as well as 20 non-serrated adenomas, 20 carcinoma in adenomas (CIAs) and 18 early pure colorectal carcinomas without any adenoma component (EPCs). Based on immunostaining score, high DCLK1 expression was detected in 20.0% of HPs (23.1% of microvesicular HPs and 14.3% of goblet cell HPs), 37.5% of TSAs, 7.7% of SSA/Ps, 80.0% of non-serrated adenomas, 75.0% of CIAs and 50.0% of EPCs. Negative or low DCLK1 expression was frequently observed in TSAs (P<0.005), SSA/Ps (P<0.00001) and EPCs (P<0.04) compared with non-serrated adenomas and CIAs. In addition, negative or low DCLK1 expression was significantly more frequent in SSA/Ps (92.3%) compared with TSAs (62.5%; P<0.05). Thus, the expression pattern of DCLK1 between the serrated pathway and ACS differed, indicating that DCLK1 expression may perform a secondary role in serrated tumorigenesis. In addition, the data indicates that EPCs may contain tumors derived from the serrated pathway as well as the ACS.

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Protein expression of Fragile Histidine Triad and cyclooxgenase-2 in serrated neoplasia of the colorectum

Cited by 3 publications

References 34 publications

Sessile Serrated Polyps Without Dysplasia Thrives With Asymmetric Relocation of Cell Proliferation-domains

Sessile Serrated Polyps Without Dysplasia Thrives With Asymmetric Relocation of Cell Proliferation-domains

Effect of interventional embolotherapy on FHIT and p16 expression in hepatocellular carcinoma patients

Expression of doublecortin and CaM kinase‑like‑1 protein in serrated neoplasia of the colorectum

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