Shannon Elf, PhD

  • Assistant Professor of Ben May Department of Cancer Research
  • Research and Scholarly Interests: Calreticulin, Hematopoietic Malignancies, Leukemia, Acute Myeloid, Metabolism, Myeloproliferative Disorders, Targeted Molecular Therapies, Unfolded Protein Response
  • Websites: Elf Lab, Research Network Profile
  • Contact: shannonelf@uchicago.edu

Although the genes that drive the development of myeloid blood cancers have largely been defined, there are currently few effective targeted treatment strategies for these diseases. The development of imatinib to treat BCR/ABL-­positive chronic myeloid leukemia remains the only true success story, with the majority of targeted therapies for myeloid malignancies demonstrating unimpressive clinical activity. This illuminates the need to exploit the molecular understanding that has been gained in the last decade through cancer exome sequencing to identify novel therapeutic vulnerabilities in myeloid malignancies.



Research in the Elf Lab focuses on identifying unique molecular dependencies in myeloid blood cancers that can be targeted for therapeutic intervention, with the long­-term goal of improving upon current treatment regimens for these diseases. Currently, our work focuses on understanding the role of the unfolded protein response (UPR) in myeloproliferative neoplasms (MPN) and acute myeloid leukemia (AML). Using molecular, biochemical, and cellular approaches in both in vitro and in vivo models, we aim to dissect the molecular mechanisms underlying UPR activation in specific subsets of MPN and AML, and to use this mechanistic insight to develop rationally designed therapies to target the UPR in these challenging diseases.

Harvard Medical School / Brigham & Women’s Hospital
Boston, MA
Postdoctoral training - Hematology
2019

Emory University
Atlanta, GA
Ph.D. - Molecular & Systems Pharmacology
2013

Bowdoin College
Brunswick, ME
A.B. - Biology & Music, English minor
2003

Increased CXCL4 expression in hematopoietic cells links inflammation and progression of bone marrow fibrosis in MPN.
Gleitz HFE, Dugourd AJF, Leimkühler NB, Snoeren IAM, Fuchs SNR, Menzel S, Ziegler S, Kröger N, Triviai I, Büsche G, Kreipe H, Banjanin B, Pritchard JE, Hoogenboezem R, Bindels EM, Schumacher N, Rose-John S, Elf S, Saez-Rodriguez J, Kramann R, Schneider RK. Increased CXCL4 expression in hematopoietic cells links inflammation and progression of bone marrow fibrosis in MPN. Blood. 2020 Oct 29; 136(18):2051-2064.
PMID: 32726410

"All Our Wisdom is Stored in the Trees" - Degrading BCR-ABL with Berberis Vulgaris.
Elf SE. "All Our Wisdom is Stored in the Trees" - Degrading BCR-ABL with Berberis Vulgaris. Clin Cancer Res. 2020 Aug 01; 26(15):3899-3900.
PMID: 32398325

Defining the requirements for the pathogenic interaction between mutant calreticulin and MPL in MPN.
Elf S, Abdelfattah NS, Baral AJ, Beeson D, Rivera JF, Ko A, Florescu N, Birrane G, Chen E, Mullally A. Defining the requirements for the pathogenic interaction between mutant calreticulin and MPL in MPN. Blood. 2018 02 15; 131(7):782-786.
PMID: 29288169

Tetrameric Acetyl-CoA Acetyltransferase 1 Is Important for Tumor Growth.
Fan J, Lin R, Xia S, Chen D, Elf SE, Liu S, Pan Y, Xu H, Qian Z, Wang M, Shan C, Zhou L, Lei QY, Li Y, Mao H, Lee BH, Sudderth J, DeBerardinis RJ, Zhang G, Owonikoko T, Gaddh M, Arellano ML, Khoury HJ, Khuri FR, Kang S, Doetsch PW, Lonial S, Boggon TJ, Curran WJ, Chen J. Tetrameric Acetyl-CoA Acetyltransferase 1 Is Important for Tumor Growth. Mol Cell. 2016 12 01; 64(5):859-874.
PMID: 27867011

