Human melanoma: Development and progression

Herlyn, Meenhard

doi:10.1007/bf00046337

Cited by 141 publications

(105 citation statements)

References 22 publications

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“…Another receptor tyrosine kinase locus, EGFR (HER-1) which shows marked sequence similarity with Xmrk-2 (Wittbrodt et al, 1989), has been previously implicated in the formation of human melanoma (see Kraehn et al, 1995, for review). Human EGFR has been mapped to chromosomal region 7p11-13 (Davies et al, 1980), a region frequently rearranged in melanomas (Herlyn, 1990). Overexpression of EGFR was shown to be associated with spontaneous metastases of a human melanoma cell line in nude mice (Huang et al, 1996), and expression of EGFR is related to speci®c stages of melanocytic cellular di erentiation and melanoma progression (de Wit et al, 1992;Real et al, 1986).…”

Section: Discussionmentioning

confidence: 99%

Comparative structure and characterization of a CDKN2 gene in a Xiphophorus fish melanoma model

Kazianis

Coletta

et al. 1999

Oncogene

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We have cloned, sequenced, and characterized the RNA expression properties of a ®sh CDKN2 gene from Xiphophorus helleri and X. maculatus. This gene, termed CDKN2X, shows a high degree of amino acid sequence similarity to members of the mammalian CDKN2 gene family, which includes the tumor suppressor loci CDKN2A (P16) and CDKN2B (P15). Comparative sequence analysis suggests that ®sh CDKN2X is similarly related to all four mammalian gene family members, and may represent a descendant of an ancestral prototypic CDKN2 gene. CDKN2X was mapped to a region on autosomal Xiphophorus linkage group V (LG V) known to contain the DIFF gene that acts as a tumor suppressor of melanoma formation in X. helleri/X. maculatus backcross hybrids. Thus, CDKN2X may be a candidate for the tumor suppressor DIFF gene. Here we have sequenced CDKN2X in both Xiphophorus species and have characterized its expression in normal and melanotic tissues within control and backcross hybrid ®sh. A simultaneous expressional analysis of the Xmrk-2 tyrosine kinase receptor gene, which is strongly implicated in melanomagenesis in this system, was also performed. RT ± PCR analyses revealed that both genes were highly expressed in melanomas. For CDKN2X, this result contrasts numerous ®ndings in human tumors including human melanoma in which either CDKN2A (P16) deactivation or LOH was observed.

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Section: Discussionmentioning

confidence: 99%

Comparative structure and characterization of a CDKN2 gene in a Xiphophorus fish melanoma model

Kazianis

Coletta

et al. 1999

Oncogene

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“…Metastatic cell lines WM9 and WM164 were derived from an intermediate stage metastatic lesion. WM136 1A was obtained from a late lesion with concomitant distant metastases at the time of tumor removal (16,17). The above cell cultures were grown in tumor medium (MCDE 153/L-15, 4:1, Sigma) supplemented with 2% fetal bovine serum and insulin (5 g/ml, Sigma).…”

Section: Methodsmentioning

confidence: 99%

A Cell Binding Domain from the α3 Chain of Type IV Collagen Inhibits Proliferation of Melanoma Cells

Han¹,

Ohno²,

Brassart‐Pasco³

et al. 1997

Journal of Biological Chemistry

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Our previous studies have shown that a peptide corresponding to the residue sequence 185-203 of the NC1 domain of the ␣3 chain of basement membrane collagen (type IV) inhibits the activation of polymorphonuclear leukocytes. Peptides from the same region of the ␣1, ␣2, ␣4, and ␣5(IV) chains did not exhibit this property. Because of the intimate relationship between metastasizing neoplastic cells and vascular as well as epithelial basement membranes, we measured the cell adhesionpromoting activity of peptides from the NC1 domain of type IV collagen and their effect on proliferation of human melanoma cells. We found that peptide ␣3(IV)185-203 (CNYYSNSYSFWLASLNPER) not only promotes adhesion of human melanoma cells but also inhibits their proliferation. Adhesion increased by 50 -60% over control. Melanoma cell proliferation was inhibited by 40% when cells were grown in a medium containing 5 g/ml peptide for 5 days. Studies showed that replacement of serine in position 189 or 191 by alanine resulted in significantly reduced adhesion. Similarly, serine replacement resulted in reduced ability to inhibit proliferation. Our data suggest that a region of the NC1 domain of the ␣3(IV) chain, contained within the sequence 185-203, not only specifically promotes adhesion but also inhibits proliferation of melanoma cells. These properties appear to be dependent on the presence of the triplet sequence -SNS-(residues 189 -191), which is unique to the ␣3 chain and may represent an important functional epitope.

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“…1 The development of malignant melanoma, with the exception of nodular type melanoma, is assumed to be a multistep process involving the conversion of a melanocyte into a nevus, a dysplastic nevus, a radial growth phase primary melanoma, a vertical growth phase primary melanoma and a metastatic melanoma. 3 When the disease is confined to the epidermis and when it is thin (o1 mm), there is very little risk for metastatic spread and surgical resection almost universally results in a cure. 4,5 However, with increasing thickness melanomas acquire metastatic potential and metastatic melanomas are universally fatal because of general resistance to adjuvant therapies, such as radiotherapy and/or chemotherapy.…”

Section: Introductionmentioning

confidence: 99%

A cancer terminator virus eradicates both primary and distant human melanomas

Sarkar

et al. 2008

Cancer Gene Ther

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The prognosis and response to conventional therapies of malignant melanoma inversely correlate with disease progression. With increasing thickness, melanomas acquire metastatic potential and become inherently resistant to radiotherapy and chemotherapy. These harsh realities mandate the design of improved therapeutic modalities, especially those targeting metastases. To develop an approach to effectively treat this aggressive disease, we constructed a conditionally replication-competent adenovirus in which expression of the adenoviral E1A gene, necessary for replication, is driven by the cancer-specific promoter of progression-elevated gene-3 (PEG-3) and which simultaneously expresses mda-7/IL-24 in the E3 region of the adenovirus (Ad.PEG-E1A-mda-7), a cancer terminator virus (CTV). This CTV produces large quantities of MDA-7/IL-24 protein as a function of adenovirus replication uniquely in cancer cells. Infection of Ad.PEG-E1A-mda-7 (CTV) in normal human immortal melanocytes and human melanoma cells demonstrates cancer cell-selective adenoviral replication, mda-7/IL-24 expression, growth inhibition and apoptosis induction. Injecting Ad.PEG-E1A-mda-7 CTV into xenografts derived from MeWo human metastatic melanoma cells in athymic nude mice completely eliminated not only primary treated tumors but also distant non-treated tumors (established in the opposite flank), thereby implementing a cure. These provocative findings advocate potential therapeutic applications of this novel virus for treating patients with advanced melanomas with metastases.

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Human melanoma: Development and progression

Cited by 141 publications

References 22 publications

Comparative structure and characterization of a CDKN2 gene in a Xiphophorus fish melanoma model

Comparative structure and characterization of a CDKN2 gene in a Xiphophorus fish melanoma model

A Cell Binding Domain from the α3 Chain of Type IV Collagen Inhibits Proliferation of Melanoma Cells

A cancer terminator virus eradicates both primary and distant human melanomas

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