Murine models of malignant melanoma

Tietze, Maja Katrin; Chin, Lynda

doi:10.1016/s1357-4310(00)01781-0

Cited by 18 publications

(15 citation statements)

References 5 publications

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“…Cell lysates from A431 and B16 cell lines were used as positive controls. B16 is a well-characterized mouse melanoma cell line that has been employed in a number of in vivo and in vitro tumor models [23,24]. We observed similar levels of STAT1 in lysates from both A431 and B16 cells; however, the AGS-1 cell line did not contain any demonstrable STAT1 protein by this assay (Fig.…”

Section: Immunoblot Analysis Of Ags-1 Cell Line For Stat1mentioning

confidence: 58%

The antitumor effects of interferon-alpha are maintained in mice challenged with a STAT1-deficient murine melanoma cell line

Badgwell

Lesinski

Magro

et al. 2004

Journal of Surgical Research

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Section: Immunoblot Analysis Of Ags-1 Cell Line For Stat1mentioning

confidence: 58%

The antitumor effects of interferon-alpha are maintained in mice challenged with a STAT1-deficient murine melanoma cell line

Badgwell

Lesinski

Magro

et al. 2004

Journal of Surgical Research

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“…196 Thus, activities of two important tumor suppressors, p53 and Rb, are essentially sabotaged in the majority of melanoma by mutations in genes that encode proteins intrinsic to these regulatory pathways. 231 Expression of the apoptosis suppressor gene bcl-2 was detected in 16 of 18 human cutaneous melanomas examined by Morales-Ducret et al 1995, 162 but the bcl-2 gene product was also found in resting melanocytes in normal skin. On the other hand, atypical bcl-2 overexpression has been detected in human uveal melanoma.…”

Section: Pathogenesismentioning

confidence: 95%

“…Mutations in INK4a, INK4b, and Waf-1 are more common. 160,231 INK4a and INK4b encode proteins p16 INK4a and p15 INK4b that are cyclin-dependent kinase inhibitors (CDKI) regulated by Rb. Entry into mitosis is triggered by cyclin-dependent kinases; therefore, INK4a and INK4b mutations ultimately remove the ability to inhibit mitosis and allow uncontrolled proliferation.…”

Section: Pathogenesismentioning

confidence: 99%

A Comparative Review of Melanocytic Neoplasms

2002

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Abstract. Melanoma is a devastating disease frequently encountered within both veterinary and human medicine. Molecular changes linked with neoplastic transformation of melanocytes include mutations in genes that encode proteins intrinsic to the regulatory pathways of two tumor suppressor proteins (retinoblastoma protein and p53), proto-oncogene mutation to oncogenes, altered expression of epithelial cadherin and CD44 adhesion molecules, and upregulation of angiogenic factors and other growth factors. Histologic evaluation of the primary mass is the most common means of diagnosis, with cytology used more frequently to document metastasis. Melanoma's highly variable histologic and cytologic patterns can make diagnosis by either method problematic. Adherent epithelioid morphology, including signet ring forms, and nonadherent round and spindle forms are recognized, with pigmentation an inconsistent finding. The site of the tumor, the thickness of the primary tumor or depth of invasion, and the number of mitotic figures per high-power field or per millimeter are used histologically to predict biologic behavior, whereas site and degree of pleomorphism are typically used for cytologic preparations. Diagnosis of amelanotic melanoma can be aided by ancillary diagnostic techniques. Tumor cells are usually positive for vimentin, S100, neuron-specific enolase, and Melan-A, and negative for cytokeratin. Melan-A as a positive marker is not as sensitive as the others are but is likely more specific. Monoclonal antibodies to human melanosome-specific antigens 1 and 5 cross-react with canine antigens for a combined sensitivity rate of 83%. Mouse monoclonal antibody IBF9 specifically recognizes canine melanoma antigen and also has good sensitivity. Serologic markers, including cytokines, cell adhesion molecules, and melanoma-inhibitory activity, are being investigated as potential sentinels of melanoma. Currently, there is no single diagnostic technique capable of differentiating benign from malignant melanocytic neoplasms or predicting survival time.

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“…These results suggest that high levels of SKI can also alter cellular senescence induced by RB complexes containing the PML protein [28]. Thus, high levels of SKI can cause lesions in the RB pathway similar to deletions or mutations of p16 INK4a , an event associated with mouse and human melanoma genesis and/or progression (reviewed in [29][30][31]). …”

Section: Ski Is a Potent Inhibitor Of The Retinoblastoma (Rb) Proteinmentioning

confidence: 99%

SKI pathways inducing progression of human melanoma

Reed

Lin

Chen

et al. 2005

Cancer Metastasis Rev

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The proteins SKI and SnoN are implicated in processes as diverse as differentiation, transformation and tumor progression. Until recently, SKI was solely viewed as a nuclear protein with a principal function of inhibiting TGF-beta signaling through its association with the Smad proteins. However, new studies suggest that SKI plays additional roles not only inside but also outside the nucleus. In normal melanocytes and primary non-invasive melanomas, SKI localizes predominantly in the nucleus, whereas in primary invasive melanomas SKI displays both nuclear and cytoplasmic localization. Intriguingly, metastatic melanoma tumors display nuclear and cytoplasmic or predominantly cytoplasmic SKI distribution. Cytoplasmic SKI is functional, as it associates with Smad3 and prevents its nuclear localization mediated by TGF-beta. SKI can also function as a transcriptional activator, targeting the beta -catenin pathway and activating MITF and NrCAM, two proteins involved in survival, migration and invasion. Intriguingly, SKI appears to live a dual life, one as a tumor suppressor and another as a transforming protein. Loss of one copy of mouse ski increases susceptibility to tumorigenesis in mice, whereas its overexpression is associated with cancer progression of human melanoma, esophageal, breast and colon. The molecular reasons for such dramatic change in SKI function appear to result from new acquired activities. In this review, we discuss the mechanisms by which SKI regulates crucial pathways involved in the progression of human malignant melanoma.

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Murine models of malignant melanoma

Cited by 18 publications

References 5 publications

The antitumor effects of interferon-alpha are maintained in mice challenged with a STAT1-deficient murine melanoma cell line

The antitumor effects of interferon-alpha are maintained in mice challenged with a STAT1-deficient murine melanoma cell line

A Comparative Review of Melanocytic Neoplasms

SKI pathways inducing progression of human melanoma

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