Differential expression of CD66a (BGP), a cell adhesion molecule of the carcinoembryonic antigen family, in benign, premalignant, and malignant lesions of the human mammary gland.

CD66a, also known as biliary glycoprotein (BGP), is a member of the carcinoembryonic antigen (CEA) family and the human homologue of the rat cell-CAM. There is evidence that aberrant expression or loss of CD66a in tumor tissue is of biological significance. No data about its expression in breast carcinoma cells and only sparse information about the expression of CD66a in normal breast are available thus far. In this study we used monoclonal antibodies to analyze the expression of CD66a and CEA in normal tissue, benign lesions, and in noninvasive and invasive carcinomas of the mammary gland. In normal tissue and benign lesions, CD66a was consistently expressed at the apical sites of epithelial cells and in myoepithelia, whereas CEA was absent or was restricted only to some apical membranes within the ductal tree. The specific staining of myoepithelia was most evident in pseudoinfiltrative radial scars and sclerosing adenosis. However, the apical expression of CD66a disappeared with the development of the malignant phenotype in noninvasive and invasive carcinomas, and changed gradually from low- to high-grade noninvasive carcinomas into a predominant uniform membrane staining all around the atypical cells. CEA expression was irregular in intensity and distribution. The native apical CD66a staining was partially preserved in some highly differentiated invasive carcinomas with a better prognosis, such as tubular and papillary carcinomas. These findings indicate that loss of CD66a expression rather than a change in staining patterns coincides with the development of the malignant phenotype.

[Unilateral systematic linear porokeratosis. Immuno- and lectin histochemistry]. / Unilaterale systematische lineäre Porokeratose. Immun- und Lektinhistochemie.

An uncommon case of unilateral systemic linear porokeratosis in a women aged 22 years is reported in this paper. The results obtained from frozen-section investigations into lectin binding were indicative of reduced epidermal fucosylation and sialinization beneath the cornoid lamella. The basal stratum failed to react with a polyclonal antibody against calmodulin. Epidermal reaction, with AS-6 staining against urokinase, was of higher intensity. The above findings, as a whole, are likely to suggest accelerated keratinocyte migration to the stratum corneum in cases of linear porokeratosis and and should actually support assignment of the latter to the group of dermatoses with transepidermal elimination.

The initial steps of tumor progression in melanocytic lineage: a histochemical approach.

Antigen expression was studied by immunohistochemistry in 133 human melanocytic skin lesions to gain insight into the initial steps of tumor development, i.e. in particular the change from melanocytes to benign nevi. We refer to the proposed progression model of Clark and co-workers. The following types of antigens were investigated: (i) intermediate filament antigens (vimentin), (ii) melanoma-associated antigens (HMB-45, NKI/C3, MA-930, LS59), (iii) proliferation-associated antigens (S-100, Ki67, Ro/SSA, calmodulin), (iv) progression-associated antigens (HLA-DR, ICAM-1), and (v) basal membrane antigens (bullous pemphigoid antigen, laminin, fibronectin, collagen type IV). The intensity of expression and the topography of immunoreactive pigment cells were compared with the stage of tumor progression. Special attention was paid to the early steps of this process, i.e. the disturbance of the epidermal melanin unit and the development of melanocytic ("nevocellular")nevi. A dramatic shift of antigen expression (antigen types [i] to [v]) was noted in benign nevi compared with melanocytes. Nevi with cellular atypia disclosed a tendency towards an increased percentage of tumor cells reactive for melanoma- and progression-related antigens (types [ii] and [iv]). However, there was no clear cut level of distinction of antigen expression (types [i] to [v]) between benign and primary malignant melanocytic tumors. So-called dysplastic nevi resembled benign tumors or melanocytes rather than malignant melanoma. Metastatic melanoma of skin showed a relatively high number of Ki67-positive, cycling melanoma cells. The results have a bearing on the concepts of melanocytic nevus ontogenesis and "maturation". It appears that melanocytes lose maturity on their way down to the dermis in contrast to traditional concepts (Abtropfung); this might be of importance for our understanding of melanoma development in association with melanocytic nevi. Our findings are discussed with regard to Clark's model of tumor progression.

