Lalita Shevde
University of Alabama at Birmingham, AL·Medicine & Clinical Research
Breast tumors become dangerous when their cells loosen their grip on neighbors and on the surrounding scaffold, rebuild their internal skeleton, and start to invade. What allows a cell to make that switch is a change in the molecular programs it runs.
- Fields
Medicine & Clinical Research
Biochemistry
Pharmacology
- Topics
breast cancer
metastasis
Merlin
- Grants
- 3 known grants, through Feb 2028
What they work on
- Test whether blocking abnormally activated Hedgehog signaling reduces the invasive and metastasis-prone behavior of Merlin-deficient mammary tumors, using mammary-specific Nf2-knockout mouse tumors and tumor-derived organoids.
- Determine whether deregulated tryptophan metabolism, a route tumors use to dampen immune attack, is a targetable vulnerability in Merlin-deficient breast cancer models.
- Identify how the hexosamine biosynthetic pathway, fed by glucose, places the sugar modification O-GlcNAc on GLI transcription factors, and how this amplifies Hedgehog signaling to drive invasion and chemoresistance.
- Evaluate how an elevated O-GlcNAc landscape reshapes mammary tumors and their immune microenvironment, using two syngeneic mouse models plus human triple-negative breast cancer and patient-derived xenograft systems, and test whether inhibiting GLI uncouples these effects.
- Coordinate cancer research training through the Cancer Training and Career Development Office, expanding education activities, supporting early-stage investigators with mentorship and grant-writing programs, and creating pathways into cancer research careers at all training stages.
More about the research
Two projects in this lab trace two such programs, one set off by the loss of a tumor-suppressing protein that normally keeps cells anchored and growth in check, the other by a sugar modification that reflects how much glucose a tumor cell is consuming. Both converge on Hedgehog signaling, a developmental pathway reawakened in cancer, and both ask whether the resulting dependencies can be attacked therapeutically. A third award coordinates cancer research training at the institution's comprehensive cancer center.
Why it matters
Merlin protein is lost in advanced and metastatic breast tumors, yet no targeted drugs exist for Merlin-deficient cancers, including those of the nervous system; testing Hedgehog and tryptophan-metabolism strategies could supply translatable options extendable to other Merlin-deficient tumor types. Clarifying how glucose-driven O-GlcNAcylation activates Hedgehog signaling could explain why some breast tumors invade and resist chemotherapy, pointing to metabolic or GLI-directed interventions. The training award builds the cancer research and clinical workforce for the center's region.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Shiaw-Yih Lin
University of Texas MD Anderson Cancer Center, TX·Medicine & Clinical Research
Test whether scarce DNA building blocks (dNTPs) cause RNA to be misinserted into TNBC genomes, and whether blocking RNase H2 leaves these errors in place, causing lethal replication stress. Also identify how tumors resist the inhibitor.
Benjamin Allen
University of Michigan, MI·Genetics
Test how loss of Gli1, Gli2 or Gli3 — the transcription factors that execute Hedgehog signaling — individually and in combination affects pancreatic tumor growth, using new pancreatic fibroblast cell lines in co-transplantation assays with tumor cells.
Ozgur Sahin
Medical University of South Carolina, SC·Pharmacology
Test whether the collagen cross-linking function of lysyl oxidase (LOX) causes broad chemotherapy resistance in triple negative breast cancer, using CRISPR LOX knockout and reconstitution plus MALDI mass spectrometry imaging of drug penetration.
The school
University of Alabama at Birmingham: 45 labs on PI Pages, $866M a year on research, 166 research doctorates a year.
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