bromochloroacetic-acid and Keratoacanthoma

Topics: Carcinoma, Squamous Cell; Humans; Keratins; Keratoacanthoma; Keratosis; Photography; Skin Neoplasms; Warts

Approximately 700 cases of keratinizing cystic squamous lung lesions in rats were investigated by light microscopy in order to clarify the nomenclature and classification of these lesions. The structure of benign keratinizing cystic squamous cell tumours of the lung was compared to that of cystic squamous lesions in the skin of rats, with consideration of data from the literature. We conclude that the reviewed keratinizing cystic squamous cell lesions of the lung are true neoplasms and that the growth pattern of these cystic lesions is inconsistent with that of a simple cyst. In the development of squamous lung cancer, a continuum of proliferation from exaggerated metaplasia through benign cystic tumours to invasive squamous cell carcinomas can be observed.

Topics: Animals; Epidermal Cyst; Keratins; Keratoacanthoma; Lung Neoplasms; Rats; Skin Diseases; Terminology as Topic

We here report the case of a 54-year old woman presenting with a swelling in the left forearm occurred eight weeks before and rapidly increasing in volume. Clinical examination showed ulcero-budding painless purplish skin lesion measuring 2 cm along its longer axis (A). The patient underwent simple biopsy. Histological examination showed dyskeratosic, disorganized, hyperplastic epithelium with cytonuclear abnormalities, suggesting malignant transformation. Given the absence of infiltration in the chorion and the presence of hyperkeratosis, the diagnosis of keratoacanthoma was made. Resection of the tumor was indicated to confirm or deny this diagnosis. Histological examination revealed a protruding epithelial tumor-like lesion circumscribed by two species of lateral "bird beaks" delineating a crater filled with many layers of keratin. The crater was bordered by hyperplastic epithelium. The crater base was characterized by irregular papillomatous projections as well as by few cellular strands which seemed to shred in the underlying dermis. These were basophilic made up of cells displaying a certain degree of cytonuclear abnormalites arranged in one or two peripheral areas and, in their center, some eosinophilic, keratin, homogeneous cells, few mitoses as well as many horny globes, most often completely keratinized (B). The diagnosis of keratoacanthoma was retained. Keratoacanthoma is a well defined anatomo-clinical entity which can be very difficult to distinguish from squamous cell carcinoma, whose incidence is three times higher. A distinction between these two lesions is necessary due to their different management.

Topics: Biopsy; Carcinoma, Squamous Cell; Diagnosis, Differential; Female; Forearm; Humans; Keratins; Keratoacanthoma; Middle Aged; Skin Neoplasms

This is a case report of a cutaneous horn, which was difficult to diagnose as benign or malignant. It demonstrates how these lesions can be approached in terms of diagnosis and management.

Topics: Carcinoma, Squamous Cell; Cheek; Diagnosis, Differential; Facial Neoplasms; Humans; Keratins; Keratoacanthoma; Male; Middle Aged; Radiotherapy, Adjuvant; Skin Neoplasms

Ligand activation of peroxisome proliferator-activated receptor (PPAR)-beta/delta and inhibition of cyclooxygenase-2 (COX-2) activity by nonsteroidal anti-inflammatory drugs can attenuate skin tumorigenesis. There is also evidence that attenuation of skin tumorigenesis by inhibition of COX-2 activity occurs through PPARbeta/delta-independent mechanisms. The present study examined the hypothesis that combining ligand activation of PPARbeta/delta with inhibition of COX-2 activity will cooperatively inhibit chemically induced skin tumor progression using both in vivo and ex vivo models. A two-stage chemical carcinogenesis bioassay was performed in wild-type and Pparbeta/delta-null mice. After 22 weeks, cohorts of both mouse lines were divided into four experimental groups: (1) control, (2) topical application of the PPARbeta/delta ligand GW0742, (3) dietary administration of the COX-2 inhibitor nimesulide, or (4) both GW0742 and nimesulide. Ligand activation of PPARbeta/delta did not influence skin tumor progression, while a modest decrease in skin tumor multiplicity was observed with dietary nimesulide. Interestingly, the combined treatment of GW0742 and nimesulide increased the efficacy of the decrease in papilloma multiplicity for 6 weeks in wild-type mice, but this effect was not found at later time points and was not found in similarly treated Pparbeta/delta-null mice. Neoplastic keratinocyte lines cultured with GW0742 and nimesulide also exhibited enhanced inhibition of cell proliferation coincident with increased expression of Keratin messenger RNAs. Results from these studies support the hypothesis that combining ligand activation of PPARbeta/delta with inhibition of COX-2 activity can inhibit chemically induced skin tumor progression by modulating differentiation.

