Strategies for multiple signalling inhibition

G. Tortora, R. Bianco, G. Daniele

Research output: Contribution to journalArticle

Abstract

Cancer cells hyperactivate signalling molecules, including EGFR, Akt and the angiogenic factor VEGF to escape apoptosis, thus contributing also to resistance to treatment. While single signalling inhibitors have produced limited advantages in clinical trials, their combination with conventional treatments is more effective; however, the rate of responses is generally around 20%. A major limitation is represented by the activation of escape pathways, due to an intensive cross-talk and redundancy of signals in the transduction network. A novel and more rational approach is the combination of multiple signalling inhibitors, according to the molecular context of disease, in combination with selected conventional treatments.

Original languageEnglish
Pages (from-to)41-43
Number of pages3
JournalJournal of Chemotherapy
Volume16
Issue numberSUPPL. 4
Publication statusPublished - Nov 2004

Fingerprint

Angiogenesis Inducing Agents
Vascular Endothelial Growth Factor A
Signal Transduction
Clinical Trials
Apoptosis
Neoplasms

Keywords

  • EGFR
  • Therapeutic strategies
  • VEGF

ASJC Scopus subject areas

  • Pharmacology (medical)
  • Microbiology (medical)

Cite this

Tortora, G., Bianco, R., & Daniele, G. (2004). Strategies for multiple signalling inhibition. Journal of Chemotherapy, 16(SUPPL. 4), 41-43.

Strategies for multiple signalling inhibition. / Tortora, G.; Bianco, R.; Daniele, G.

In: Journal of Chemotherapy, Vol. 16, No. SUPPL. 4, 11.2004, p. 41-43.

Research output: Contribution to journalArticle

Tortora, G, Bianco, R & Daniele, G 2004, 'Strategies for multiple signalling inhibition', Journal of Chemotherapy, vol. 16, no. SUPPL. 4, pp. 41-43.
Tortora G, Bianco R, Daniele G. Strategies for multiple signalling inhibition. Journal of Chemotherapy. 2004 Nov;16(SUPPL. 4):41-43.
Tortora, G. ; Bianco, R. ; Daniele, G. / Strategies for multiple signalling inhibition. In: Journal of Chemotherapy. 2004 ; Vol. 16, No. SUPPL. 4. pp. 41-43.
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