The changes in the expression levels of follicular markers in keratoacanthoma depend on the stage: keratoacanthoma is a follicular neoplasm exhibiting infundibular/isthmic differentiation without expression of <scp>CK15</scp>

Misago, Noriyuki; Takai, Toshihiro; Toda, Shuji; Narisawa, Yutaka

doi:10.1111/cup.12317

Cited by 29 publications

(63 citation statements)

References 48 publications

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“…Additionally, KA did not express other keratins, including K7, K8, K15, K18, and K19. 9,30,31 The presence of the K1 and K10 pair was in the upper area of the ORS and may be associated with epithelial maturation once it is expressed in terminally differentiating epidermal keratinocytes and infundibular cells, 31,32 and K6 and K16 are observed in hyperproliferative epithelia or the beginning of the ORS differentiation. 31 K14 is frequently present in the proliferative basal layer of stratified epithelia and hair follicle cells, such as ORS and stem cells located at the hair follicle bulge.…”

Section: Discussionmentioning

confidence: 99%

“…17,18 In addition, K19 is usually negative for labial epidermis but positive in the labial mucosa epithelium, 17 and interestingly, it was negative for KA. 9,30,31 In addition to the keratins and ORS markers, our study analyzed markers in the specialized cell layers of the hair follicle. Hair cortex keratin was observed in the cortex and precortex of the hair follicle.…”

Section: Discussionmentioning

confidence: 99%

“…7,47,48 There are several reports of differential expression of molecular markers, such as laminin-32, nuclear factor kappa B/p50, cortactin, glut-1, Bcl-x, beta-catenin, CD44, anti-P2 X7, K10, E-cadherin, transforming growth factor-a, peanut agglutinin, peanut lectin receptor, and carcinoembryonic antigen, in KAs and SCCs. 22,31,40,43,44,[49][50][51][52][53][54][55][56][57][58][59][60][61][62] KAs were consistently positive for K6, K10, and K14. K10 and K14 were observed in specialized cells within the ORS of the hair follicle and in the interfollicular epithelium.…”

Section: Discussionmentioning

confidence: 99%

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Histogenesis of keratoacanthoma: histochemical and immunohistochemical study

Wagner

Dillenburg

Meurer

et al. 2015

Oral Surgery, Oral Medicine, Oral Pathology and Oral Radiology

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Histogenesis of keratoacanthoma: histochemical and immunohistochemical study

Wagner

Dillenburg

Meurer

et al. 2015

Oral Surgery, Oral Medicine, Oral Pathology and Oral Radiology

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“…Typical KA is a symmetrical, crateriform, exo‐endophytic lesion composed of contiguous, dilated, infundibular structures that have a central large keratotic horn and overhanging epithelial lips. Proliferation of large pale pink cells with a glassy appearance (follicular isthmic differentiation) is a common feature in KA that is more prominent in well‐developed lesions . Besides these features of KA, CFV also showed more verrucous features that differed from those of typical KA.…”

Section: Discussionmentioning

confidence: 99%

Clinicopathological study of crateriform verruca: Crateriform epithelial lesions histopathologically distinct from keratoacanthoma

Ogita

Ansai

Misago³

et al. 2016

The Journal of Dermatology

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Keratoacanthoma (KA) is a distinct clinicopathological entity, but it is often confused with other crateriform tumors. This study re-examined the clinicopathological features of 380 crateriform epithelial tumors with a central keratin plug. Seventy-six tumors (20%) had histopathological features that differed from solitary KA and were more verruca-like, and we designated these lesions as crateriform verruca (CFV). We performed clinicopathological re-examination of these neoplasms with a crateriform architecture and epithelial lip-like structures similar to KA, which also displayed histopathological features reminiscent of verruca vulgaris, such as finger-like exophytic projections with hyperkeratosis and acanthosis, focal hypergranulosis and arborization. Clinical data on CFV were also summarized. The main histopathological differences from KA were that CFV showed proliferation of keratinocytes with a similar size and regular arrangement, and the base of CFV was well demarcated without endophytic growth. Interestingly, some CFV were partly composed of epithelial cells with large pink cytoplasm in the upper malpighian layer between papillomatous projections. Furthermore, areas of trichilemmal-like keratinization without formation of the granular layer were seen in some lesions. These types of CFV were hardly distinguishable from KA, unless it is recognized that CFV may contain trichilemmal keratinization-like areas accompanied by large epithelial cells with eosinophilic cytoplasm. We have proposed the term CFV for these verrucous neoplasms to differentiate them from KA.

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“…Recent studies showed CK15 staining in the outermost layer of the hair bulge of normal human scalp samples, as well as in the proximal isthmus, infundibulum, outermost layer of the sub-bulge, the basal interfollicular epidermis and eccrine glands [59,60,61]. Exploration of the literature data on development of scarring alopecia led us to the understanding that clones C8⁄144B and LHK15 of anti-CK15 antibodies are mostly used [62], and LHK15 antibody, recognized as a marker for bulge epithelial stem cells in humans [63], was selected for this study. Other investigators have shown that bulge cells may serve as frame builders in the follicular construction of a hair [64], and the opinion that loss of stem cells in the bulge area of the hair follicle is the reason for alopecia has been established [7,22,23].…”

Section: Discussionmentioning

confidence: 99%

Eradication of damaged keratinocytes in cutaneous lichen planus forms demonstrated by evaluation of epidermal and follicular expression of CK15, indices of apoptosis and regulatory protein S100

Upeniece

Groma

Skuja

et al. 2016

pjp

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The study of cytoskeleton arrangement and its contribution to survival of cell-tocell contacts appears to be essential for understanding of numerous cellular and tissue processes. Applying CK15, S100 labeling and TUNEL reaction to cutaneous lichen planus subtypes, we found CK15 expression in the outer and inner root sheath of hair follicles, the basal epidermal layer, and eccrine glands. Its follicular expression was decreased in nearby inflammatory infiltrates. The CK15 immunopositivity was mostly described as weak (92.3%) for lichen planus but equally subdivided into weak, moderate and strong in lichen planopilaris (χ 2 = 32.514; df = 4; p < 0.001). The greatly varying apoptotic index was the highest in the lichen planopilaris involving the scalp: 81.2 ±10.7; 87.8 ±10.7 and 88.0 ±10.5 for the basal, spinous and upper epidermal layers, respectively. S100 positive epidermal and follicular cells did not differ in the lesions demonstrated in the study groups; still immunoreactivity was more pronounced in the scalp region of lichen planopilaris. Damage of cell-to-cell contacts was confirmed by electron microscopy. Apart from immunocyte-mediated keratinocyte death, cytoskeleton-based injury and loss of cellto-cell and matrix contacts may be of great importance, leading to eradication of degrading cells and thus contributing to the pathogenesis of lichen planus.

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The changes in the expression levels of follicular markers in keratoacanthoma depend on the stage: keratoacanthoma is a follicular neoplasm exhibiting infundibular/isthmic differentiation without expression of CK15

Cited by 29 publications

References 48 publications

Histogenesis of keratoacanthoma: histochemical and immunohistochemical study

Histogenesis of keratoacanthoma: histochemical and immunohistochemical study

Clinicopathological study of crateriform verruca: Crateriform epithelial lesions histopathologically distinct from keratoacanthoma

Eradication of damaged keratinocytes in cutaneous lichen planus forms demonstrated by evaluation of epidermal and follicular expression of CK15, indices of apoptosis and regulatory protein S100

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