cDNA array technology in melanoma: An overview

Baldi, Alfonso; Santini, Daniele; Luca, Antonio De; Paggi, Marco G.

doi:10.1002/jcp.10255

Cited by 17 publications

(9 citation statements)

References 47 publications

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“…Our differential gene expression data showed minimal overlap with previously described microarray experiments in which also gene expression patterns were studied in cutaneous melanoma progression (Brem et al, 2001;Baldi et al, 2003b;Carr et al, 2003;Dooley et al, 2003;Rumpler et al, 2003;Becker et al, 2004;Nambiar et al, 2004). This could be explained by the fact that design of our custom made oligonucleotide arrays was based on previously found differential gene expression in melanoma cell lines.…”

Section: Discussionsupporting

confidence: 66%

Analysis of differential gene expression in human melanocytic tumour lesions by custom made oligonucleotide arrays

et al. 2005

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Melanoma is one of the most aggressive types of cancer and resection of the tumour prior to dissemination of tumour cells is still the most effective treatment. Therefore, early diagnosis of melanocytic lesions is important and identification of novel (molecular) markers would be helpful to improve diagnosis. Moreover, better understanding of molecular targets involved in melanocytic tumorigenesis could possibly lead to development of novel interventions. In this study, we used a custom made oligonucleotide array containing 298 genes that were previously found to be differentially expressed in human melanoma cell lines 1F6 (rarely metastasising) and Mel57 (frequently metastasising). We determined differential gene expression in human common nevocellular nevus and melanoma metastasis lesions. By performing nine dye-swap array experiments, using individual as well as pooled melanocytic lesions, a constant differential expression could be detected for 25 genes in eight out of nine or nine out of nine array analyses. For at least nine of these genes, namely THBD, FABP7, H2AFJ, RRAGD, MYADM, HR, CKS2, NCK2 and GDF15, the differential expression found by array analyses could be verified by semiquantitative and/or real-time quantitative RT -PCR. The genes that we identified to be differentially expressed during melanoma progression could be potent targets for diagnostic, prognostic and/ or therapeutic interventions.

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Section: Discussionsupporting

confidence: 66%

Analysis of differential gene expression in human melanocytic tumour lesions by custom made oligonucleotide arrays

et al. 2005

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“…Patients with similar clinical and anatomic-pathologic prognostic factors may progress in different manners, sometimes progressing favorably, sometimes with disease dissemination, probably because of the intrinsic properties of these tumor cells. A number of studies have examined molecular factors that may explain such differences, particularly focusing on genetic changes involved in tumorigenesis and melanoma progression 2, 17– 19…”

Section: Introductionmentioning

confidence: 99%

Primary Cutaneous Melanoma: An 18-Year Study

Anger

Friedhofer

Fukutaki

et al. 2010

Clinics

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BACKGROUND:Primary cutaneous melanoma still constitutes the main cause of skin cancer death in developed countries, and its incidence in recent years has been increasing in a steady, worrisome manner.OBJECTIVES:This study evaluated the clinical, epidemiological and demographic aspects of this disease, and correlated them with patient prognosis.METHODS:Using epidemiologic and clinical data, we analyzed 84 patients with mild to severe primary cutaneous melanoma treated between 1990 and 2007. Slides containing surgical specimens were analyzed, and new slides were made from archived paraffin sections when necessary.RESULTS:The melanoma incidence was higher in areas of sun exposure, with lesions commonly observed in the trunk for males, and lower limbs for females. In addition to Breslow’s thickness and ulceration (p = 0.043 and p < 0.001, respectively), the mitotic rate per mm2 also correlated with worse patient outcome (p = 0.0007). The sum of ulceration (0 when absent or 1 when present), the Breslow index (1 when <1 mm, 2 when >1 mm and <4 mm, 3 when >4 mm) and the mitotic index (0 when absent or 1 when ≥1 per mm2) allowed the establishment of a prognostic score: if the sum was equal to or over three, nearly all (91.7%) patients had systemic disease. The 5-year survival was approximately seventy percent.CONCLUSION:Because American Join Committee of Cancer Staging will update the classification of malignant tumors (TNM) staging in the near future, and introduce mitosis as a prognostic factor, our results show the importance of such a feature. Additional studies are necessary to confirm the importance of a prognostic score as proposed herein.

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“…With cDNA hybridization arrays, it is now possible to simultaneously examine changes in the expression of thousands of genes. Gene expression profiles identify “signatures” of neoplastic transformation and progression (Bittner et al, 2000; Alizadeh et al, 2001; Baldi et al, 2003).…”

mentioning

confidence: 99%

cDNA‐array profiling of melanomas and paired melanocyte cultures

Mischiati

Natali²,

Sereni

et al. 2006

Journal Cellular Physiology

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Three paired (from the same donor) sets of melanoma cells and normal melanocytes, established as early-passage cultures from metastatic lesions and the uninvolved skin of three patients, were comparatively cDNA profiled by macroarrays (approximately 1,200 genes) and reverse transcription (RT)-PCR. While 145 gene products were significantly (at least twofold) upregulated or downregulated in at least 1 pair, and 23 were in at least 2 pairs, only 3 (the signal transducer and activator of transcription STAT2, collagen type VI, and CD9) were concordantly modulated (downregulation) in all 3 pairs. Array results were validated by RT-PCR on a small panel of surgically removed nevocellular nevi and metastatic melanoma lesions, and by immunohistochemistry on a large panel of benign and malignant lesions of the nevomelanocytic lineage. The three gene products were downregulated at different stages of melanoma progression. STAT2 was detectable in nevi (5/5) and most primary melanomas (11/12), but was lost in 10/15 metastatic lesions. Collagen type VI was expressed in nevi (5/5) and primary melanomas below a Breslow thickness of 1 mm (3/3), but was lost in 24/24 primary melanomas above this threshold, and in metastatic melanomas (10/10). The tetraspanin CD9 molecule was expressed in 18/18 nevi, but was lost in 20/28 primary melanomas (including thin lesions), and in 24/52 metastatic lesions. These data provide the proof of principle that cDNA profiling of paired melanocyte/melanoma cultures sorts out novel, early signatures of melanocyte transformation that could contribute to the clinical management of patients at high risk of metastatic disease.

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cDNA array technology in melanoma: An overview

Cited by 17 publications

References 47 publications

Analysis of differential gene expression in human melanocytic tumour lesions by custom made oligonucleotide arrays

Analysis of differential gene expression in human melanocytic tumour lesions by custom made oligonucleotide arrays

Primary Cutaneous Melanoma: An 18-Year Study

cDNA‐array profiling of melanomas and paired melanocyte cultures

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