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Related Experiment Video

Updated: Mar 7, 2026

A Robust Discovery Platform for the Identification of Novel Mediators of Melanoma Metastasis

A Robust Discovery Platform for the Identification of Novel Mediators of Melanoma Metastasis

Published on: March 8, 2022

Melanoma genome evolution across species.

Emily R Kansler¹, Akanksha Verma², Erin M Langdon¹

¹Memorial Sloan Kettering Cancer Center, Cancer Biology & Genetics, New York, USA.

|February 9, 2017

Summary

Cross-species oncogenomics in zebrafish identified conserved genetic alterations in melanoma progression and vemurafenib resistance. Targeting these shared changes may offer new therapeutic strategies for human melanoma patients.

Keywords:

Cancer Drug-resistance Melanoma Zebrafish

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Area of Science:

Oncogenomics
Comparative genomics
Cancer biology

Background:

Melanoma evolution is complex, with genetic heterogeneity driving tumor progression and drug resistance.
High mutation rates in human melanoma, particularly from UV radiation, obscure key evolutionary events.
Cross-species oncogenomics, comparing animal models to human cancers, aids in identifying conserved, mechanistically important alterations.

Purpose of the Study:

To utilize a zebrafish model for cross-species genomic analysis of melanoma tumor progression and drug resistance.
To identify conserved genetic and transcriptomic alterations between zebrafish and human melanoma.

Main Methods:

Initiation of zebrafish transgenic melanoma with BRAF^V600E and p53^-/- genetic lesions.
Whole genome sequencing of tumors before and after vemurafenib treatment to identify DNA mutations.
Transcriptome analysis to assess changes in gene expression, focusing on signaling pathways.
Comparison of identified zebrafish alterations with a panel of human melanoma genomic and transcriptomic data.

Main Results:

Zebrafish tumors accumulated over 3,000 mutations during progression.
Drug-resistant tumors acquired specific DNA mutations in BUB1B, PINK1, and COL16A1.
Significant transcriptomic reorganization occurred, involving over 800 genes and altered cAMP/PKA signaling.
Identified DNA and RNA alterations showed significant enrichment in human vemurafenib-resistant melanoma.

Conclusions:

Conserved genetic alterations between zebrafish and human melanoma suggest potential therapeutic targets.
Targeting these conserved alterations may provide novel therapeutic strategies for melanoma.
Zebrafish cancer models offer a powerful platform for informing human cancer genomics and drug discovery.