Proteomic and histopathological characterization of the interface between oral squamous cell carcinoma invasion fronts and non-cancerous epithelia

Abé, Tatsuya; Maruyama, Satoshi; Yamazaki, Manabu; Xu, Bin; Babkair, Hamzah; Sumita, Yoshimasa; Cheng, Jun; Yamamoto, Tadashi; Saku, Takashi

doi:10.1016/j.yexmp.2017.02.018

Cited by 13 publications

(12 citation statements)

References 38 publications

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“…Emergence of K17 has been shown to be required for cell proliferation of cancer cells and their larger size 3 . Additionally, our recent proteome analysis findings confirmed that loss of K13 and emergence of K17 were more exclusively specific to oral CIS and squamous cell carcinoma (SCC) as compared to other keratin subtypes 4 . We have also noticed the presence of K17-positive (+) cell-debris-like speckles scattered in tissue specimens obtained from oral lichen planus cases, which were obviously benign and not candidates for differential diagnosis from any malignant lesions.…”

Section: Introductionsupporting

confidence: 61%

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Keratin 17-positive Civatte bodies in oral lichen planus—distribution variety, diagnostic significance and histopathogenesis

Abé

Kitagawa

Yoshimoto

et al. 2020

Sci Rep

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Although emergence of keratin 17 (K17) and reciprocal loss of K13 are immunohistochemical hallmarks for oral mucosal malignancy, we report here findings of K17-positive (+) speckles, possibly equivalent to Civatte bodies, in benign oral lichen planus. Sixty-two biopsy samples from oral lichen planus cases were subjected to immunohistochemical examinations to analyze the distribution as well as histopathogenesis of Civatte bodies. K17 was irregularly positive among oral lichen planus-affected epithelial cells, and K17-positive (+) filamentous structures were irregularly distributed within the cytoplasm in confocal images. K17+ speckles were identified as Civatte bodies, and they were mainly distributed in the interface between epithelial cells and lymphocytic infiltrates (type A, 52.8%), followed by distribution within the epithelial layer (type B, 24.7%) or within the lamina propria with lymphocytic infiltration (type C, 22.5%). Apoptotic figures were often engulfed by macrophages and clearly distinguished from Civatte bodies by the presence TUNEL signals. These results indicate that K17 is a sensitive immunohistochemical marker for Civatte bodies and useful for differential diagnosis of oral lichen planus from other oral mucosal lesions. Civatte bodies are generated from denucleation of K17+ epithelial cells during the process of cell death via dyskeratosis, which is possibly related to blood capillary collapse.

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Section: Introductionsupporting

confidence: 61%

“…For the control experiments, the primary antibodies were replaced with pre-immune IgGs. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) was performed as described elsewhere 4 . K17+ speckles were compared with Civatte bodies seen in serial HE-stained sections.…”

Section: Methodsmentioning

confidence: 99%

Keratin 17-positive Civatte bodies in oral lichen planus—distribution variety, diagnostic significance and histopathogenesis

Abé

Kitagawa

Yoshimoto

et al. 2020

Sci Rep

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“…Sections were preincubated with 10% normal horse serum in phosphate‐buffered saline, incubated with a rabbit polyclonal antibody against PRMT5 (HPA005525, Sigma‐Aldrich, St. Louis, MO, USA) at a dilution of 1:100, a mouse monoclonal antibody against CK10/13 (clone DE‐K13, DakoCytomation, Glostrup, Denmark) specifically detecting CK13 on paraffin sections at a dilution of 1:200, a mouse monoclonal antibody against CK17 (clone E3, DakoCytomation) at a dilution of 1:100, a mouse monoclonal antibody against E‐cadherin (clone 36, BD Biosciences, Franklin Lakes, NJ, USA) at a dilution of 1:400, and a pre‐diluted mouse monoclonal antibody against vimentin (clone V9, DakoCytomation) at 4 °C overnight. The linked primary antibody was detected with DAKO EnVision+ Dual Link System‐HRP (Agilent Technologies, Santa Clara, CA, USA) according to the manufacturer's instructions.…”

Section: Methodsmentioning

confidence: 99%

Expression of protein arginine methyltransferase‐5 in oral squamous cell carcinoma and its significance in epithelial‐to‐mesenchymal transition

