Comparative genome hybridization analysis of laser‐capture microdissected <i>in situ</i> melanoma

Vincek, Vladimir; Xu, Suying; Fan, Yao Shan

doi:10.1111/j.1600-0560.2009.01299.x

Cited by 10 publications

(6 citation statements)

References 29 publications

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“…The reason for this difference may be that the majority cases in our study was in‐situ melanomas, while previous studies mainly included invasive lesions. And comparative genome hybridisation test has revealed that compared with invasive melanoma, in‐situ melanoma harbored relatively limited chromosomal aberrations 22 . Similar to the results of Romano et al 19 .…”

Section: Discussionsupporting

confidence: 80%

Clinicopathological, immunohistochemical and fluorescence in‐situ hybridisation features of early subungual melanoma: an analysis of 65 cases

Ren

Cai

et al. 2020

Histopathology

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Aims Very limited data are available concerning the clinicopathological and molecular features of early subungual melanoma (SM), especially with regard to the Asian population. The aim of this study was to investigate the clinical, histological, immunohistochemical and chromosomal features of early SM. Methods and results Fifty‐two in‐situ and 13 thin (Breslow thickness ≤1.0 mm) SM cases were retrospectively reviewed. All patients presented with longitudinal melanonychia involving a single digit, and the thumb was the most affected digit (35 of 65, 53.8%). Microscopically, most cases showed small to medium nuclear enlargement (58 of 65) and mild to moderate nuclear atypia (57 of 65). Hyperchromatism and irregular contours of nuclei were persistent features in all cases. The variation of melanocyte count (the number of melanocytes per mm dermal‐epithelial junction) ranged from 31 to 255. Intra‐epithelial mitoses were identified in 34 cases (52.3%). Statistically, features of in‐situ lesions including higher melanocyte count (>70), presence of multinucleated melanocytes, inflammatory infiltrate and cutaneous adnexal extension, were associated with early invasion. Melan‐A, human melanoma B (HMB)45, mouse monoclonal melanoma antibody (PNL2) and SOX10 antibodies (>95.0%) showed superior diagnostic sensitivity to S‐100 protein (83.1%). Fluorescence in‐situ hybridisation (FISH) results were positive in 15 of 23 successfully analysed cases. Conclusions To the best of our knowledge, this is the largest single‐institution study of early SM in an Asian population, and the largest cohort tested by FISH. Early SM mainly showed small to medium nuclear enlargement and mild to moderate nuclear atypia. High melanocyte count, hyperchromatism and irregular contours of nuclei and intra‐epithelial mitoses are crucial diagnostic parameters. Immunohistochemistry, especially SOX10 staining, and FISH analysis are valuable in the diagnosis of SM.

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Section: Discussionsupporting

confidence: 80%

Clinicopathological, immunohistochemical and fluorescence in‐situ hybridisation features of early subungual melanoma: an analysis of 65 cases

Ren

Cai

et al. 2020

Histopathology

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“…In conclusion, the relevance of RB1 to melanoma is not in question and this is highlighted by a recent CGH study that found that RB1 ‐loss is an early and defining change in melanoma (Vincek et al., 2009). However, our data shows that Rb1 ablation alone does not lead to a short‐term or long‐term loss of melanocyte homeostasis and apoptosis either in vivo or in vitro, irrespective of the developmental stage at which the recombination event driving deletion occurs.…”

Section: Resultsmentioning

confidence: 99%

Melanocyte homeostasis in vivo tolerates Rb1 loss in a developmentally independent fashion

Tonks

Mould

Schroder

et al. 2010

Pigment Cell Melanoma Res

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SummaryThere has been uncertainty regarding the precise role that the pocket protein Rb1 plays in murine melanocyte homeostasis. It has been reported that the TAT-Cre mediated loss of exon 19 from a floxed Rb1 allele causes melanocyte apoptosis in vivo and in vitro. This is at variance with other findings showing, either directly or indirectly, that Rb1 loss in melanocytes has no noticeable effect in vivo, but in vitro leads to a semi-transformed phenotype. In this study, we show that Rb1-null melanocytes lacking exon 19 do not undergo apoptosis and survive both in vitro and in vivo, irrespective of the developmental stage at which Cre-mediated ablation of the exon occurs. Further, Rb1 loss has no serious long-term ramifications on melanocyte homeostasis in vivo, with Rb1-null melanocytes being detected in the skin after numerous hair cycles, inferring that the melanocyte stem cell population carrying the Cre-mediated deletion is maintained. Consequently, whilst Rb1 loss in the melanocyte is able to alter cellular behaviour in vitro, it appears inconsequential with respect to melanocyte homeostasis in the mouse skin.

