Types Of Skin Tumors Research Articles

Specific distribution patterns of hCDC47 expression in cutaneous diseases.

hCDC47 is a human member of the MCM family, which has been implicated to be concerned with the regulatory machinery causing DNA to replicate once per cell cycle. In a previous paper, we described hCDC47 expression as being localized in the proliferative component of normal tissues, and showed greater expression in squamous cell skin carcinomas than in seborrheic keratosis. In the present study, we compared its expression in another type of skin tumor and various non-neoplastic cutaneous proliferative diseases. Two patterns of distribution of hCDC47-positive cells were observed. Keratoacanthomas showed a peripheral pattern in which only the cells located the basal cell layers were positive. Psoriasis vulgaris also showed this peripheral type of location, with the cells in the suprabasal layers also occasionally expressing hCDC47. Verruca vulgaris demonstrated a diffuse pattern, with positive epithelial cells distributed throughout the layers. Basal cell carcinomas also showed a similar pattern. The keratoacanthomas showed the highest hCDC47 positive cell rate (43.1%), followed by verruca vulgaris (42.5%), psoriasis vulgaris (23.4%), and basal cell carcinoma (17.3%). Our results suggest participation of hCDC47 in these proliferative disorders involving keratinocytes.

Expression of moesin and its associated molecule CD44 in epithelial skin tumors.

Moesin, one of the ERM (ezrin; radixin; moesin) family members, is directly associated with the cytoplasmic domain of CD44, which is now thought to be related to the metastatic potential of tumor cells. Using immunohistochemistry we investigated the expression of moesin in normal epidermis and various kinds of epithelial skin tumors: squamous cell carcinoma, verrucous carcinoma, Bowen's disease, solar keratosis, keratoacanthoma, basal cell carcinoma, and extramammary Paget's disease. Normal skin showed positive epidermal staining for moesin with the exception of the stratum corneum. The expression of moesin varied with the type of skin tumor. In basal cell carcinoma, Bowen's disease, and extramammary Paget's disease, moesin expression was either faint or negative. In contrast to Bowen's disease, invasive squamous cell carcinoma showed more intense and heterogeneous staining of the cytoplasm and the cell membrane. Verrucous carcinoma was weakly positive, with a tendency for the moesin to be distributed in the cell membrane. The staining pattern of moesin varied among the different kinds of epithelial skin tumors, and its expression was generally similar to that of the standard form of CD44. These results suggest that moesin is closely inter-related with CD44 in epithelial skin cells as seen in other cellular systems, and that the variable pattern of moesin staining among the skin tumor cells could reflect expression disorders associated with the transformation.

XPA-deficiency in hairless mice causes a shift in skin tumor types and mutational target genes after exposure to low doses of U.V.B.

Xeroderma pigmentosum (XP) patients with a defect in the nucleotide excision repair gene XPA, develop tumors with a high frequency on sun-exposed areas of the skin. Here we describe that hairless XPA-deficient mice also develop skin tumors with a short latency time and a 100% prevalence after daily exposure to low doses of U.V.B. Surprisingly and in contrast to U.V.B.-exposed repair proficient hairless mice who mainly develop squamous cell carcinomas, the XPA-deficient mice developed papillomas with a high frequency (31%) at a U.V. dose of 32 J/m2 daily. At the highest daily dose of 80 J/m2 mainly squamous cell carcinomas (56%) and only 10% of papillomas were found in XPA-deficient hairless mice. p53 gene mutations were examined in exons 5, 7 and 8 and were detected in only 3 out of 37 of these skin tumors, whereas in tumors of control U.V.B.-irradiated wild type littermates this frequency was higher (45%) and more in line with our previous data. Strikingly, a high incidence of activating ras gene mutations were observed in U.V.B.-induced papillomas (in 11 out of 14 tumors analysed). In only two out of 14 squamous cell carcinomas we found similar ras gene mutations. The observed shift from squamous cell carcinomas in wild type hairless mice to papillomas in XPA-deficient hairless mice, and a corresponding shift in mutated cancer genes in these tumors, provide new clues on the pathogenesis of chemically- versus U.V.B.-induced skin carcinogenesis.

