. Author manuscript; available in PMC: 2018 Jun 11.

Published in final edited form as: Expert Opin Pharmacother. 2015 May;16(7):983–998. doi: 10.1517/14656566.2015.1032246

Table 2.

Targeting ‘driver’ signaling pathways identified in GSE-A of triple negative breast cancer subtypes.

Subtypes	‘Driver’ pathways	Representative cell lines	Agents
BL1	Cell cycle, DNA damage response	HCC2157^, HCC1599^‡, HCC1937^, HCC1143, HCC3153^*, MDA-MB-468, HCC38	Cisplatin, Poly(ADP-ribose)polymerase inhibitors (veliparib, olaparib)
BL2	Cell cycle, DNA damage response, growth factor signaling	SUM149PT^*, CAL-851, HCC70, HCC1806, HDQ-P1
Immunomodulary	Immune signaling, cytokine signaling, antigen presentation	HCC1187, DU4475
Mesenchymal	Cell motility, ECM receptor interactions, cell differentiation	BT-549, CAL-51^§, CAL-120	Abl/Src inhibitor (dasatinib), PI3K/mTOR inhibitor (NVP-BEZ235)
Mesenchymal-stem cell-like	Cell motility, cell differentiation, growth factor signaling	Hs578T, MDA-MB-157, SUM159PT^§, MDA-MB-436^*, MDA-MB-231
Luminal androgen receptor	Steroid synthesis and metabolism	MDA-MB-453^§, SUM185PE^§, CAL-148^§, MFM-223^§	Bicalutamide, Hsp90 inhibitor (17-DMAG), PI3K/mTOR inhibitor (NVP-BEZ235)

BRCA2 mutant,

^‡

BRCA1 mutant,

^§

PIK3CA mutant.

Data taken from [13].

BL: Basal-like; ECM: Extracellular matrix; GSE-A: Gene set enrichment analysis; mTOR: Mammalian target of rapamycin; PI3K: Phosphatidylinositide 3-kinase.