KRAS, EGFR AND PIK3CA mutation in triple negative breast carcinomas

Creative Commons License

ERDOĞAN G., ÖZCAN M., KARAVELI F. S., PEŞTERELİ H. E.

INTERNATIONAL JOURNAL OF MEDICAL RESEARCH & HEALTH SCIENCES, cilt.5, sa.3, ss.95-104, 2016 (ESCI) identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 5 Sayı: 3
  • Basım Tarihi: 2016
  • Dergi Adı: INTERNATIONAL JOURNAL OF MEDICAL RESEARCH & HEALTH SCIENCES
  • Derginin Tarandığı İndeksler: Emerging Sources Citation Index (ESCI)
  • Sayfa Sayıları: ss.95-104
  • Anahtar Kelimeler: triple negative breast carcinoma, EGFR, KRAS, PIK3CA, GROWTH-FACTOR RECEPTOR, CANCER SUBTYPES, BASAL-LIKE, ACTIVATING MUTATIONS, ONCOGENIC MUTATIONS, TARGETED THERAPY, EXPRESSION, IDENTIFICATION, BIOMARKERS, CETUXIMAB
  • Akdeniz Üniversitesi Adresli: Evet

Özet

Triple negative breast carcinoma is defined by the absence of oestrogen receptor (ER) and progesterone receptor (PR) expression and the lack of HER2 gene amplification. It comprise 10-17 % of all breast cancers. Though EGFR gene mutaion is rare in triple negative breast cancers, 47-70 % expressed EGFR protein. PIK3CA mutation is a frequent event in breast cancers. We aim to investigate EGFR, KRAS and PIK3CA mutation in triple negative breast carcinomas by pyrosequencing and compare the results with hormone receptor positive and HER2 overexpressed breast carcinomas which were identified by immunohistochemistry. No mutations in Exon 18, 19, 20 and 21 of EGFR gene were detected in all groups. KRAS mutation was identified in only one case. PIK3CA mutations were detected in 9 of TNBC (23.7 %), 5 of hormone receptors positive, HER2-negative tumors (50 %) In HER2-positive tumors, no mutations were detected in PIK3CA gene. Our results revealed that PIK3CA inhibitors might be a new candidate in the targeted treatment of triple negative breast cancers that were resistant to chemotherpy. These results should be supported by large series with survival analysis.

Abstract

Triple negative breast carcinoma is defined by the absence of oestrogen receptor (ER) and progesterone receptor (PR) expression and the lack of HER2 gene amplification. It comprise 10-17 % of all breast cancers. Though EGFR gene mutaion is rare in triple negative breast cancers, 47-70 % expressed EGFR protein. PIK3CA mutation is a frequent event in breast cancers. We aim to investigate EGFR, KRAS and PIK3CA mutation in triple negative breast carcinomas by pyrosequencing and compare the results with hormone receptor positive and HER2 overexpressed breast carcinomas which were identified by immunohistochemistry. No mutations in Exon 18, 19, 20 and 21 of EGFR gene were detected in all groups. KRAS mutation was identified in only one case. PIK3CA mutations were detected in 9 of TNBC (23.7 %), 5 of hormone receptors positive, HER2-negative tumors (50 %) In HER2-positive tumors, no mutations were detected in PIK3CA gene. Our results revealed that PIK3CA inhibitors might be a new candidate in the targeted treatment of triple negative breast cancers that were resistant to chemotherpy. These results should be supported by large series with survival analysis.