Abstract:

Breast atypical ductal hyperplasia (ADH) has the risk of progression into breast cancer, and there are characteristic molecular biological and genetic changes in ADH, which is to some extent similar to ductal carcinoma in situ (DCIS). The increase of cell proliferation index, hormone receptor expression and cell growth regulating factors may promote the formation of ADH. Chromosome abnormality and epigenetic changes may lead to the formation of ADH, among which 16p, 17q chromosome abnormality and promoter methylation of cancer related gene may be the early events of ADH. Studies have confirmed that ADH is the precursor of low grade ductal carcinoma in situ (LG-DCIS) which shares the similar molecular biological characteristics and genetic performance with ADH, and can progress to low grade invasive ductal carcinoma (LG-IDC) through LG-DCIS stage. Studies have also pointed out that ADH is not the precursor of high grade ductal carcinoma in situ (HG-DCIS), and high grade invasive ductal carcinoma (HG-IDC) has different pathogenesis. With the abnormal expression of cell adhesion molecule, extracellular matrix produces a large number of matrix protease which results in reduced cell-to-cell adhesion and degradation of basement membrane, and ultimately promotes the development of ADH to IDC.

Key words: atypical ductal hyperplasia, molecular features, genetics, extracellular matrix