Skin Abnormalities in Neurofibromatosis 2

To determine the prevalence, distribution, and histopathological conditions of skin abnormalities in neurofibromatosis 2 (NF2). Case series. Hospital neurology department. Consecutive sample of 88 patients with NF2 referred through workshops and publications, genetic counseling, and referral from neurosurgical departments; 81 patients met the National Institutes of Health, Bethesda, Md, NF2 diagnostic criteria and the diagnosis was established by mutation or segregation analyses in 7 patients. Prevalence, distribution, and type of skin abnormalities; histopathological features of 29 skin tumors selected primarily for medical indications. Fifty-two patients (59.1%) had 458 skin tumors, which were the first presenting sign in 27.3% of patients and usually appeared as flat dysplastic tumors or subcutaneous spherical nodular tumors of the peripheral nerves, on the limbs and trunk. Although 29 patients (33.0%) had café au lait spots, only 2 patients had as many as 6 spots. compared with patients with milder disease, patients with more severe disease had a significantly greater prevalence of skin tumors (24.0% and 71.0%, P < .001), more than 10 skin tumors (0.0% and 27.4%, P = .004), flat dysplastic skin tumors (8.0% and 54.8%, P < .001), and subcutaneous spherical nodular tumors (24.0% and 58.1%, P = .004). The histologically analyzed tumors were predominantly schwannomas, but 5 were neurofibromas and 2 were mixed tumors. The prevalence of some skin tumor types in NF2 is high and varies with disease severity, and schwannomas predominate in sampled tumors. The occurrence of neurofibromas is surprising, but could be explained by an interaction between neurofibromin and the NF2 gene product in regulating the ras proto-oncogene.

Solid tumors after heart transplantation: Lethality of lung cancer

Prolonged nonspecific immunosuppression after solid-organ transplantation is associated with an increased risk of certain cancers. This study examined the development of solid-organ tumors after cardiac transplantation. Thirty-eight solid tumors were identified in 36 (5.9%) of 608 cardiac transplant recipients who survived more than 30 days. Two patients had two types of skin tumors (basal cell and squamous cell). The tumors included the following types: skin (15), lung (10), breast (1), bladder (2), larynx (2), liver (1), parotid (1), testicle (1), uterus (2), melanoma (2), and Merkel's cell (1). Four immunosuppression regimens based on cyclosporin A or FK 506 were used during this period. There was no association between the incidence of solid tumors and the use of lympholytic therapy. After the diagnosis of tumor was made, the actuarial 2-year survival rates of recipients with skin, lung, and other solid tumors were 71%, 22%, and 23%, respectively. Eight of 10 patients with lung cancer were in stage IIIA or higher at the time of diagnosis. Skin and lung tumors are the most frequent solid tumors in heart transplant recipients. Skin tumors (except Merkel's cell carcinoma and melanoma) usually have a benign course, whereas lung and other tumors developing in cardiac transplant recipients carry a poor prognosis. Advanced disease stage at the time of diagnosis is responsible for the dismal outcome of recipients in whom solid tumors develop. Close postoperative tumor surveillance after cardiac transplantation is warranted.

Mutation and expression of TP53 in malignant melanomas.

Mutations of the TP53 gene are the most common genetic alterations in human malignancies. Overexpression of the p53 protein has been reported in high frequencies in all types of skin cancer. To determine the role of TP53 in the pathogenesis of malignant melanoma, we investigated the expression of p53 in 12 cell lines and 145 primary and metastatic lesions by immunohistochemistry. Overexpression of p53 was predominantly detected in the cytoplasm of the cells in 96 (66%) tumor and 12 (93%) cell lines. In contrast to findings in other tumor types, in melanomas immunoreactive cells were found in clusters or as scattered single cells. In primary melanomas, the frequency of p53 overexpression did not correlate with tumor thickness. Nucleotide sequencing of TP53 genes of 24 melanoma tumors/cell lines demonstrated point mutations in seven samples, all coding for mutant p53 protein species. The frequency of TP53 alterations of 20%-30% is lower than in other skin tumor types. Notably, immunohistochemistry was not a suitable method to distinguish overexpression of wild-type p53 from mutant species, since cell lines/tumors with TP53 mutations did not show distinctive staining patterns. The mutation pattern in six out of seven lesions was similar to that caused by ultraviolet light damage. This finding may be regarded a further indication for a pathogenetic role of UV light damage in at least a subgroup of malignant melanomas.

