Table 1.

Metabolic changes in the intrinsic subtypes of breast cancer. Empty squares stand for no data. Abbreviations: ASCT2/SLC1A5, amino acid transporter-2; ER, estrogen receptor; GDH/H6PD, glutamate dehydrogenase; GLS1, glutaminase 1; HER2, human epidermal growth factor 2 receptor; PgR, progesterone receptor; SLC, solute carrier transporters.

	Breast Cancer	Luminal A	Luminal B		HER2+	TNBC (~Basal-like)	Ref.
			HER2−	HER2+
Receptor Status according to [1]	N/A	ER+, HER2−, Ki67 low, PgR high Low-Risk Molecular Signature (If Available)	ER+, HER2−, either Ki67high or PgR low High-Risk Molecular Signature (If Available)	ER+, HER2+, any Ki67, any PgR	HER2+, ER−, and PgR−	HER2-, ER-, and PgR−	[1]
Cholesterol and oxysterol metabolism	Lipid and cholesterol metabolism supports tamoxifen resistance. Increases in serum cholesterol is a risk factor for breast cancer.	27-hydroxycholesterol supports the growth of ER+ breast cancer cells	27-hydroxycholesterol supports the growth of ER+ breast cancer cells	27-hydroxycholesterol supports the growth of ER+ breast cancer cells			[62,63,64,65,66,67,68]
Glycolysis	upregulated	low	intermediate/low	intermediate/low	intermediate/low	high	[69,70,71,72]
Pentose-phosphate pathway	upregulated	low	low	low	high	highest	[73]
Glutamine-proline-glycine metabolism	upregulated to serve energy homeostasis and protein and nucleotide biosynthesis	SLC6A14, SLC7A11 upregulated	High expression of glutamine-proline enzymes in Mychigh tumors SLC6A14, SLC7A11 upregulated	High expression of glutamine-proline enzymes in Myc high tumors SLC6A14, SLC7A11 upregulated	highest expression of GLS1, GDH, ASCT, SLC7A5, SLC1A5 upregulated highest level of glutamine metabolism among the intrinsic types	SLC7A11, SLC1A5 upregulated increased glutamine uptake	[37,38,39,74,75]
Protein translation	upregulated	highest	high	high			[76,77,78]