Topics: 9,10-Dimethyl-1,2-benzanthracene; Animals; Anticarcinogenic Agents; Carcinoma, Squamous Cell; Cell Differentiation; Cell Line, Tumor; Cell Proliferation; Cyclooxygenase 2 Inhibitors; Dinoprostone; Disease Models, Animal; Female; Keratinocytes; Keratins; Keratoacanthoma; Ligands; Mice; Mice, Inbred C57BL; Mice, Knockout; Papilloma; PPAR delta; PPAR-beta; RNA, Messenger; Skin Neoplasms; Sulfonamides; Thiazoles; Time Factors

Keratoacanthoma (KA) is a common keratinizing squamous cell neoplasm of unknown origin characterized by rapid growth and spontaneous involution. Trauma-induced forms have been observed with various types of skin injury. To our knowledge, reports of KA arising at tattoo sites are scarce in the literature. A 41-year-old woman with no medical history presented for a rapidly growing nodule confined to the red part of a tattoo located on the scapula. Histology showed a keratin-filled cuplike crater with an epithelial proliferation (hyperkeratosis, parakeratosis, no keratinocyte atypia). An inflammatory infiltrate in the dermis composed of lymphocytes and histiocytes intermixed with red ink-related exogenous pigments was noted. Lack of papillomatosis and viral inclusions ruled out the diagnosis of viral wart, absence of granulomatous reaction ruled out deep fungal or mycobacterial infection and lack of cytological atypia and frank architectural abnormalities did not favour a squamous cell carcinoma. KA should be included in the list of cutaneous complications related to tattooing. Diagnosis can be challenging as differential diagnoses include pseudoepitheliomatous hyperplasia and squamous cell carcinoma. Removal of the entire area, thorough histological examination and careful follow up are mandatory.

Topics: Adult; Carcinoma, Squamous Cell; Coloring Agents; Diagnosis, Differential; Female; Histiocytes; Humans; Keratinocytes; Keratins; Keratoacanthoma; Lymphocytes; Skin Diseases; Skin Neoplasms; Tattooing

To clarify the histogenesis of keratoacanthoma, we studied keratin (K) expression in keratoacanthoma (KA) using 10 different anti-keratin antibodies against K1, K7, K8, K10, K14, K15, K16, K17, K18 and K19 and anti-filaggrin (filament aggregating protein) antibody. In the centre of KA, K1 and K10 expressions were declined, and K14 and K16 were detected in the tumour cells, suggesting differentiation towards the outer root sheath beneath the orifice of the sebaceous duct. These results suggest that KA differentiates towards the outer root sheath beneath the opening of the sebaceous duct.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Female; Filaggrin Proteins; Gene Expression Regulation, Neoplastic; Humans; Intermediate Filament Proteins; Keratin-1; Keratin-10; Keratin-14; Keratin-16; Keratins; Keratoacanthoma; Male; Middle Aged; Sebaceous Gland Neoplasms; Sebaceous Glands; Skin

The incidence of skin cancer is increased in transplant recipients. UV radiation, papillomaviruses, and immunosuppression participate in the pathogenesis of these tumors. In addition, donor cells may leave the grafted organ, reach peripheral tissues and either induce immune phenomena or possibly take part in tissue remodeling. Herein, we investigated the possible involvement of donor cells in the development of skin tumors in kidney allograft recipients. We analyzed a series of 48 malignant and benign cutaneous tumors developing in 14 females who had been grafted with a male kidney. The number of male cells was measured on microdissected material by quantitative PCR for Y chromosome. In the samples with high levels of male cells, fluorescent in situ hybridization (FISH) with X and Y probes and/or immuno-FISH with anticytokeratin antibodies were carried out. Male cells were detected in 5/15 squamous cell carcinomas and Bowen disease (range 4-180 copies), 3/5 basal cell carcinomas (91-645), 6/11 actinic keratosis (7-102), 2/4 keratoacanthoma (22-41), and 2/5 benign cutaneous lesions (14-55). In a basal cell carcinoma specimen with a high number of male cells, FISH showed that most cells within the tumoral buds were XY. In this lesion, immuno-FISH showed the presence of XY cytokeratin-positive cells indicating that the tumor nests contained male keratinocytes. In contrast, in other female transplants, male cells present in the tumors were not epithelial. In conclusion, stem cells originating from a grafted kidney may migrate to the skin, differentiate, or fuse as keratinocytes that could, rarely, undergo cancer transformation.

