Abstract
Atypical lobular hyperplasia manifests as a clonal proliferation of dis-cohesive epithelial cells emerging from terminal duct lobular units. Neoplasm appears reminiscent of lobular carcinoma in situ (LCIS) although cellular quantification is reduced. Characteristically, the incidentally discovered lesion is associated with dysfunction or decimation of E-cadherin. Additionally designated as lobular intraepithelial neoplastic 1 (LIN1), tumefaction exemplifies a female preponderance. Typically, adult subjects are implicated. Tumefaction is commonly encountered within the fifth decade although no age of disease emergence is exempt. Atypical lobular hyperplasia is detected within<1% of core needle biopsies adopted for evaluating BI-RADS 4 lesions [1,2]. Atypical lobular hyperplasia may incriminate bilateral breasts wherein specific lesion localization is absent. Tumefaction exhibits loss of chromosome 16qand deletion of CDH1 genes with loss of function of E-cadherin, a Tran’s membrane cell adhesion molecule. Alternatively, altered function of E-cadherin may occur. Exceptionally, various adhesion proteins are implicated wherein E-cadherin molecule appears stable [1,2]. Characteristically, atypical lobular hyperplasia is a diploid neoplasm. Tumefaction exhibits loss of heterozygosis (LOH) at chromosome 16q. A subset of neoplasms demonstrates methylation of CDH1 gene. Several tumefaction express loss of chromosome 22q and 16p, gain of chromosome 2p11.2, 5q32- 33.1 (CSF1R), 6q, 11q13 or 14q32.33.
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