Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027627 (metastases)
 103,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Lentigo maligna (LM) and lentigo maligna melanoma (LMM) are distinct entities from other forms of melanoma, occurring predominantly on the skin of the head and neck in elderly people, having a slow growth rate and a low metastatic potential (10%). Twenty-three patients with LM were treated with conventional fractionated irradiation, 18 were locally controlled and two failed locally both of whom, however, were salvaged with further treatment. Three patients are not evaluable because of short follow-up time. Median time to complete regression of the lesion is seven months. Twenty-eight patients with LMM have been irradiated, 23 are locally controlled, two locally recurred (both retrieved with subsequent treatment), and three are inevaluable because of short follow-up time. One patient with a level 5 LMM has developed regional and distant metastases. It is concluded that irradiation is a simple effective method of treatment for this form of melanoma.
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PMID:Conventional fractionated radiotherapy for 51 patients with lentigo maligna and lentigo maligna melanoma. 686 69

I. A brief description is given of the general aspects of skin melanomas, including some personal observations. II. Immunologic facts are mentioned demonstrating: A) The existence of specific circulating antibodies demonstrated by immunofluorescence techniques, by the useful action of blood from patients with duly controlled melanoma injected into other melanoma patients, and by the verification that blood serum from a melanoma patient inhibits cultures thereof. B) As regards cell-mediated immunity, this is normal when a melanoma cure is obtained, and abnormal when no cure takes place. C) There exist melanoma remissions in patients treated with specific or non-specific (BCG) antigens. Spontaneous regression has also been observed in some melanomas. III. A case is presented: a) with spontaneous regression of facial malignant lentigo; b) manifestation of a cervical lymph node metastasis after the primitive tumor had subsided; c) low-degree cell-mediated immunity recuperated spontaneously in an exaggerated manner after radical neck dissection in which none of the lymph nodes proved metastatic; d) manifestation of herpes zoster while the patient presented her best immunologic index; and 2) 11 years' survival since the melanoma made its appearance, and more than 2 years (up to March 1979) since the manifestation of the lymph node metastases.
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PMID:[Melanoma (Hutchinson's lentigo maligna) having spontaneous regression. A case of immunologic importance]. 702 50

This report reviews experience with radiation therapy in 77 patients with melanoma of the head and neck, a lesion traditionally but incorrectly considered to be radiation-resistant. Thirteen patients with lentigo malignum and 18 patients with lentigo malignum melanoma have been primarily irradiated. In 11 of the 13 patients, the lentigo malignum has been locally controlled with no recurrence from 6 months to 5 years following treatment. One patient had a local recurrence and was salvaged with further radiation therapy, and one patient had residual tumor after irradiation and was salvaged with simple excision. Seventeen of 18 patients primarily irradiated had lentigo malignum melanomas that have been locally controlled from 6 months to 6 years after irradiation. One patient had a local recurrence and was salvaged by excisional surgery. There have been no deaths from lentigenous melanoma, and the cosmetic results of treatment are excellent. We concluded that radiation therapy is a simple, effective out-patient treatment for lentigo maligna and lentigo maligna melanoma. Nonlentigenous melanoma was irradiated after incisional biopsy in 6 patients; local control was obtained in 4 patients although 1 died of distant metastases. Fifteen patients were irradiated after excisional biopsy (margins inadequate); 14 of 15 had local control although 6 died of metastases. Only 2 of 16 patients irradiated for recurrent melanoma were controlled. Analysis of local control versus irradiation fraction size revealed that 17/24 (71%) achieved local control with a dose per fraction of greater than 400 rad as compared with 3 of 12 (25%) in those being irradiated with a dose of less than 400 rad per fraction. We concluded that nonlentigenous melanoma is not radiation resistant and that local excision followed by radiation therapy with a large dose per fraction deserves further study, particularly in melanomas of the head and neck where wide local excision is not possible due to age of the patient or location of the tumor. Nine mucosal melanomas have primarily irradiated and four have been locally controlled.
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PMID:Radiation therapy for melanomas of the head and neck. 711 48

