Marcus Goncalves
New York University, NY·Medicine & Clinical Research
What we eat and how our bodies handle sugar and insulin can shape both obesity and cancer. Fructose, found in table sugar, honey and high-fructose corn syrup (HFCS), is eaten in larger amounts today than ever recorded, and obesity raises insulin levels and the risk of dying from some cancers.
- Fields
Medicine & Clinical Research
Biochemistry
Physiology
- Topics
fructose
obesity
colorectal cancer
- Grants
- 3 known grants, through Jul 2028
What they work on
- Test whether fructose enlarges intestinal villi and boosts fat uptake by blocking PKM2, a sugar-metabolism enzyme, by genetically and pharmacologically altering ketohexokinase and PKM2 in mouse intestines.
- Define how pyruvate kinase activity controls fat metabolism in enterocytes, the gut's absorptive cells, using dietary and drug interventions in mice and intestinal organoids, which are lab-grown mini-guts.
- Determine whether PKM2 mediates the growth of larger, more aggressive intestinal tumors in mice given high-fructose corn syrup, using genetic and drug manipulation of PKM2.
- Test whether fructose 1-phosphate blocks PKM2 to help colorectal cancer cells survive low oxygen, using cell and human organoid cultures with KHK and PKM2 manipulated.
- Measure how fructose 1-phosphate binds and inhibits purified pyruvate kinase forms, using biochemical activity and structural assays of enzyme kinetics and subunit assembly.
- Examine how a very low carbohydrate diet, with or without a PI3K inhibitor, changes insulin/PI3K signaling, growth and cell-death markers in blood and tumors from endometrial cancer patients.
- Test whether canagliflozin, which prevents high blood sugar, or diazoxide, which prevents high insulin, improves the tumor response to PI3K inhibitors in patient-derived endometrial cancer xenografts in mice.
More about the research
The lab's grants study how these diet-driven signals change metabolism in the gut, in intestinal tumors and in endometrial cancer, and how blocking those signals could be used for treatment.
Why it matters
Obesity and high sugar intake are common and are tied to colorectal and endometrial cancer. This work could point to PKM2-activating drugs as a new way to fight obesity and fructose-driven colorectal cancer. It could also support combining insulin-lowering diets or drugs with PI3K inhibitors for patients with endometrial cancer. The grants note that such diet and drug strategies could be brought into clinical practice quickly if they succeed.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Suryavathi Viswanadhapalli
University of Texas Health Science Center at San Antonio, TX·Medicine & Clinical Research
Determine how LIF/LIFR signaling, a growth-factor pathway linked to poor survival, drives endometrial cancer progression, using global genomic approaches in endometrial cancer cells.
Jun He
Thomas Jefferson University, PA·Biochemistry
Determine how suppression of the microRNA miR-152 confers resistance to doxorubicin chemotherapy and radiation in triple-negative breast cancer cells, and test whether EZH2 and DNA hypermethylation are responsible for silencing miR-152.
Yaguang Xi
University of Georgia, GA·Pharmacology
Determine how the oncogenic microRNA miR-10b and its target gene NR4A3 contribute to the experimental compound LG007's activity against triple-negative breast cancer.
The school
New York University: 72 labs on PI Pages, $1.5B a year on research, 540 research doctorates a year.
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