Epidemiologic aspects of uveal melanoma

Egan, Kathleen M.; Seddon, Johanna M.; Glynn, Robert J.; Gragoudas, Evangelos S.; Albert, Daniel M.

doi:10.1016/0039-6257(88)90173-7

Cited by 468 publications

(275 citation statements)

References 121 publications

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“…24 -27 Uveal melanoma is the most common primary intraocular tumor, with an annual incidence of 6 per 1 million. 28 Although the genes responsible for this cancer type are unknown, cytogenetic analyses and CGH have revealed abnormalities of chromosomes 3, 6 and 8. Loss of chromosome 3, overrepresentation of 6p, loss of 6q, amplification of 8q and overrepresentation of chromosome 8 are the most characteristic.…”

Section: Resultsmentioning

confidence: 99%

Assessment of genomic instability in breast cancer and uveal melanoma by random amplified polymorphic DNA analysis

Papadopoulos

Benter

Anastassiou

et al. 2002

Intl Journal of Cancer

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Some types of cancer have been associated with abnormal DNA fingerprinting. We used random amplified polymorphic DNA (RAPD) to generate fingerprints that detect genomic alterations in human breast cancer. Primers were designed by choosing sequences involved in the development of DNA mutations. Seventeen primers in 44 different combinations were used to screen a total of 6 breast cancer DNA/normal DNA pairs and 6 uveal melanoma DNA/normal DNA pairs. Forty-five percent of these combinations reliably detected quantitative differences in the breast cancer pairs, while only 18% of these combinations detected differences in the uveal melanoma pairs. Fourteen (32%) and 12 (27%) primers generated a smear or did not produce any band patterns in the first and second cases, respectively. Taking into account the ability of RAPD to screen the whole genome, our results suggest that the genomic damage in breast cancer is significantly higher than in uveal melanoma. Our study confirms other reports that the molecular karyotypes produced with random priming, called amplotypes, are very useful for assessing genomic damage in cancer. Genomic instability is a hallmark of neoplastic transformation and a herald of genomic damage. The existence of an additional type of genomic instability has been described, the microsatellite mutator phenotype pathway. Progress in molecular cancer genetics has facilitated the detection of these mutations. In the last decade, representation differential analysis and comparative genomic hybridization (CGH) were added to methods like flow cytometry, restriction fragment length polymorphisms of polymorphic minisatellite loci and allelotyping, a PCR amplification of informative microsatellite loci.Another promising approach has been introduced, arbitrarily primed PCR 1 combined with random amplified polymorphic DNA (RAPD). 2 Both PCR-based techniques, called amplotyping, use fingerprinting to quantitatively and qualitatively evaluate band alterations. 3 This random priming method allows comparison of normal and tumor tissues at a minimum of 20 -40 genome sites in a single PCR, though evidence suggests that the number of compared loci runs into the hundreds if we take into account that a gel band consists of many comigrating fragments. 4,5 It also includes internal controls and detects moderate gains of chromosomal sequences (trisomy/tetrasomy) that would otherwise escape detection.Previously, we addressed the problems of reproducibility and contamination in random priming. In the present work, we used RAPD fingerprinting to assess the genomic damage present in breast cancer and in uveal melanoma cells. For this task, we designed primers based on sequences that are supposed to play an important role in the mechanisms leading to DNA alterations. Human gene mutations appear to be caused by multiple mechanisms whose relative importance is probably governed by local primary and secondary DNA structure. 7 We have searched for consensus sequences located in the immediate vicinity of gene mutations and for "hot s...

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Section: Resultsmentioning

confidence: 99%

Assessment of genomic instability in breast cancer and uveal melanoma by random amplified polymorphic DNA analysis

Papadopoulos

Benter

Anastassiou

et al. 2002

Intl Journal of Cancer

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“…1 Although cutaneous and uveal melanomas share a neural crest origin, they differ significantly in their epidemiological, 2 cytogenetic 3 , metastatic [4][5][6] and immunological 4 characteristics. One of the remarkable differences between cutaneous and uveal melanomas is their metastatic behavior.…”

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confidence: 99%

“…[7][8][9][10] Although there have been advances in the treatment of primary uveal melanomas, the 5-year survival rate for uveal melanoma patients has not improved in the past 30 years. 1,10 Moreover, no therapeutic modality prevents the metastasis of uveal melanoma or prolongs the survival of patients. 11 Studies have suggested a correlation between the expression of CD54 and the progression of skin and uveal melanomas.…”

mentioning

confidence: 99%

Effect of an anti‐CD54 (ICAM‐1) monoclonal antibody (UV3) on the growth of human uveal melanoma cells transplanted heterotopically and orthotopically in SCID mice

