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The Metabolic Profiles in Hematological Malignancies

  • Tao Liu
  • Xing-Chun Peng
  • Bin LiEmail author
Review Article
  • 45 Downloads

Abstract

Leukemia is one of the most aggressive hematological malignancies. Leukemia stem cells account for the poor prognosis and relapse of the disease. Decades of investigations have been performed to figure out how to eradicate the leukemia stem cells. It has also been known that cancer cells especially solid cancer cells use energy differently than most of the cell types. The same thing happens to leukemia. Since there are metabolic differences between the hematopoietic stem cells and their immediate descendants, we aim at manipulating the energy sources with which that could have an effect on leukemia stem cells while sparing the normal blood cells. In this review we summarize the metabolic characteristics of distinct leukemias such as acute myeloid leukemia, chronic myeloid leukemia, T cell lymphoblastic leukemia, B-cell lymphoblastic leukemia, chronic lymphocytic leukemia and other leukemia associated hematological malignancies such as multiple myeloma and myelodysplastic syndrome. A better understanding of the metabolic profiles in distinct leukemias might provide novel perspectives and shed light on novel metabolic targeting strategies towards the clinical treatment of leukemias.

Keywords

Hematological malignancies Leukemia stem cells Metabolism 

Abbreviations

AML

Acute myeloid leukemia

CML

Chronic myeloid leukemia

T-ALL

T-cell lymphoblastic leukemia

B-ALL

B-cell lymphoblastic leukemia

CLL

Chronic lymphocytic leukemia

MM

Multiple myeloma

MDS

Myelodysplastic syndrome

LSCs

Leukemia stem cells

OXPHOS

Oxidative phosphorylation

FAO

Fatty acid oxidation

PPP

Pentose phosphate pathway

Glut1

Glucose transporter 1

Ara-C

Arabinofuranosyl cytidine

2-DG

2-Deoxy-d-glucose

RTKs

Receptor tyrosine kinases

ROS

Reactive oxygen species

CSCs

Cancer stem cells

PPARγ

Proliferator-activated receptor gamma ligands

CPT1

Carnitine O-palmitoyltransferase I

GAT

Gonadal adipose tissue

GA

Glutaminase

IDH1/2

Isocitrate dehydrogenase 1 and 2

PHGDH

Phosphoglycerate dehydrogenas

I-ASP

l-Asparaginase

GS

Glutamine synthase

ASNS

Asparagine synthetase

PRC2

Polycomb repressive complex 2

Notes

Acknowledgements

This study was supported by grants from Project of Shanghai Municipal Health Bureau (Surface Program, SHXH201402).

Authors’ Contribution

All authors read and approved the final manuscript. BL designed the manuscript and TL and XP wrote the review.

Compliance with Ethical Standards

Conflict of interest

The authors declare that they have no conflict of interest.

Ethics approval and consent to participate

All authors are compliant with ethical standards.

Consent for publication

All authors approve the manuscript for publication.

Availability of data and materials

Data and materials related to this work are available upon request.

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Copyright information

© Indian Society of Hematology and Blood Transfusion 2019

Authors and Affiliations

  1. 1.Department of PathologyPeople’s Hospital of LonghuaShenzhenPeople’s Republic of China
  2. 2.Department of Pathology, Shanghai Xuhui Central Hospital, Zhongshan-Xuhui Hospital, Fudan University, Shanghai Clinical CenterCASShanghai CityPeople’s Republic of China

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