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Future Oncol. 2019 Mar 19. doi: 10.2217/fon-2018-0555. [Epub ahead of print]

A breast one-patient panel of heterogeneous genomes reveals genetic alterations driving DCIS into invasive lesions.

Yang M1, Xu Z2,3, Zhang QZ4,5, Wang K1, Ji XY4,6, Xu J7, Zhang JY8, Niu G4,5.

Author information

1
Department of Breast Cancer, Cancer Center, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou 510080, PR China.
2
Department of Ophthalmology, The First Affiliated Hospital of Guangdong Pharmaceutical University, Guangzhou 510080, PR China.
3
Department of Ophthalmology, General hospital of southern theatre command, Guangzhou 510010, PR China.
4
Phil Rivers Technology, Beijing 10095, PR China.
5
Department of Cancer Genomics, LemonData Biotech (Shenzhen) Ltd, Shenzhen 518000, PR China.
6
College of Animal Science, Inner Mongolia Agricultural University, Hohhot 010018, China.
7
Breast Disease Center, Guangdong Women & Children Hospital, Guangzhou 511400, PR China.
8
Pathology Department, Guangdong Women & Children Hospital, Guangzhou 511400, PR China.

Abstract

AIM:

Utilize breast cancer samples in the same patient to indicate breast cancer development.

PATIENTS & METHODS:

We performed whole-exome analysis of spatially independent ductal carcinoma in situ (DCIS) and invasive ductal carcinoma samples from the same breast.

RESULTS:

In VEGF pathway, we observed two genes disrupted in DCIS, while another four (including ACTN2) mutated in invasive ductal carcinoma. When looked up TCGA database, we identified seven breast cancer patients with ACTN2 somatic mutations and observed a dramatic decrease in the overall survival time in ACTN2 mutant patients (p = 0.0182). A further finding in the TCGA database shows that breast cancer patients with ≥2 mutated genes in VEGF pathways showed worse prognosis (p = 0.0013).

CONCLUSION:

TCGA database and special case could inform each other to reveal DCIS developmental rules.

KEYWORDS:

ACTN mutation; VEGF pathway; ductal carcinoma ; invasive ductal carcinoma; precision medicine

PMID:
30888194
DOI:
10.2217/fon-2018-0555

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