Immunohistochemical staining of a large series of human cutaneous melanocytic lesions using the method selected showed differential EGFR expression in various stages of melanocytic tumor progression: 19% of common nevocellular nevi; 61% of dysplastic nevi, 89% of primary cutaneous melanomas, and 91% of melanoma metastases showed staining of the melanocytic cells.
In contrast, MGSA mRNA was constitutively expressed in the absence of exogenous growth factors in cultures established from benign intradermal and dysplastic nevi and melanoma lesions in different stages of tumor progression.
MoAb PAL-M1 reacted with all 15 melanoma metastases (MM), with 14 of 19 primary cutaneous melanomas (PCM), 9 of 35 dysplastic nevi (DN), and 2 of 26 NN.
MoAb PAL-M1 reacted with all 15 melanoma metastases (MM), with 14 of 19 primary cutaneous melanomas (PCM), 9 of 35 dysplastic nevi (DN), and 2 of 26 NN.
MoAb PAL-M1 reacted with all 15 melanoma metastases (MM), with 14 of 19 primary cutaneous melanomas (PCM), 9 of 35 dysplastic nevi (DN), and 2 of 26 NN.
We found that cathepsin D was expressed in all of the dysplastic nevi and primary and metastatic melanomas tested but in only 18% of nevocellular nevi (five of 27), whereas normal melanocytes showed no cathepsin D expression.
An increase in immunoreactive TGF alpha in nevocytes was noted in both benign and dysplastic nevi from dysplastic nevus patients, as compared to benign nevi from normal patients.
We studied the effect of biologically relevant doses (comparable to 2-3 MED (minimal erythemal dose) for in vivo irradiated full-thickness skin) of monochromatic UVB light of 302 nm on cultured melanocytes derived from foreskin, common melanocytic nevi, and dysplastic nevi.
We studied the effect of biologically relevant doses (comparable to 2-3 MED (minimal erythemal dose) for in vivo irradiated full-thickness skin) of monochromatic UVB light of 302 nm on cultured melanocytes derived from foreskin, common melanocytic nevi, and dysplastic nevi.
We studied the effect of biologically relevant doses (comparable to 2-3 MED (minimal erythemal dose) for in vivo irradiated full-thickness skin) of monochromatic UVB light of 302 nm on cultured melanocytes derived from foreskin, common melanocytic nevi, and dysplastic nevi.
We studied the effect of biologically relevant doses (comparable to 2-3 MED (minimal erythemal dose) for in vivo irradiated full-thickness skin) of monochromatic UVB light of 302 nm on cultured melanocytes derived from foreskin, common melanocytic nevi, and dysplastic nevi.
We studied the effect of biologically relevant doses (comparable to 2-3 MED (minimal erythemal dose) for in vivo irradiated full-thickness skin) of monochromatic UVB light of 302 nm on cultured melanocytes derived from foreskin, common melanocytic nevi, and dysplastic nevi.
We have analyzed expression of nm23 polypeptide in acquired melanocytic nevi (n = 19), dysplastic nevi (n = 19), malignant melanomas (n = 22) and metastases of malignant melanomas (n = 47) in situ.
Although the first English-language report of melanoma in 1820 contained a description of a melanoma-prone family, seminal studies by investigators at the National Cancer Institute and the University of Pennsylvania identified dysplastic nevi (DN) as an important melanoma precursor, suggested an autosomal dominant mode of inheritance for both melanoma and DN, and proposed that a melanoma-susceptibility gene (CMM1) was located on chromosome 1p36.
An absence of linkage between chromosome 9p markers and the 358delGCDKN2A mutation and DN was detected, indicating genetic heterogeneity for DN and CMM in this family.
Therefore, these data suggest that deletion of p16 may play an important role in the development of dysplastic nevus as an early event and that the changes may represent an early event in the development of malignant melanoma.
Therefore, these data suggest that deletion of p16 may play an important role in the development of dysplastic nevus as an early event and that the changes may represent an early event in the development of malignant melanoma.
To determine whether IFN-alpha, used for adjuvant therapy of high-risk, resected melanoma, induces changes in Stat3 in atypical nevi, patients with a clinical history of melanoma who have multiple atypical nevi were treated for 3 months with low-dose IFN-alpha.