Shuaiying Cui, PhD
Associate Professor
Boston University Chobanian & Avedisian School of Medicine
Medicine
Hematology & Medical Oncology

PhD, University of Science and Technology of China
BS, Anhui University



Dr. Cui's research has focused on the development of novel agents that can elicit developmental stage-specific gene silencing or reprogramming in hematopoietic stem cells and progenitors through a series of epigenetic chromatin modifications by nucleosome remodeling, histone deacetylation and demethylation. Such agents can be applied to the treatment of the patients with hematologic disorders such as sickle cell disease and beta-thalassemia, as well as acute myeloid leukemia (Blood cancer), which arise from congenital defects in genome. The findings from these preclinical studies could also help to establish therapeutic indications in other hematological malignancies.

Diversity, Equity, Inclusion and Accessibility

If you are not sure what is DEIA. Here are the definitions from https://www.bmc.org/glossary-culture-transformation.

Diversity: Each individual is unique, and groups of individuals reflect multiple dimensions of identity: race, sex and gender, socio-economic status, sexuality, age, ability, national origin, religious beliefs, cognitive styles, personality, appearance, and much more. Valuing diversity means embracing and celebrating the rich dimensions of difference that exist in groups and eliminating interpersonal and institutional biases based on these differences.

Equity: The state in which differences in life outcomes are not predicted by one’s race, sex and gender, and other dimensions of identity, with specific emphasis on populations bearing the burden of inequities (e.g., people of color, women, LGBTQIA+ individuals). Valuing equity means engaging those most impacted by structural inequity in the creation and implementation of institutional policies, practices, and messages that eliminate unfair differences in outcomes, so everyone has the means and opportunity to improve the quality of their lives. Equity is both a process and an outcome.
Equity does not mean equality. Although both aim to achieve fairness, an equality approach treats everyone the same regardless of need, while an equity approach treats people differently and appropriately dependent on need.

Inclusion: The fundamental and authentic integration of historically and currently excluded individuals and/or groups (e.g., Black, Indigenous, people of color, women, transgender and gender non-binary individuals, and the intersection of structurally marginalized identities) into positions, processes, activities, and decision and policy making in a way that shares power, values input and engenders belonging. In terms of understanding inclusion, we must understand who is excluded.

Accessibility: The "ability to access" the functionality of a system or entity, and gain the related benefits. The degree to which a product, service, or environment is accessible by as many people as possible. Accessible design ensures both direct (unassisted) access and indirect access through assistive technology (e.g., computer screen readers). Universal design ensures that an environment can be accessed, understood, and used to the greatest extent possible by all people.

I am deeply committed to develop and disseminate DEIA in the current academic environment.

I serve on the Diversity Equity Inclusion and Accessibility Committee and Anti-Racism Committee in the Department of Medicine, Section of Hematology and Medical Oncology to promote DEIA-related activities through recruiting and mentoring a diverse group of research fellows, graduate and undergrad students as well as creating and maintaining a DEIA work environment in the research laboratory.

I am also a member of Graduate Medical Sciences Awards Committee and Admissions Committee where I dedicate to improving DEIA activities.

Member
Boston University
Center for Excellence in Sickle Cell Disease





Modulation of LSD1 and PGC-1a pathways by small molecule compounds for fetal hemoglobin induction
09/01/2023 - 08/31/2025 (PI)
Doris Duke Charitable Foundation

Targeting PGC-1a for the treatment of sickle cell disease
07/01/2022 - 05/31/2025 (PI)
National Heart, Lung, and Blood Institute/NIH/DHHS
5R01HL155451-02

Inhibition of LSD1 by small molecule inhibitors stimulates fetal hemoglobin synthesis for sickle…
09/01/2019 - 08/31/2024 (PI)
Doris Duke Charitable Foundation

LSD1 inhibition for the treatment of beta-globin disorders
02/01/2021 - 08/31/2023 (PI)
Doris Duke Charitable Foundation

Interactions between fetal hemoglobin regulation networks
07/01/2021 - 06/30/2023 (PI)
Doris Duke Charitable Foundation

Cui American Society of Hematology Junior Faculty Scholar Award in Basic/Translational Research
07/01/2017 - 06/30/2019 (PI)
American Society of Hematology

Regulating transcriptional co-activator PGC-1a for the treatment of sickle cell disease
05/12/2017 - 06/30/2018 (PI)
Pfizer, Inc

LSD1 Inhibition for the treatment of beta-globin disorders
07/01/2016 - 06/30/2018 (PI)
American Heart Assoc


Title

Publications listed below are automatically derived from MEDLINE/PubMed and other sources, which might result in incorrect or missing publications. Faculty can login to make corrections and additions.

iCite Analysis       Copy PMIDs To Clipboard

  1. Sun Y, Benmhammed H, Al Abdullatif S, Habara A, Fu E, Brady J, Williams C, Ilinski A, Sharma A, Mahdaviani K, Alekseyev YO, Campbell JD, Steinberg MH, Cui S. PGC-1a agonism induces fetal hemoglobin and exerts antisickling effects in sickle cell disease. Sci Adv. 2024 Aug 02; 10(31):eadn8750.View Related Profiles. PMID: 39083598; PMCID: PMC11290485; DOI: 10.1126/sciadv.adn8750;
     
