Laurianne Van Landeghem
North Carolina State University, NC·Medicine & Clinical Research
Advanced colon cancer often stops responding to chemotherapy, and this resistance largely explains why few patients survive five years. Chemotherapy drugs are designed to stop cancer cells from dividing and make them self-destruct.
- Fields
Medicine & Clinical Research
Physiology
Pharmacology
- Topics
colon cancer
colorectal cancer
chemoresistance
- Grants
- 1 known grant, through Mar 2028
What they work on
- Determine whether enteric glial cells help colon cancer stem cells resist chemotherapy by releasing FSTL3, using primary human cell cultures and 3D co-culture platforms.
- Test whether glial protection works by boosting DNA repair through the MRN-ATM pathway, a central DNA-repair system, in cancer stem cells exposed to chemotherapy drugs.
- Determine whether blocking FSTL3 production in enteric glia makes colon tumors more sensitive to chemotherapy in vivo, using GFAP-CreERT2 mice that allow gene deletion only in glial cells.
- Profile how chemotherapy-activated enteric glia change tumor signaling, using GFAP-hM3Dq mice whose glia can be switched on by a drug, single-cell RNA sequencing and mass spectrometry.
More about the research
They overlook protective signals coming from the healthy cells around the tumor. One such neighbor is the enteric glial cell (EGC), a support cell of the gut's nervous system that normally helps the colon lining stay sealed and heal.
Why it matters
Chemotherapy resistance is a main reason patients with advanced colon cancer die. If blocking FSTL3, a protein released by enteric glial cells, makes tumors sensitive to chemotherapy again, it could point to combination treatments that pair a targeted therapy with standard chemotherapy to improve outcomes for these patients.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Daniela Matei
Northwestern University, IL·Medicine & Clinical Research
Identify DNA-packing and epigenetic features unique to ovarian cancer stem cells by combining Hi-C, ATAC-seq, ChIP-seq and single-cell RNA sequencing with nanoscale chromatin imaging.
Xunlei Kang
University of Missouri-Columbia, MO·Medicine & Clinical Research
Determine how DPP4, a cell-surface enzyme, controls the location, survival and self-renewal of human AML stem cells, using colony-forming assays and mice carrying human AML cells.
Stefanie Galban
University of Michigan, MI·Medicine & Clinical Research
Determine how ALDH1A3 and ALDH2, enzymes marking cancer stem cells, are controlled by the H3 K27M histone mutation and by IL1β from microglia, using isogenic DIPG models in vitro and in vivo.
The school
North Carolina State University: 40 labs on PI Pages, $717M a year on research, 603 research doctorates a year.
Reach out
A start for your email. Fill in the brackets.