Ronen Lab

The goal of the research performed in the Ronen lab is to develop and mechanistically validate robust noninvasive translatable magnetic resonance (MR)–based biomarkers that can be used to identify oncogenic events associated with cancer, and to monitor response to a broad range of therapies including chemotherapy, targeted therapies, immunotherapies etc.

To this end, our research uses multinuclearMR spectroscopy (MRS), imaging (MRI) and spectroscopic imaging (MRSI) to probe preclinical cell and animal models of cancer. Putative biomarkers are mechanistically validated using established biochemical, cell and molecular biological methods.


2013 Imaging Research Symposium

Myriam Chaumeil receives the Hasegawa Award for excellence in biomedical imaging, October 2013







Employment Opportunities for staff positions are posted through the UCSF Department of Human Resources

Rotations and Post-doctoral Opportunities

Rotations provide an opportunity to explore research opportunities in the Ronen Lab and are currently available in several areas of ongoing research. For further information, please contact Dr. Ronen.

Post-doctoral Opportunities (doc)


Complete list of publications can be found at Dr. Sabrina Ronen's UCSF profile under "Publications."

Or visit a full list of publications at the NCBI website,


Myriam Chaumeil, PhD
Assistant Researcher


Marina Radoul, PhD
Post Doctoral Fellow



Jose-Luis Izquierdo-Garcia, PhD
Post Doctoral Fellow


Chloe Najac, PhD
Post Doctoral Fellow   


Pavithra Viswanath, PhD        


Pia Eriksson
Lab Manager



Caroline Guglielmetti
Visiting graduate student



Cathy Devine


Research Directions 

Pyruvate metabolism as a biomarker of PI3K signaling in cancer (Funding: NIH R01)

The PI3K pathway is mutated in over 30% of human cancers and in 88% of glioblastoma (GBM) cases. We hypothesized that because the PI3K pathway mediates the expression of enzymes controlling the glycolytic pathway, probing the last step of the glycolytic pathway using hyperpolarized 13C MRS will inform on the status of PI3K signaling. We have confirmed this hypothesis and shown that the pyruvate to lactate conversion is inhibited following PI3K inhibition in breast cancer and GBM cells. Furthermore, we have now shown that response to treatment with PI3K pathway inhibitors, and increased survival, are better predicted by pyruvate metabolism than by tumor size in orthotopic tumor-bearing mice (see figure). Future work will focus on translating our findings to patients. This research will validate a novel radiation free imaging method to monitor the effect of PI3K inhibitors in vivo.

Monitoring the mutational status and activity of isocitrate dehydrogenase (IDH) in glioma (Funding: NIH R21, NIH R01)

Mutant  forms of IDH have recently been discovered in over 70% of grade II, III and secondary GBM. Recent studies indicate that the IDH mutation is an early oncogenic event and inhibiting mutant IDH activity is being considered as a novel therapeutic approach in the treatment of tumors that harbor this mutation. Our work is focused on developing and validating hyperpolarized 13C and 1H MRS-based approaches for monitoring IDH mutational status and activity, as well as metabolic reprogramming associated with IDH mutation. These approaches could help both in development of novel IDH inhibitors and in monitoring the effect of such inhibitors in future trials.

IDH mutation causes metabolic reprogramming. Metabolic profiling clearly discriminates between wild-type (blue) and mutant IDH cells (red) in both U87 (A) and NHA (B) cell lines.

Non-invasive in vivo assessment of IDH1 mutational status using hyperpolarized [1-13C] α-ketoglutarate in glioma (a) T2-weighted anatomical MR image of the head of a U87IDHmut (top) and a U87IDHwt (bottom) tumor-bearing animal overlaid with the grid used for 2D 13C CSI acquisition. The tumors appear as hyperintense regions. (b) Corresponding heatmap of hyperpolarized [1-13C] α-KG at 20s post injection. (c) Corresponding heatmap of hyperpolarized [1-13C] 2-HG at 20s post injection, illustrating the presence of this metabolite in IDH1 mutant tumors only. From Chaumeil M. M. et al, Nature Communications (2013)

Choline-containing metabolites as biomarkers of cancer (Funding: NIH R01)

Clinical studies demonstrate that phosphocholine (PC) and total-choline-containing metabolite (tCho) levels are elevated in virtually all cancer types. Research in the lab has shown that PC synthesis is modulated by signaling via Ras, MAPK and PI3K. To further our understanding of the link between oncogenic signaling and PC levels, we are investigating the precise mechanism by which oncogenes affect choline metabolism in breast, prostate and brain cancer. This work will serve to validate PC as a biomarker of oncogenic transformation and will test the value of PC as a marker of response to novel oncogene-targeted therapies.

(A) PC level as measured by 1H MRS in cell lysates as a function of time for control GS-2 cells and GS-2 cells treated with LY294002, everolimus, and temozolomide. (B) 31P MR spectrum of perfused control GS-2 cells. PC levels decreased following inhibition of PI3K by LY294002, in line with the observed drop in ChoK activity (A). From Venkatesh HS Neuro Oncol. 2012

Metabolic alterations as a readout for response to therapy in recurrent GBM (Funding: NIH PO1).

The goal of this collaborative study is to determine if treatment-induced alterations in metabolism detected by hyperpolarized 13C magnetic resonance spectroscopic imaging (MRSI) can be used as a biomarker to assess target inhibition, and early response in recurrent glioblastoma (GBM). Current studies are focused on investigating response to a range of therapies in pairs of sensitive and resistant cells. Early findings indicate that metabolic alterations inform on response as well as development of resistance. Future work is expected to include animal and patient studies.

Determining the metabolomic profile of pancreatic cancer (Funding:Schwartz Pancreatic Cancer fund)

By investigating cell lines, pancreatic juices, mouse models and patients biopsies, this study is focused on identifying 13C MRS detectable metabolic alterations and characteristic 1H MRS-based metabolomic signatures of pancreatic cancer. Our findings indicate a 1H MRS-detectable alteration in lipid metabolism and studies are underway to understand the significance of these observations.