Identification of Novel Deletion Loci at 1p36 and 9p22-21 in Melanocytic Dysplastic Nevi and Cutaneous Malignant Melanomas

Hussein, Mahmoud R.; Roggero, Eduardo; Tuthill, Ralph J.; Wood, Gary S.; Sudilovsky, Oscar

doi:10.1001/archderm.139.6.816

Cited by 24 publications

(21 citation statements)

References 5 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…All the four cases of OMM, one case of SCCM and three cases of DMM resulted wild type for 1p36, while 1p36 deletion was observed in all the three cases of CMM. This finding is consistent with previously reported data showing that deletion of 1p36 is a frequent finding in CMMs [5,6], while it has not been described in OMM and in DMM.…”

Section: Discussionsupporting

confidence: 93%

See 1 more Smart Citation

Genetic markers of oral malignant melanoma analysed by fluorescence in situ hybridisation (FISH)

et al. 2011

View full text Add to dashboard Cite

Oral malignant melanoma (OMM) is a rare condition, and our knowledge about morphological and genetic modifications is scanty and incomplete. The aim of this study is to report morphological and fluorescent in situ hybridisation (FISH) data obtained in four cases of OMM. FISH results were also compared with those of cutaneous malignant melanoma (CMM, three cases), desmoplastic cutaneous melanoma (DMM, four cases) and spindle cells cutaneous melanoma (SCCM, one case). All the OMM cases showed a combined radial and vertical growth pattern, with the invasive component characterised by malignant spindle cells intermingled among collagen bundles. Two cases of OMM resulted positively stained with p16, in contrast with frequent loss of immunoreactivity in CMM. Three OMM were suitable for FISH analysis: 9p21 locus was deleted in 1/3, 1p36 resulted deleted 3/3, while EGFR gene showed a relative deletion. Similar genetic alterations were found in DMM and SCMM, but not in CMM. Ultrastructural findings further enhanced differences between OMM and CMM; OMM displayed, mature-staged melanosomes only within in situ component. In conclusion, OMM presents a morphological and genetic profile similar to DMM; and SCCM, however, displays some differences from CMM.

show abstract

Section: Discussionsupporting

confidence: 93%

“…Several genetic alterations including 9p21, 1p36 deletions and EGFR amplification have been described in the literature as characteristic of CMM [4][5][6]. On the contrary, data on genetic alterations in OMM are still scanty.…”

Section: Introductionmentioning

confidence: 99%

Genetic markers of oral malignant melanoma analysed by fluorescence in situ hybridisation (FISH)

et al. 2011

View full text Add to dashboard Cite

show abstract

“…Several observations support the view that the development of malignant melanoma involves a series of pathologically and experimentally defined events [3,23,24]. One such event is activation of the RAS/RAF/ERK pathway, a signaling cascade important in mediation of cellular responses to growth signals via mutations of the genes BRAF and NRAS as well as mutations of other RAS genes [9,13,16].…”

Section: Discussionmentioning

confidence: 83%

Oncogenic BRAF-positive dysplastic nevi and the tumor suppressor IGFBP7—challenging the concept of dysplastic nevi as precursor lesions?

et al. 2010

View full text Add to dashboard Cite

“…Deletions of the 1p36 region are also prevalent in other tumors (Bello et al, 2000;Benn et al, 2000;Mora et al, 2000;Sun et al, 2001), including pheochromocytomas, parathyroid adenomas, hepatocellular car-cinomas, meningiomas, and neuroblastomas. A variety of cytogenetic abnormalities affecting 1p36 and other regions of 1p have been reported in melanomas (Mertens et al, 1997;Poetsch et al, 1999;Zhang et al, 1999;Nelson et al, 2000;Hussein et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

Deletion mapping suggests that the 1p22 melanoma susceptibility gene is a tumor suppressor localized to a 9‐mb interval

Walker

Indsto

Sood

et al. 2004

Genes Chromosomes & Cancer

View full text Add to dashboard Cite

Loss of the short arm of chromosome 1 is frequently observed in many tumor types, including melanoma. We recently localized a third melanoma susceptibility locus to chromosome band 1p22. Critical recombinants in linked families localized the gene to a 15-Mb region between D1S430 and D1S2664. To map the locus more finely we have performed studies to assess allelic loss across the region in a panel of melanomas from 1p22-linked families, sporadic melanomas, and melanoma cell lines. Eighty percent of familial melanomas exhibited loss of heterozygosity (LOH) within the region, with a smallest region of overlapping deletions (SRO) of 9 Mb between D1S207 and D1S435. This high frequency of LOH makes it very likely that the susceptibility locus is a tumor suppressor. In sporadic tumors, four SROs were defined. SRO1 and SRO2 map within the critical recombinant and familial tumor region, indicating that one or the other is likely to harbor the susceptibility gene. However, SRO3 may also be significant because it overlaps with the markers with the highest 2-point LOD score (D1S2776), part of the linkage recombinant region, and the critical region defined in mesothelioma. The candidate genes PRKCL2 and GTF2B, within SRO2, and TGFBR3, CDC7, and EVI5, in a broad region encompassing SRO3, were screened in 1p22-linked melanoma kindreds, but no coding mutations were detected. Allelic loss in melanoma cell lines was significantly less frequent than in fresh tumors, indicating that this gene may not be involved late in progression, such as in overriding cellular senescence, necessary for the propagation of melanoma cells in culture.

show abstract

Identification of Novel Deletion Loci at 1p36 and 9p22-21 in Melanocytic Dysplastic Nevi and Cutaneous Malignant Melanomas

Cited by 24 publications

References 5 publications

Genetic markers of oral malignant melanoma analysed by fluorescence in situ hybridisation (FISH)

Genetic markers of oral malignant melanoma analysed by fluorescence in situ hybridisation (FISH)

Oncogenic BRAF-positive dysplastic nevi and the tumor suppressor IGFBP7—challenging the concept of dysplastic nevi as precursor lesions?

Deletion mapping suggests that the 1p22 melanoma susceptibility gene is a tumor suppressor localized to a 9‐mb interval

Contact Info

Product

Resources

About