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The Metabolism of Renal Cell Carcinomas and Liver Cancer

  • Chapter
The Heterogeneity of Cancer Metabolism

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

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Abstract

According to data from the American Cancer Society, cancer is one of the deadliest health problems globally. Annually, renal cell carcinoma (RCC) and liver cancer cause more than 100,000 and 800,000 deaths worldwide, respectively [1–4], creating an urgent need to develop effective therapeutic treatments to increase patient survival outcomes. New therapeutic treatments are expected to address a major factor contributing to cancer’s resistance to standard therapies: oncogenic heterogeneity. Because gene expression can vary tremendously among different types of cancers, different patients of the same tumor type, and even within individual tumors, various metabolic phenotypes can emerge, making single-therapy approaches insufficient. This heterogeneity translates into changes in the landscape of metabolic enzymes and biomolecules within both the cancer cell and tumor microenvironment. Novel strategies targeting the diverse metabolism of cancers aim to overcome this obstacle, and though some have yielded positive results, it remains a challenge to uncover all of the distinct metabolic profiles of RCC and liver cancer. Nonetheless, the metabolic-oriented research focusing on these cancers has offered different, fresh new perspectives, which are expected to contribute heavily to the development of new therapeutic treatments.

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Abbreviations

α-KG:

α-Ketoglutarate

ACC:

Acetyl-CoA carboxylase

AMPK:

AMP-activated protein kinase

ATP:

Adenosine triphosphate

ccRCC:

Clear-cell renal cell carcinoma

CL:

Cardiolipin

COX5B:

Cytochrome C oxidase subunit 5B

DEN:

Diethylnitrosamine

ePC:

Ether-type phosphatidylcholine

ePE:

Ether-type PE

ERRα:

Estrogen-related receptor Α

FASN:

Fatty acid synthase

FH:

Fumarate hydratase

G6PH:

Glucose-6-phosphate dehydrogenase

GLS2:

Glutaminase 2

Glu:

Glutamine

GLUT1:

Glucose transporter 1

GLUT2:

Glucose transporter 2

HCC:

Hepatocellular carcinoma

HIF:

Hypoxia-inducible factor

HIF-1α:

Hypoxia-inducible factor 1-alpha

HK2:

Hexokinase 2

LCSCs:

Liver cancer stem cells

LDHA:

Lactate dehydrogenase A

LRH-1:

Liver receptor homolog 1

Me1:

Malic enzyme 1

MIR21:

MicroRNAs-21

mTORC1:

Mechanistic target of rapamycin complex 1

NADPH:

Nicotinamide adenine dinucleotide phosphate

Non-LCSCs:

Non-liver cancer stem cells

PE:

Phosphatidylethanolamine

PGK1:

Phosphoglycerate kinase 1

PGLS:

6-Phosphogluconolactonase

PI3K:

Phosphatidylinositol-3 kinases

PTEN:

Phosphatase and tensin homolog deleted in chromosome 10

RCC:

Renal cell carcinoma

ROS:

Reactive oxygen species

SM:

Sphingomyelin

STF-31:

4-[[[[4-(1,1-Dimethylethyl)phenyl]sulfonyl]amino]methyl]-N-3-pyridinyl-benzamide

TALDO:

Transaldolase

TKT:

Transketolase

TSC2:

Tuberous sclerosis 2

VEGFR:

Vascular endothelial growth factor receptor

VHL :

Von Hippel-Lindau tumor suppressor gene

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Author information

Authors and Affiliations

  1. Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, USA

    Tu Nguyen

  2. Department of Pathology and Oncology, Johns Hopkins University School of Medicine, Baltimore, MD, USA

    Anne Le

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  1. Tu Nguyen
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Correspondence to Anne Le .

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  1. Johns Hopkins Medicine, Baltimore, MD, USA

    Anne Le MD, HDR

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Nguyen, T., Le, A. (2018). The Metabolism of Renal Cell Carcinomas and Liver Cancer. 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_8

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