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A case of morphea coexisting with extragenital lichen sclerosus et atrophicus
( Yu Jin Lee ),( Yeon Seok Lee ),( Young Shin Kim ),( Tae Young Han ),( Jae Eun Choi ),( June Hyunkyung Lee ) 대한피부과학회 2021 대한피부과학회 학술발표대회집 Vol.72 No.2
Morphea is a chronic inflammatory disease characterized by hypopigmented sclerotic plaques, which becomes softened and atrophic. Extragenital lichen sclerosus et atrophicus (LSEA) is an inflammatory dermatosis that presents with porcelain-white plaques. Coexistence of morphea and LESA has been occasionally identified in literatures. A 26-year-old woman presented with asymptomatic multiple hyper- and hypopigmented atrophic patches with focal porcelain-white sclerotic lesions on trunk and right axilla since childhood. She denied any traumatic history. Routine laboratory tests were normal except for speckled patterned anti-nuclear antibody (ANA). Histologically, perivascular inflammatory infiltrate of lymphocytes and plasma cells, and swollen collagen bundles were observed, which suggest morphea. In addition, thinned epidermis and subepidermal cleavage with interface change, and a wide band of hyalinization at the dermo-epidermal junction were also observed, which suggest LSEA. According to clinicopathological findings, she was diagnosed with morphea coexisting with extragenital LSEA. The coexistence of both conditions may suggest that these lesions share a spectrum of common pathologic process. While the cause of either disease is unknown, several factors such as Borrelia infection, autoimmunity, and trauma have been considered as etiologies. Herein, we report an uncommon case of a patient with morphea coexisting with extragenital LSEA.
Choi, Hee June;Lee, Ji Min;Kim, Hyunkyung;Nam, Hye Jin;Shin, Hi-Jai R.;Kim, Dongha;Ko, Enyoung;Noh, Dong-Young;Kim, Keun II;Kim, Jung Hwa;Baek, Sung Hee Sookmyung Women's University Research Institute of 2011 여성과 건강 Vol.6 No.2
B-cell lymphoma 3 (Bc13) is a proto-oncogene upregulated in a wide range of cancers, including breast cancer. Although Bc13 is known to promote cell proliferation and inhibit apoptosis, the molecular mech¬anisms underlying the proto-oncogenic function of Bc13 have not been completely elucidated. To gain insight into the oncogenic role of Bc13, we applied a proteomic approach, which led to the identification of C-terminal binding protein 1 (CtBP1) as a binding partner of Bc13. A PXDLS/R motif embedded in Bc13 was found to mediate the interaction between Bc13 and CtBP1, which caused the stabilization of CtBP1 by blocking proteasome-dependent degradation. Apoptotic stimuli-induced degradation of CtBP1 was sig¬nificantly abolished by the upregulation of Bc13, leading to the sustained repression of pro-apoptotic gene expression and subsequent inhibition of apoptosis. Intriguingly, a strong positive correlation between the protein levels of Bc13 and CtBP1 was detected in breast cancer patient samples. Our study reveals a novel combinatorial role for Bc13 and CtBP1, providing an explanation for the acquisition of resistance to apop¬tosis in cancer cells, which is a major requirement for cancer development.