Topics: Bowen's Disease; Carcinoma, Basal Cell; Carcinoma, Squamous Cell; Cell Differentiation; Cell Fusion; Chromosomes, Human, X; Chromosomes, Human, Y; Female; Humans; Immunoenzyme Techniques; In Situ Hybridization, Fluorescence; Karyotyping; Keratinocytes; Keratins; Keratoacanthoma; Keratosis; Kidney Transplantation; Male; Reverse Transcriptase Polymerase Chain Reaction; Skin Diseases; Skin Neoplasms; Stem Cells; Tissue Donors; Transplantation, Homologous

Topics: Carcinoma, Squamous Cell; Diagnosis, Differential; Humans; Immunohistochemistry; Keratins; Keratoacanthoma; Protein Precursors; Skin Neoplasms

The most frequent consideration in the clinical and histologic differential diagnosis of keratoacanthoma is squamous cell carcinoma. In the present study, cytokeratin 10 expression and proliferation rate as measured by Ki-67 expression were compared between 50 clinically and histologically diagnosed keratoacanthomas and 50 squamous cell carcinomas. Tissue sections from the skin were immunohistochemically stained with anti-cytokeratin 10 and anti-Ki-67 monoclonal antibodies. The distribution of cytokeratin 10 expression and proliferative cell count were analyzed. Study results showed higher cytokeratin 10 expression in keratoacanthomas than in squamous cell carcinomas and different distribution of staining in the two entities. The analysis of cytokeratin 10 expression showed a much wider range of values and statistically higher median (p<0.001) in keratoacanthomas than in squamous cell carcinomas. Additionally, the proliferation index of keratinocytes as measured by Ki-67 expression was significantly higher in squamous cell carcinomas than in keratoacanthomas (p<0.01). These results may prove helpful in histologic differentiation of these disorders.

Topics: Carcinoma, Squamous Cell; Diagnosis, Differential; Humans; Keratins; Keratoacanthoma; Ki-67 Antigen; Skin Neoplasms

The antibody 34-betaE12 stains selectively the keratins of basal cells. The aim of this study is to investigate the staining pattern of 34-betaE12 in borderline (keratoacanthomas and solar keratosis), and benign lesions (seborrheic keratoses). The proliferation index Ki-67 staining was also evaluated in these and also in malignant (basal and squamous cell carcinomas) cases. The staining pattern where the 34-betaE12 positive cells found in the basal, suprabasal epidermal layers was called "focal"; and the staining in all layers including upper spinous layer was called "diffuse". Mean proliferation index and the distribution pattern of Ki-67 immunohistochemical expression were assessed. Basal and suprabasal expression of 34-betaE12 significantly predominated in the normal parts of the epidermis, in eight out of 11 seborrheic keratoses (%73), one out of the 19 keratoacanthomas (%5), two out of 11 solar keratosis (18%). Statistical analysis revealed significant differences between mean level of Ki-67 expression of malignant (squamous cell carcinoma, basal cell carcinoma), benign (seborrheic keratoses) and premalignant (solar keratoses, keratoacanthomas) lesions (p<0.01). The distribution of staining pattern for Ki-67 paralleled to the staining pattern of 34-betaE12. Basal cell status assessment completed by 34-betaE12 may resolve some, but not all of the problems in terms of determining the presence of dysplasia.

Topics: Cell Division; Humans; Immunohistochemistry; Keratins; Keratoacanthoma; Keratosis; Keratosis, Seborrheic; Ki-67 Antigen; Precancerous Conditions; Skin

We report two patients with keratoacanthoma, simple in one and multiple in the other, displaying typical histological features except for intravascular spread. Although this spread points to malignancy, it did not allow to rule out the diagnosis of keratoacanthoma. These aggressive histological features, as well as perineural invasion, are not linked to malignant clinical course, according to the literature. Intravascular spread suggests that keratoancanthoma could be considered as a peculiar form of well differentiated squamous cell carcinoma. Comparison between clinical and pathological observations should lead to more specific diagnosis.

Topics: Adult; Aged; Carcinoma, Squamous Cell; Female; Humans; Keratins; Keratoacanthoma; Male; Neoplasm Invasiveness; Skin Neoplasms; Treatment Outcome

Topics: Carcinoembryonic Antigen; Epithelial Cells; Hair Follicle; Humans; Hyperplasia; Keratins; Keratoacanthoma; Melanoma; Mouth Mucosa; Skin; Skin Neoplasms

Skin malignancies can originate in burn scars (Marjolin's ulcer). The most common is squamous cell carcinoma, usually appearing years after injury. Split-thickness skin graft donor sites as a source of malignant transformation are far less frequent and demonstrate a shorter interval between surgery and tumor onset. Keratoacanthomas have rarely been reported to arise in such scars. We describe the simultaneous occurrence of keratoacanthomas on a spontaneously healed second-degree burn on the flank and in the scar of a skin graft donor site on the thigh, 4 months after a 40% total body surface area burn.