Human eccrine sweat glands--a histochemical approach.

Histogenesis of eccrine sweat glands is incompletely understood. Histochemistry of the human eccrine sweat gland of adult skin by the use of lectins as well as antibodies to neuroglandular antigen (NGA) and urokinase was in favour of a relative independent differentiation from interfollicular epidermis. Expression of NGA by sweat glands is a feature unique among skin appendages. The possible impact of our findings for sweat gland histogenesis is briefly discussed.

[Pachyonychia congenita. Presentation of a case and histological-histochemical findings]. / Pachyonychia congenita. Falldarstellung und histologisch-histochemische Befunde.

We report on two cases of pachyonychia congenita, Jadassohn-Lewandowsky type, in a father and daughter. Histopathological examination revealed thickened, aggregated bundles of tonofilaments and an increased number of atypical keratohyalin granula, which is suggestive of an altered keratinization. Immunohistological staining with antibodies to cytokeratins (A45-B/B3, A51-B/H4, A53-B/A2, RPN 1161) was unchanged. Filaggrin could not be detected. Basal cells immunoreactive for calmodulin were markedly reduced or even absent in the rete ridges. Staining with a monoclonal antibody against Ki67 made epidermal cell hyperproliferation seem unlikely. The epidermal lectin binding was normal. C3 was detectable in vessel walls mainly of the stratum reticulare. The findings are discussed with reference to pachyonychia pathogenesis.

[A combination of psoriasis vulgaris and nevus cell nevus--clinical, histopathologic and histochemical findings]. / Kombination von Psoriasis vulgaris und Nävuszellnävus--Klinische, histopathologische und histochemische Befunde.

In a study on 76 patients suffering from psoriasis, we found melanocytic nevi (MCN) within psoriatic lesions in 7%, and in perilesional areas of about 2 cm in 13% of the patients. Under magnification (operating microscope), we failed to detect any signs of psoriasis in both the epidermis covering the MCN and the adjacent epidermis. Histopathologically, 6 out of 7 MCN examined did not show any psoriatic alterations of the epidermis, and in all the 7 cases, the adjacent epidermis was free of psoriasis. Using unfixed frozen sections in histochemistry, we studied the lectin binding of FITC-labeled ConA and UEA I in 5 MCN. The epidermal reaction was comparable to that of psoriatic lesions. In contrast to psoriatic lesions, there was no staining of the spinous layer with a polyclonal antiserum against calmodulin, but only the staining of basal cells as in non-lesional psoriasis. We discuss possible 'protective' factors against psoriasis.

[Histochemical studies of transepidermal elimination of nevus cells in nevus cell nevi of the corium]. / Histochemische Untersuchungen zur transepidermalen Elimination von Nävuszellen bei korialen Nävuszellnävi.

Dermal nevocytic nevi (NN) were histochemically studied with the help of FITC-conjugated lectins as well as antisera against keratin and plasminogen activators of the urokinase type. 3 out of 18 NN showed interpenetrating nevus cells in atrophic parts of the epidermis. These cells revealed strong lectin reactivity both with Con A (cytoplasmatic binding) and WGA/RCA II (membraneous binding). In addition we found membraneous reaction with anti-urokinase, whereas there was no anti-keratin staining. Our findings suggest active transepidermal elimination of nevus cells in dermal nevocytic nevi.

[Lectin histochemical studies of nevus cell nevi of the corium]. / Lektinhistochemische Untersuchungen korialer Nävuszellnävi.

