A tumoros cachexia molekuláris háttere.

Translated title of the contribution: Molecular mechanisms of cancer cachexia

Adám Lelbach, G. Müzes, J. Fehér

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

Molecular mechanisms of cancer cachexia. Cancer cachexia is a complex, multifactorial syndrome characterised by a critical weight loss, anorexia, asthenia and anaemia. Most of the patients with advanced cancer suffer from cancer cachexia. The cachectic state is closely associated with progressive expansion of the tumour and leads to a malnutrition status due to the induction of anorexia and decreased food intake. In addition, the competition for nutrients between the tumour and the host leads to malnutrition state, too, which promotes severe metabolic disturbances in the host, including hypermetabolism which leads to an increased energetic inefficiency. Although, the search for the cachectic factors has a long history, we are still far away from knowing the complete answer. The main aim of the present paper is to summarise the different catabolic mediators involved in cancer cachexia. Better understanding of the pathomechanism of cancer cachexia can lead to the discovery of new, effective strategies of the therapy for the future.

Original languageHungarian
Pages (from-to)2329-2334
Number of pages6
JournalOrvosi Hetilap
Volume145
Issue number46
Publication statusPublished - Nov 14 2004

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Cachexia
Neoplasms
Anorexia
Malnutrition
Asthenia
Anemia
Weight Loss
Eating
History
Food

ASJC Scopus subject areas

  • Medicine(all)

Cite this

A tumoros cachexia molekuláris háttere. / Lelbach, Adám; Müzes, G.; Fehér, J.

In: Orvosi Hetilap, Vol. 145, No. 46, 14.11.2004, p. 2329-2334.

Research output: Contribution to journalArticle

Lelbach, A, Müzes, G & Fehér, J 2004, 'A tumoros cachexia molekuláris háttere.', Orvosi Hetilap, vol. 145, no. 46, pp. 2329-2334.
Lelbach, Adám ; Müzes, G. ; Fehér, J. / A tumoros cachexia molekuláris háttere. In: Orvosi Hetilap. 2004 ; Vol. 145, No. 46. pp. 2329-2334.
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