Amyloid in basal cell carcinoma and seborrheic keratosis.

The frequency of amyloid substance was studied in two different types of skin tumours: basal cell carcinoma and seborrheic keratosis. In 9 out of 49 cases of seborrheic keratosis amyloid substance was found. In the basal cell carcinomas, 194 out of 260 cases showed amyloid deposits, a rate that is higher than that previously reported. The basal cell carcinoma material was further studied regarding the amount of amyloid, mitotic rate, degree of apoptosis and the age of the patients. There was no correlation between the amount of amyloid and the mitotic rate, or the degree of apoptosis. There was a slightly higher incidence of amyloid-positive cases among elderly patients.

Localization of Endogenous β‐Galactoside‐Binding Lectin as a Means to Distinguish Malignant from Benign Skin Tissue

The immunolocalization of a 30-kd endogenous lectin, referred to as galaptin, was studied in various skin tumor types. Basal cell carcinomas expressed little or no galaptin, whereas nonmalignant basaloid cells, squamous cell carcinomas, melanoma, nevi, and stroma showed more prominent galaptin immunostaining. Therefore, the immunodetection of galaptin may aid the dermatopathologist in difficult histologic diagnosis.

Epithelial distribution of a myelomonocytic antigen LI in relation to cutaneous malignancies and melanocytic naevi.

The distribution of LI antigen in four common skin tumours was examined immunohistochemically in 40 samples of formalin-fixed routine biopsy material. Presence of LI in the dermis depended on the extent and composition of the inflammatory infiltrate; LI was found mainly in reactive histiocytes and neutrophils. Intense epidermal staining was seen adjacent to squamous cell carcinoma, basal cell carcinoma and malignant melanoma, but not adjacent to melanocytic naevi. In specimens of melanocytic naevi, LI staining around pilosebaceous units was weak or absent. Around the three malignant types of lesion, epidermal LI positivity faded distally--thereby indicating the extent of the tumour. LI was, in addition, expressed by the most highly differentiated cells in squamous cell carcinomas, whereas the other neoplasms were negative. Antibody to LI may, thus, be a useful adjunct for distinction between various types of skin tumours.

Fibroepithelioma of Pinkus Overlying Breast Cancer

To the Editor.— Although much has been written about the association of cutaneous tumors with internal malignant neoplasms, opinions vary widely. One of the problems with these studies is the attempt to associate one type of skin tumor with all types of internal malignant neoplasms. For example, the question of increased association of Bowen's disease with internal malignant neoplasms has been answered affirmatively,1negatively,2and positively only for females.3Pairing of a specific skin tumor with all internal malignant neoplasms seems unrewarding. Perhaps more definite answers may result from pairing a particular skin tumor with one specific internal malignant neoplasm. I report herein two cases of fibroepithelioma of Pinkus in the skin overlying breast cancer. Report of Cases.—Case 1.— A 52-year-old woman was admitted to the hospital because of a mass in her right breast. She had first noticed the mass four weeks prior to

'Atrichosis', a new hairless gene with cyst formation in rats.

A new hairless gene in the Donryu strain of the rat has been designated atrichosis (at). Histological sections demonstrated that atrichotic skin was quite similar to that found in human skin with multiple follicular cysts, which is one type of skin tumor in humans.

Lymphocyte stimulation in the cellular inflammatory reaction of some human skin tumours.

