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Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 1063))

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Abstract

Despite advances in screening, therapy, and surveillance that have improved survival rates, breast cancer is still the most commonly diagnosed cancer and the second leading cause of cancer mortality among women [1]. Breast cancer is a highly heterogeneous disease rooted in a genetic basis and reflected in clinical behavior. The diversity of breast cancer hormone receptor status and the expression of surface molecules has guided therapy decisions for decades; however, subtype-specific treatment often yields diverse responses due to varying tumor evolution and malignant potential. Although understanding the mechanisms behind breast cancer heterogeneity is still a challenge, available evidence suggests that studying its metabolism has the potential to give valuable insight into the causes of these variations, as well as viable targets for intervention.

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Abbreviations

3HP:

3-Phosphohydroxypyruvate

3PG:

3-Phosphoglycerate

αKG:

Alpha-ketoglutarate

CK:

Choline kinase

COMT:

Catechol-O-methyltransferase

D-2HG:

D-2-hydroxyglutarate

E2:

17b-Estradiol

ER:

Estrogen receptor

GLUT:

Glucose transporter

GSTP:

Glutathione S-transferase P

HER2:

Human epidermal growth factor receptor 2

PCho:

Phosphocholine

PHGDH:

Phosphoglycerate dehydrogenase

PR:

Progesterone receptor

PSAT1:

Phosphoserine aminotransferase 1

PSPH:

Phosphoserine phosphatase

PtdCho:

Phosphatidylcholine

TCA:

Tricarboxylic acid

TNBC:

Triple-negative breast cancer

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Correspondence to Anne Le .

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Tan, J., Le, A. (2018). Breast Cancer Metabolism. In: Le, A. (eds) The Heterogeneity of Cancer Metabolism. Advances in Experimental Medicine and Biology, vol 1063. Springer, Cham. https://doi.org/10.1007/978-3-319-77736-8_6

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