Topics: Burns; Cicatrix; Dermis; Eosinophils; Epidermis; Fibrosis; Humans; Keratins; Keratoacanthoma; Lymphocytes; Male; Middle Aged; Skin Transplantation

Verruciform xanthoma is a rare clinicopathologic entity of uncertain etiology that occurs primarily in the oral mucosa. Aggregates of foam cells in the submucosal stroma or papillary dermis in association with verrucous epithelial hyperplasia are the hallmark of this lesion. Extraoral (cutaneous) occurrence of verruciform xanthoma is much rarer and has been reported mostly in the genital skin. Five cases of extraoral cutaneous verruciform xanthoma (three from the scrotum, one from the penis, and one from the nose) and one histologic "simulant" (from skin of the nose) were studied. The lesions were solitary, raised, or polypoid with cup-shaped craters filled with parakeratotic cells that blended into keratinocytes of an acanthotic and papillomatous epidermis. There was a neutrophilic infiltrate of varying intensity between plump parakeratotic cells and keratinocytes, near the surface of the epidermis. Aggregates of foam cells were present in the papillary dermis, which was highly vascular. A plasma cell predominant infiltrate was seen at the base in a bandlike fashion. Despite the architectural resemblance of verruciform xanthoma to verrucous mucocutaneous lesions related to human papillomavirus infection, it was not detected by either immunohistochemistry, in situ hybridization, polymerase chain reaction, or Southern blot analysis in any case. The foam cells were weakly positive for cytokeratin and for Factor XIIIa but negative for S-100 protein. The KP1 and Mac 387 immunostain showed focal weak staining in foam cells. We postulate that a cascade of events pursue after initial keratinocytic damage attracting neutrophils, with subsequent phagocytosis of necrotic keratinocytic debris by dermal dendrocytes, eventually leading to the ultimate manifestation of the lesion as verruciform xanthoma. The etiologic agent remains elusive, but based on our findings, we conclude that verruciform xanthoma is most likely not a human papillomavirus-associated squamoproliferative lesion and that the foam cells, a histologic hallmark of the lesion, are most likely derived from dermal dendritic cells.

Topics: Adult; Aged; Biomarkers; Female; Genital Diseases, Male; Humans; Immunohistochemistry; In Situ Hybridization; Keratins; Keratoacanthoma; Male; Middle Aged; Nose Diseases; Papillomaviridae; Polymerase Chain Reaction; Psoriasis; Transglutaminases; Xanthomatosis

Topics: Child; Connective Tissue; Diagnosis, Differential; Epithelium; Follow-Up Studies; Gingival Diseases; Granuloma, Pyogenic; Humans; Keratins; Keratoacanthoma; Male; Maxilla

Specimens of trichilemmal cyst, malignant trichilemmoma, keratoacanthoma, and epidermal cyst were examined to characterize keratin peptides in hair-follicle-derived tumors. Keratins were extracted from the specimens and analyzed by two-dimensional gel electrophoresis and densitometry; the results were then compared with those for normal epidermis, the outer root sheath of hair follicles, psoriatic epidermis, and various nonfollicular cutaneous epithelial tumors. The specific nonfollicular tumors examined were squamous cell carcinoma, Bowen disease, actinic keratosis, eccrine porocarcinoma, and sebaceous carcinoma. Immunohistochemistry also was performed with a few anti-keratin monoclonal antibodies. As a general rule, K6 and K16 were expressed in hyperproliferative conditions, such as epidermal tumors, and K17 was coexpressed in the same lesions. The ratio of K16 to K17 in many epithelial skin tumors has been unclear until now. K17 content exceeded K16 content in most follicular tumors, whereas in almost all the nonfollicular tumors and the psoriatic epidermis, K17 levels were less than or about equal to K16 levels. There was a significant difference in the ratio of K16 to K17 between follicular and nonfollicular skin tumors. These results indicate that alterations in the content of these keratins may be associated with follicular differentiation.

