Brooke Emerling, PhD - Sanford Burnham Prebys

Emerling received her B.A. from the University of California Santa Cruz and her PhD 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 Sanford Burnham Prebys 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

Related Disease
Breast Cancer, Cancer

Phenomena or Processes
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.

Press Release: Study offers new approach to starve p53 deficient tumors

9/25/18 Public Lecture – SBP Insights: Breast Cancer – Register Here

Still from video of Brooke Emerling, PhD

Select Publications

Showing 2 of 2

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

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Funding Awards and Collaborative Grants

Honors and Recognition

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

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

Biography

Funding Awards and Collaborative Grants

Honors and Recognition

Research

Select Publications

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

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