Connecting the Metabolic and Immune Responses to Cancer

被引：51

作者：

Flint, Thomas R. ^{[1
,2
]}

Fearon, Douglas T. ^{[1
,3
,4
]}

Janowitz, Tobias ^{[1
,5
]}

机构：

[1] Univ Cambridge, Canc Res UK Cambridge Inst, Li Ka Shing Ctr, Cambridge CB2 0RE, England

[2] Univ Cambridge, Sch Clin Med, Addenbrookes Hosp, Cambridge CB2 0SP, England

[3] Cold Spring Harbor Lab, POB 100, Cold Spring Harbor, NY 11724 USA

[4] Weill Cornell Med Coll, New York, NY 10021 USA

[5] Univ Cambridge, Addenbrookes Hosp, Dept Oncol, Cambridge CB2 0QQ, England

来源：

TRENDS IN MOLECULAR MEDICINE | 2017年 / 23卷 / 05期

基金：

英国惠康基金;

关键词：

CELL LUNG-CANCER; SKELETAL-MUSCLE UCP2; WHITE ADIPOSE-TISSUE; ANTITUMOR IMMUNITY; GENE-EXPRESSION; PD-1; BLOCKADE; WEIGHT-LOSS; ANTI-PD-L1; ANTIBODY; ACTRIIB ANTAGONISM; CTLA-4;

D O I：

10.1016/j.molmed.2017.03.001

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Separate research fields have advanced our understanding of, on the one hand, cancer immunology and, on the other hand, cachexia, the fatal tumor-induced wasting syndrome. A link between the host's immune and metabolic responses to cancer remained unexplored. Emerging work in preclinical models of colorectal and pancreatic cancer has unveiled tumor-induced reprogramming of liver metabolism in cachexia that leads to suppression of antitumor immunity and failure of immunotherapy. As research efforts in metabolism and immunology in cancer are rapidly expanding, it is timely to discuss the metabolic and immunological determinants of the cancer-host interaction. We also present the hypothesis that the convergence of host metabolism and antitumor immunity may offer a platform for biomarker-driven investigations of new combination therapies.

引用

页码：451 / 464

页数：14

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