Topics: Epidermis; Hair; Humans; Immunohistochemistry; Keratins; Keratoacanthoma; Neoplasms, Basal Cell; Psoriasis; Skin Neoplasms

Topics: Antigens, Neoplasm; Carcinoma, Squamous Cell; Cell Nucleus; Cytoplasm; Epidermis; Gene Expression Regulation; Gene Expression Regulation, Neoplastic; Humans; Keratinocytes; Keratins; Keratoacanthoma; Ki-67 Antigen; Neoplasm Proteins; Nuclear Proteins; Precancerous Conditions; Skin Neoplasms; Tumor Suppressor Protein p53

Keratoacanthomas are benign skin tumors that grow rapidly but eventually regress. They occur most commonly in sun-exposed skin and are histologically remarkably similar to squamous cancers. Since mutations of the p53 tumor suppressor gene are found frequently in cutaneous squamous cell carcinomas, we hypothesized that p53 mutations might contribute to the development of keratoacanthomas. To address this question, we did p53 immunohistochemistry with a polyclonal rabbit antiserum, CM-1, that binds both mutant and wild-type p53 proteins. Although wild-type p53 protein degrades rapidly and is generally undetected by immunohistochemistry, mutant p53 protein has a longer half-life and accumulates to detectable levels. We tested 26 formalin-fixed keratoacanthomas and 4 normal skin biopsies. Positive nuclear staining was detected in 20 of 26 (77%) of the keratoacanthomas and in none of the normal skin samples. Nuclear staining occurred in the outermost layer of the neoplasms and not in the keratin-filled central cores. Since nuclear p53 protein within a cutaneous squamous cell carcinoma usually correlates with missense mutation, these data suggest that p53 mutations contribute to the development of this benign neoplasm. The histologic similarity to squamous cell carcinoma and the accumulation of p53 protein suggest progression toward malignancy, but the invariable regression of these tumors suggests an arrest at some point in multistage carcinogenesis. If this model is correct, then genetic analysis of keratoacanthomas may provide clues to the later stages of squamous carcinogenesis including local invasion and metastasis.

Topics: Animals; Carcinoma, Squamous Cell; Cell Nucleus; Coloring Agents; Disease Progression; Fixatives; Formaldehyde; Genes, p53; Half-Life; Humans; Image Processing, Computer-Assisted; Immunohistochemistry; Keratins; Keratoacanthoma; Mutation; Neoplasm Regression, Spontaneous; Rabbits; Remission, Spontaneous; Skin; Skin Neoplasms; Sunlight; Tumor Suppressor Protein p53

Recent research observations suggest that the keratoacanthoma (KA) is a form of resolving squamous cell carcinoma (SCC). The mechanism by which this resolution takes place has not been fully explored, although it may have an immunological basis. To investigate this, we compared 15 clinically and histologically diagnosed KAs and 15 SCCs with regard to cellular infiltrate and keratin expression. We found that KAs have significantly higher numbers of CD3+ and CD4+ cells invading their epidermal component than SCCs. The T lymphocytes infiltrating KAs were more immunologically active, as greater numbers expressed the interleukin-2 receptor (IL-2R) than those in SCCs. It is of interest that CD36 was expressed by a significantly greater proportion of tumour cells within KAs than SCCs. This was also the case for the intercellular adhesion molecule ICAM-1, and the differentiation marker keratin 10. Overall, these findings suggest that KA regression is immunologically mediated, with activated (IL-2R+) CD4+ T lymphocytes and adhesion molecules playing a pivotal role in the immune response.

Topics: Aged; Aged, 80 and over; Antigens, CD; Carcinoma, Squamous Cell; CD3 Complex; CD36 Antigens; CD4 Antigens; Epidermis; Humans; Immunohistochemistry; Intercellular Adhesion Molecule-1; Keratins; Keratoacanthoma; Lymphocyte Activation; Middle Aged; Platelet Membrane Glycoproteins; Receptors, Interleukin-2; Remission, Spontaneous; Skin Diseases; Skin Neoplasms; T-Lymphocytes

A case of keratoacanthoma (KA) with glandular proliferation was reported. The tumor was a firm, dome-shaped, elevated nodule on the cheek of an 82-year-old Japanese male. Generally, the tumor showed the typical histopathological features of KA; slight nuclear atypia and mitotic figures were present in a cup-shaped proliferation of keratinocytes and, in the center of the lesion, a keratin-filled crater with nests of dyskeratotic and acantholytic cells was seen. In the bottom of the lesion, a glandular structure forming branching, thin lumina was observed. The epithelium of the lumina was made up of two or more layers of columnar or cuboidal cells without keratinization. Tall columnar cells with oval nuclei were located in the luminal row and small cuboidal cells with round nuclei and scanty cytoplasm were in the outer layer. Immunohistochemical staining revealed that only the glandular structure was carcinoembryonic antigen positive. Lectin binding patterns observed in the glandular proliferation were similar to those reported for the apocrine gland. KA sometimes exhibits an adenoid structure in its lesion because of acantholytic changes. However, KA associated with true glandular proliferation has not been reported as far as we know, and our case is the first reported one. KA is thought to be a tumor of follicular origin, and the glandular proliferation observed in the present case seemed to have certain characteristics that suggest its apocrine origin.

