이재웅 (고려대학교, Yale School of Medicine)

한빛사논문

조회302

고려대학교, Yale School of Medicine

CV File 258 kb

Progr Lipid Res, Volume 95, July 2024, 101288 | https://doi.org/10.1016/j.plipres.2024.101288 Leveraging altered lipid metabolism in treating B cell malignancies

Jaewoong Lee^a,b,c,d, Arya Mani ^e,f, Min-Jeong Shin ^a,b,c, Ronald M. Krauss ^g

^aSchool of Biosystems and Biomedical Sciences, College of Health Science, Korea University, Seoul 02841, Republic of Korea

^bDepartment of Integrated Biomedical and Life Science, Korea University, Seoul 02841, Republic of Korea

^cInterdisciplinary Program in Precision Public Health, Korea University, Seoul 02841, Republic of Korea

^dCenter of Molecular and Cellular Oncology, Yale University, New Haven, CT 06511, USA

^eDepartment of Internal Medicine, Section of Cardiovascular Medicine, Yale University, New Haven, CT 06511, USA

^fDepartment of Genetics, Yale University, New Haven, CT 06511, USA

^gDepartment of Pediatrics and Medicine, University of California San Francisco, San Francisco, CA 94143, USA

Corresponding authors: Jaewoong Lee, Ronald M. Krauss

Abstract

B cell malignancies, comprising over 80 heterogeneous blood cancers, pose significant prognostic challenges due to intricate oncogenic signaling. Emerging evidence emphasizes the pivotal role of disrupted lipid metabolism in the development of these malignancies. Variations in lipid species, such as phospholipids, cholesterol, sphingolipids, and fatty acids, are widespread across B cell malignancies, contributing to uncontrolled cell proliferation and survival. Phospholipids play a crucial role in initial signaling cascades leading to B cell activation and malignant transformation through constitutive B cell receptor (BCR) signaling. Dysregulated cholesterol and sphingolipid homeostasis support lipid raft integrity, crucial for propagating oncogenic signals. Sphingolipids impact malignant B cell stemness, proliferation, and survival, while glycosphingolipids in lipid rafts modulate BCR activation. Additionally, cancer cells enhance fatty acid-related processes to meet heightened metabolic demands. In obese individuals, the obesity-derived lipids and adipokines surrounding adipocytes rewire lipid metabolism in malignant B cells, evading cytotoxic therapies. Genetic drivers such as MYC translocations also intrinsically alter lipid metabolism in malignant B cells. In summary, intrinsic and extrinsic factors converge to reprogram lipid metabolism, fostering aggressive phenotypes in B cell malignancies. Therefore, targeting altered lipid metabolism has translational potential for improving risk stratification and clinical management of diverse B cell malignancy subtypes.

논문정보

형식Review Paper
게재일2024년 07월 (BRIC 등록일 2024-07-07)
연구진국내(교신)+국외 연구진
분야 생명과학 > 면역학

댓글 작성 로그인

CV 열람하기

연락처 보기