PIPages
Labs

Laura Calvi

University of Rochester, NY·Medicine & Clinical Research

Cells do not become cancerous, or stay healthy, in isolation: the surrounding tissue — its immune cells, support cells and signals — strongly influences whether disease starts, spreads and responds to treatment. Work here centers on the bone marrow, the tissue where blood and immune cells are made, and on how that environment changes with age.

Fields

Medicine & Clinical Research

Physiology

Microbiology & Immunology

Topics

clonal hematopoiesis

myelodysplastic syndromes

bone marrow niche

Grants
3 known grants, through Feb 2030

What they work on

  1. Test whether pre-leukemic mutant blood cells form clones and progress to myelodysplastic syndromes more readily in an aged marrow environment, by transplanting mouse models of clonal hematopoiesis into young versus aged recipient mice.
  2. Determine whether overexpressing SIRT6, a regulator of genome stability that silences mobile DNA elements, in marrow macrophages and multipotent stromal cells slows microenvironmental aging, clonal expansion and progression to myeloid neoplasms.
  3. Test whether blocking LINE1 retrotransposition with nucleoside reverse transcriptase inhibitors (NRTIs), drugs developed for HIV, reduces marrow inflammation and slows clonal expansion, and use this to uncover niche regulators of clonal progression.
  4. Define how bone marrow mesenchymal stromal cells engulf dying cells (efferocytosis) in vivo, including the role of the phosphatidylserine receptor BAI1 that recognizes apoptotic cells, using transgenic and aged mice.
  5. Determine whether excessive efferocytosis causes oxidative stress, mitochondrial dysfunction and senescence in mesenchymal stromal cells, reducing their ability to become bone-forming osteoblasts.
  6. Establish the role of stromal cell efferocytosis in normal bone-immune interactions and in age-related bone loss, using aging and genetic mouse models.
  7. Pursue program-level goals of disrupting and reprogramming cancer-promoting tissue microenvironments and restoring tissue homeostasis after cancer and cancer treatment injury, using genetic models and patient-derived specimens.

More about the research

Two linked ideas run through the projects: that an aged marrow environment becomes inflamed and drives mutated blood cell clones toward malignancy, and that the marrow's stromal support cells lose function with age in ways that cost the skeleton bone. A third, broader effort coordinates cancer microenvironment research across a cancer center.

Why it matters

Mutated blood-cell clones are common in older adults and raise the risk of bone marrow failure, myeloid cancer and cardiovascular disease, while age-related bone loss causes widespread fractures and disability. Identifying inflammation from mobile DNA elements and overloaded dead-cell clearance as drivers could point to preventive strategies, including repurposed reverse transcriptase inhibitors. The cancer microenvironment program aims to translate findings on tumor-supporting tissues into trials and to reduce treatment-related injury in cancer survivors.

Known grants

From NIH and NSF research grants. Labs often have other funding we can't see.

Cancer Microenvironment Research Program

NIH · Mar 2025 – Feb 2030

Mechanisms of marrow microenvironmental aging and their impact of progression of clonal hematopoiesis

NIH · Jul 2022 – Mar 2027

Efferocytosis by Bone Marrow Stromal Cells and Bone Aging

NIH · Jun 2022 – Feb 2027

Closest labs

Teresa V Bowman

Albert Einstein College of Medicine, NY·Genetics

Test whether DDX41 insufficiency cooperates with age-associated activity of cGAS, an inflammation-triggering DNA sensor, to impair blood stem and progenitor cells in germline ddx41 heterozygous zebrafish that develop MDS-like disease.

Golam Mohi

University of Virginia, VA·Medicine & Clinical Research

Determine how loss of PTPN1, a signal-shutting enzyme deleted with chromosome 20q, cooperates with the JAK2V617F mutation to drive myeloproliferative neoplasm progression and bone marrow fibrosis.

Lukasz Gondek

Johns Hopkins University, MD·Medicine & Clinical Research

Determine the cancer-causing potential of donor-derived CHIP in transplant recipients, using a cohort of 1,857 donors over 40 and serial recipient samples to separate true driver mutations from background aging mutations.

The school

University of Rochester: 38 labs on PI Pages, $492M a year on research, 308 research doctorates a year.

More about University of Rochester

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