Iranian Journal of Pathology

Relationship Between PIK3CA Amplification and P110α and CD34 Tissue Expression as Angiogenesis Markers in Iranian Women with Sporadic Breast Cancer

Document Type : Original Research

Authors

Shadi Hosseini 1
Farkhondeh Behjati 1
Maryam Rahimi 1
Nazanin Taheri 1
Hamid Reza Khorram Khorshid 1
Fatemehte Aghakhani Moghaddam 1
Saghar Ghasemi Frouzabadi 1
Masoud Karimlou 2
Fereidoon Sirati 3
Elahe Keyhani 1

1 Genetics Research Center, University of Social Welfare and Rehabilitation Sciences, Tehran, Iran

2 Dept. of Epidemiology and Biostatistics, Tehran Medical Sciences Branch, Islamic Azad University, Tehran, Iran

3 Cancer Institute, Tehran University of Medical Sciences, Tehran, Iran

Abstract
Background and Objective: The PI3K/AKT/mTOR pathway is known to play an important role in regulating angiogenesis both in normal and breast cancer (BC) tissues. PIK3CA amplification was reported in various malignancies, including approximately 10% of BC cases. The aim of this study was to identify the frequency of PIK3CA amplification in Iranian female patients suffering from BC. Additionally, possible association between PIK3CA amplification and P110α expression with microvascular density (MVD) was examined.
Methods: DNA samples were extracted from paraffin embedded tumor tissue blocks and copy number changes were evaluated by MLPA Technique. The results were analyzed by coffalyzer software. The tissue expression of P110α and CD34 was assessed using immunohistochemistry.
Results: Ten out of 40 samples (17.5%) showed amplification in PIK3CA gene and 22 out of 40 samples (55%) showed overexpression in P110α. For CD34, from 40 samples, 20 (50%), 15 (37.5%) and 5 (12.5%) had scores 1+, 2+ and 3+, respectively.
Conclusion: No significant association was detected between gain of PIK3CA copy number and P110α or CD34 tissue expression.

Keywords

PIK3CA
Amplification
P110α
MVD
Breast cancer

Subjects

Iranian Journal of Pathology
Volume 13, Issue 4
Autumn 2018
Pages 447-453

  • Receive Date 22 June 2017
  • Accept Date 13 September 2018

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