Multiple bone metastases from basal cell carcinoma.
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Adult↗
Biomedical subjects
J Alcalay
Publications and source records attributed to J Alcalay.
Basal cell carcinoma occurring at the site of a strawberry hemangioma.
A twenty-seven-year-old white woman presented with a basal cell carcinoma at the former site of a strawberry hemangioma. The strawberry hemangioma had been treated in infancy with dry ice. The lesion spontaneously regressed and left no visible scar. To our knowledge, this is the first reported association of basal cell carcinoma and strawberry hemangioma.
Basal Cell Carcinoma↗
Antigen-presenting activity of draining lymph node cells from mice painted with a contact allergen during ultraviolet carcinogenesis.
The induction of skin cancers in mice by chronic UV irradiation is accompanied by a decrease in the numbers of Ia+ and Thy-1+ dendritic cells in the epidermis early in the course of UV irradiation. Subsequently, the number of Ia+ cells, but not Thy-1+ cells, increases until the time of tumor development. To assess the functional significance of these changes in cutaneous immune cells, and to help define the role these cells may play in immune surveillance against skin cancers, we tested the afferent immunologic capability of the skin during the development of UV-B radiation-induced skin cancers. Afferent immune function was measured by testing the Ag-presenting capacity of draining lymph node (DLN) cells from mice sensitized epicutaneously with dinitrofluorobenzene. A reduced contact hypersensitivity response was induced in mice immunized with DLN cells from UV-irradiated mice that had been sensitized with hapten on UV-irradiated skin. This decreased reactivity was present during the entire latent period of tumor development. However, in tumor-bearing mice, the DLN cells from UV-irradiated, sensitized animals exhibited normal Ag-presenting activity. DLN cells from UV-irradiated mice sensitized on ventral, unirradiated skin exhibited normal Ag-presenting activity. The lowest amount of Ag-presenting activity in the draining lymph nodes of UV-irradiated mice correlated temporally with the lowest number of Ia+, adenosine triphosphatase+ dendritic epidermal cells in the UV-irradiated skin. At least during the early part of the tumor latent period, an increase in the number of these cells was paralleled by an increase in the Ag-presenting activity of the DLN cells. In contrast, the number of Thy-1+ dendritic epidermal cells in UV-irradiated skin did not correlate with the Ag-presenting activity. Thus, the decrease in the number of identifiable epidermal Langerhans cells early in the course of chronic UV irradiation correlated with a decrease in Ag-presenting activity after sensitization through the UV-irradiated skin. These studies demonstrate that the afferent arm of the cutaneous immune response is impaired in the site of tumor development throughout the latent period of UV carcinogenesis.
Animals↗
[Sunlight, ultraviolet radiation and the skin: summary of the National Institute of Health Consensus Development Conference].
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Humans↗
Intraoperative nasal ala stabilization using the Foley catheter.
The authors describe a technique of intraoperative nasal ala stabilization to aid excision of skin lesions on the nasal ala and the surrounding skin. The fixation is achieved by inserting a Foley catheter into the nasal antrum and inflating the balloon. The inflated balloon produces pressure against the surrounding walls, allows convenient excision of skin lesions with good hemostasis, and is comfortable for the patient.
Catheterization↗
Ultraviolet radiation-induced damage to human Langerhans cells in vivo is not reversed by ultraviolet A or visible light.
Exposure of human skin in vivo to UVB radiation induces pyrimidine dimers in DNA and alters the morphology and function of epidermal Langerhans cells. Cells in human skin have been reported to contain a photoreactivation repair mechanism that, following exposure to UVA or visible light, repairs UVB-induced pyrimidine dimers. The purpose of this study was to determine whether exposure to photoreactivating light would also reverse the UVB-induced morphologic alterations in human Langerhans cells. The skin of eight healthy volunteers was exposed to a low dose of UVB radiation (between 0.75 and 1.5 times the minimal erythema dose), and immediately thereafter exposed to photoreactivating light from either BLB fluorescent lamps (UVA radiation) or incandescent bulbs (visible light). After exposure to UVB radiation, the number of ATPase+ epidermal Langerhans cells was reduced in all subjects to between 21% and 65% of that in unirradiated skin, and the majority of the remaining cells exhibited morphologic alterations. Exposure of the UVB-irradiated skin to photoreactivating light did not reverse or reduce these effects. We conclude that UVB-induced morphologic alterations of human Langerhans cells are not subject to photoreactivation. These results imply either that pyrimidine dimers are not involved in these effects of UVB irradiation, or that photoreactivation does not occur in human Langerhans cells in situ.
