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Melanoma FISH Probes

BCL2 inhibits apoptosis and provides a growth advantage to metastatic melanoma cells. The gene is a key regulator of apoptosis pathways blocking the effective oligomerization of Bax and Bak, thereby protecting against cell death.

Activating BRAF mutations occur in about half of cutaneous melanoma cases with non-chronic sun damage. The gene plays an important role in MAPK signaling, which is known to be deregulated across melanoma subtypes.

CCND1, which regulates G1/S phase transition, is influenced by upstream melanoma oncogenes BRAF and NRAS. The gene is frequently amplified in acral melanomas, especially in lesions with chronic sun damage.

The CDK4 pathway is deregulated in 90% of melanomas. CDK4 inhibits retinoblastoma protein, and phosphorylates other proteins that promote cell-cycle progression. CDK4 overactivation inhibits both cell senescence and apoptosis.

CDKN2A acts as a critical tumor suppressor in melanoma, as evidenced by frequent loss of function mutations and deletions.

PAX3 is considered a biomarker for non-chronic-sun-damaged melanoma. Studies have shown that the gene drives CXCRF/MET proto-oncogene tyrosine kinase expression in melanoma, promoting tumor growth and metastasis.

In most melanomas, PD-1 expression is upregulated on T-cells in response to an increased load of tumor neoantigens. Tumor cells respond by increasing PDL-1 expression on their surfaces, effectively escaping immune surveillance.

Amplifications in the p arm of chromosome 6 are common across all melanoma subtypes. RREB1 lies in one of the frequently amplified regions, 6p25.

A recent study detected TERT gene amplification in 44.9% (257/573) of acral melanoma patients, while TERT promoter mutations can be found in up to 50% of cutaneous melanomas. TERT operates downstream of RAS-ERK, a central oncogenic pathway in melanoma.