PMID- 26060045
OWN - NLM
STAT- MEDLINE
DCOM- 20160526
LR  - 20181202
IS  - 1532-2807 (Electronic)
IS  - 1219-4956 (Linking)
VI  - 21
IP  - 4
DP  - 2015 Sep
TI  - Determination of HER2 and p53 Mutations by Sequence Analysis Method and 
      EGFR/Chromosome 7 Gene Status by Fluorescence in Situ Hybridization for the 
      Predilection of Targeted Therapy Modalities in Immunohistochemically Triple 
      Negative Breast Carcinomas in Turkish Population.
PG  - 1223-7
LID - 10.1007/s12253-015-9956-1 [doi]
AB  - Triple negative breast cancer (TNBC), an agressive subtype accounts nearly 15 % 
      of all breast carcinomas. Conventional chemotherapy is the only treatment 
      modality thus new, effective targeted therapy methods have been investigated. 
      Epidermal growth factor receptor (EGFR) inhibitors give hope according to the 
      recent studies results. Also therapeutic agents have been tried against aberrant 
      p53 signal activity as TNBC show high p53 mutation rates. Our aim was to detect 
      the incidence of mutations/amplifications identified in TNBC in our population. 
      Here we used sequence analysis to detect HER2 (exon 18-23), p53 (exon 5-8) 
      mutations; fluorescence in situ hybridization (FISH) method to analyse 
      EGFR/chromosome 7 centromere gene status in 82 immunohistochemically TNBC. 
      Basaloid phenotype was identified in 49 (59.8 %) patients. EGFR amplification was 
      noted in 5 cases (6.1 %). All EGFR amplified cases showed EGFR overexpression by 
      immunohistochemistry (IHC). p53 mutations were identified in 33 (40.2 %) cases. 
      Almost 60 % of the basal like breast cancer cases showed p53 mutation. Only one 
      case showed HER2 mutation (exon 20:g.36830_3). Our results showed that gene 
      amplification is not the unique mechanism in EGFR overexpression. IHC might be 
      used in the decision of anti-EGFR therapy in routine practice. p53 mutation rate 
      was lower than the rates reported in the literature probably due to ethnic 
      differences and low sensitivity of sanger sequences in general mutation 
      screening. We also established the rarity of HER2 mutation in TNBC. In conclusion 
      EGFR and p53 are the major targets in TNBC also for our population.
FAU - Pala, Emel Ebru
AU  - Pala EE
AD  - Izmir Tepecik Training and Research Hospital Pathology Department, Gaziler 
      Caddesi, Yenisehir, Izmir, 35000, Turkey, emelozkok@yahoo.com.
FAU - Bayol, Umit
AU  - Bayol U
FAU - Keskin, Elif Usturali
AU  - Keskin EU
FAU - Ozguzer, Alp
AU  - Ozguzer A
FAU - Kucuk, Ulku
AU  - Kucuk U
FAU - Ozer, Ozge
AU  - Ozer O
FAU - Koc, Altug
AU  - Koc A
LA  - eng
PT  - Journal Article
DEP - 20150610
PL  - Switzerland
TA  - Pathol Oncol Res
JT  - Pathology oncology research : POR
JID - 9706087
RN  - 0 (TP53 protein, human)
RN  - 0 (Tumor Suppressor Protein p53)
RN  - EC 2.7.10.1 (EGFR protein, human)
RN  - EC 2.7.10.1 (ERBB2 protein, human)
RN  - EC 2.7.10.1 (ErbB Receptors)
RN  - EC 2.7.10.1 (Receptor, ErbB-2)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - Chromosomes, Human, Pair 7/*genetics
MH  - ErbB Receptors/*genetics
MH  - Exons/genetics
MH  - Female
MH  - Gene Amplification/genetics
MH  - Gene Dosage/genetics
MH  - Humans
MH  - Immunohistochemistry/methods
MH  - In Situ Hybridization, Fluorescence/methods
MH  - Middle Aged
MH  - Mutation/*genetics
MH  - Receptor, ErbB-2/*genetics
MH  - Sequence Analysis/methods
MH  - Triple Negative Breast Neoplasms/*genetics
MH  - Tumor Suppressor Protein p53/*genetics
MH  - Turkey
MH  - Young Adult
EDAT- 2015/06/11 06:00
MHDA- 2016/05/27 06:00
CRDT- 2015/06/11 06:00
PHST- 2014/10/10 00:00 [received]
PHST- 2015/05/26 00:00 [accepted]
PHST- 2015/06/11 06:00 [entrez]
PHST- 2015/06/11 06:00 [pubmed]
PHST- 2016/05/27 06:00 [medline]
AID - 10.1007/s12253-015-9956-1 [doi]
PST - ppublish
SO  - Pathol Oncol Res. 2015 Sep;21(4):1223-7. doi: 10.1007/s12253-015-9956-1. Epub 
      2015 Jun 10.