Wang

Coleman

Pop

et al. 2005

Intl Journal of Cancer

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We have shown that administration of a novel anti-CD54 monoclonal antibody (UV3) results in long-term survival of SCID mice bearing human myeloma xenografts. Previous studies have demonstrated a link between the expression of CD54 and the progression of uveal melanoma. Our study assessed the expression of CD54 on 7 human uveal melanoma cell lines and 3 cell lines established from uveal melanoma metastases. In vivo studies examined the efficacy of systemic and local administration of UV3 antibody on the progression of uveal melanoma cells transplanted either heterotopically or orthotopically into SCID mice. Five of the 7 primary uveal melanoma cell lines and all 3 of the metastases cell lines expressed CD54. Intraperitoneal injection of either IgG or F(ab 0 ) 2 fragments of UV3 significantly inhibited the growth of subcutaneous and intraocular melanomas. Subconjunctival injection of either IgG or F(ab 0 ) 2 fragments of UV3 produced a significant reduction in the growth of intraocular melanomas, even if the antibody was administered after the appearance of intraocular tumors. The results indicate that both primary and metastatic human uveal melanoma cells express CD54. The marked inhibition of intraocular and subcutaneous uveal melanoma progression suggests that UV3 antibody is a promising therapeutic agent for further evaluation in patients with uveal melanoma. This is especially noteworthy, as no existing therapeutic modality prevents metastasis of uveal melanoma or prolongs the survival of patients with uveal melanoma. ' 2005 Wiley-Liss, Inc.Key words: anterior chamber; eye; CD54; immunotherapy; uveal melanoma Uveal melanoma is the most common intraocular malignancy in adults and occurs with a frequency of 6 to 7 cases per one million adults. 1 Although cutaneous and uveal melanomas share a neural crest origin, they differ significantly in their epidemiological, 2 cytogenetic 3 , metastatic 4-6 and immunological 4 characteristics. One of the remarkable differences between cutaneous and uveal melanomas is their metastatic behavior. Although skin melanomas metastasize to almost any organ, uveal melanoma displays a propensity to spread to the liver. Indeed, liver metastases are present in up to 95% of the patients who die from uveal melanomas. [7][8][9][10] Although there have been advances in the treatment of primary uveal melanomas, the 5-year survival rate for uveal melanoma patients has not improved in the past 30 years. 1,10 Moreover, no therapeutic modality prevents the metastasis of uveal melanoma or prolongs the survival of patients. 11 Studies have suggested a correlation between the expression of CD54 and the progression of skin and uveal melanomas. 12,13 Expression of CD54 was detected in 81-85% of human uveal melanoma specimens. 13,14 Reduced expression of CD54 in primary uveal melanomas has been associated with increased metastatic disease. 13 CD54 is an important ligand for leukocytes and is believed to be involved in immune surveillance. 15,16 Intravenous administration of MAb against human CD54 (U...

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“…[33][34][35] Approximately, 35% of patients with uveal melanoma develop metastases. 36 Histologic sections of aggressive choroidal melanomas and their metastases contain perfusion channels that are associated with extracellular matrix.…”

Section: Discussionmentioning

confidence: 99%

A gene transfer comparative study of HSA-conjugated antiangiogenic factors in a transgenic mouse model of metastatic ocular cancer

et al. 2006

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Different antiangiogenic and antimetastatic recombinant adenoviruses were tested in a transgenic mouse model of metastatic ocular cancer (TRP1/SV40 Tag transgenic mice), which is a highly aggressive tumor, developed from the pigmented epithelium of the retina. These vectors, encoding amino-terminal fragments of urokinase plasminogen activator (ATF), angiostatin Kringles (K1-3), endostatin (ES) and canstatin (Can) coupled to human serum albumin (HSA) were injected to assess their metastatic and antiangiogenic activities in our model. Compared to AdCO1 control group, AdATF-HSA did not significantly reduce metastatic growth. In contrast, mice treated with AdK1-3-HSA, AdES-HSA and AdCan-HSA displayed significantly smaller metastases (1.1971.19, 0.8771.5, 0.4370.56 vs controls 4.0475.12 mm 3 ). Moreover, a stronger inhibition of metastatic growth was obtained with AdCan-HSA than with AdK1-3-HSA (P ¼ 0.04). Median survival was improved by 4 weeks. A close correlation was observed between the effects of these viruses on metastatic growth and their capacity to inhibit tumor angiogenesis. Our study indicates that systemic antiangiogenic factors production by recombinant adenoviruses, particularly Can, might represent an effective way of delaying metastatic growth via inhibition of angiogenesis.

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Epidemiologic aspects of uveal melanoma

Cited by 468 publications

References 121 publications

Assessment of genomic instability in breast cancer and uveal melanoma by random amplified polymorphic DNA analysis

Assessment of genomic instability in breast cancer and uveal melanoma by random amplified polymorphic DNA analysis

Effect of an anti‐CD54 (ICAM‐1) monoclonal antibody (UV3) on the growth of human uveal melanoma cells transplanted heterotopically and orthotopically in SCID mice

A gene transfer comparative study of HSA-conjugated antiangiogenic factors in a transgenic mouse model of metastatic ocular cancer

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