We tested 418 neoplasms along the whole spectrum of primary lung tumor histotypes for epidermal growth factor receptor (EGFR) and K-ras mutations. Clinicopathologic data from 154 patients undergoing treatment with EGFR tyrosine kinase inhibitors (TKIs) were retrospectively studied. A scoring system assigning a score for each positive or negative characteristic (+1, female sex, nonsmoking status, adenocarcinoma histotype, Asian ethnicity, and EGFR mutation; −1, current smoker and K-ras mutation; and 0, male sex, ex-smoker, nonadenocarcinoma histotype, and no mutations) was elaborated and tested with EGFR-TKI response.Salivary gland–type, mucin-rich, and neuroendocrine tumors do not harbor EGFR mutations. A subset of nonmucinous adenocarcinomas, not necessarily of the bronchioloalveolar type, is related to EGFR mutations. Three probability groups significantly correlating with response to EGFR-TKIs were identified. Of note, the addition of molecular results did not significantly change the predictive value obtained by the combination of clinicopathologic characteristics alone in this scoring system. K-ras mutations, significantly associated with the mucin-secreting type of adenocarcinoma, consistently predict lack of response in white patients.

EGFR and K-ras mutations along the spectrum of pulmonary epithelial tumors of the lung and elaboration of a combined clinicopathologic and molecular scoring system to predict clinical responsiveness to EGFR inhibitors / Sartori, G; Cavazza, A; Sgambato, A; Marchioni, A; Barbieri, F; Longo, L; Bavieri, M; Murer, B; Meschiari, E; Tamberi, S; Cadioli, A; Luppi, F; Migaldi, Mario; Rossi, G.. - In: AMERICAN JOURNAL OF CLINICAL PATHOLOGY. - ISSN 0002-9173. - ELETTRONICO. - 131:(2009), pp. 478-489.

EGFR and K-ras mutations along the spectrum of pulmonary epithelial tumors of the lung and elaboration of a combined clinicopathologic and molecular scoring system to predict clinical responsiveness to EGFR inhibitors.

MIGALDI, Mario;
2009

Abstract

We tested 418 neoplasms along the whole spectrum of primary lung tumor histotypes for epidermal growth factor receptor (EGFR) and K-ras mutations. Clinicopathologic data from 154 patients undergoing treatment with EGFR tyrosine kinase inhibitors (TKIs) were retrospectively studied. A scoring system assigning a score for each positive or negative characteristic (+1, female sex, nonsmoking status, adenocarcinoma histotype, Asian ethnicity, and EGFR mutation; −1, current smoker and K-ras mutation; and 0, male sex, ex-smoker, nonadenocarcinoma histotype, and no mutations) was elaborated and tested with EGFR-TKI response.Salivary gland–type, mucin-rich, and neuroendocrine tumors do not harbor EGFR mutations. A subset of nonmucinous adenocarcinomas, not necessarily of the bronchioloalveolar type, is related to EGFR mutations. Three probability groups significantly correlating with response to EGFR-TKIs were identified. Of note, the addition of molecular results did not significantly change the predictive value obtained by the combination of clinicopathologic characteristics alone in this scoring system. K-ras mutations, significantly associated with the mucin-secreting type of adenocarcinoma, consistently predict lack of response in white patients.
131
478
489
EGFR and K-ras mutations along the spectrum of pulmonary epithelial tumors of the lung and elaboration of a combined clinicopathologic and molecular scoring system to predict clinical responsiveness to EGFR inhibitors / Sartori, G; Cavazza, A; Sgambato, A; Marchioni, A; Barbieri, F; Longo, L; Bavieri, M; Murer, B; Meschiari, E; Tamberi, S; Cadioli, A; Luppi, F; Migaldi, Mario; Rossi, G.. - In: AMERICAN JOURNAL OF CLINICAL PATHOLOGY. - ISSN 0002-9173. - ELETTRONICO. - 131:(2009), pp. 478-489.
Sartori, G; Cavazza, A; Sgambato, A; Marchioni, A; Barbieri, F; Longo, L; Bavieri, M; Murer, B; Meschiari, E; Tamberi, S; Cadioli, A; Luppi, F; Migaldi, Mario; Rossi, G.
File in questo prodotto:
File Dimensione Formato  
EGFR.pdf

non disponibili

Tipologia: Post-print dell'autore (bozza post referaggio)
Dimensione 875.96 kB
Formato Adobe PDF
875.96 kB Adobe PDF   Visualizza/Apri   Richiedi una copia
Pubblicazioni consigliate

Caricamento pubblicazioni consigliate

Licenza Creative Commons
I metadati presenti in IRIS UNIMORE sono rilasciati con licenza Creative Commons CC0 1.0 Universal, mentre i file delle pubblicazioni sono rilasciati con licenza Attribuzione 4.0 Internazionale (CC BY 4.0), salvo diversa indicazione.
In caso di violazione di copyright, contattare Supporto Iris

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11380/616197
Citazioni
  • ???jsp.display-item.citation.pmc??? 13
  • Scopus 61
  • ???jsp.display-item.citation.isi??? 49
social impact