The clinical and histologic records of 46 consecutive patients were reviewed who during the period 1980-1993 had recurrence from melanoma in the scar after limited surgery for a skin tumor. They constituted about 50% of all patients admitted with local recurrence from melanoma during this period. At reexamination of the primary tumors, 16 were found to be malignant melanomas and 9 were nevi (four atypical and five benign). Twenty-one were missing, 11 of which had never been set for histologic examination. The median thickness of nine measurable melanomas was 0.66 mm. The recurrences in scar consisted of 34 primary melanomas: 18 superficial spreading, 4 nodular, 3 lentigo malignant, and 9 unclassified. Twelve tumors were dermal melanoma metastases. The median thickness of the 25 measurable melanomas was 0.78 mm. The 5-year overall survival was 69%. At the closing date of the study 15 patients had died, 13 of them because of disseminated melanoma. A comparison of the survival curves from this study with those from other series of melanomas with comparable tumor thickness indicates a considerably worse prognosis than is expected with such thin tumors. We believe that the considerable number of local recurrences in the form of a new primary in a scar following limited surgery supports the theory of limited field change around a primary melanoma. Furthermore, limited procedures for primary melanoma, if followed by a recurrence in the scar, worsen the prognosis.
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PMID:Local melanoma recurrences in the scar after limited surgery for primary tumor. 763 85

In the present study, we investigated the expression of the tumour suppressor protein p53 in 113 primary and 43 metastatic malignant melanomas by immunohistochemistry, and correlated the findings with clinicopathological parameters such as histological melanoma subtype, thickness of primary melanomas (Breslow thickness) and patient outcome. In primary melanomas, the polyclonal anti-p53 antibody CM-1 detected immunoreactivity in 70% of the lesions, predominantly in the cytoplasm. Signals were observed in this cellular compartment in 57% of the melanomas, whereas in 32% nuclear p53 over-expression was detected. Immunohistochemistry, using the monoclonal antibody DO-1, revealed lower staining frequencies. However, both antibodies showed congruent results in approximately 80% of the cases. Overall, immunoreactivity was observed in 73% of superficial spreading melanomas, but only in 52% of lentigo maligna melanomas. This difference (P < 0.001) was mainly due to a lower frequency of cytoplasmic immunoreactivity (P < 0.002). There was no difference with respect to cytoplasmic and nuclear immunoreactivity between thin (< 1 mm thickness) and thicker primary melanomas. Staining frequencies detected in metastatic lesions seemed to be lower than in primary tumours. In 103 primary melanomas, follow-up data for at least 5 years were available. In 71% (54 of 76) of the primary melanomas which did not recur, and in 78% (21 of 27) of tumours with subsequent metastases, p53 over-expression was detected by CM-1. However, this difference was not statistically significant. The results of the present study indicate that immunoreactivity to anti-p53 antibodies is a common observation in malignant melanomas, with staining signals predominantly found in the cytoplasm of cells.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Expression of p53 protein in malignant melanoma: clinicopathological and prognostic implications. 766 36

DNA from formalin-fixed and paraffin-processed samples from 100 melanocytic lesions (39 malignant melanomas, 18 cases of dysplastic naevi, and 43 congenital naevi) was extracted, and the sequences around codons 12/13 and 61 of the N-ras oncogene were amplified using the polymerase chain reaction. The amplified product was then analysed both by dot-blotting and by direct sequencing for point mutations. By the dot-blotting technique, mutations were seen in 18 of 100 lesions. These were in one of five distant metastases (20%), in one of three nodal metastases (33%), in four of 31 (13%) primary melanomas, in none of 18 dysplastic naevi, and in 12 of 43 (28%) congenital naevi, all at codon 61. On direct sequencing, nine of 18 mutations were confirmed, in two of 31 (6%) primary tumours, one distant metastasis, and six of 43 (14%) congenital naevi. Of the 23 superficial spreading melanomas examined, eight were on sun-exposed skin. A superficial spreading melanoma, in which the N-ras mutation at codon 61 was confirmed, was on non-exposed skin, and an unconfirmed mutation was from an exposed site. One of three nodular melanomas with a confirmed mutation was on a light-exposed site, and the other two nodular melanomas were from non-exposed areas. All four lentigo maligna melanomas were from exposed sites, and one of these had an unconfirmed mutation. The only acral lentiginous melanoma, which had no mutation, was from a sun-exposed area.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Point mutations in the N-ras oncogene in malignant melanoma and congenital naevi. 804 23