Targeting 6-phosphogluconate dehydrogenase in the oxidative PPP sensitizes leukemia cells to antimalarial agent dihydroartemisinin.
Elf S, Lin R, Xia S, Pan Y, Shan C, Wu S, Lonial S, Gaddh M, Arellano ML, Khoury HJ, Khuri FR, Lee BH, Boggon TJ, Fan J, Chen J. Targeting 6-phosphogluconate dehydrogenase in the oxidative PPP sensitizes leukemia cells to antimalarial agent dihydroartemisinin. Oncogene. 2017 01 12; 36(2):254-262.
PMID: 27270429

Mutant Calreticulin Requires Both Its Mutant C-terminus and the Thrombopoietin Receptor for Oncogenic Transformation.
Elf S, Abdelfattah NS, Chen E, Perales-Patón J, Rosen EA, Ko A, Peisker F, Florescu N, Giannini S, Wolach O, Morgan EA, Tothova Z, Losman JA, Schneider RK, Al-Shahrour F, Mullally A. Mutant Calreticulin Requires Both Its Mutant C-terminus and the Thrombopoietin Receptor for Oncogenic Transformation. Cancer Discov. 2016 Apr; 6(4):368-81.
PMID: 26951227

Inhibition of human copper trafficking by a small molecule significantly attenuates cancer cell proliferation.
Wang J, Luo C, Shan C, You Q, Lu J, Elf S, Zhou Y, Wen Y, Vinkenborg JL, Fan J, Kang H, Lin R, Han D, Xie Y, Karpus J, Chen S, Ouyang S, Luan C, Zhang N, Ding H, Merkx M, Liu H, Chen J, Jiang H, He C. Inhibition of human copper trafficking by a small molecule significantly attenuates cancer cell proliferation. Nat Chem. 2015 Dec; 7(12):968-79.
PMID: 26587712

6-Phosphogluconate dehydrogenase links oxidative PPP, lipogenesis and tumour growth by inhibiting LKB1-AMPK signalling.
Lin R, Elf S, Shan C, Kang HB, Ji Q, Zhou L, Hitosugi T, Zhang L, Zhang S, Seo JH, Xie J, Tucker M, Gu TL, Sudderth J, Jiang L, Mitsche M, DeBerardinis RJ, Wu S, Li Y, Mao H, Chen PR, Wang D, Chen GZ, Hurwitz SJ, Lonial S, Arellano ML, Khoury HJ, Khuri FR, Lee BH, Lei Q, Brat DJ, Ye K, Boggon TJ, He C, Kang S, Fan J, Chen J. 6-Phosphogluconate dehydrogenase links oxidative PPP, lipogenesis and tumour growth by inhibiting LKB1-AMPK signalling. Nat Cell Biol. 2015 Nov; 17(11):1484-96.
PMID: 26479318

Metabolic Rewiring by Oncogenic BRAF V600E Links Ketogenesis Pathway to BRAF-MEK1 Signaling.
Kang HB, Fan J, Lin R, Elf S, Ji Q, Zhao L, Jin L, Seo JH, Shan C, Arbiser JL, Cohen C, Brat D, Miziorko HM, Kim E, Abdel-Wahab O, Merghoub T, Fröhling S, Scholl C, Tamayo P, Barbie DA, Zhou L, Pollack BP, Fisher K, Kudchadkar RR, Lawson DH, Sica G, Rossi M, Lonial S, Khoury HJ, Khuri FR, Lee BH, Boggon TJ, He C, Kang S, Chen J. Metabolic Rewiring by Oncogenic BRAF V600E Links Ketogenesis Pathway to BRAF-MEK1 Signaling. Mol Cell. 2015 Aug 06; 59(3):345-358.
PMID: 26145173

Distinct effects of concomitant Jak2V617F expression and Tet2 loss in mice promote disease progression in myeloproliferative neoplasms.
Chen E, Schneider RK, Breyfogle LJ, Rosen EA, Poveromo L, Elf S, Ko A, Brumme K, Levine R, Ebert BL, Mullally A. Distinct effects of concomitant Jak2V617F expression and Tet2 loss in mice promote disease progression in myeloproliferative neoplasms. Blood. 2015 Jan 08; 125(2):327-35.
PMID: 25281607

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