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Colorectal Cancer FISH Probes

BRAF mutations can be found in about 10% of CRC patients. CRC cells use BRAF amplification to maintain signaling of the oncogenic ERK pathway required for proliferation and therapeutic resistance.

EGFR amplification is associated with metastatic CRC; it is required for tumor cell proliferation, with cells likely addicted to aberrant EGFR signaling for growth.

ERBB2 amplification is an emerging biomarker in colon cancer. Studies show that ERBB2 amplification/overexpression occurs rarely in stage II & III CRC, rising in stage IV and further in KRAS/BRAF WT tumors.


MET encodes a receptor tyrosine kinase that regulates invasive tumor growth through the coordination of cell proliferation, survival, EMT, and migration/invasion. Recent meta-analyses indicate that the MET protein is overexpressed in up to 78% of CRC.

Loss of PTEN, a tumor suppressor that downregulates the PI3K pathway, drives metastasis in CRC. While PTEN deletion has been found in 20-49% of early-stage CRC, the gene is deleted in up to 83% of metastatic cases.


RET is a proposed tumor suppressor in CRC. Inactivation of RET has been shown to promote the formation of CRC by downregulating RET-induced apoptosis in tumor cells.

WWTR1 promotes CRC progression via co-regulation with two of its downstream target genes, AXL and CTGF. Upregulation of the signaling pathway leads to aberrant cell migration, angiogenesis, and calcium signaling.

ZNF217 lies on the q arm of chromosome 20, a region amplified in over 20% of locally advanced CRC. Amplification likely contributes to CRC progression by stimulating uncontrolled cell proliferation and overcoming cell senescence.