Atypical uterine polyps show morphologic and molecular overlap with mullerian adenosarcoma but follow a benign clinical course

Histological and molecular analysis of cellular leiomyoma with sclerosis: linked to HMGA2 overexpression

“…The phenomenon that ~96% of CLM‐S in our series display HMGA2 overexpression by IHC, yet more than half did not contain a detectable abnormality in HMGA2 by FISH, suggests that other mechanisms potentially lead to HMGA2 overexpression in CLM‐S similar to hydropic LM 6 . Based on recent studies on whole genome sequencing, HMGA2 overexpression can be caused by copy number gain or gene amplification in chromosome 12q15 where HMGA2 is located 18,19 . Prior works have demonstrated that down‐regulation of the 3 ' UTR for HMGA2 and disrupting tumour suppression by microRNA let‐7 contributes to oncogenesis 20–22 .…”

“…6 Based on recent studies on whole genome sequencing, HMGA2 overexpression can be caused by copy number gain or gene amplification in chromosome 12q15 where HMGA2 is located. 18,19 Prior works have demonstrated that down-regulation of the 3' UTR for HMGA2 and disrupting tumour suppression by microRNA let-7 contributes to oncogenesis. [20][21][22] Ultimately, FISH testing and related data/results may be limited for HMGA2, and interpretations should incorporate variables accordingly.…”