Computer Image Analysis Reveals C-Myc as a Potential Biomarker for Discriminating between Keratoacanthoma and Cutaneous Squamous Cell Carcinoma

Abstract

The distinction between Keratoacanthoma (KA) and Cutaneous Squamous Cell Carcinoma (cSCC) is critical yet usually challenging to discriminate clinically and histopathologically. One approach to differentiate KA from cSCC is through assessing the immunohistochemical staining patterns of the three indicators, β-catenin, C-Myc, and CyclinD1, which are critical molecules that play important roles in the Wnt/β-catenin signaling pathway. Ki-67, as a proliferation biomarker for human tumor cells, was also assessed as an additional potential marker for differentiating KA from cSCC. In this report, these four indicators were analyzed in 42 KA and 30 cSCC cases with the use of the computer automated image analysis system. Computer automated image analysis is a time-based and cost-effective method of determining IHC staining in KA and cSCC samples. We found that C-Myc staining was predominantly localized in the nuclei of basal cells within KA patients, whereas cSCC staining was predominantly localized in the nuclei of diffuse cells. This C-Myc staining pattern has a sensitivity of 78.6% and a specificity of 66.7% for identifying KA. Moreover, positive rates of distinct expression patterns of C-Myc and Ki-67 may also serve as a means to clinically distinguish KA from cSCC. Taken together, our results suggest that these markers, in particular C-Myc, may be useful in differentiating KA from cSCC.

Gene expression landscape of cutaneous squamous cell carcinoma progression

“…The reduced proliferative capacity of KA was further supported by increased NOTCH signaling and lower levels of MYC activation ( Figure S4 ). These findings agree with previous reports demonstrating inactivating NOTCH mutations in growing KA but not regressing lesions (63,64) and suggest that the KA in our cohort were collected during the terminal differentiation/involution phase rather than the initial growth phase.…”

Upregulation of miR-194-5p or silencing of PRC1 enhances radiotherapy sensitivity in esophageal squamous carcinoma cells

“…The Wnt/β-catenin signaling pathway is an evolutionarily conserved pathway that has been shown to promote tumorigenesis and metastasis in certain cancers, including ESCC [ 35 , 36 ]. Aberrant activation of the Wnt/β-catenin signaling pathway leads to the accumulation of β-catenin in the nucleus, which promotes the transcription of many oncogenes, such as C-myc, CyclinD1 and MMP-2 [ [37] , [38] , [39] ]. Previous studies have found that PRC1 increases lymph node metastasis in lung adenocarcinoma by activating the Wnt/β-catenin signaling pathway [ 21 ].…”