Multiple bone metastases from basal cell carcinoma.
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Adult↗
Biomedical subjects
L H Goldberg
Publications and source records attributed to L H Goldberg.
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↗
Ras gene mutation and amplification in human nonmelanoma skin cancers.
Our previous studies have shown that human skin cancers occurring on sun-exposed body sites frequently contain activated Ha-ras oncogenes capable of inducing morphologic and tumorigenic transformation of NIH 3T3 cells. In this study, we analyzed human primary squamous cell carcinomas (SCCs) and basal cell carcinomas (BCCs) occurring on sun-exposed body sites for mutations in codons 12, 13, and 61 of Ha-ras, Ki-ras, and N-ras oncogenes by amplification of genomic tumor DNAs by the polymerase chain reaction, followed by dot-blot hybridization to synthetic oligonucleotide probes designed to detect single base-pair mutations. In addition to the primary human skin cancers, we also analyzed Ha-ras-positive NIH 3T3 transformants for mutations in the Ha-ras oncogene. The results indicated that all three NIH 3T3 transformants, 11 of 24 (46%) SCCs, and 5 of 16 (31%) BCCs contained mutations at the second position of Ha-ras codon 12 (GGC----GTC), predicting a glycine-to-valine amino acid substitution, whereas only 1 of 40 skin cancers (an SCC) displayed a mutation in the first position of Ki-ras codon 12 (GGT----AGT), predicting a glycine-to-serine amino acid change. In addition, three of the SCCs contained highly amplified copies of the N-ras oncogene in their genomic DNA. Interestingly, two of the SCCs containing amplified N-ras sequences also had G----T mutations in codon 12 of the Ha-ras oncogene. These studies demonstrate that mutations in codon 12 of the Ha-ras oncogene occurred at a high frequency in human skin cancers originating on sun-exposed body sites, whereas mutation in codon 12 of Ki-ras or amplification of N-ras occurred at a low frequency. Since the mutations in the Ha-ras and Ki-ras oncogenes were located opposite potential pyrimidine dimer sites (C-C), it is likely that these mutations were induced by ultraviolet radiation present in sunlight.
Adult↗
Mutations in the p53 tumor suppressor gene in human cutaneous squamous cell carcinomas.
In this study, we analyzed 10 human squamous cell carcinomas (SCCs) for alterations in the p53 tumor suppressor gene in exons 4 through 9 by single-strand conformation polymorphism (SSCP) analysis. We found that 2 of 10 SCCs displayed unusual SSCP alleles at exon 7 of the p53 gene. Subsequent cloning and sequencing of PCR-amplified exon 7 DNA from these two tumors revealed that one had a G----A transition at the first position of codon 244, predicting a glycine-to-serine amino acid change, while the other tumor exhibited a G----T base change at the second nucleotide of codon 248, predicting an arginine-to-leucine substitution. Because the mutations in the p53 tumor suppressor gene in both tumors were located opposite potential pyrimidine dimer sites (C-C), it is consistent with these mutations having been induced by the ultraviolet radiation present in sunlight. These studies demonstrate that inactivation of the p53 tumor suppressor gene, as well as activation of ras oncogenes, may be involved in the pathogenesis of some human skin cancers.
Base Sequence↗
Presence of human papilloma virus type 16 DNA sequences in human nonmelanoma skin cancers.
The presence of human papillomaviruses (HPV) has been shown to be associated with the development and progression of invasive cancers of the genital tract, skin, and head and neck. In this study we analyzed 37 human nonmelanoma skin cancers (21 squamous cell carcinomas and 16 basal cell carcinomas) for the presence of HPV sequences. The polymerase chain reaction (PCR) was employed using primers designed to amplify DNA encoding the E6-E7 region of HPV types 6b/11, 16, and 18. HPV type 6b/11 and 18 sequences were absent from the DNA of all 37 tumors examined. However, HPV type 16 sequences were detected in four of 21 squamous cell carcinomas (SCC) (19%) and three of 16 basal cell carcinomas (BCC) (19%) as indicated on agarose gel electrophoresis by the presence of a single specific DNA band of predicted length. Furthermore, HPV type 16 sequences were absent in the DNA of normal skin from these seven skin cancer patients. The presence of HPV type 16 sequences in the seven skin tumors was confirmed by dot blot hybridization of PCR-amplified material to 32P-labeled HPV type 16, but not to HPV type 6/11 or 18-specific probes. These data indicate that HPV type 16, but not 6b/11 or 18, is associated with development of some human nonmelanoma skin cancers.
Adult↗
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↗
Hypersensitivity of skin fibroblasts from basal cell nevus syndrome patients to killing by ultraviolet B but not by ultraviolet C radiation.
