Practice Locations

UCHealth University of Colorado Hospital (UCH)
12605 E. 16th Ave Aurora, CO 80045


Michael Alberti, MD, PhD

Molecular Genetic

Board Certified


Practice Locations

UCHealth University of Colorado Hospital (UCH)
12605 E. 16th Ave, Aurora, CO 80045


Provider Expertise

Clinical Interest for Patients

My main clinical interests include clinical pathology and molecular/genetic pathology, particularly the genetics of myeloid malignancies (MDS, MPN, AML).


  • Molecular Genetic ( 2017 )
  • Clinical ( 2016 )

Education & Training

Medical Schools

MD, University of Alabama School of Medicine (2013)

Undergraduate Schools

BS, California Lutheran University (CA) (2005)

Graduate Schools

PhD, University of Alabama at Birmingham (2011)

Residency Program

UCLA Medical Center Program (2016)


Washington University in St. Louis (2017)

Professional Memberships

Academy of Clinical Laboratory Physicians and Scientists (ACLPS), Member

American Association for the Advancement of Science (AAAS), Member

American Physician Scientists Association (APSA), Member

American Society of Hematology (ASH), Member

Association for Molecular Pathology (AMP), Member

International Society for Experimental Hematology (ISEH), Member

Research & Grants


Distinct roles of U2AF1 mutations in MDS pathogenesis (2021)

Distinct roles of U2AF1 mutations in myelodysplastic syndrome pathogenesis (2021)

Research Interests for Patients

As a physician-scientist I am interested in understanding the genetic and molecular basis of splicing factor gene mutations in clonal hematopoiesis and myeloid malignancies, such as myelodysplastic syndromes (MDS). My postdoctoral work demonstrated that mutations in the U2AF1 splicing factor gene provide an ideal model for these studies as they occur at one of two hotspot codons (S34 and Q157) in separate zinc finger domains, and each of these mutations are associated with different clinical features, outcomes, alternative splicing, and co-occurring gene mutations in MDS patients. Complimentary experiments using U2af1(S34F/+) and U2af1(Q157R/+) small animal models support these observations and have also revealed differential activation of several key signaling pathways. The goal of our lab's research program is focused on answering the following questions: (1) Why are splicing factor mutations highly enriched in clonal myeloid malignancies (e.g., MDS) compared to other types of cancer? (2) What are the individual and shared mechanisms by which different splicing factor mutations induce MDS? (3) What are the dynamics facilitating acquisition of additional mutations in the context of splicing factor mutant disease?

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