Erinn Rankin
Stanford University, CA·Pharmacology
Cancer cells rewire their metabolism to fuel rapid growth, and both projects here target the same control switch over that rewiring: an enzyme called FTO (fat-mass and obesity-associated protein). FTO is a demethylase, meaning it strips a chemical tag called m6A off messenger RNA.
- Fields
Pharmacology
Medicine & Clinical Research
Biochemistry
- Topics
m6A
RNA demethylase
epitranscriptomics
- Grants
- 2 known grants, through Feb 2028
What they work on
- Test whether FTO, an enzyme that removes m6A chemical tags from RNA, drives glutamine rewiring in VHL-deficient kidney cancer by raising levels of SLC1A5, the protein that imports glutamine into cells.
- Determine whether FTO inhibitors create an exploitable metabolic vulnerability in clear cell renal cell carcinoma, testing tumors that respond to the HIF-2 blocker belzutifan and tumors that have become resistant to it.
- Measure the anti-tumor effect of combining FTO blockade with radiation across cervical, non-small cell lung and head and neck tumor models, using both gene knockdown and small-molecule FTO inhibitors.
- Distinguish whether FTO inhibition sensitizes cancer cells to radiation through reduced glutamine metabolism, impaired handling of oxidative stress, or weaker DNA damage repair, using knockdown and gain-of-function approaches.
- Test whether switching off FTO spares normal tissue, assessing acute and late radiation injury in bone marrow, intestine, salivary gland, oral mucosa and lung in mice with global conditional FTO inactivation.
More about the research
Those tags help decide how long an RNA lasts and how much protein it makes, so removing them changes which genes a cell effectively uses, a layer of regulation known as the epitranscriptome. One project asks how FTO sustains kidney cancer; the other asks whether blocking FTO makes tumors easier to kill with radiation. Both converge on glutamine, an amino acid tumors consume heavily, and on SLC1A5, the transporter protein that pulls glutamine into cells.
Why it matters
Kidney cancer is among the ten most common cancers, and survival for advanced clear cell renal cell carcinoma remains about 11%, so new targets that kill the cancer cells themselves are needed. If FTO controls glutamine supply through SLC1A5, FTO inhibitors already in clinical development could offer a treatment option for tumors that never respond, or stop responding, to belzutifan. In cervical, lung and head and neck cancers, the same drugs could make radiotherapy more effective without adding harm to healthy tissue, which would widen the safety margin for patients receiving radiation.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Yin Xi
University of Texas Southwestern Medical Center, TX·Medicine & Clinical Research
Measure blood flow in clear cell renal cell carcinoma with arterial spin labeling (ASL) MRI and test whether it matches tumor regions with molecular changes that drive new blood vessel growth, such as HIF and VEGF activity.
Joshua T Mendell
University of Texas Southwestern Medical Center, TX·Biochemistry
Determine how altering dihydrouridine synthase (DUS) activity changes D modifications on tRNAs, overall tRNA metabolism and the PTMD mRNA-decay pathway in human and mouse ccRCC cells.
Sunil Sudarshan
University of Alabama at Birmingham, AL·Biochemistry
Determine the molecular mechanism by which the oncometabolite L-2-hydroxyglutarate promotes the mRNA mark N6-methyladenosine (m6A) in renal cell carcinoma, and establish what this RNA hypermethylation does to gene expression.
The school
Stanford University: 87 labs on PI Pages, $1.6B a year on research, 739 research doctorates a year.
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