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 cancer.

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

To tackle this goal, our research will bring 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.



  • Cancer biology & cancer 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 other diseases and drugs on cancer development. Some cancer processes are involved in other common diseases, with implications for personalized cancer risk forecasting and prevention. Repurposing drugs that treat other common diseases has the potential to accelerate discovery of new cancer treatments.

The natural history of cancer

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

Connecting other health conditions to cancer

Diabetes, obesity, and immunodeficiency are just a few of the health conditions that can impact cancer. Using genomic data, we can learn about disease mechanisms contributing to cancer.

Learning how drugs affect cancer tissue

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