Rachel Melamed

Assistant Professor of Biology

University of Massachusetts at Lowell


I an assistant professor at UMass Lowell in the Biology department, also affiliated with the Center of Biomedical and Health Research in Data Sciences. I’m excited to work with Biology students at all levels to make discoveries about the origins of disease.

My goal is to discover health conditions, medical treatments, or other exposures that change risk of disease, by linking health data to molecular data. These results can uncover how the disease works and identify interventions to prevent and treat it.

To tackle this goal, our research brings together many kinds of data, including health records, biobanks, cancer genomics projects, and massive experimental studies of drugs. We will use methods inspired by computer science and epidemiology.



  • Disease biology & disease genomics
  • Data science
  • Epidemiology & causal inference


  • Postdoc in Biomedical Data Science

    University of Chicago

  • PhD in Biomedical Informatics

    Columbia University

  • BA in Computer Science

    Brown University

Research interests

Cancer is essentially a human tissue that has gone rogue, weaponized and retrofitted to ensure its own survival in a hostile environment–the human body. The work of this lab is inspired by certain key aspects of this process:

  • Cells are constantly at risk of DNA damage, which accumulate over divisions, figure, above (A). But this damage only results in cancer when driver mutations affect certain well-defined hallmark biological processes.

  • But, the growth that can be caused by any one mutation is limited (B). Instead, yet more damage is required to other key cellular processes (C) for cancer to develop. Cancers occur more with age, a result of the process of trial and error as cancers evolve a combination these abilities.

  • Besides acquired mutations, other infuences on cancer development affect some of the same biological processes. This can suggest new ways to understand the disease (figure, below).

    • Some people are born with very high genetic risk, (D) , such as people with the inherited BRCA mutation. But, other more common genetic variation can influence cancer risk more subtly.

    • Other health conditions can change risk of cancer, (E). For example, obesity has been shown to increase risk of cancer, possibly by effects on inflammation, hormones, or levels of insulin.

    • Certain drugs used for other diseases have been discovered to have a secondary affect on cancer (F). Aspirin is an anti-inflammatory drug, and it has been shown to reduce risk of cancer. Other drugs increase risk of cancer.


A major goal of the lab is to learn influences of health history and drugs on disease development. Diseases can share common causes and deveolopment patterns, with implications for personalized disease risk forecasting and prevention. Repurposing common drugs has the potential to accelerate discovery of new disease treatments.

The natural history of cancers and dementias

We use large health records data to learn how drugs, diseases, and other types of expsosures could change risk of disease or change disease outcome. These studies complement our work using genomic data to understand these effects.

Leveraging the shared basis of diseases

Genetic diseases, lifestyle, and chronic diseases can impact the development of late-onset diseases like cancer and dementias. Using genomic data, we can learn about disease mechanisms contributing to the development of these diseases of later life.

Learning how drugs affect disease tissue

This project aims to use big experimental datasets to understand the effects of drugs on gene function in disease, and how these effects impact disease pathways.