Using 11 different kinds of lectins, we histochemically studied 18 dermal nevocytic nevi (NCN). The investigation included both unfixed frozen sections and pretreated sections fixed with acetone (pretreatment: chloroform/methanol, Triton X-100, neuraminidase). In this way, we hoped to get some information both on the expression of surface glycoconjugates and the chemical nature of the sites of lectin binding. Our results argue for an abundance of glucosyl, mannosyl, galactosyl, and N-acetyl galactosamine residues on the surface of nevus cells. In comparison to keratinocytes, we found a greater sensitivity to chloroform/methanol, which suggests a relative increase of glycolipids. Dermal NCN showed heterogenic lectin binding: The highest intensity was seen in the marginal nevus cells, the lowest in the central cells of epidermal nests. Dermal cells showed a moderate binding intensity. Epidermal cells lying above the NCN disclosed some modifications of their lectin binding pattern. In contrast to normal epidermis, basal keratinocytes failed to bind LCA; suprabasal cells showed cytoplasmic staining. In some NCN, we observed an intensive perinuclear staining of the upper keratinocytes with granular ConA. Our results suggest (1) a modified lectin binding pattern of nevus cells depending on their microenvironment, as well as (2) a distinctly altered lectin binding of keratinocytes in the adjacent epidermis.

[Lectin histochemical study of epidermal nevi]. / Lektinhistochemische Untersuchung epidermaler Naevi.

3 epidermal nevi were investigated by means of FITC-labeled lectins (LCA, RCA II, ConA, WGA). In comparison with normal skin, we observed selective modifications of the lectin-binding patterns. These findings suggest an increased presence of GlcNAc residues.

[Effect of dithranol therapy on membrane, basement membrane and nuclear markers in psoriasis lesions]. / Einfluss der Dithranoltherapie auf Membran-, Basal-membran- und Kernmarker in der Psoriasisläsion.

We investigated the effects of anti-psoriatic therapy with dithranol (1/20-1%) in salicylic acid (0.5%) in white petrolatum on lesional skin. FITC-labeled lectins and pemphigus vulgaris antibodies (PV) served as analytical means to study the glycocalyx. Antibodies of bullous pemphigoid (BP) were used as basal membrane markers. Nuclear antigens were recorded according to the binding of speckled, anti-nuclear antibodies (ANA) as well as antibodies to dsDNA. With some lectins, dithranol therapy resulted in pronounced fluorescence of the lower parts of the basal cells. ConA was fixed by the basal cell layer. To a lesser degree, ANA were fixed by nuclei of keratinocytes. PV antibodies were not fixed at all.

[Effect of neutral solvents on lectin binding of healthy and psoriatic epidermis]. / Einfluss neutraler Lösungsmittel auf die Lektinbindung gesunder und psoriatischer Epidermis.

We studied the influence of neutral solvents on epidermal lectin binding in normal and lesional psoriatic skin. 1% solution of Tween 80 or Triton X-100 had no effect on the binding of the following lectins: PHA, ConA, and LCA. The HPA staining of the str. spinosum in normal skin, however, was completely removed by neutral solvents. In psoriatic skin, str. spinosum staining with HPA was resistant. Our results are discussed in the light of an altered keratinocyte maturation in psoriasis.

[Lectin binding of psoriatic skin]. / Untersuchungen zur Lektinbindung psoriatischer Haut.

The aim of our study was the characterization of epidermal lectin binding pattern in psoriatic vs. non-psoriatic skin in order to reveal possible alterations of the glycocalyx composition of psoriatic keratinocytes. We used fluoroisothiocyanate-labeled lectins of Canavalia ensiformis (ConA), Phaseolus vulgaris (PHA), Lens culinaris (LCA), and Helix pomatia (HPA). The binding pattern of psoriatic (involved and non-lesional) skin did not differ from the control samples in ConA, PHA, and LCA. In psoriasis, there was a prominent HPA binding to the dermo-epidermal junction and to a lesser degree, intercellular epidermal near the uppermost cell layers. In seborrheic keratosis, in contrast, there was no fluorescence of the dermo-epidermal junction or the first layers of the epidermis. The most pronounced binding was observed perinuclear in the upper epidermis. The results are discussed in the light of an altered keratinocyte maturation in psoriasis.