Topics: Aged; Aged, 80 and over; Apocrine Glands; Carcinoembryonic Antigen; Cheek; Epidermis; Epithelium; Facial Dermatoses; Humans; Keratinocytes; Keratins; Keratoacanthoma; Male

The expression of differentiation associated high PM Keratin polypeptides of the oral mucosa lesions were studied by immunohistochemical and immunoblotting techniques applied to adjacent sections of each biopsy specimen. The material studied included specimens of leukoplakia, verrucous carcinoma, squamous cell carcinoma, adenocarcinoma and keratoacanthoma. Little or no expression of 65-67 Kd keratins was evident in squamous cell carcinoma and adenocarcinoma. Hyperkeratotic (both benign and dysplastic) lesions such as verrucous carcinoma, leukoplakia, and keratoacanthoma, showed great variations in the intensity of 65-67 bands and a very irregular immunohistochemical staining pattern. Increased amounts of horny substance was usually accompanied by absence of, or decreased expression of 65-67 Kd keratins, thus indicating a change in the polypeptide composition of the horny layer in pathological conditions of the oral epithelium.

Topics: Adenocarcinoma; Antigens, Differentiation; Carcinoma, Squamous Cell; Carcinoma, Verrucous; Cell Differentiation; Electrophoresis, Polyacrylamide Gel; Humans; Immunoblotting; Immunoenzyme Techniques; Immunohistochemistry; Keratins; Keratoacanthoma; Leukoplakia, Oral; Mouth Mucosa; Mouth Neoplasms

The tissue labelling of a panel of monoclonal antikeratin antibodies (LL001, LL002, LL003, LP2K, BA17, LP34, CAM5.2, and LH1) recognising keratins 1, 5, 8, 10, 14, 18, and 19 were investigated in frozen and formalin-fixed normal skin. Antibodies LL001, LL003, BA17, LP34, CAM5.2, and LH1 were found to be reactive in formalin-fixed material and were used to study 23 basal cell carcinomas, 8 squamous cell carcinomas, 5 keratoacanthomas, 5 Bowen's disease, and 6 clear cell acanthomas. All these tumours demonstrated a loss of keratin 10 expression as demonstrated by loss of labelling with LH1. Keratin 14 expression, as demonstrated by LL001, was reduced but present in all the tumours except squamous cell carcinomas and keratoacanthomas where increased labelling was observed in the more differentiated areas of these tumours. Simple epithelial keratin expression was demonstrated by positive labelling with CAM5.2 and keratin 19 by BA17 in a third of basal cell carcinomas and squamous cell carcinomas. Three of the five keratoacanthomas labelled with BA17, indicating the presence of keratin 19 in these lesions. These results support the concept that keratin expression is a phenotypic marker of the state of differentiation or malignant transformation and that patterns of keratin expression are not specific to any particular premalignant or malignant disorder.

Topics: Antibodies, Monoclonal; Axilla; Bowen's Disease; Carcinoma, Basal Cell; Carcinoma, Squamous Cell; Freezing; Humans; Immunohistochemistry; Keratins; Keratoacanthoma; Reference Values; Skin; Skin Neoplasms; Tissue Fixation

Among carcinomas, signet-ring morphologic characteristics have been regarded as pathognomonic of adenocarcinoma. This report presents the case of a poorly differentiated cutaneous squamous cell carcinoma with a monodispersed, invasive signet-ring component. Kreyberg stains had negative results for mucin. Immunohistochemical analysis demonstrated that concentric rings in the signet-ring cells were composed of keratin. To the best of the authors' knowledge, this is the first report of signet-ring squamous cell carcinoma. Another feature that bears emphasis is that this squamous cell carcinoma led to the death of the patient, even though it originated in a field of actinic keratosis.

Topics: Adenocarcinoma, Mucinous; Aged; Carcinoma, Squamous Cell; Forehead; Humans; Immunohistochemistry; Keratins; Keratoacanthoma; Keratosis; Neoplasm Recurrence, Local; Skin Neoplasms; Staining and Labeling

Topics: Epidermis; Humans; Keratins; Keratoacanthoma; Skin Diseases

We examined seven invasive squamous cell carcinomas, five squamous cell carcinomas in situ, four keratoacanthomas, two actinic keratoses, and two seborrheic keratoses by indirect immunofluorescence. We used a panel of three antibodies: one directed against filaggrin, one against involucrin, and one against peptidylarginine deiminase. Anti-involucrin stained all the lesions studied, but the pattern within a given category of lesions was variable and consistent differences between the categories were not observed. Similarly, the antibodies against peptidylarginine deiminase and filaggrin were not able to distinguish differences between the various types of tumors. We conclude that in tumors of epidermis, benign or malignant, products of differentiation are expressed independently of histologic atypia or clinical aggressiveness. Therefore, markers of differentiation do not appear to be reliable indexes for distinguishing benign from malignant lesions.

