Videos
Dr. Christine Seidman of the Harvard Medical School has uncovered the genetic basis of many human cardiovascular disorders, from cardiomyopathy and heart failure to congenital heart malformations. In this interview, she speaks about her early intrigue with atrial natriuretic factor and her more current gene-intensive investigations. She also shares many more stories about her interest in the ear, an early inspirational patient, and her thoughts on work-life balance.
Tsonwin Hai and colleagues discuss how the transcription factor ATF3 acts as a key regulator of the host immune response and as a contributor to co-option of the host by cancer cells to promote metastasis. Highlights:
- ATF3 is expressed in immune mononuclear cells in human breast tumors and is associated with worse clinical outcomes.
- Host ATF3 expression facilitates breast cancer metastasis.
- ATF3 alters the host systemic environment, increasing the number of tumor-associated macrophages.
- Cancer-induced ATF3 expression in mononuclear cells alters gene expression and bioactivity to contribute to host-enhanced metastasis.
Professor Stephen O’Rahilly’s research has led to an increased understanding of the genetic causes of human obesity and insulin resistance. Using modern biochemical approaches and classical clinical observation in humans with profound metabolic disorders, O’Rahilly, from the Departments of Medicine and Clinical Biochemistry at the University of Cambridge, has shown that a person’s appetite and feeding behavior can be linked to specific genes. His work has challenged long-held dogmas and led to new treatment avenues. The full interview includes many more stories about how you can learn more from reading Chekhov than medical school and why he has stayed in Cambridge all these years.
More than almost any other scientist in the field of obesity and metabolism research, the work of Bruce Spiegelman, from the Dana-Farber Cancer Institute and Harvard Medical School, has informed potential targets for drug discovery that could burn fat and even turn fat into muscle. He was the first to suggest that inflammation underscores insulin resistance, and also the first to find the key regulator of adipogenesis, PPAR-γ.
Brett Monia and Stefano Rivella discuss how reduction of TMPRSS6 expression with antisense oligonucleotides ameliorates iron metabolism disorders in mice. Highlights:
- Iron metabolism is a complex and heavily regulated process that is required for basic physiological functions, including hematopoiesis and host immune responses.
- Hemochromatosis and β-thalassemia are iron overload disorders caused by low levels of hepcidin, the hormone that regulates iron absorption.
- Antisense oligonucleotides (ASOs) lowered Tmprss6 RNA and elevated hepcidin levels.
- TMPRSS6 ASO treatment reversed anemia and iron overload in a mouse model of β-thalassemia.
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