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Charting epimutation dynamics in human hematopoietic differentiation Xiaohuan Qina

Blood Science 2024年第3期6卷 1-10页

作者： Jiayi Lu Peng Wu Chunyong Zhang Lei Shi Ping Zhu State Key Laboratory of Experimental Hematology National Clinical Research Center for Blood DiseasesHaihe Laboratory of Cell EcosystemDepartment of Stem Cell and Regenerative MedicineInstitute of Hematology and Blood Diseases HospitalChinese Academy of Medical Sciences and Peking Union Medical CollegeTianjinChina The Province and Ministry Co-sponsored Collaborative Innovation Center for Medical Epigenetics Key Laboratory of Immune Microenvironment and Disease(Ministry of Education)Department of Biochemistry and Molecular BiologySchool of Basic Medical SciencesTianjin Medical UniversityTianjinChina

DNA methylation plays a critical role in hematopoietic *** is a stochastic variation in DNA methylation that induces epigenetic ***,the effects of epimutations on normal hematopoiesis and hematopoietic diseases remain *** this study,we developed a Julia package called EpiMut that enabled rapid and accurate quantification of *** was used to evaluate and provide an epimutation landscape in steady-state hematopoietic differentiation involving 13 types of blood cells ranging from hematopoietic stem/progenitor cells to mature *** showed that substantial genomic regions exhibited epigenetic variations rather than significant differences in DNA methylation levels between the myeloid and lymphoid *** dynamics of epimutations were observed during the differentiation of each ***,we found that epimutation significantly enriched signals associated with lineage ***,epimutations in hematopoietic stem cells(HSCs)derived from various sources and acute myeloid leukemia were related to the function of HSCs and malignant cell *** together,our study comprehensively documented an epimutation map and uncovered its important roles in human hematopoiesis,thereby offering insights into hematopoietic regulation.

关键词： DNA methylation epimutation Hematopoietic differentiation Hematopoietic stem cell

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Epigenetic reduction of DNA repair in progression to gastrointestinal cancer

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World Journal of Gastrointestinal Oncology 2015年第5期7卷 30-46页

作者： Carol Bernstein Harris Bernstein Department of Cellular and Molecular Medicine College of Medicine University of Arizona

Deficiencies in DNA repair due to inherited germ-line mutations in DNA repair genes cause increased risk of gastrointestinal(GI) cancer. In sporadic GI cancers, mutations in DNA repair genes are relatively rare. However, epigenetic alterations that reduce expression of DNA repair genes are frequent in sporadic GI cancers. These epigenetic reductions are also found in field defects that give rise to cancers. Reduced DNA repair likely allows excessive DNA damages to accumulate in somatic cells. Then either inaccurate translesion synthesis past the un-repaired DNA damages or error-prone DNA repair can cause mutations. Erroneous DNA repair can also cause epigenetic alterations(i.e., epimutations, transmitted through multiple replication cycles). Some of these mutations and epimutations may cause progression to cancer. Thus, deficient or absent DNA repair is likely an important underlying cause of cancer. Whole genome sequencing of GI cancers show that between thousands to hundreds of thousands of mutations occur in these cancers. epimutations that reduce DNA repair gene expression and occur early in progression to GI cancers are a likely source of this high genomic instability. Cancer cells deficient in DNA repair are more vulnerable than normal cells to inactivation by DNA damaging agents. Thus, some of the most clinically effective chemotherapeutic agents in cancer treatment are DNA damaging agents, and their effectiveness often depends on deficient DNA repair in cancer cells. Recently, at least 18 DNA repair proteins, each active in one of six DNA repair pathways, were found to be subject to epigenetic reduction of expression in GI cancers. Different DNA repair pathways repair different types of DNA damage. Evaluation of which DNA repair pathway(s) are deficient in particular types of GI cancer and/or particular patients may prove useful in guiding choice of therapeutic agents in cancer therapy.

关键词： Epigenetic DNA damage DNA repair DNA repair deficiency disorders epimutation Genomicinstability Germ-line mutation MicroRNAs Precancerousconditions Gastrointestinal cancer

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