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Breast Cancer FISH Probes

In breast cancer, estrogen has been shown to stimulate overexpression of the BCL2 antiapoptotic protein. Therefore, BCL2-positive expression in breast cancer is considered a sign of estrogen receptor (ER) functional activity, and associated with ER+ biological/clinical features.

Breast cancer is the most common cancer in patients harboring germline BRCA1 or BRCA2 mutations, with a lifetime risk ranging from 46% to 87%. Truncating mutations are considered major oncogenic drivers, and have been found throughout BRCA2.

CCND1 gene amplification is observed in about 5-20% of invasive breast cancer cases, and overexpression of its protein in some 40-90% of patients. The gene is a primary contributor to estrogen-induced BC, as ER signaling is mediated through transcriptional activation of CCND1 and MYC.

CDK4 mediates pathways that play a key role in the proliferation of both normal breast epithelium and breast cancer cells. The gene's protein binds CCND1, which is a transcriptional target of estrogen receptor, to promote transition of ER+ cells from G1 to S phase.

CHEK1 regulates a DNA damage response pathway critical to maintenance of genome stability. CHEK1's interaction with BRCA1 (one of the most well-established breast cancer suppressor genes) at the G2M checkpoint has been implicated as evidence of its significance in BC.

CREB1 is overexpressed in BC tumors. The gene is a transcriptional activator of several antiapoptotic genes, including BRCA1 and BCL2. Recent studies point to CREB1 as an enhancer of aromatase transactivation in BC cells.

EGFR's downstream signaling pathways are essential to cell cycle regulation and survival of breast epithelial cells. Overactivation of these pathways is associated with BC development and therapeutic resistance.

ERBB2 is one of the most well-studied oncogenes in breast cancer. Amplification of the gene results in deregulated RAS/RAF/MAPK pathways that monitor cell survival and proliferation, leading to the development of particularly aggressive tumors.

Gain of function mutations in ESR1 are found in around 20% of patients with metastatic ER+ disease who have received endocrine therapy. These mutations are clustered in a hotspot within the ligand-binding domain of the ER, and result in ligand-independent ER activity.

ETV6/NTRK3 fusion is a genetic hallmark of secretory breast carcinoma (SBC), occurring in over 90% of cases. The fusion gene encodes a chimeric tyrosine kinase with powerful transforming activity in several cell lineages, including fibroblasts and breast epithelial cells. It also activates RAS-MAPK and PI3K-Akt pathways crucial to breast cell proliferation and survival.

FGFR1 amplification is found in roughly 10% of breast cancer patients. Tumor cell lines with FGFR1 overexpression and amplification display enhanced ligand-dependent signaling, with increased activation of the MAPK and PI3K-AKT signaling pathways.

Genome-wide association studies have narrowed in on variants of the tumor suppressor gene FGFR2 as a genetic risk factor for breast cancer susceptibility. FGFR2 is amplified in 5-10% of breast tumors, and is strongly associated with ER+ disease.

Ectopic expression of HMGA2 upregulates migration and invasion of breast cancer cells, and protects cells against genotoxic agents via phosphorylation of P53. The gene has been proposed as a future treatment target.

Abnormally high levels of MDM2 protein are found in approximately 38% of breast cancers. Overexpression is most prevalent in ER+ and PR+ luminal cases. The gene has been shown to both downregulate ER-beta (a tumor suppressor that reduces BC cell migration) and upregulate ER-alpha (a tumor promoter).

MYB is highly expressed in ER+ breast cancer, as it's a direct target of ER signaling. The gene is essential for breast cancer cell proliferation, suppression of apoptosis and differentiation, and epithelial-mesenchymal transition.

MYB/NFIB fusion is a major driver of adenoid cystic breast carcinoma, a rare histological subtype of triple-negative BC. The abnormality is considered an early, disease-initiating event in tumor development.


MYC plays several roles in breast cancer development and progression. The gene is a key regulator of cell proliferation and transformation; its activation of various cell cycle regulators appears to be its major contribution to oncogenesis. MYC gene amplification has been detected in approximately 15% of BC.

Recent studies have indicated the PTEN tumor suppressor is underexpressed in nearly 40% of invasive BC cases. This reduction is associated with negative estrogen and progesterone receptor status.


Cytogenetic and CGH analyses have revealed recurrent somatic deletions in the long arm of chromosome 13 in BC. RB1 is located in one of these commonly deleted regions (13q14), and is lost in approximately 20% of triple-negative BC.

TERT copy number gains have been detected in more than 20% of primary breast tumors. In BC cells, MYC binds to an ETS2 site (EtsA) in the TERT promoter and increases TERT expression.

TOP2A is co-amplified with HER2 in about half of breast cancers; the gene is located close to HER2 on chromosome 17, so these amplicons span the entire genomic region housing both genes. TOP2A encodes a topoisomerase involved in resolving topological DNA problems.

The most common mutational sites in breast cancer are in the TP53 gene; roughly 30% of tumors bear TP53 mutations, usually deletions. TP53 mutations can occur in ductal carcinoma in situ prior to development of BC, and their frequency increases with increasing tumor grade.

XIST encodes a tumor suppressor that inhibits disease by decreasing AKT phosphorylation in BC cells. Its protein has been shown to be significantly reduced in tumor cells.

ZNF217 is a candidate oncogene found on chromosome 20q13.2, a region frequently amplified in BC. Overexpression of the gene promotes EMT and deregulates apoptotic signaling in tumor cells.