Oncogenic <i>SF3B1</i> mutations alter the splicing of mRNA noncoding regions to induce a novel therapeutic vulnerability

M Michal Sekrecki (1Division of Hematology, Department of Medicine, Stanford University School of Medicine, Stanford, CA) A Agata Sekrecka (1Division of Hematology, Department of Medicine, Stanford University School of Medicine, Stanford, CA) R Rohan R. Lattupally (1Division of Hematology, Department of Medicine, Stanford University School of Medicine, Stanford, CA) K Kenny Le (1Division of Hematology, Department of Medicine, Stanford University School of Medicine, Stanford, CA) X Xiaokang Jin (Department of Chemistry) C Chen Mozes (2Department of Chemistry, Northwestern University, Chicago, IL) B Brendan G. Dwyer (Department of Chemical and Systems Biology, ChEM-H, and Stanford Cancer Institute, Stanford School of Medicine) Z Zhe Zhuang (Department of Chemical and Systems Biology, ChEM-H and Stanford Cancer Institute, Stanford Medical School) B Bryan A. Romero (Department of Chemical and Systems Biology, ChEM-H, and Stanford Cancer Institute, Stanford School of Medicine) J Jose M. B. Pineda (1Division of Hematology, Department of Medicine, Stanford University School of Medicine, Stanford, CA) X Xunhong Cao (1Division of Hematology, Department of Medicine, Stanford University School of Medicine, Stanford, CA) L Linh Nguyen V Vicky Chen C Crystal M. Zhou (1Division of Hematology, Department of Medicine, Stanford University School of Medicine, Stanford, CA) J Jared A. Wallace (1Division of Hematology, Department of Medicine, Stanford University School of Medicine, Stanford, CA) K Kailee Tanaka C Charu Tiwari (1Division of Hematology, Department of Medicine, Stanford University School of Medicine, Stanford, CA) A Austin Gabel (6Department of Genome Sciences and Medical Scientist Training Program, University of Washington, Seattle, WA) W Won Jun Kim R Robert F. Stanley (7Molecular Pharmacology Program, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, NY) S Salima Benbarche (Molecular Pharmacology Program, Sloan Kettering Institute) J Jaspreet Thind (Department of Cell Biology and Genetics, Texas A&M University Health Science Center) A Abhinaya Muruganandham (8Department of Cell Biology and Genetics, Texas A&M University Health Science Center, Bryan, TX) T Tian Yi Zhang (1Division of Hematology, Department of Medicine, Stanford University School of Medicine, Stanford, CA) P Peter L. Greenberg (1Division of Hematology, Department of Medicine, Stanford University School of Medicine, Stanford, CA) J Jason R. Gotlib (1Division of Hematology, Department of Medicine, Stanford University School of Medicine, Stanford, CA) G Gabriel Mannis (1Division of Hematology, Department of Medicine, Stanford University School of Medicine, Stanford, CA) W William E. Shomali (1Division of Hematology, Department of Medicine, Stanford University School of Medicine, Stanford, CA) G Giselle Salmasi (1Division of Hematology, Department of Medicine, Stanford University School of Medicine, Stanford, CA) C Calvin Kuo T Tait Shanafelt (1Division of Hematology, Department of Medicine, Stanford University School of Medicine, Stanford, CA) I Irtisha Singh (Interdisiplinary program in Genetics and Genomics, College of Agriculture and Life Sciences, Texas A&M University) D Daichi Inoue F Finn K. Hansen (11Department of Pharmaceutical and Cell Biological Chemistry, Pharmaceutical Institute, University of Bonn, Bonn, Germany) N Nathanael S. Gray C Capucine van Rechem (4Department of Pathology, Stanford University School of Medicine, Stanford, CA) B Bita Fakhri (1Division of Hematology, Department of Medicine, Stanford University School of Medicine, Stanford, CA) X Xiaoyu Zhang S Sydney X. Lu (1Division of Hematology, Department of Medicine, Stanford University School of Medicine, Stanford, CA)

Abstract

Abstract Oncogenic mutations of SF3B1 are common in myeloid cancers, chronic lymphocytic leukemia (CLL), and select solid tumors. Their mechanistic basis for promoting oncogenesis has been investigated in detail, with the stereotyped missplicing of messenger RNA (mRNA) protein coding sequences most intensively studied. These changes, in genes such as MAP3K7, BRD9, and ABCB7, typically lead to loss of function, thus contributing to cancer pathogenesis. Here, we systematically analyzed the impact of mutant SF3B1 on noncoding regions of mRNA transcripts across disease types, in both cell lines and primary patient specimens. This identified numerous novel and highly reproducible splicing alterations in such regions. Studies of a target gene, DCAF16, revealed multiple complex mutation-induced alterations in its 5′ and 3′ untranslated regions (UTRs). Remarkably, these were mechanistically associated with increased DCAF16 protein levels in SF3B1-mutant cells, representing, to our knowledge, the first time that oncogenic SF3B1 has been found to increase levels of a target protein in a gain-of-function manner. DCAF16 is a substrate recognition adapter for the DDB1/CUL4 E3 ubiquitin ligase complex. Novel protein degrader small molecules that coopt DCAF16 to degrade BRD4 as a neosubstrate demonstrated preferential selectivity for SF3B1-mutant cancers and CLL primary patient specimens due to increased DCAF16 protein levels. In turn, this reveals the therapeutic relevance of mutant SF3B1 dysregulation of transcript UTRs and uncovers a novel strategy for the treatment of these important neoplasms.

