Brooke Emerling, Ph.D.

Brooke Emerling's Research Focus

Breast Cancer, Cancer
Cancer Biology, Cancer Metabolism, Cell Signaling, Metabolic Processes, Signal Transduction

Research in the Emerling Lab is focused on understanding key signaling and metabolic pathways involved in the regulation of cellular function under pathological conditions such as cancer. Our research program centers around dissecting the roles of the family of non-canonical phosphatidylinositol kinases, called the phosphatidylinositol-5-phosphate 4-kinases (PI5P4Ks), in cancer metabolism using a multi-disciplinary approach integrating human, mouse, and worm models. Currently, a major research project in the Emerling Lab is determining the role of the PI5P4Ks in p53 mutant cancers, especially the triple-negative breast cancer subgroup where targeted therapies have not been effective.

Brooke Emerling's Bio

Emerling received her B.A. from the University of California Santa Cruz and her Ph.D. in molecular and cellular biology from Northwestern University. Emerling did her postdoctoral training at Harvard Medical School. She then became an Instructor of Cancer Biology in Medicine at Weill Cornell Medical College in New York City, where she continued her research on lipid kinase signaling and cancer metabolism. In August 2016, Brooke joined the faculty at SBP Medical Discovery Institute as an Assistant Professor in the Cancer Metabolism and Signaling Networks Program.
 

Funding Awards and Collaborative Grants

Breast Cancer Research Foundation - AACR Career Development Award for Translational Breast Cancer Research
Mary Kay Foundation Innovative Translational Grant Award
Department of Defense Breast Research Program Breakthrough Award
 

Honors and Recognition

2014: NextGen Star – AACR Early-Career Speaker Award
2013-2016: Mastercard Ajay Banga Scientist Award
2013: AACR – Aflac Travel Fellowship Award


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Publications

Phosphatidylinositol-5-Phosphate 4-Kinases Regulate Cellular Lipid Metabolism By Facilitating Autophagy.

Lundquist MR, Goncalves MD, Loughran RM, Possik E, Vijayaraghavan T, Yang A, Pauli C, Ravi A, Verma A, Yang Z, Johnson JL, Wong JCY, Ma Y, Hwang KS, Weinkove D, Divecha N, Asara JM, Elemento O, Rubin MA, Kimmelman AC, Pause A, Cantley LC, Emerling BM

Mol Cell 2018 May 3 ;70(3):531-544.e9

The Lipid Kinase PI5P4Kβ Is an Intracellular GTP Sensor for Metabolism and Tumorigenesis.

Sumita K, Lo YH, Takeuchi K, Senda M, Kofuji S, Ikeda Y, Terakawa J, Sasaki M, Yoshino H, Majd N, Zheng Y, Kahoud ER, Yokota T, Emerling BM, Asara JM, Ishida T, Locasale JW, Daikoku T, Anastasiou D, Senda T, Sasaki AT

Mol Cell 2016 Jan 21 ;61(2):187-98

Depletion of a putatively druggable class of phosphatidylinositol kinases inhibits growth of p53-null tumors.

Emerling BM, Hurov JB, Poulogiannis G, Tsukazawa KS, Choo-Wing R, Wulf GM, Bell EL, Shim HS, Lamia KA, Rameh LE, Bellinger G, Sasaki AT, Asara JM, Yuan X, Bullock A, Denicola GM, Song J, Brown V, Signoretti S, Cantley LC

Cell 2013 Nov 7 ;155(4):844-57

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Endogenous spacing enables co-processing of microRNAs and efficient combinatorial RNAi.

Amen AM, Loughran RM, Huang CH, Lew RJ, Ravi A, Guan Y, Schatoff EM, Dow LE, Emerling BM, Fellmann C

Cell Rep Methods 2022 Jul 18 ;2(7):100239

Mechanistic roles of mutant p53 governing lipid metabolism.

Loughran RM, Emerling BM

Adv Biol Regul 2022 Jan ;83:100839

Expanding role of PI5P4Ks in cancer: A promising druggable target.

Arora GK, Palamiuc L, Emerling BM

FEBS Lett 2022 Jan ;596(1):3-16

A Functional Precision Oncology Approach to Identify Treatment Strategies for Myxofibrosarcoma Patients.

Pauli C, De Boni L, Pauwels JE, Chen Y, Planas-Paz L, Shaw R, Emerling BM, Grandori C, Hopkins BD, Rubin MA

Mol Cancer Res 2022 Feb ;20(2):244-252

PI5P4Ks drive metabolic homeostasis through peroxisome-mitochondria interplay.

Ravi A, Palamiuc L, Loughran RM, Triscott J, Arora GK, Kumar A, Tieu V, Pauli C, Reist M, Lew RJ, Houlihan SL, Fellmann C, Metallo C, Rubin MA, Emerling BM

Dev Cell 2021 Jun 7 ;56(11):1661-1676.e10

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