Adult↗
Excision repair of pyrimidine dimers induced by simulated solar radiation in the skin of patients with basal cell carcinoma.
One prominent lesion induced in DNA by ultraviolet (UV) radiation is the cyclobutyl pyrimidine dimer formed between adjacent pyrimidines on the same DNA strand. We investigated whether people who have developed basal cell carcinoma on sun-exposed skin have an altered ability to repair UV-induced pyrimidine dimers in DNA. Twenty-two patients with at least one basal cell carcinoma, aged 31-84 years, and 19 healthy volunteers, aged 25-61 years, took part in the study. Both groups were given one minimal erythema dose (MED) of simulated solar radiation on the lower back. DNA was extracted from the irradiated skin 0 to 6 h later, and the number of UV-induced pyrimidine dimers was determined using a dimer-specific endonuclease. At time 0, the average number of dimers per unit of DNA was similar in the two groups. After 6 h, an average of 22 +/- 4% of the dimers were removed in the group with basal cell carcinoma compared to 33 +/- 4% in the cancer-free group. In the basal cell carcinoma group, only 23% of the patients repaired more than 30% of the dimers after 6 h, compared with 53% of the cancer-free subjects (p less than 0.05). We conclude that patients who develop basal cell carcinoma on sun-exposed skin may have a decreased ability to repair pyrimidine dimers induced in skin exposed to simulated solar radiation.
Adult↗
The effect of photochemotherapy with 4,4',6 trimethylangelicin on murine cutaneous immune cells.
The effect of photochemotherapy with 4,4',6 trimethylangelicin (TMA), a new monofunctional furocoumarin with a high antiproliferative activity, was studied on murine dendritic epidermal cells. Female mice (C3H/HeN[MTV-]) were treated topically with the drug three times a week for 4 consecutive weeks followed each time by 1 J/cm2 of UVA radiation. At the end of the treatment almost total depletion of ATPase+, Ia+ and Thy-1+ dendritic epidermal cells was observed, associated with marked hyperpigmentation but no gross or microscopic phototoxicity. Although 4,4',6 TMA is not phototoxic in mice, it affects the cutaneous immune cells.
Animals↗
The needle-scratch technique.
An easy, convenient method of marking the borders of a cutaneous tumor before excision is presented. It enables the physician to see the preoperative clinical borders of a tumor without worry of erasing the inked borders with cleansing solution.
Basal Cell Carcinoma↗
Effects of a new bifunctional psoralen, 4,4',5'-trimethylazapsoralen and ultraviolet-A radiation on murine dendritic epidermal cells.
Although some psoralens are therapeutically active in the treatment of cutaneous hyperproliferative diseases when combined with UVA (320-400 nm) radiation, the toxic effects of these compounds have led physicians to seek new photochemotherapeutic agents. One such agent is 4,4',5'-trimethylazapsoralen (TMAP), a new bifunctional psoralen compound. We investigated the effects of repetitive treatments with TMAP plus UVA radiation on the number of dendritic immune cells in murine epidermis and on the induction of phototoxicity. Mice treated 3 times per week for 4 weeks with 129 microgram TMAP plus 10 kJ/m2 UVA radiation exhibited no gross or microscopic evidence of phototoxicity. During this treatment, the numbers of ATPase+, Ia+, and Thy-l+ dendritic epidermal cells were greatly reduced, and by the end of the treatment period, few dendritic immune cells could be detected. We conclude that morphological alterations of cutaneous immune cells can occur in the absence of overt phototoxicity, and that TMAP plus low-dose UVA radiation decreases the numbers of detectable Langerhans cells and Thy-1+ cells in murine skin.
Animals↗
Photocarcinogenesis in mice by 4,4',6 trimethylangelicin plus UVA radiation.
The carcinogenic effect of a new monofunctional psoralen 4,4',6-trimethylangelicin (TMA) plus UVA radiation was examined in C3H/HeN mice and compared with that of the parent compound angelicin. TMA carcinogenic effects were also compared with the previously reported effects of 8-methoxypsoralen. Using 2 different doses of TMA (25 micrograms and 250 micrograms) combined with 1 J/cm2 of UVA radiation, we found that 42% and 52% of the mice (respectively) developed tumors on the treated site. A dose of angelicin (215 micrograms) equimolar to the highest dose of TMA combined with 1 J/cm2 of UVA radiation produced tumors in 28% of the mice (P greater than 0.05). All tumors were squamous cell carcinomas. No metastases were found in any of the mice. We conclude that, although TMA + UVA radiation is carcinogenic in mice, it seems to be an equally active, but less phototoxic and less carcinogenic psoralen than 8-methoxypsoralen. The parent compound angelicin is not significantly less carcinogenic, and its clinical efficacy is poor.
