Table 4.

Therapeutic implications for fusions reported in breast cancer.

FUSION	ONCOGENIC FUNCTION	PREVALENCE IN OTHER CANCERS	POTENTIAL DRUGS/THERAPIES	BREAST CANCER SUBTYPE
ETV6-NTRK368,104–108	Promotes transformation and tumor formation	Mesoblastic nephroma, congenital fibrosarcoma, acute myeloid leukemia, salivary gland secretory carcinoma	Small molecule broad-spectrum kinase inhibitors, NTRK inhibitors, IGF1R/INSR inhibitors	Secretory breast cancer
ESR1-CCDC17095	Increases cell motility, anchorage-independent growth, reduced endocrine sensitivity and xenograft tumor formation	ND	Precise oncogenic pathways involved under investigation	ER+ (luminal B)
MAGI3-AKT396	Constitutive activation of the AKT3 kinase domain and downstream signaling, loss of contact inhibition	ND	ATP-competitive Akt inhibitors, mTOR inhibitors	TNBC
ERBB2-fusions89,109	ND	ND	HER2-targeting agents	Relapsed invasive lobular breast cancer, invasive carcinoma
SCNN1A-TNFRSF1A93	ND	ND	Unknown	ER+, TNBC, breast cancer cell lines
CTSD-IFITM1093	siRNA knockdown decreases live cells	ND	Unknown	ER+, TNBC, breast cancer cell lines
EML4-ALK112,113	Growth inhibition in some cell lines upon EML4 or ALK siRNA knockdown	Colorectal cancer, NSCLC	ALK inhibitors	Basal, luminal, and HER2+ breast cancers, inflammatory breast cancer, breast cancer cell lines
ERC1–RET3,34	ND	Thyroid cancer	RET inhibitors	Invasive carcinoma
TBL1XR1–PIK3CA3,98	ND	Prostate adenocarcinoma	PI3K, AKT or mTOR inhibitors	Invasive carcinoma, metaplastic breast cancer

Abbreviations: ND, not determined; ER+, estrogen receptor positive; TNBC, triple negative breast cancer; siRNA, small interfering RNA; NSCLC, non-small cell lung cancer.