Driver mutations and differential sensitivity to targeted therapies: a new approach to the treatment of lung adenocarcinoma

Nicolo' Gebbia, Giuseppe Bronte, Viviana Bazan, Antonio Russo, Laura La Paglia, Sergio Siragusa, Sergio Siragusa, Corrado Ficorella, Vincenzo Adamo, Giuseppe Colucci, Daniele Santini, Sergio Rizzo

Risultato della ricerca: Article

95 Citazioni (Scopus)

Abstract

The adenocarcinoma of the lung has recently shown peculiar molecular characteristics, which relate with both carcinogenesis and response to targeted drugs. Several molecular alterations have been defined as "driver mutations". These are responsible for both the initiation and maintenance of the malignancy. The epidermal growth factor receptor (EGFR) pathway is the main regulator of cell function and cancer development. It has a widely defined role in the occurrence of driver mutations. Up till now EGFR gene mutations, KRAS gene mutations and EML4-ALK fusion genes are the most widely recognized alterations involved in both the biology and the clinical management of lung adenocarcinoma. In this review we report the molecular bases that have led to the clinical application of the detection for such genetic impairments. Subsequently we discuss the clinical studies regarding the prognostic role and the predictive value for response to anti-EGFR tyrosine kinase inhibitors (TKI) of the same mutations. We also provide a potential algorithm as a guide in the choice of the best treatment for patients with adenocarcinoma.
Lingua originaleEnglish
pagine (da-a)21-29
Numero di pagine9
RivistaDefault journal
Volume36 (3)
Stato di pubblicazionePublished - 2010

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Mutation
Epidermal Growth Factor Receptor
erbB-1 Genes
Therapeutics
Gene Fusion
Protein-Tyrosine Kinases
Neoplasms
Carcinogenesis
Adenocarcinoma
Maintenance
Adenocarcinoma of lung
Pharmaceutical Preparations
Genes

All Science Journal Classification (ASJC) codes

  • Oncology
  • Radiology Nuclear Medicine and imaging

Cita questo

Driver mutations and differential sensitivity to targeted therapies: a new approach to the treatment of lung adenocarcinoma. / Gebbia, Nicolo'; Bronte, Giuseppe; Bazan, Viviana; Russo, Antonio; La Paglia, Laura; Siragusa, Sergio; Siragusa, Sergio; Ficorella, Corrado; Adamo, Vincenzo; Colucci, Giuseppe; Santini, Daniele; Rizzo, Sergio.

In: Default journal, Vol. 36 (3), 2010, pag. 21-29.

Risultato della ricerca: Article

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AU - Gebbia, Nicolo'

AU - Bronte, Giuseppe

AU - Bazan, Viviana

AU - Russo, Antonio

AU - La Paglia, Laura

AU - Siragusa, Sergio

AU - Siragusa, Sergio

AU - Ficorella, Corrado

AU - Adamo, Vincenzo

AU - Colucci, Giuseppe

AU - Santini, Daniele

AU - Rizzo, Sergio

PY - 2010

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N2 - The adenocarcinoma of the lung has recently shown peculiar molecular characteristics, which relate with both carcinogenesis and response to targeted drugs. Several molecular alterations have been defined as "driver mutations". These are responsible for both the initiation and maintenance of the malignancy. The epidermal growth factor receptor (EGFR) pathway is the main regulator of cell function and cancer development. It has a widely defined role in the occurrence of driver mutations. Up till now EGFR gene mutations, KRAS gene mutations and EML4-ALK fusion genes are the most widely recognized alterations involved in both the biology and the clinical management of lung adenocarcinoma. In this review we report the molecular bases that have led to the clinical application of the detection for such genetic impairments. Subsequently we discuss the clinical studies regarding the prognostic role and the predictive value for response to anti-EGFR tyrosine kinase inhibitors (TKI) of the same mutations. We also provide a potential algorithm as a guide in the choice of the best treatment for patients with adenocarcinoma.

AB - The adenocarcinoma of the lung has recently shown peculiar molecular characteristics, which relate with both carcinogenesis and response to targeted drugs. Several molecular alterations have been defined as "driver mutations". These are responsible for both the initiation and maintenance of the malignancy. The epidermal growth factor receptor (EGFR) pathway is the main regulator of cell function and cancer development. It has a widely defined role in the occurrence of driver mutations. Up till now EGFR gene mutations, KRAS gene mutations and EML4-ALK fusion genes are the most widely recognized alterations involved in both the biology and the clinical management of lung adenocarcinoma. In this review we report the molecular bases that have led to the clinical application of the detection for such genetic impairments. Subsequently we discuss the clinical studies regarding the prognostic role and the predictive value for response to anti-EGFR tyrosine kinase inhibitors (TKI) of the same mutations. We also provide a potential algorithm as a guide in the choice of the best treatment for patients with adenocarcinoma.

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KW - Tyrosine kinase inhibitors

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