  2. Sun Y, Habara A, Le CQ, Nguyen N, Chen R, Murphy GJ, Chui DHK, Steinberg MH, Cui S. Pharmacologic induction of PGC-1a stimulates fetal haemoglobin gene expression. Br J Haematol. 2022 Apr; 197(1):97-109.View Related Profiles. PMID: 35118652
     
  3. Aygun B, Bello A, Thompson AA, Davis L, Sun Y, Luo HY, Cui S, Chui DHK. Clinical phenotypes of three children with sickle cell disease caused by HbS/Sicilian (dß)0 -thalassemia deletion. Am J Hematol. 2022 04; 97(4):E156-E158.View Related Profiles. PMID: 35045200; DOI: 10.1002/ajh.26470;
     
  4. Li X, Chen M, Liu B, Lu P, Lv X, Zhao X, Cui S, Xu P, Nakamura Y, Kurita R, Chen B, Huang DCS, Liu DP, Liu M, Zhao Q. Transcriptional silencing of fetal hemoglobin expression by NonO. Nucleic Acids Res. 2021 09 27; 49(17):9711-9723. PMID: 34379783; PMCID: PMC8464040; DOI: 10.1093/nar/gkab671;
     
  5. Le CQ, Myers G, Habara A, Jearawiriyapaisarn N, Murphy GJ, Chui DHK, Steinberg MH, Engel JD, Cui S. Inhibition of LSD1 by small molecule inhibitors stimulates fetal hemoglobin synthesis. Blood. 2019 05 30; 133(22):2455-2459.View Related Profiles. PMID: 30992270; PMCID: PMC6543516; DOI: 10.1182/blood.2018892737;
     
  6. Tang B, Wang S, Wang SG, Wang HJ, Zhang JY, Cui SY. Invertebrate Trehalose-6-Phosphate Synthase Gene: Genetic Architecture, Biochemistry, Physiological Function, and Potential Applications. Front Physiol. 2018; 9:30. PMID: 29445344; PMCID: PMC5797772; DOI: 10.3389/fphys.2018.00030;
     
  7. Morrison TA, Wilcox I, Luo HY, Farrell JJ, Kurita R, Nakamura Y, Murphy GJ, Cui S, Steinberg MH, Chui DHK. A long noncoding RNA from the HBS1L-MYB intergenic region on chr6q23 regulates human fetal hemoglobin expression. Blood Cells Mol Dis. 2018 03; 69:1-9.View Related Profiles. PMID: 29227829; PMCID: PMC5783741; DOI: 10.1016/j.bcmd.2017.11.003;
     
  8. de Medeiros AS, Wyman AR, Alaamery MA, Allain C, Ivey FD, Wang L, Le H, Morken JP, Habara A, Le C, Cui S, Lerner A, Hoffman CS. Identification and characterization of a potent and biologically-active PDE4/7 inhibitor via fission yeast-based assays. Cell Signal. 2017 Dec; 40:73-80.View Related Profiles. PMID: 28867658; PMCID: PMC5651194; DOI: 10.1016/j.cellsig.2017.08.011;
     
  9. Jagadeeswaran R, Vazquez BA, Thiruppathi M, Ganesh BB, Ibanez V, Cui S, Engel JD, Diamond AM, Molokie RE, DeSimone J, Lavelle D, Rivers A. Pharmacological inhibition of LSD1 and mTOR reduces mitochondrial retention and associated ROS levels in the red blood cells of sickle cell disease. Exp Hematol. 2017 06; 50:46-52. PMID: 28238805; PMCID: PMC6263958; DOI: 10.1016/j.exphem.2017.02.003;
     
  10. Cui S, Engel JD. Reactivation of Fetal Hemoglobin for Treating ß-Thalassemia and Sickle Cell Disease. Adv Exp Med Biol. 2017; 1013:177-202. PMID: 29127681; DOI: 10.1007/978-1-4939-7299-9_7;
     
Showing 10 of 26 results. Show More

This graph shows the total number of publications by year, by first, middle/unknown, or last author.

Bar chart showing 26 publications over 14 distinct years, with a maximum of 4 publications in 2017

YearPublications
20051
20061
20102
20112
20131
20143
20153
20163
20174
20181
20191
20211
20222
20241

2023-2024 Boston University Chobanian & Avedisian School of Medicine: Wing Tat Lee Awards
2023-2026 Doris Duke Charitable Foundation: Sickle Cell Disease/Advancing Cures Award
2019-2022 Doris Duke Charitable Foundation: Sickle Cell Disease/Advancing Cures Award
2017-2018 American Society of Hematology: Scholar Awards
2017-2018 Pfizer: ASPIRE US Sickle Cell Disease Competitive Research Awards
2013-2017 American Heart Association: Award for National Scientist Development Grant

Available to Mentor as: (Review Mentor Role Definitions):
  • Advisor
  • Career Mentor
  • Co-Mentor or Peer Mentor
  • Diversity Mentor
  • Education Mentor
  • Project Mentor
  • Research / Scholarly Mentor
  • Work / Life Integration Mentor
Contact for Mentoring:
  • Email (see 'Contact Info')
  • Phone (see 'Contact Info')

650 Albany St Evans Biomed Research Ctr
Boston MA 02118
Google Map

(617) 638-7530 (fax)

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