Article Details

Journal Blood
Volume / Issue Vol. 147, Issue 17
Published April 23, 2026
Pages 1941-1957
ISSN 0006-4971
Publisher Elsevier BV

Journal Info

Blood

Elsevier BV

ISSN: 0006-4971 Health Sciences

Authors (39)

M

Michal Sekrecki

1Division of Hematology, Department of Medicine, Stanford University School of Medicine, Stanford, CA

A

Agata Sekrecka

1Division of Hematology, Department of Medicine, Stanford University School of Medicine, Stanford, CA

R

Rohan R. Lattupally

1Division of Hematology, Department of Medicine, Stanford University School of Medicine, Stanford, CA

K

Kenny Le

1Division of Hematology, Department of Medicine, Stanford University School of Medicine, Stanford, CA

X

Xiaokang Jin

Department of Chemistry

C

Chen Mozes

2Department of Chemistry, Northwestern University, Chicago, IL

B

Brendan G. Dwyer

Department of Chemical and Systems Biology, ChEM-H, and Stanford Cancer Institute, Stanford School of Medicine

Z

Zhe Zhuang

Department of Chemical and Systems Biology, ChEM-H and Stanford Cancer Institute, Stanford Medical School

B

Bryan A. Romero

Department of Chemical and Systems Biology, ChEM-H, and Stanford Cancer Institute, Stanford School of Medicine

J

Jose M. B. Pineda

1Division of Hematology, Department of Medicine, Stanford University School of Medicine, Stanford, CA

X

Xunhong Cao

1Division of Hematology, Department of Medicine, Stanford University School of Medicine, Stanford, CA

L

Linh Nguyen

V

Vicky Chen

C

Crystal M. Zhou

1Division of Hematology, Department of Medicine, Stanford University School of Medicine, Stanford, CA

J

Jared A. Wallace

1Division of Hematology, Department of Medicine, Stanford University School of Medicine, Stanford, CA

K

Kailee Tanaka

C

Charu Tiwari

1Division of Hematology, Department of Medicine, Stanford University School of Medicine, Stanford, CA

A

Austin Gabel

6Department of Genome Sciences and Medical Scientist Training Program, University of Washington, Seattle, WA

W

Won Jun Kim

R

Robert F. Stanley

7Molecular Pharmacology Program, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, NY

S

Salima Benbarche

Molecular Pharmacology Program, Sloan Kettering Institute

J

Jaspreet Thind

Department of Cell Biology and Genetics, Texas A&M University Health Science Center

A

Abhinaya Muruganandham

8Department of Cell Biology and Genetics, Texas A&M University Health Science Center, Bryan, TX

T

Tian Yi Zhang

1Division of Hematology, Department of Medicine, Stanford University School of Medicine, Stanford, CA

P

Peter L. Greenberg

1Division of Hematology, Department of Medicine, Stanford University School of Medicine, Stanford, CA

J

Jason R. Gotlib

1Division of Hematology, Department of Medicine, Stanford University School of Medicine, Stanford, CA

G

Gabriel Mannis

1Division of Hematology, Department of Medicine, Stanford University School of Medicine, Stanford, CA

W

William E. Shomali

1Division of Hematology, Department of Medicine, Stanford University School of Medicine, Stanford, CA

G

Giselle Salmasi

1Division of Hematology, Department of Medicine, Stanford University School of Medicine, Stanford, CA

C

Calvin Kuo

T

Tait Shanafelt

1Division of Hematology, Department of Medicine, Stanford University School of Medicine, Stanford, CA

I

Irtisha Singh

Interdisiplinary program in Genetics and Genomics, College of Agriculture and Life Sciences, Texas A&M University

D

Daichi Inoue

F

Finn K. Hansen

11Department of Pharmaceutical and Cell Biological Chemistry, Pharmaceutical Institute, University of Bonn, Bonn, Germany

N

Nathanael S. Gray

C

Capucine van Rechem

4Department of Pathology, Stanford University School of Medicine, Stanford, CA

B

Bita Fakhri

1Division of Hematology, Department of Medicine, Stanford University School of Medicine, Stanford, CA

X

Xiaoyu Zhang

S

Sydney X. Lu

1Division of Hematology, Department of Medicine, Stanford University School of Medicine, Stanford, CA