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口腔上皮发育异常和口腔鳞状细胞癌中[具体物质]免疫组化表达的相关性

A correlation of immunohistochemical expression of and in oral epithelial dysplasia and oral squamous cell carcinoma.

作者信息

Pandya Jay Ashokkumar, Boaz Karen, Natarajan Srikant, Manaktala Nidhi, Nandita K P, Lewis Amitha J

机构信息

Department of Oral Pathology and Microbiology, Ambika Dental Clinic and Oral Histopathology Laboratory, Bharuch, Gujarat, India.

Department of Oral Pathology and Microbiology, Manipal College of Dental Sciences, Manipal University, Mangalore, Karnataka, India.

出版信息

J Cancer Res Ther. 2018 Apr-Jun;14(3):666-670. doi: 10.4103/0973-1482.180683.

Abstract

PURPOSE

Oral epithelial dysplasia (OED) occurs on exposure of epithelial cells to carcinogens and genetic alteration. Once the reversible cell damage is surpassed, cells either undergo apoptosis or transform into malignancy, chiefly oral squamous cell carcinoma (OSCC). Progressive accumulation of genetic errors (including mutations in TP53 and CDKN1A) is associated with the initiation and progression of potentially malignant oral lesions toward frank malignancy. The present study attempted to correlate the immunohistochemical expression of CDKN1A and TP53 with increasing severity of OED along with increased aggressiveness of OSCC as reflected in the clinicopathologic variables.

MATERIALS AND METHODS

Tissue sections from forty biopsy-proven cases of OED and OSCC were stained with anti-TP53 and anti-CDKN1A mouse monoclonal antibodies. One hundred cells in each case were counted under high power magnification.

RESULTS

Poorly differentiated OSCC showed the highest TP53 expression (mean = 70.285), with least expression seen in mild dysplasia (mean = 22.125) (P < 0.001). Higher TP53 count was seen in cases with margin involvement, without recurrence and lymph node involvement and in cases which died of disease. CDKN1A expression was seen only in five cases and that too focally in the cytoplasm, thereby warranting removal of analysis of CDKN1A positivity from the study.

CONCLUSION

The expression of TP53 in OED highlights its role in initial carcinogenesis. Although the role of CDKN1A in the cell cycle has been documented, its relationship to various clinical and pathological variables of OSCC and its different treatment modalities could not be adequately assessed.

摘要

目的

口腔上皮发育异常(OED)发生于上皮细胞暴露于致癌物及基因改变时。一旦可逆性细胞损伤被超越,细胞要么发生凋亡,要么转变为恶性肿瘤,主要是口腔鳞状细胞癌(OSCC)。遗传错误(包括TP53和CDKN1A突变)的逐步积累与潜在恶性口腔病变向明显恶性肿瘤的起始和进展相关。本研究试图将CDKN1A和TP53的免疫组化表达与OED严重程度增加以及OSCC临床病理变量所反映的侵袭性增加相关联。

材料与方法

对40例经活检证实的OED和OSCC病例的组织切片用抗TP53和抗CDKN1A小鼠单克隆抗体进行染色。在高倍镜下对每个病例的100个细胞进行计数。

结果

低分化OSCC显示出最高的TP53表达(平均值 = 70.285),轻度发育异常中表达最低(平均值 = 22.125)(P < 0.001)。在切缘受累、无复发和淋巴结受累以及死于疾病的病例中,TP53计数较高。仅在5例病例中观察到CDKN1A表达,且仅在细胞质中呈局灶性表达,因此有必要从研究中去除对CDKN1A阳性的分析。

结论

TP53在OED中的表达突出了其在初始致癌过程中的作用。尽管CDKN1A在细胞周期中的作用已有文献记载,但其与OSCC各种临床和病理变量及其不同治疗方式的关系无法得到充分评估。

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