Basal cell nevus syndrome (BCNS) is an autosomal dominant genetic disorder in which the afflicted individuals are extremely susceptible to sunlight-induced skin cancers, particularly basal cell carcinomas. However, the cellular and molecular basis for BCNS is unknown. To ascertain whether there is any relationship between genetic predisposition to skin cancer and increased sensitivity of somatic cells from BCNS patients to killing by UV radiation, we exposed skin fibroblasts established from unexposed skin biopsies of several BCNS and age- and sex-matched normal individuals to either UV-B (280-320 nm) or UV-C (254 nm) radiation and determined their survival. The results indicated that skin fibroblasts from BCNS patients were hypersensitive to killing by UV-B but not UV-C radiation as compared to skin fibroblasts from normal individuals. DNA repair studies indicated that the increased sensitivity of BCNS skin fibroblasts to killing by UV-B radiation was not due to a defect in the excision repair of pyrimidine dimers. These results indicate that there is an association between hypersensitivity of somatic cells to killing by UV-B radiation and the genetic predisposition to skin cancer in BCNS patients. In addition, these results suggest that DNA lesions (and repair processes) other than the pyrimidine dimer are also involved in the pathogenesis of sunlight-induced skin cancers in BCNS patients. More important, the UV-B sensitivity assay described here may be used as a diagnostic tool to identify presymptomatic individuals with BCNS.
Basal Cell Nevus Syndrome↗
Treatment of solitary keratoacanthomas with oral isotretinoin.
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Administration, Oral↗
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 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↗
Deletion of the c-Ha-ras-1 allele in human skin cancers.
Previous studies have shown that c-Ha-ras-1 and other genes located on the short arm of chromosome 11 are frequently lost in a number of human tumors. We investigated whether similar losses of the c-Ha-ras-1 allele occurred in human squamous cell carcinomas (SCCs) and basal cell carcinomas (BCCs). DNAs were isolated from 35 pairs of skin tumors (25 BCCs and 10 SCCs) and matching normal skin from the same patients and analyzed for c-Ha-ras gene polymorphism by Southern blot hybridization. Sixteen BCC patients and 1 SCC patient were constitutionally heterozygous for the c-Ha-ras gene in their normal skin DNA. Of these 17 patients, five patients (four with BCC and one with SCC) (29%) showed loss of one of the c-Ha-ras alleles in their tumor DNA. One of the constitutionally heterozygous BCC patients exhibited deletion of the 6.6-kb c-Ha-ras allele and an extra copy of the 7.8-kb allele. In summary, loss of heterozygosity at the c-Ha-ras locus occurred frequently (29%) in the 17 human skin cancers studied. However, our finding that 90% of the patients with SCC, as opposed to 36% of the patients with BCC, had only one of the c-Ha-ras alleles in their normal skin tissue requires further study. Whether c-Ha-ras homozygosity has any bearing on genetic susceptibility to SCC remains to be established.
Alleles↗
Effectiveness of isotretinoin in preventing the appearance of basal cell carcinomas in basal cell nevus syndrome.
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Adult↗
Management of basal cell carcinoma. Which option is best?
Basal cell carcinoma, the most common type of skin cancer, can be treated successfully by a variety of methods. The most commonly employed techniques are curettage with electrodesiccation, scalpel excision, Mohs' chemosurgery, cryosurgery, and radiation therapy, all of which have advantages and disadvantages. The primary care physician needs to be aware of available forms of therapy, problems with recurrent lesions, and the importance of adequate follow-up.
Basal Cell Carcinoma↗
The sensitivity of Langerhans cells to simulated solar radiation in basal cell carcinoma patients.
The role of Langerhans cells (LC) in host resistance against the induction and growth of nonmelanoma skin cancers is still obscure. The purpose of this study was to investigate the sensitivity of LC to simulated solar radiation in patients with basal cell carcinoma (BCC). Thirty-four patients (31-74 years old) with at least one histologically diagnosed BCC on a sun-exposed area and 21 healthy volunteers (29-62 years old) were included in the study. Patients and control subjects were given 10 graded doses of simulated solar UV radiation (10-75 mJ/cm2) on the lower back using a 12S solar simulator with a WG 320 filter. Twenty-four hours later, the minimal erythema dose (MED) was determined and shave biopsies were taken from the site given 1.25 X MED and from adjacent, unirradiated skin. Epidermal sheets were stained for LC using the ATPase method. The mean value of the MED of the BCC patients was 25 +/- 2 mJ/cm2 and that of controls was 29 +/- 3 mJ/cm2 (p greater than 0.05). The number of ATPase+ LC was significantly decreased (p less than 0.05), and their morphology was altered in the irradiated skin of nearly all individuals. However, there was no significant difference in the average reduction of LC in the patients (32% +/- 3%) compared with that of control subjects (32% +/- 4%). The depletion of LC ranged from 0% to 74% in different individuals, all of whom were given 1.25 MED. Furthermore, no correlation was found between the percentage decrease in ATPase+ cells and the dose of UV radiation required to produce erythema. Our results indicate that the ability of UV radiation to cause erythema was unrelated to the magnitude of its effects on LC number or morphology. Second, the morphologic alterations of LC in BCC patients after UV irradiation do not differ from those observed in normal individuals. Third, as a group, patients with BCC do not have a significantly lower MED than cancer-free subjects.
Adult↗
Facial nerve palsy as a result of squamous cell carcinoma of the skin.
Perineural invasion is increasingly recognized as a significant mode of tumor spread in squamous cell carcinoma (SCC) of the skin. Clinically, it is very difficult to diagnose perineural involvement in the majority of patients due to the lack of symptoms. The occasional propensity for perineural invasion from SCCs of the skin of the head and neck region is well documented and, although SCCs arising from actinically damaged skin reportedly have a low incidence of metastasis or deep invasion, failure to recognize this potential mode of spread could result in fatal consequences.
Carcinoma, Squamous Cell↗