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Breast Cancer Metabolism

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

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.

Keywords

Breast cancer Estrogen receptor status Metabolic fingerprint Choline metabolism Estrogen metabolism Serine biosynthesis Glycolytic upregulation 

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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Copyright information

© Springer International Publishing AG, part of Springer Nature 2018

Authors and Affiliations

  1. 1.Department of PathologyJohns Hopkins University School of MedicineBaltimoreUSA
  2. 2.Department of Pathology and OncologyJohns Hopkins University School of MedicineBaltimoreUSA

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