Amano

Matsubara

Yoshimoto

et al. 2018

Pathology International

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Protein arginine methyltransferases (PRMT) 5, a member of type II arginine methyltransferases, catalyzes the symmetrical dimethylation of arginine residues on histone and non-histone substrates. Although the overexpression of PRMT5 has been reported in various cancers, its role in oral squamous cell carcinoma (OSCC) has not been elucidated. In the present study, we immunohistochemically examined the expression of PRMT5 in surgically resected oral epithelial dysplasia (OED, n = 8), oral intraepithelial neoplasia (OIN)/carcinoma in situ (CIS) (n = 11) and OSCC (n = 52) with or without contiguous OED lesions. In the normal epithelium, PRMT5 was weakly expressed in the cytoplasm of basal layer cells. In OED, OIN/CIS, and OSCC, its expression consistently and uniformly increased in the cytoplasm of dysplastic and cancer cells. Moreover, nuclear and cytoplasmic localization was detected in the invasive front of cancer cells, particularly in cases showing poor differentiation or aggressive invasion patterns. The concomitant nuclear and cytoplasmic expression of PRMT5 correlated with the loss of E-cadherin and cytokeratin 17, and the upregulation of vimentin, features that are both indicative of epithelial-to-mesenchymal transition. PRMT5 may play a role from early oncogenesis through to the progression of OSCC, particularly in the aggressive mode of stromal invasion.

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“…Regarding CK13, we have also previously reported that the reciprocal immunohistochemical expression pattern of CK17 and CK13 in the oral mucosal epithelia corresponds to the grades of malignancy in oral squamous cell malignancies. Furthermore, we evaluated their immunohistochemical profiles by referring to the presence or absence of positivity as follows: the CK17+/CK13 − pattern indicated carcinoma in situ or squamous cell carcinoma, while the CK17−/CK13 + pattern meant normal and dysplastic epithelia [ 11 , 12 ]. CK13 positivity can be a hallmark of squamous epithelium within the normal keratinization processes [ 11 , 12 ].…”

Section: Discussionmentioning

confidence: 99%

Central mucoepidermoid carcinoma arising directly from a glandular odontogenic cyst of the mandible: a case report

et al. 2021

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Background Central mucoepidermoid carcinoma (MEC) is a rare salivary gland tumor that affects the jawbone. Glandular odontogenic cyst (GOC) is also a rare odontogenic developmental cyst with glandular differentiation. GOC shares some histological features with central MEC, and a pre-existing GOC can develop into central MEC. Here, we present a rare case of central MEC developed directly from a pre-existing GOC of the mandible. Case presentation A 67-year-old Japanese man presented with a cystic lesion in the right third molar region. Histologically, the biopsy specimen demonstrated both typical findings of a GOC component lined with non-keratinized squamous epithelium and a recognizable component of central MEC consisting of polycystic nests with mucous cells, intermediate cells, and epidermoid cells in the cyst wall. The results from the immunohistochemistry for cytokeratin (CK) profiling demonstrated that, while both central MEC and GOC expressed CKs 7, 14, 18, and 19, CK13 was interestingly exclusively expressed in GOC. Fluorescence in-situ hybridization (FISH) revealed the rearrangement of the Mastermind like (MAML)-2 gene in both the MEC and GOC components. Conclusions Our case suggests that central MEC and GOC may be in the same spectrum of diseases caused by the rearrangement of the MAML-2 gene. However, given that the expression profile of CK13 was completely different between central MEC and GOC, they can be considered as separate tumors. Overall, we demonstrated a rare case in which central MEC may have originated directly from the GOC.

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Proteomic and histopathological characterization of the interface between oral squamous cell carcinoma invasion fronts and non-cancerous epithelia

Cited by 13 publications

References 38 publications

Keratin 17-positive Civatte bodies in oral lichen planus—distribution variety, diagnostic significance and histopathogenesis

Keratin 17-positive Civatte bodies in oral lichen planus—distribution variety, diagnostic significance and histopathogenesis

Expression of protein arginine methyltransferase‐5 in oral squamous cell carcinoma and its significance in epithelial‐to‐mesenchymal transition

Central mucoepidermoid carcinoma arising directly from a glandular odontogenic cyst of the mandible: a case report

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