On our way to targeted therapy for cachexia in cancer?

被引:23
作者
Boddaert, Manon S. A. [1 ]
Gerritsen, Winald R. [1 ]
Pinedo, Herbert M. [1 ]
机构
[1] Vrije Univ Amsterdam Med Ctr, Ctr Canc Amsterdam, Dept Med Oncol, NL-1081 HV Amsterdam, Netherlands
关键词
cachexia; cancer; pathogenesis; targeted therapy;
D O I
10.1097/01.cco.0000228738.85626.ac
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Purpose of review Cachexia, the occurance of involuntary weight loss due to loss of adipose tissue and skeletal muscle mass, is among the most common and devestating symptoms in patients with advanced cancer. It is a significant factor contributing to the poor performance status and high mortality rate of these patients, and is a distressing problem for both patients and their families. Despite extensive research in an attempt to better understand the mechanisms involved, progress in the management of cancer cachexia has been slow. Recent findings The pathogenic mechanisms of cachexia and anorexia are multifactorial, but cytokines and tumour-derived factors are known to play a significant role, thereby representing suitable therapeutic targets. Moreover, recent advances in the field of molecular biology have shed light on other mediators involved in the mechanisms leading to muscle wasting, thus increasing potential targets for new therapies. Summary This review will focus on recent findings in relation to the molecular pathways leading to muscle wasting that have improved our current understanding of cachexia and will direct the future management of cachexia in cancer towards targeted therapies.
引用
收藏
页码:335 / 340
页数:6
相关论文
共 56 条
[1]   Cancer cachexia is regulated by selective targeting of skeletal muscle gene products [J].
Acharyya, S ;
Ladner, KJ ;
Nelsen, LL ;
Damrauer, J ;
Reiser, PJ ;
Swoap, S ;
Guttridge, DC .
JOURNAL OF CLINICAL INVESTIGATION, 2004, 114 (03) :370-378
[2]   Ubiquitin-proteasome-dependent proteolysis in skeletal muscle [J].
Attaix, D ;
Aurousseau, E ;
Combaret, L ;
Kee, A ;
Larbaud, D ;
Ralliere, C ;
Souweine, B ;
Taillandier, D ;
Tilignac, T .
REPRODUCTION NUTRITION DEVELOPMENT, 1998, 38 (02) :153-165
[3]   The effect of an oral nutritional supplement enriched with fish oil on weight loss in patients with pancreatic cancer [J].
Barber, MD ;
Ross, JA ;
Voss, AC ;
Tisdale, MJ ;
Fearon, KCH .
BRITISH JOURNAL OF CANCER, 1999, 81 (01) :80-86
[4]   Viral mediated expression of insulin-like growth factor I blocks the aging-related loss of skeletal muscle function [J].
Barton-Davis, ER ;
Shoturma, DI ;
Musaro, A ;
Rosenthal, N ;
Sweeney, HL .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1998, 95 (26) :15603-15607
[5]   Akt/mTOR pathway is a crucial regulator of skeletal muscle hypertrophy and can prevent muscle atrophy in vivo [J].
Bodine, SC ;
Stitt, TN ;
Gonzalez, M ;
Kline, WO ;
Stover, GL ;
Bauerlein, R ;
Zlotchenko, E ;
Scrimgeour, A ;
Lawrence, JC ;
Glass, DJ ;
Yancopoulos, GD .
NATURE CELL BIOLOGY, 2001, 3 (11) :1014-1019
[6]   Identification of ubiquitin ligases required for skeletal muscle atrophy [J].
Bodine, SC ;
Latres, E ;
Baumhueter, S ;
Lai, VKM ;
Nunez, L ;
Clarke, BA ;
Poueymirou, WT ;
Panaro, FJ ;
Na, EQ ;
Dharmarajan, K ;
Pan, ZQ ;
Valenzuela, DM ;
DeChiara, TM ;
Stitt, TN ;
Yancopoulos, GD ;
Glass, DJ .
SCIENCE, 2001, 294 (5547) :1704-1708
[7]   ABC of palliative care - Anorexia, cachexia, and nutrition [J].
Bruera, E .
BRITISH MEDICAL JOURNAL, 1997, 315 (7117) :1219-1222
[8]   The potential role of proteasome inhibitors in the treatment of lung cancer [J].
Bunn, PA .
CLINICAL CANCER RESEARCH, 2004, 10 (12) :4263S-4265S
[9]   IKKβ/NF-κB activation causes severe muscle wasting in mice [J].
Cai, DS ;
Frantz, JD ;
Tawa, NE ;
Melendez, PA ;
Oh, BC ;
Lidov, HGW ;
Hasselgren, PO ;
Frontera, WR ;
Lee, J ;
Glass, DJ ;
Shoelson, SE .
CELL, 2004, 119 (02) :285-298
[10]   NF-κB-mediated MyoD decay during muscle wasting requires nitric oxide synthase mRNA stabilization, HuR protein, and nitric oxide release [J].
Di Marco, S ;
Mazroui, R ;
Dallaire, P ;
Chittur, S ;
Tenenbaum, SA ;
Radzioch, D ;
Marette, A ;
Gallouzi, IE .
MOLECULAR AND CELLULAR BIOLOGY, 2005, 25 (15) :6533-6545