By labelling dermal infiltrate cells with H3-thymidine, two types of skin tumours can be distinguished: one type with many labelled cells in the infiltrate (H3-thymidine labelling index, H3-I), the other with few labelled cells. Type I includes malignant melanoma (H3-I = 2.2%) and hemangioendothelioma (2.8%). Type II includes metastases of malignant melanoma (1%), squamous cell carcinoma (1.1%), basel cell epithelioma (0.5%), nevus cell nevus (0.6%), and nevoid lentigo (0.4). The number of labelled cells in the cellular reaction of Type II tumours does not differ significantly from that in normal human corium (0.75%), though there may be a dense cellular reaction. DNA-synthesizing cells were classified with the aid of characteristical stainings and histochemical methods. A vast majority of them were found to be lymphocytes. Our research underlines the special importance of cellular inflammatory reaction, i.e. cellular immunity, im malignant melanoma and probably in hemangioendothelioma.

Possible usefulness of hypotrichotic rats for studies on skin tumorigenesis.

A new strain of hypotrichotic (hairless or partially hairless) rats was studied to determine whether such animals would be suitable for studies on radiation-induced skin carcinogenesis. Breeding experiments revealed that the condition is inherited in a simple Mendelian recessive manner, and that the hypotrichotic dams are defective in milk supply for nourishing their young. Histological. sections of hypotrichotic skin demonstrated the presence of hair-follicle and sebaceous gland cysts in young adults. Observations of older hypotrichotic rats showed that some of these microscopical cysts proliferate to form visible epidermal tumors. Notwithstanding this undesirable feature, the choice of hypotrichotic rats for studies of the types of skin tumors induced by ionizing radiation might well provide more meaningful data than that derived from normal rats or mice, particularly where the effects are to be extrapolated to man.

The Trend of Morality from Primary Malignant Tumors of Skin

There is an approximate balance between the rising incidence of the common types of skin tumors and improving recognition and treatment of them. As a result, the death rate from primary malignant tumors of the skin in white people in the U.S. is currently stable. In recent years the death rate in the elderly has fallen, while it has risen in the middle-aged and young. As a result, the mean age of death has declined and the loss of expected life from these tumors has increased. Currently, about two-thirds of the deaths are due to malignant melanoma.

Radiation-Induced Hair-Follicle Damage and Tumor Formation in Mouse and Rat Skin&lt;xref ref-type="fn" rid="FN2"&gt;2&lt;/xref&gt;

The dorsal skin of 158 Swiss Millerton mice was irradiated with electrons in single exposures at 6 dose levels from 500–4,000 rods. The mice were observed for skin-tumor formation every 4 weeks for 88 weeks. At death each tumor was examined histologically, and whole-skin mounts were used to determine the survival of intact hair follicles and the incidence of atrophic follicles. These data were compared with the dose-response characteristics for tumor induction and hair-follicle survival in the rat from previous experiments. The incidence of epithelial skin tumors was markedly lower in mice than in rats. This difference was due to the failure of mice to develop adnexal tumors, which are the predominant type of skin tumor in the rat. The radiation sensitivity of mouse skin for hair-follicle destruction was at least twice that of the rat. The relatively low level of atrophic follicle formation in the mouse skin as a consequence of radiation damage may be related to the failure to develop adnexal skin tumors.—J Natl Cancer Inst 49: 1131–1137, 1972.

Skin Tumours of Cats

SUMMARY An account is given of a series of 125 cutaneous tumours of cats, with reference to their age and sex incidence and site of origin, their clinical and pathological features and their malignancy. Special mention is made of the tumours of particular importance in this series, which were: baso-squamous tumours (in 36 cats), squamous-cell carcinomas (in 22), ceruminous-gland tumours (in 8), fibromas (in 11), and fibrosarcomas and spindle-cell sarcomas (in 21). At least 22 of the baso-squamous tumours were pigmented. Eighteen of the squamous-cell carcinomas affected the head region, no fewer than 10 of them occurring on the ear-flap. Four of the cats with ear-flap tumours were white. The findings are briefly discussed, and a comparison made with the incidence and types of skin tumours in dogs.