Topics: Carcinoma, Squamous Cell; Filaggrin Proteins; Fluorescent Antibody Technique; Humans; Hydrolases; Intermediate Filament Proteins; Keratins; Keratoacanthoma; Precancerous Conditions; Protein Precursors; Protein-Arginine Deiminase Type 4; Protein-Arginine Deiminases; Skin; Skin Neoplasms

Fifteen keratoacanthomas and fifteen squamous cell carcinomas of the skin were examined by immunoperoxidase methods for involucrin and both 45- and 63-kilodalton keratins. Keratoacanthomas showed a relatively homogeneous staining pattern for involucrin; all cells except basal cells stained with mild to moderate intensity. Squamous cell carcinomas disclosed a highly irregular involucrin staining pattern with marked variation in staining intensity from cell to cell. Staining patterns for keratin proteins did not appear to distinguish between keratoacanthomas and squamous cell carcinomas. The 45-kilodalton keratin pattern showed diffuse staining within both keratoacanthomas and squamous cell carcinomas, and the 63-kilodalton keratin pattern consisted of focal staining, mostly of dyskeratotic cells. These results suggest that involucrin may serve as a diagnostic aid in differentiating between squamous cell carcinomas and keratoacanthomas. In addition, other lesions in the differential diagnosis of keratoacanthoma and squamous cell carcinoma were also examined for involucrin.

Topics: Adult; Aged; Carcinoma, Squamous Cell; Epidermis; Histocytochemistry; Humans; Immunoenzyme Techniques; Keratins; Keratoacanthoma; Middle Aged; Neoplasm Proteins; Protein Precursors; Sebaceous Glands; Skin Diseases; Skin Neoplasms; Sweat Glands

UV induced keratoacanthoma-like lesions in mice were studied grossly, light microscopically and electron microscopically. The tumours varied in their degree of cell organization and keratinization but all exhibited downward growth and had a continuous basement membrane. Ultrastructurally, the keratinocytes displayed villous distortion of their plasma membranes, and at times the basal lamina of the epidermal-dermal junction showed focal discontinuation. The keratoacanthoma-like lesions in mice had similarities of appearance to keratoacanthoma in man but showed no regression and regularly progressed to squamous cell carcinoma. This clinical course is dissimilar to that of keratoacanthoma in man which suggests that the use of the term is inappropriate for these UV induced tumours. Moreover, in the context of our experimental system and a dynamic picture of tumour development where tumour types can be seen as stably arising and continuing entities or, a progressive sequence for which squamous cell carcinoma represents an end stage, it is not appropriate to view the keratoacanthoma-like lesion in mice as an entity distinct from the spectrum of UV induced tumours progressing from benignity to malignancy.

Topics: Animals; Carcinoma, Squamous Cell; Epidermis; Humans; Keratins; Keratoacanthoma; Mice; Mice, Hairless; Microscopy, Electron; Neoplasms, Radiation-Induced; Skin; Skin Diseases; Skin Neoplasms; Ultraviolet Rays

In normal skin, cytokeratin polypeptides are expressed in different cell-type-specific patterns, in the keratinocytes of the different epidermal cell strata as well as in different lateral epithelial domains. Using light microscopically controlled microdissection of defined regions from frozen sections of biopsies, we have prepared cytoskeletons of various benign and malignant keratinocyte-derived tumors of human skin and analyzed their cytokeratin polypeptide patterns by two-dimensional gel electrophoresis. Premalignant fibroepitheliomas and basal cell epitheliomas display a relatively simple cytokeratin pattern (cytokeratins nos. 5, 14, 15, and 17). Pseudocarcinomatous hyperplasia, some squamous cell carcinomas, and a certain subtype of condylomata acuminata present a hair-follicle-like pattern (nos. 5, 6, 14, 16, 17). In addition to these components, variable, mostly low amounts of cytokeratins nos. 1 (Mr 68,000), and 11 are detected in most squamous cell carcinomas, in keratoacanthomas, verruca vulgaris, and another type of condylomata acuminata. In molluscum contagiosum, verruca plana, solar keratosis, and seborrheic keratosis, the cytokeratin expression is shifted more towards the normal epidermal pattern (polypeptides nos. 1, 2, 5, 10, 11, 14, 15 and traces of nos. 6 and 16 in the latter two tumors). No tumor-specific cytokeratins have been found. We conclude that keratinocyte-derived skin tumors contain various combinations of cytokeratins of the subset typical for normal keratinocytes of skin, but no cytokeratins typical for internal, simple epithelia. Different groups of tumors can be distinguished by their specific cytokeratin patterns. Possible applications of cytokeratin typing in clinical diagnosis are discussed.

