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Title : Exploring a New Classification System for Breast Carcinoma Based on the Presence of DCIS and Benign Breast Disease: Findings from a Pathological Study
Name : Aeree Kim
University : Korea University College of Medicine
Country : Korea
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Breast carcinoma is a diverse disease with varying morphological, phenotypical, and biological characteristics, which impact disease progression and therapeutic responsiveness. Molecular classification has greatly impacted clinical management and prediction of clinical outcomes, but it is not perfect. Ductal carcinoma in situ (DCIS) is a non-obligate precursor of invasive breast cancer (IBC) and is associated with 45-78% of all invasive breast cancers. However, not all IBC are preceded by DCIS, even though carcinogenesis starts from a single ductal epithelial cell.
My paper in 2017 dealt with multifocal tumors which can be of different origins despite being closely located to each other, and phenotypes of multifocal breast cancer are heterogeneous. Further study using whole-exome sequencing revealed that a DCIS lesion in the breast of one patient displayed a greater amount of genetic aberration than the accompanying IBC, which can imply that a subset of DCIS was as advanced or more advanced than the synchronous IBC. We demonstrated genetic intra-tumoral heterogeneity in DCIS lesions coexisting with IBC. My colleague and I recently demonstrated that the Luminal B type is the most common of the heterogeneous phenotypes through immunohistochemical analysis.
Many benign breast diseases, such as ductal hyperplasia, fibroadenoma, papilloma, and lobular hyperplasia, are associated with breast cancer. Currently, we use a widely accepted classification system based on pathological and molecular phenotype. However, we are exploring the potential of a more meticulous classification of breast cancer based on the presence or absence of DCIS and/or depending on the type of benign breast disease.
For this study, in 2019, we roughly mapped 500 pathological samples of breast cancer patients at Korea University Guro Hospital. Pathological evaluations were carefully conducted and analyzed not only for breast cancer but also for accompanying DCIS and benign breast disease. This new classification could provide valuable insight into the carcinogenesis of breast cancer as well as set a new paradigm for screening, diagnosing, and treating patients.
Title : The Role of Histone Mutations in Human Disease
Name : Kui Ming Chan
University : City University of Hong Kong
Country : China
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Histones are small nuclear proteins essential for DNA packaging and epigenetic gene regulation. Recent studies on the different histone mutations identified in cancer patients have revealed multiple oncohistones in driving different types of cancers. In addition to the oncogenic mutations in genes encode histone H3 (H3K27M, H3G34V/R and H3K36M), where the mutations occur in the tail domain and affect gene expression via modulating histone post-translational modifications, additional histone onco-mutations were identified in other histone genes within the histone fold domain and affect gene expression via distinct mechanisms. In this meeting, I will present our latest findings on the 3 newly identified cancer-associated mutations in histone H2B and reveal their mechanisms in altering gene expression and cancer development.
Biography
Dr Kui Ming Chan graduated with BSc and received his PhD at the department of Biochemistry, the University of Hong Kong (HKU). He then moved to Mayo Clinic (Rochester MN, USA) for postdoctoral training and obtained the Edward C. Kendall Research Fellowship in Biochemistry before rejoining HKU as Research Assistant Professor in June 2013. In February 2015 he joined the Department of Biomedical Sciences (BMS), City University of Hong Kong as a tenure-track Assistant Professor and was promoted to Associate Professor in 2021. Dr Chan is interested in understanding the role of epigenetics in regulating gene expression under physiological and pathological conditions. His group is currently focusing on 1) identifying new cancer driving histone mutations and developing therapeutics for these diseases using different animal models and 2) the role of novel protein factors and RNA binding proteins in X Chromosome inactivation.