In order to evaluate the significance of adhesion molecules expressed on melanocytic tumours for progression and prognosis in vivo, we studied integrin expression (VLA-1 to VLA-6, CD18, CD51, CD61) on 10 naevi, 40 primary malignant melanomas, and 11 metastases by immunohistology using the APAAP technique. Evaluation was done by grouping the percentage of positive tumour cells in six categories. Statistical analysis (Wilcoxon rank test, Scheffe test) revealed significant differences in the expression of VLA-1 (P < 0.0001), VLA-2 (P = 0.0001), VLA-5 (P = 0.0093), VLA-6 (P = 0.0232), and CD61 (P = 0.0002) between naevi and primary melanomas. Comparing primary melanomas with metastases, a statistically significant decrease in the expression of VLA-1, VLA-2, and VLA-6 was detectable, as well as a significant increase in VLA-4 and VLA-5. There was no correlation between integrin expression and tumour type (superficial spreading melanoma, nodular melanoma, lentigo maligna melanoma), regression and ulceration. Changes of VLA-1, VLA-4, and VLA-6 expression correlated with the tumour thickness of the primary melanoma, but only VLA-4 and VLA-6 expression on primary melanomas correlated significantly with the development of metastases (P = 0.024 and P = 0.001). These changes of integrin expression during tumour progression particularly, the data showing an increase of VLA-4, and a decrease of VLA-6 expression support the concept that integrins are a new additional set of prognostic markers which indicate predisposition to the development of metastases.
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PMID:Tumour progression and metastatic behaviour in vivo correlates with integrin expression on melanocytic tumours. 810 45

Family physicians should be aware of the early signs of malignant melanoma, as well as measures that can be taken to prevent the disease. Etiologic factors for melanoma include sunburns, particularly those occurring early in life, giant congenital nevi, dysplastic nevi and the presence of numerous nevi. The four major subtypes of melanoma are lentigo maligna, superficial spreading melanoma, acral lentiginous melanoma and nodular melanoma. Diagnosis is based on excisional, incisional or punch biopsy. The crude five-year survival rate for malignant melanoma is 81 percent, but survival depends on stage of disease, anatomic site, the patient's age and sex, histologic factors and clinical subtype. Surgical excision is the usual treatment for primary melanoma. Surgery, radiation therapy and chemotherapy are used in the management of metastatic disease, but the prognosis following the development of metastases remains poor. Family physicians can affect survival rates by improving early detection, promoting patient awareness and self-examination, and encouraging regular physical examination of patients who are at increased risk of melanoma.
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PMID:Malignant melanoma. 827 27

The current classification of malignant melanomas gives recognition to superficial spreading melanoma, lentigo maligna melanoma, acral lentiginous melanoma, and nodular types. In addition, neurotropic and desmoplastic types are recognized. The relativity inherent in the diagnosis of melanoma, provides the basis for the classification of melanomas on the basis of size. Lesions measuring 1 mm or less in vertical dimensions are unlikely to metastasize; they qualify as borderline melanocytic neoplasia of indeterminant malignant potential. The current classification has little relevancy to the category of variant nevi with the exceptions of malignant cellular blue nevus and melanoma arising in giant congenital nevi. A classification of variant melanomas as related to variant nevi is proposed. From a different perspective, a classification of melanomas with attention to nesting and cytological patterns in vertical growth is proposed: this alternate approach gives recognition to lesions that might otherwise be classified as "nevoid" melanomas. It also provides a default category for lesions that might otherwise be assigned to the Spitz nevus-like category. All of these tools for the manipulation of the real and virtual images of melanomas have been emphasized in the concept of minimal deviation melanoma.
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PMID:Variants of melanoma. 922 May 53

The product of the p16/INK4a/CDKN2/MTS1 tumor-suppressor gene acts as a negative cell cycle regulator by inhibiting G1 cyclin-dependent kinases that phosphorylate the retinoblastoma protein. p16 is inactivated in a wide range of human malignancies, including familial melanoma. However, its expression and function in sporadic melanoma has not been extensively investigated. We studied p16 expression in 62 archival melanomas and 30 archival nevi and lentigines by immunohistochemistry. Eighteen of 26 (69%) superficial spreading melanomas, 17 of 28 (61%) nodular melanomas, all of three lentigo maligna melanomas, and all of five melanoma metastases were found to harbor less than 10% p16-positive tumor cells. In contrast, only six of 24 (25%) nevi had less than 10% positive cells. No correlation between tumor thickness and loss of p16 expression was found. Using DNA from micro-dissected tumor and matched normal tissues, five of seven (71%) p16-negative melanoma cases had 9p21 loss of heterozygosity (LOH), and one of these 9p21 LOH cases had promoter region hypermethylation of the remaining p16 allele. These data demonstrate that partial or complete loss of p16 expression is prevalent in sporadic melanoma and is frequently associated with 9p21 LOH.
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PMID:p16INK4a expression is frequently decreased and associated with 9p21 loss of heterozygosity in sporadic melanoma. 969 17


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