About The Asnani Research Lab

The Asnani Lab focuses on defining molecular mechanisms of chemotherapy-associated heart toxicity, with the goal of targeting these pathways therapeutically in patients.

Advances in the early diagnosis and treatment of cancer have led to dramatic improvements in cancer survival rates over the past few decades. It is estimated that there will be 26 million cancer survivors in the United States by the year 2040. Many of these patients are exposed to cancer treatments that cause short- and long-term cardiovascular complications, including heart failure and arrhythmia. The molecular pathways that contribute to cancer therapy-associated heart toxicity are not well understood. As a result, effective approaches to risk stratify and protect patients exposed to cardiotoxic cancer treatments are currently lacking.

The Asnani Lab aims to define the molecular mechanisms of chemotherapy-associated heart toxicity. Our ultimate goal is to target these pathways in patients to allow for the optimal treatment of cancer while simultaneously protecting the heart. Learn more about the Asnani Lab.

Research Interests

1. Molecular mechanisms of heart toxicity in patients treated for cancer

Our laboratory has established zebrafish and mouse models to define the molecular pathways that contribute to heart toxicity associated with the following commonly used cancer treatments:

  • Anthracyclines such as doxorubicin (Adriamycin)
  • Targeted therapies such as ibrutinib
2. Early biomarkers of heart toxicity in patients treated for cancer

Using high-throughput metabolite and protein profiling techniques, we have identified circulating biomarkers of early cardiac injury in patients treated with cardiotoxic cancer therapies.

3. Clinical characteristics of patients who develop heart toxicity in the setting of cancer therapy

We are developing a retrospective and prospective patient registry to identify clinical risk factors and outcomes of patients who develop cancer therapy-associated heart and blood vessel toxicity.