Animals↗
Skin diseases unique to the pregnant woman.
Skin disorders are often associated with pregnancy. Most of these disorders are physiologic but some are pathologic. The following review focuses on skin diseases that are unique to pregnancy.
Female↗
Cutaneous pigmented melanocytic tumor in a mouse treated with psoralen plus ultraviolet A radiation.
A pigmented melanocytic tumor was induced on the treated site of a C3H/HeN female mouse given repeated topical applications of 8-methoxy-psoralen and subsequent exposures to ultraviolet A radiation (PUVA) over a 7-month period. The tumor invaded the subcutaneous tissue and muscle but produced no distant metastases. To our knowledge, this is the first report suggesting a direct relationship between PUVA treatment and the induction of cutaneous melanocytic tumor in mice.
Animals↗
[Darker side of tanning from artificial radiation source].
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Animals↗
Identification of the molecular target for the suppression of contact hypersensitivity by ultraviolet radiation.
This study was conducted to explore the involvement of DNA damage in the suppression of contact hypersensitivity (CHS) by UV irradiation. The opossum, Monodelphis domestica, was used because cells of these marsupials have an enzyme that is activated by visible light (photoreactivating enzyme) and repairs ultraviolet radiation (UVR)-induced pyrimidine dimers in DNA. A single dose of 1,500 J/m2 of UVB (280-320 nm) radiation, representing 2 minimal erythema doses, was administered to the dorsal skin of opossums. This treatment prevented the opossums from developing a CHS response to dinitrofluorobenze (DNFB) applied either at the site of irradiation or an unirradiated site. In addition, this dose of UVR decreased the number of ATPase+ epidermal Langerhans cells in the dorsal epidermis to approximately 3% of that in unirradiated skin at the time of DNFB application. Treatment of the animals with wavelengths that activate the repair enzyme (320-500 nm, photoreactivating light, PRL) for 120 min immediately after UV irradiation inhibited the UVR-induced suppression of CHS almost completely. Exposure to PRL before UVR did not prevent UVR-induced suppression of CHS. PRL treatment after UV irradiation also prevented the decrease in the number of ATPase+ Langerhans cells. Measurements of lesions in DNA indicated that PRL treatment removed around 85% of the UVR-induced pyrimidine dimers. These data provide direct evidence that DNA, and most likely, the pyrimidine dimer, is the primary molecular target for the UVB-induced suppression of contact hypersensitivity to haptens applied to irradiated or unexposed skin.
Adenosine Triphosphatases↗
Alterations in Langerhans cells and Thy-1+ dendritic epidermal cells in murine epidermis during the evolution of ultraviolet radiation-induced skin cancers.
To understand the role of cutaneous immune cells in host resistance to the induction and growth of skin cancer, we investigated the number and morphology of murine dendritic epidermal cells (dEC) during the evolution of ultraviolet (UVA) UV-induced skin cancers. Female C3H/HeN mice were treated topically with 8-methoxypsoralen followed by ultraviolet A (UVA) radiation 3 times/week or irradiated with UVB radiation 3 times/week. In both psoralen plus UVA- and UVB-treated mice, ATPase+ and Ia+ Langerhans cells almost completely disappeared from the treated skin during the early latency period of tumor development (4 weeks) but reappeared in the epidermis late in the latency period (between 15 and 22 weeks). The ATPase+ cells that reappeared in the epidermis had a rounder, less dendritic morphology than normal Langerhans cells. Thy-1+ dEC were totally depleted from the epidermis in both treatment groups at the end of first week of treatment and were nearly absent from the skin during the entire latency period. After tumors appeared (29 weeks), Thy-1+ dEC were still absent or detected only in small numbers in skin surrounding the tumors. ATPase+ and Ia+ cells present in skin around the tumors constituted 60 to 80% of the number in nonirradiated skin. Mice that received UVA radiation alone developed no tumors. ATPase+ and Ia+ Langerhans cells and Thy-1+ dEC were detected in UVA-treated epidermis after 22 weeks and 43 weeks, although the numbers were lower than those in unirradiated mice. Most psoralen plus UVA-induced tumors (81%) were squamous cell carcinomas, whereas only 24% of UVB-induced tumors were of this histological type. Our results demonstrate that UV-induced skin cancers developed in the presence of ATPase+ and Ia+ cells in the epidermis and in the absence of Thy-1+ dEC.
Adenosine Triphosphatases↗