Topics: Carcinoma, Basal Cell; Carcinoma, Squamous Cell; Condylomata Acuminata; Electrophoresis, Polyacrylamide Gel; Humans; Keratins; Keratoacanthoma; Keratosis; Molecular Weight; Molluscum Contagiosum; Papilloma; Peptides; Skin; Skin Neoplasms; Warts

We report an interesting case of generalized papular and nodular lesions with central keratinous plugs and severe hyperkeratotic-acanthotic histopathology with arthritis in a 19-year-old male patient who had suffered from a similar disease 2 years earlier. Papules and nodules erupted a few days after the arthritis and this was noticed during both episodes. On healing, nodules fell spontaneously leaving behind insignificant hyperpigmented scars.

Topics: Adult; Arthritis; Humans; Keratins; Keratoacanthoma; Keratosis; Male; Skin; Skin Diseases

Human keratoacanthomas are benign, hyperkeratotic skin tumors which, until now, have not been studied by the combined techniques of scanning electron microscopy (SEM) and transmission electron microscopy (TEM). Correlation of the results obtained by these two methods revealed the tridimensional anatomy of the tumor and illustrated the origin of keratin plugs within the tumor. Tumor cells were modified keratinocytes which differed from normal keratinocytes in that they were larger and sometimes contained vacuoles and intracellular desmosomes. the presence of vacuoles among the tonofilaments and tonofibrils indicated that the keratinization process was altered in the tumor cells. Keratin plugs arose from hair follicles and extrafollicular tumor cells. Hairs usually degenerated following histogenesis of the plugs. Extrafollicular plugs originated about foci of degenerating tumor cells and leukocytes. Keratin plugs, regardless of their mode of origin, were surrounded by concentric lamellae of tumor cells. Keratinized tumor cells in the plugs and at the free surface of the lesion had a "honeycomb" appearance. This resulted from prominent microridges and microgrooves which interdigitated extensively and produced a "tongue and groove" effect. As reported for several animal models of keratoacanthomas, there was no evidence that sweat ducts, sebaceous glands, or Langerhans cells were involved in the pathogenesis of the human keratoacanthoma. The findings supported the view that the human keratoacanthoma arises from hair follicles.

Topics: Adult; Aged; Epidermis; Female; Hair; Humans; Keratins; Keratoacanthoma; Male; Microscopy, Electron; Microscopy, Electron, Scanning; Middle Aged

In the case of viral acanthomas, the stratum spinosum and granulosum presents ballooned cells which contain all transitional stages from multivesicular bodies (MVB) to keratinosomes. A particularity in condylomata acuminata are the "wagon-wheel" bodies. These structures are typical for the non keratinazed squamous epithelium. The participation of intercellular extruded "wagon-wheel" bodies, MVB and atypical keratinosomes on an irregular baso-apical diffusion-barrier in the epidermis of cases with viral acanthomas has been discussed. On the basis of the relation seen between MVB and the Golgi-apparatus, their transition to partially atypical keratinosomes in cases of viral acanthomas and their "expulsion" into the intercellular space could indicate that in keratinozytes the enzymatically regulated feed-back between the cellular surface and the capability to synthesize is changed by viral agents. The interference appears to manifest itself in the Golgi-apparatus and also appears to be "specified" by the terrain present.

Topics: Condylomata Acuminata; Cytoplasm; Epidermal Cells; Epidermis; Extracellular Space; Golgi Apparatus; Humans; Keratins; Keratoacanthoma; Male; Membranes; Microscopy, Electron; Viruses

Topics: Adult; Edema; Humans; Hyalin; Keratins; Keratoacanthoma; Male; Melanins; Melanocytes; Pigments, Biological; Skin Neoplasms

Topics: Basement Membrane; Carcinoma; Dermatology; Diagnosis, Differential; Esterases; Fluorescent Antibody Technique; Glycogen; Histocytochemistry; Humans; Keratins; Keratoacanthoma; Keratosis; Lupus Erythematosus, Discoid; Mast-Cell Sarcoma; Psoriasis; Skin; Skin Diseases; Skin Neoplasms; Sweat Glands; Urticaria

Topics: Animals; Humans; Keratins; Keratoacanthoma; Lip; Lip Neoplasms; Mollusca