PMID- 20472851
OWN - NLM
STAT- MEDLINE
DCOM- 20100601
LR  - 20220330
IS  - 1943-7722 (Electronic)
IS  - 0002-9173 (Print)
IS  - 0002-9173 (Linking)
VI  - 133
IP  - 6
DP  - 2010 Jun
TI  - EGFR mutation is a better predictor of response to tyrosine kinase inhibitors in 
      non-small cell lung carcinoma than FISH, CISH, and immunohistochemistry.
PG  - 922-34
LID - 10.1309/AJCPST1CTHZS3PSZ [doi]
AB  - About 10% of patients with non-small cell lung carcinoma (NSCLC) respond to 
      epidermal growth factor receptor (EGFR)-targeted tyrosine kinase inhibitors 
      (TKIs). More than 75% of "responders" have activating mutations in EGFR. However, 
      mutation analysis is not widely available, and proposed alternatives (in situ 
      hybridization and immunohistochemical analysis) have shown inconsistent 
      associations with outcome. Fluorescence in situ hybridization (FISH), chromogenic 
      in situ hybridization (CISH), immunohistochemical analysis, and DNA sequencing 
      were compared in this study of 40 NSCLC samples from TKI-treated patients. 
      Response rates were 12 of 19 in EGFR-mutant vs 1 of 20 EGFR wild-type tumors (P = 
      .0001), 7 of 19 FISH+ vs 4 of 17 FISH- tumors (not significant [NS]), 5 of 16 
      CISH+ vs 6 of 21 CISH- tumors (NS), and 3 of 9 immunohistochemically positive vs 
      7 of 22 immunohistochemically negative tumors (NS). EGFR mutation was associated 
      with improved progression-free survival (P = .0004). Increased copy number (FISH 
      or CISH) and protein expression (immunohistochemical) did not independently 
      predict outcome. Thus, EGFR sequence analysis was the only method useful for 
      predicting response and progression-free survival following TKI therapy in NSCLC.
FAU - Sholl, Lynette M
AU  - Sholl LM
AD  - Department of Pathology, Brigham and Women's Hospital, 75 Francis St., Boston, MA 
      02115, USA.
FAU - Xiao, Yun
AU  - Xiao Y
FAU - Joshi, Victoria
AU  - Joshi V
FAU - Yeap, Beow Y
AU  - Yeap BY
FAU - Cioffredi, Leigh-Anne
AU  - Cioffredi LA
FAU - Jackman, David M
AU  - Jackman DM
FAU - Lee, Charles
AU  - Lee C
FAU - Janne, Pasi A
AU  - Janne PA
FAU - Lindeman, Neal I
AU  - Lindeman NI
LA  - eng
GR  - R01 CA114465/CA/NCI NIH HHS/United States
GR  - R01 CA114465-05/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PL  - England
TA  - Am J Clin Pathol
JT  - American journal of clinical pathology
JID - 0370470
RN  - 0 (Protein Kinase Inhibitors)
RN  - EC 2.7.10.1 (ErbB Receptors)
RN  - EC 2.7.10.1 (Protein-Tyrosine Kinases)
SB  - IM
CIN - Am J Clin Pathol. 2010 Jul;134(1):7-9. PMID: 20551260
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - Carcinoma, Non-Small-Cell Lung/*drug therapy/*genetics
MH  - ErbB Receptors/*genetics
MH  - Female
MH  - Humans
MH  - Immunohistochemistry
MH  - In Situ Hybridization
MH  - In Situ Hybridization, Fluorescence/methods
MH  - Lung Neoplasms/*drug therapy/*genetics
MH  - Male
MH  - Middle Aged
MH  - Mutation
MH  - Protein Kinase Inhibitors/*therapeutic use
MH  - Protein-Tyrosine Kinases/metabolism
MH  - Retrospective Studies
MH  - Sensitivity and Specificity
MH  - Sequence Analysis, DNA
PMC - PMC3156055
MID - NIHMS299356
EDAT- 2010/05/18 06:00
MHDA- 2010/06/02 06:00
PMCR- 2011/08/15
CRDT- 2010/05/18 06:00
PHST- 2010/05/18 06:00 [entrez]
PHST- 2010/05/18 06:00 [pubmed]
PHST- 2010/06/02 06:00 [medline]
PHST- 2011/08/15 00:00 [pmc-release]
AID - 133/6/922 [pii]
AID - 10.1309/AJCPST1CTHZS3PSZ [doi]
PST - ppublish
SO  - Am J Clin Pathol. 2010 Jun;133(6):922-34. doi: 10.1309/AJCPST1CTHZS3PSZ.