Targeting phosphoinositide 3-kinase signalling in lung cancer

Wojtalla, Anna; Arcaro, Alexandre (2011). Targeting phosphoinositide 3-kinase signalling in lung cancer. Critical reviews in oncology, hematology, 80(2), pp. 278-90. Boca Raton, Fla.: Elsevier 10.1016/j.critrevonc.2011.01.007

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Lung cancer is the leading cause of cancer-related mortality worldwide and more than 1 million people annually die in consequence of lung cancer. Although an improvement in lung cancer treatment could be achieved, especially in the last decade, the development of additional therapeutic strategies is urgently required in order to provide improved survival benefit for patients. Lung cancer formation is caused by genetic modifications commonly caused by tobacco smoking. Numerous studies have demonstrated the role of extracellular growth factors in lung cancer cell proliferation, metastasis, and chemoresistance. Mutations and amplifications in molecules related to receptor tyrosine signalling, such as EGFR, ErbB2, c-Met, c-Kit, VEGFR, PI3K, and PTEN are only some of the alterations known to contribute to the development of lung cancer. The phosphoinositide 3-kinase (PI3K) pathway, fundamental for cell development, growth, and survival, is known to be frequently altered in neoplasia, including carcinomas of the lung. Based on the high frequency of alterations, which include mutations and amplifications, leading to over-activation of certain upstream/downstream mediators, targeting components of the PI3K signalling pathway is considered to be a promising therapeutic approach in cancer treatment. In this article we will summarize the current knowledge about the involvement of PI3K signalling in lung cancer and discuss the development of targeted therapies involving PI3K pathway inhibitors.

Item Type:

Journal Article (Further Contribution)

Division/Institute:

04 Faculty of Medicine > Department of Gynaecology, Paediatrics and Endocrinology (DFKE) > Clinic of Paediatric Medicine

UniBE Contributor:

Wojtalla, Anna and Arcaro, Alexandre

ISSN:

1040-8428

Publisher:

Elsevier

Language:

English

Submitter:

Factscience Import

Date Deposited:

04 Oct 2013 14:24

Last Modified:

06 Dec 2013 13:29

Publisher DOI:

10.1016/j.critrevonc.2011.01.007

PubMed ID:

21316260

Web of Science ID:

000296683200008

URI:

https://boris.unibe.ch/id/eprint/8328 (FactScience: 213849)

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