Residual dysplastic and other nevi in superficial spreading melanoma. Clinical correlations and association with sun damage

1989 ◽  
Vol 83 (5) ◽  
pp. 935
Author(s):  
Black W. C. ◽  
Hal G. Bingham
Keyword(s):  
Superficial Spreading ◽  
Superficial Spreading Melanoma ◽  
Clinical Correlations

scholarly journals Evolution of superficial spreading melanoma to resemble desmoplastic melanoma: case report

2021 ◽  
Author(s):  
Martin G. Cook ◽  
Barry W. E. M. Powell ◽  
Megan E. Grant ◽  
Adele C. Green
Keyword(s):  
Case Report ◽  
Clinical Management ◽  
Unusual Case ◽  
Primary Site ◽  
Mixed Tumor ◽  
Superficial Spreading ◽  
Superficial Spreading Melanoma ◽  
Desmoplastic Melanoma ◽  
Mixed Features ◽  
Melanoma Case

AbstractDesmoplastic melanoma commonly occurs on the head and neck in a pure form, but occasionally, it occurs in a mixed tumor with another type, usually superficial spreading melanoma (SSM), and rarely as a metastasis from a primary SSM. We report here a primary SSM on the leg of a 32-year-old male which metastasised to lymph nodes, and 10 years later recurred at the primary site initially with mixed features but evolving to resemble a uniformly desmoplastic, deeply invasive melanoma. This unusual case has implications for clinical management and is additionally notable for its reversal in behavior, from metastatic to local infiltrative type, correlating with the change in morphology.

scholarly journals Cutaneous Melanomas Arising during Childhood: An Overview of the Main Entities

2021 ◽  
Vol 8 (3) ◽  
pp. 301-314
Author(s):  
Arnaud de la Fouchardière ◽  
Felix Boivin ◽  
Heather C. Etchevers ◽  
Nicolas Macagno
Keyword(s):  
Lymph Node ◽  
Regional Lymph Node ◽  
Germline Mutations ◽  
Epithelioid Cells ◽  
Superficial Spreading ◽  
Superficial Spreading Melanoma ◽  
Cancer Predisposition Syndrome ◽  
Specific Morphology ◽  
Genetic Features ◽  
Molecular Assessment

Cutaneous melanomas are exceptional in children and represent a variety of clinical situations, each with a different prognosis. In congenital nevi, the risk of transformation is correlated with the size of the nevus. The most frequent type is lateral transformation, extremely rare before puberty, reminiscent of a superficial spreading melanoma (SSM) ex-nevus. Deep nodular transformation is much rarer, can occur before puberty, and must be distinguished from benign proliferative nodules. Superficial spreading melanoma can also arise within small nevi, which were not visible at birth, usually after puberty, and can reveal a cancer predisposition syndrome (CDKN2A or CDK4 germline mutations). Prognosis is correlated with classical histoprognostic features (mainly Breslow thickness). Spitz tumors are frequent in adolescents and encompass benign (Spitz nevus), intermediate (atypical Spitz tumor), and malignant forms (malignant Spitz tumor). The whole spectrum is characterized by specific morphology with spindled and epithelioid cells, genetic features, and an overall favorable outcome even if a regional lymph node is involved. Nevoid melanomas are rare and difficult to diagnose clinically and histologically. They can arise in late adolescence. Their prognosis is currently not very well ascertained. A small group of melanomas remains unclassified after histological and molecular assessment.

NATURAL HISTORY OF A SUPERFICIAL SPREADING MELANOMA

1993 ◽  
Vol 32 (4) ◽  
pp. 293-296 ◽  
Author(s):  
CARLIN MCLAUGHLIN ◽  
HENRY C. MAGUIRE ◽  
MICHAEL J. MASTRANGELO
Keyword(s):  
Natural History ◽  
Superficial Spreading ◽  
Superficial Spreading Melanoma ◽  
History Of

The unique molecular signatures of nodular and superficial spreading melanoma

2009 ◽  
Vol 27 (15_suppl) ◽  
pp. 9047-9047
Author(s):  
A. E. Rose ◽  
J. Wang ◽  
A. Pearlman ◽  
N. Doudican ◽  
E. Hernando ◽  
...  
Keyword(s):  
Gene Expression ◽  
Copy Number ◽  
Expression Profiles ◽  
Snp Array ◽  
Mapk Signaling ◽  
Data Sets ◽  
Molecular Signatures ◽  
Superficial Spreading ◽  
Superficial Spreading Melanoma ◽  
Public Data

9047 Background: Primary nodular melanoma (NM) patients have a relatively poor prognosis compared to superficial spreading melanoma (SSM) patients. The disparity is generally attributed solely to NM's advanced thickness at presentation. In this study we attempted to define molecular signatures of NM and SSM that may explain their clinical differences. Methods: We performed an in silico gene expression analysis of 2 public data sets consisting of 36NM and 54 SSM primary melanoma tissues (CCR 2007;13 and JNCI 2006;98). We then utilized DNA microarray to generate gene expression profiles of a panel of 22 melanoma cell lines (2SSM, 4 NM, 12 met, 4 melanocytes). Differentially expressed genes and over-represented pathways in NM and SSM were identified based on a pooled analysis of the 3 data sets. We then used SNP array to define genomic alterations unique to NM and SSM but not altered in normal melanocytes. Finally, we correlated SNP array with gene expression. Results: Genes significantly overexpressed (p<0.05) in NM showed over-representation of pathways related to MAPK signaling (p=0.05) and cytoskeleton organization (p=0.02), while SSM showed over-representation of cell communication (p=0.05) and primary metabolic processes (p=0.002). Notable correlations between gene expression and copy number alteration in NM include increased copy number/overexpression of SOX5 (transcription factor related to embryonic development and cell fate) and the downregulation/deletion of ST14 (suppression of tumorigenicity 14). SSM demonstrated concordance of increased copy number/overexpression of EZR (cell adhesion protein implicated in human cancer) as well as PALLD (a protein related to motility, adhesion, and extracellular matrix interactions). Notable SSM genes showing correlation between downregulation/deletion include BNIP3 (a pro-apoptotic protein) and MTAP (often co- deleted with tumor suppressor p16). Conclusions: Simultaneous integration of gene expression with SNP array revealed molecular signatures characteristic of NM and SSM. These results suggest that NM and SSM are distinct biologic entities and that molecularly targeted adjuvant therapy may be more effective if tailored to the molecular signatures of melanoma subtypes. Validation is necessary to draw further conclusions. No significant financial relationships to disclose.

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