Photo of Masako  Nakanishi, PhD

Masako Nakanishi, PhD

Assistant Professor-in-Residence
Academic Office Location:
Center for Molecular Oncolgy
UConn Health
263 Farmington Avenue
Farmington, CT 06030-3101
Phone: 860-679-8703
Fax: 860-679-7639
Website(s):

Center for Molecular Oncology

Cell Biology Graduate Program

 The Rosenberg/Nakanishi laboratory focuses on the chemoprevention of colorectal cancer (CRC) and inflammatory bowel diseases (IBDs). A key focus of our work is the role of bioactive lipid signaling in colon carcinogenesis. We also investigate therapeutic interventions and nutritional strategies to modulate cancer risk.

 

Education
DegreeInstitutionMajor
BSShippensburg UniversityBiotechnology
PhDUniversity of Connecticut Health CenterBiomedical Science

Post-Graduate Training
TrainingInstitutionSpecialty
PostdoctoralUniversity of Connecticut Health CenterPostdoctoral Fellow

My primary focus is on elucidating the role of PGE2 signaling in colon carcinogenesis and inflammation. We utilize a range of animal models of colon cancer to investigate the mechanisms by which PGE2 promotes tumor growth and mucosal inflammation.


We are also exploring the chemopreventive benefits of natural products, including walnuts and omega-3 fatty acids, in preclinical mouse models. These intervention studies have expanded into clinical trials, with the goal of advancing translational approaches for colorectal cancer prevention.


In recent years, our work has expanded to investigate the role of estrogen in BRAF-mutated sessile serrated CRC. Sessile serrated lesions (SSLs) are more commonly observed in postmenopausal women. Estrogen is thought to confer chemoprotection against CRC in healthy women, protection that is likely lost during menopause. We are examining whether activation of estrogen signaling through ERβ agonist can restore its anti-tumorigenic activities. An overarching goal of this work is to evaluate the chemopreventive potential of ERβ activation in combination with BRAF inhibition in the at-risk colon, particularly in postmenopausal women. 

Role of PGE2 on CRC development: Genetic deletion of PGE2 synthase (Ptges) significantly suppress CRC in multiple mouse models, suggesting an alternative strategy to reduce PGE2 levels.  We are currently examining the potential mechanisms of tumor suppression using multiple mouse models.  


Differential susceptibility to colonic ulceration in Ptges deficient mice: Ptges KO mice develop colonic ulceration in a strain-specific manner.  We are examining the mechanisms of induction/protection of ulcer development, which may represent different susceptibility to NSAIDs in human population.


Role of estrogen in BRAF-mutated sessile serrated CRC: Sessile serrated lesions (SSLs) are more frequently detected in postmenopausal women. We will evaluate the efficacy of combinatorial therapy with an ERβ agonist and a BRAF inhibitor in SSLs using both in vitro and in vivo models.


 

Accepting Lab Rotation Students: Fall Block 2026, Spring Block 2027

Journal Articles

Conference Papers

  • Gene deletion of mPGES-1 results in a significant reduction in tumor stage and burden in the BBN mouse model of bladder cancer. Highly Rated Abstract, Top 2%
    Nakanishi M, Choudhary S, Hegde P, Pilbeam C, Rosenberg D, Taylor JA. 2010 Jan;51596-597

Reviews