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Dipali Sharma, PhD
Associate Professor of Oncology
Kimmel Cancer Center
Johns Hopkins University, School of Medicine
- Seeking to understand the molecular links between obesity and breast cancer and to develop new strategies to counter these changes.
- Laboratory studies are ongoing to characterize the complex effects of obesity on fat tissue, the micobiome and tumor growth.
- These studies could lead to a natural approach that could potentially lower the risk of breast cancer.
Obesity increases the risk of several cancers including breast cancer after menopause. Understanding the relationship between obesity and breast cancer can provide clues to better prevention strategies. Dr. Sharma's research has shown that the type of fat that surrounds the breast tumor is important in tumor growth and drug resistance. She is continuing to examine obesity-driven changes in breast tumor microenvironment to understand the underlying molecular mechanisms of these associations to develop preventive and therapeutic strategies.
Full Research Summary
According to the Centers for Disease Control and Prevention, the prevalence of obesity in 2018 is 35-40 percent in all states and the numbers are increasing. A five-unit increase in BMI associates with a 12 percent increase in breast cancer risk. Obese Postmenopausal women have a 20-40 percent increase in risk of developing breast cancer in comparison to normal-weight women.
Dr. Sharma's team is studying how molecular changes caused by obesity promote breast cancer development, progression, and metastasis, with the goal of developing new preventive strategies.
Her recent work has shown that fat cells called WAT around the breast tumor increase growth and metastatic potential of cancer cells. The WAT cells secrete a tumor-promoting hormone called leptin, which causes the tumors to be resistant to antiestrogen therapy. Her team also observed distinct fat-induced changes in microbiota–the microorganisms around the fat tissue.
Her work in the coming year will focus on elucidating the link between microbiome, resident fat cells and breast cancer cells.
These studies will inform preventive interventions and treatment strategies.
Dr. Sharma is an Associate Professor in the Department of Oncology, Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins. She obtained her doctorate in Molecular Biology and Oncology from the University of Delhi. She then completed fellowships at both the University of Maryland and the Sidney Kimmel Comprehensive Cancer Center training under the mentorship of Dr. Nancy Davidson.
The prevalence of obesity, an epidemic of major proportions in the United States today, has risen steadily over the last several decades. Research on the biological mechanisms underpinning the link between cancer and obesity is clearly a vitally important area, with major implications for both public health and fundamental cancer research. Dr. Sharma focuses on investigating the molecular links between obesity and cancer, emphasizing aspects that have potential clinical significance. Her studies on obesity-related hormones, adipocytokines, showed that leptin promotes the proliferative response and metastatic potential as well as modulates the expression of various genes involved in cell cycle, apoptosis and metastasis. Dr. Sharma is currently examining the potential of adiponectin as an antagonist using innovative approaches including nanotechnology to investigate these important aspects in obesity-breast tumorigenesis connection. Her lab is exploring the genes, molecules, hormones and cellular processes that could cause and promote cancer in obese people. Using various physiologically relevant models and cell lines, their aim is to find molecular targets that can be disrupted to break the obesity-cancer axis. She is exploring new strategies to disrupt the obesity-cancer connection using novel small molecule inhibitors as well as bioactive food components. Her overall goal is to understand the molecular networks by which obesity affects carcinogenesis and discover novel agents to effectively disrupt obesity-cancer axis.