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“…BCL2L1 (also known as BCL-XL), located on chromosome 12q, was amplified in 40% of DM; it encodes the antiapoptotic protein Bcl-XL, which has been demonstrated to enhance CXCL8-induced angiogenesis in melanoma cells. 9 Also amplified was ARTN on chromosome 1p, which encodes the protein artemin, which is reported to promote invasion of pancreatic carcinoma, influence perineural invasion, and increase the oncogenicity and invasiveness of endometrial carcinoma. 10 Interestingly, the gene AMPK on chromosome 1p was also amplified; although adenosine monophosphate-activated protein kinase (AMPK) has proapoptotic properties, it is well known to be involved in UV-induced skin cell damage and also plays a major role in the regulation of vascular endothelial growth factor expression and has a potential role in tumor angiogenesis.…”

Section: Dna Copy Number Changesmentioning

confidence: 99%

Microarray Comparative Genomic Hybridization Detection of Copy Number Changes in Desmoplastic Melanoma and Malignant Peripheral Nerve Sheath Tumor

Pryor¹,

Brown-Kipphut²,

Iqbal³

et al. 2011

The American Journal of Dermatopathology

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Desmoplastic melanoma (DM) and malignant peripheral nerve sheath tumor (MPNST) can appear morphologically and immunophenotypically similar. We attempted to determine whether microarray comparative genomic hybridization could detect copy number differences between them to aid in the diagnosis. S-100 immunohistochemistry was performed on 5 cases of DM and 9 cases of MPNST using formalin-fixed paraffin-embedded specimens. Genomic DNA was extracted from microdissected cells. Whole genome amplification was performed on 5 of 5 DMs and 6 of 9 MPNST cases. A multiplex polymerase chain reaction assay was used to determine the quality of the DNA samples, which were run on the Spectral Chip 2600 bacterial artificial chromosome array platform. DM showed gains involving chromosomes 1p, 2p, 9q, 13q, 14q, and 20q and losses involving chromosomes 5p, 11p, 12q, 15q, and 18q. Several cancer-associated genes were involved, including gain of BCL2L1, ARTN, AMPK, NRAS, and CCNA1 and loss of IGF2, CDKN1C, PAX6, WT1, TRAF6, MAPK8IP1, and IMP3. MPNST had gains involving chromosomes 1p, 2q, and 19p and loss of chromosome 21q. Gains of MUM1, APC2, MAP2K2, JMJD2B, SP110, PTMA, GPI, and CDKN2D were detected. DM and MPNST have chromosomal alterations detected by array comparative genomic hybridization that might be useful in distinguishing these 2 tumors, although further studies with a larger sample size will be needed to test this.

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Comparative genome hybridization analysis of laser‐capture microdissected in situ melanoma

Abstract: In situ melanomas show characteristic chromosomal aberrations that are limited compared to melanomas that invade the dermis. Deletion of 13q found in in situ melanomas, which encompass the Rb1 tumor suppressor gene, might be one of the first events in the development of melanoma.

Cited by 10 publications

References 29 publications

Clinicopathological, immunohistochemical and fluorescence in‐situ hybridisation features of early subungual melanoma: an analysis of 65 cases

Clinicopathological, immunohistochemical and fluorescence in‐situ hybridisation features of early subungual melanoma: an analysis of 65 cases

Melanocyte homeostasis in vivo tolerates Rb1 loss in a developmentally independent fashion

Microarray Comparative Genomic Hybridization Detection of Copy Number Changes in Desmoplastic Melanoma and Malignant Peripheral Nerve Sheath Tumor

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