Therapy of muscle wasting in cancer: what is the future?

被引:31
作者
Muscaritoli, M
Bossola, M
Bellantone, R
Fanelli, FR
机构
[1] Univ Roma La Sapienza, Dept Clin Med, I-00185 Rome, Italy
[2] Catholic Univ Rome, Ist Clin Chirurg, Rome, Italy
关键词
cancer; cachexia; muscle wasting; therapy;
D O I
10.1097/01.mco.0000134366.07148.2e
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Purpose of review The aim of the present review is to provide insights into the future therapeutic approaches to cancer-related muscle wasting that flow from the progressive knowledge of mechanisms regulating muscle mass in health and disease. Recent findings Cancer cachexia is a severely debilitating and life-threatening paraneoplastic syndrome accounting for approximately 20% of cancer deaths. The prominent clinical feature of cancer cachexia is the progressive loss of muscle mass, which is substantially not reversible with any of the currently available nutritional, metabolic or pharmacological approaches. Cancer cachexia has long been considered a late event in the natural history of cancer patients, thus condemning them to merely palliative interventions. The accumulating evidence that the metabolic and molecular derangements ultimately leading to muscle wasting are operating early after tumour onset, even when weight loss is minimal or absent, is strengthening the view that cancer cachexia should be considered an early phenomenon. Summary Currently, despite scientific and economic efforts, the therapy of cancer-related muscle wasting has a poor success rate. Present knowledge of the intracellular mechanisms involved in muscle homeoastasis is prompting continuous research aimed at developing more effective and selective therapeutic tools for the prevention and treatment of muscle loss in cancer.
引用
收藏
页码:459 / 466
页数:8
相关论文
共 88 条
  • [1] AbuShakra S, 1997, J NEUROSCI RES, V47, P186, DOI 10.1002/(SICI)1097-4547(19970115)47:2<186::AID-JNR7>3.0.CO
  • [2] 2-B
  • [3] Potential for proteasome inhibition in the treatment of cancer
    Adams, J
    [J]. DRUG DISCOVERY TODAY, 2003, 8 (07) : 307 - 315
  • [4] Argiles J M, 1998, Curr Opin Clin Nutr Metab Care, V1, P245, DOI 10.1097/00075197-199805000-00002
  • [5] The acidosis of chronic renal failure activates muscle proteolysis in rats by augmenting transcription of genes encoding proteins of the ATP-dependent ubiquitin-proteasome pathway
    Bailey, JL
    Wang, XN
    England, BK
    Price, SR
    Ding, XY
    Mitch, WE
    [J]. JOURNAL OF CLINICAL INVESTIGATION, 1996, 97 (06) : 1447 - 1453
  • [6] BALLARD FJ, 1993, GROWTH REGULAT, V3, P40
  • [7] ACTIVATION OF THE ATP-UBIQUITIN-PROTEASOME PATHWAY IN SKELETAL-MUSCLE OF CACHECTIC RATS BEARING A HEPATOMA
    BARACOS, VE
    DEVIVO, C
    HOYLE, DHR
    GOLDBERG, AL
    [J]. AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM, 1995, 268 (05): : E996 - E1006
  • [8] The effect of an oral nutritional supplement enriched with fish oil on weight loss in patients with pancreatic cancer
    Barber, MD
    Ross, JA
    Voss, AC
    Tisdale, MJ
    Fearon, KCH
    [J]. BRITISH JOURNAL OF CANCER, 1999, 81 (01) : 80 - 86
  • [9] Bartsch W, 1993, Wien Med Wochenschr, V143, P363
  • [10] Signalling pathways involved in antiproliferative effects of IGFBP-3: a review
    Baxter, RC
    [J]. JOURNAL OF CLINICAL PATHOLOGY-MOLECULAR PATHOLOGY, 2001, 54 (03): : 145 - 148