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2.
Biomed Res Int ; 2015: 432479, 2015.
Article in English | MEDLINE | ID: mdl-26161400

ABSTRACT

Mucosal melanoma is a rare disease, which differs from its cutaneous counterpart genetically and for its clinical behaviour. Moreover this is a heterogeneous disease based on the tissue of origin. As CT7 and CT10 are highly expressed in cutaneous melanoma and are immunogenic in this disease, we analysed their expression throughout the different subtypes of mucosal melanoma and tumor development. We detected a frequent expression of CT7 in primaries and corresponding metastases (55%) as well as for CT10 (30%). This expression resulted to be heterogeneous in the same tumor specimen and moreover influenced by the tissue of origin. Our results support the role of these antigens in immunotherapy for mucosal melanoma.


Subject(s)
Antigens, Neoplasm/metabolism , Genetic Heterogeneity , Melanoma/pathology , Mucous Membrane/metabolism , Mucous Membrane/pathology , Neoplasm Proteins/metabolism , Skin Neoplasms/pathology , Humans , Melanoma/metabolism , Neoplasm Recurrence, Local/metabolism , Neoplasm Recurrence, Local/pathology , Skin Neoplasms/metabolism
3.
Praxis (Bern 1994) ; 102(4): 219-24, 2013 Feb 13.
Article in German | MEDLINE | ID: mdl-23399605

ABSTRACT

Malignant melanoma is the most common cause of death from skin cancer. Wide surgical excision of localized melanoma in its primary stages remains the main curative therapy. Identifying patients at an early tumour stage is therefore one of the most significant steps for treatment. In the last decades, molecular pathology rapidly established itself in melanoma research. We present new molecular methods, their significance and their application, especially focusing on BRAF( V600) mutation and BRAF-inhibiting tumor targeting therapy. Resistance to tumor targeting therapies and cell line experiments, which have evidenced a sub population with stem cell properties, illustrate melanoma heterogeneity. Efforts to develop drugs that target more than a single target gene are currently underway.


Subject(s)
Melanoma/pathology , Skin Neoplasms/pathology , Biopsy , Cell Line, Tumor/pathology , Diagnosis, Differential , Gene Expression Profiling , Humans , Melanoma/genetics , Neoplasm Staging , Neoplasms, Radiation-Induced/genetics , Neoplasms, Radiation-Induced/pathology , Nevus, Pigmented/genetics , Nevus, Pigmented/pathology , Prognosis , Sentinel Lymph Node Biopsy , Skin Neoplasms/genetics , Sunlight/adverse effects , Ultraviolet Rays/adverse effects
4.
Br J Cancer ; 98(12): 1922-8, 2008 Jun 17.
Article in English | MEDLINE | ID: mdl-18506141

ABSTRACT

Twenty per cent of sentinel lymph node (SLN)-positive melanoma patients have positive non-SLN lymph nodes in completion lymph node dissection (CLND). We investigated SLN tumour load, non-sentinel positivity and disease-free survival (DFS) to assess whether certain patients could be spared CLND. Sentinel lymph node biopsy was performed on 392 patients between 1999 and 2005. Median observation period was 38.8 months. Sentinel lymph node tumour load did not predict non-SLN positivity: 30.8% of patients with SLN macrometastases (> or =2 mm) and 16.4% with micrometastases (< or =2 mm) had non-SLN positivity (P=0.09). Tumour recurrences after positive SLNs were more than twice as frequent for SLN macrometastases (51.3%) than for micrometastases (24.6%) (P=0.005). For patients with SLN micrometastases, the DFS analysis was worse (P=0.003) when comparing those with positive non-SLNs (60% recurrences) to those without (17.6% recurrences). This difference did not translate into significant differences in DFS: patients with SLN micrometastasis, either with (P=0.022) or without additional positive non-SLNs (P<0.0001), fared worse than patients with tumour-free SLNs. The 2-mm cutoff for SLN tumour load accurately predicts differences in DFS. Non-SLN positivity in CLND, however, cannot be predicted. Therefore, contrary to other studies, no recommendations concerning discontinuation of CLND based on SLN tumour load can be deduced.


Subject(s)
Lymphatic Metastasis , Melanoma/pathology , Sentinel Lymph Node Biopsy , Skin Neoplasms/pathology , Adolescent , Adult , Aged , Aged, 80 and over , Female , Humans , Male , Melanoma/surgery , Middle Aged , Retrospective Studies , Skin Neoplasms/surgery
5.
Virchows Arch ; 439(6): 823-6, 2001 Dec.
Article in English | MEDLINE | ID: mdl-11787857

ABSTRACT

Distinction of spitzoid malignant melanomas (SMM) from Spitz nevi may be difficult or even impossible on the basis of conventional histology. In this report, a patient suffering from a primary lesion diagnosed as a Spitz nevus and a metastatic malignant melanoma approximately 4 years thereafter is described. A diagnosis of SMM was made subsequently upon review of the primary lesion. In the present analysis, we used comparative genomic hybridization (CGH) to define markers characteristic of SMM. The primary lesion revealed deletions on chromosomes 6q and 9p. In the metastasis, additional deletions on chromosomes 10p and 10q and gains of chromosome 7 were found. To our knowledge, no chromosomal aberration on chromosome 6 was hitherto demonstrated in benign melanocytic nevi. Findings reported in the literature suggest that human melanoma metastasis suppressor gene maps to 6q. In contrast, losses on chromosome 9p seem to be an early event in the development of melanoma. However, they are not only found in melanomas but are occasionally present in Spitz nevi as well as in atypical nevi. The CGH result with deletion of 6q in this difficult to diagnose primary melanocytic lesion strongly supports the diagnosis of malignant melanoma. To demonstrate the reliability of loss on chromosome 6q as a marker of SMM, a larger number of lesions must be investigated.


Subject(s)
Chromosomes, Human, Pair 6 , Loss of Heterozygosity , Melanoma/secondary , Nevus, Epithelioid and Spindle Cell/pathology , Skin Neoplasms/pathology , Adolescent , Biomarkers, Tumor , DNA, Neoplasm/analysis , Female , Gene Dosage , Humans , Lymph Nodes/pathology , Lymphatic Metastasis , Melanoma/genetics , Melanoma/surgery , Nevus, Epithelioid and Spindle Cell/genetics , Nevus, Epithelioid and Spindle Cell/surgery , Nucleic Acid Hybridization , Skin Neoplasms/genetics , Skin Neoplasms/surgery
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