Urbain Weyemi Looks for the Unexpected to Better Understand Cancer

November 20, 2019 • by Esther Robards-Forbes
Profile picture of Urbain Weyemi

A noted researcher at the intersection of cancer biology, neurodegeneration and epigenetics, Urbain Weyemi is joining the Department of Molecular Biosciences with the help of a recruitment grant from the Cancer Prevention and Research Institute of Texas (CPRIT). We connected with Weyemi as he makes the move from Johns Hopkins University to The University of Texas at Austin.

How do you describe your research to non-scientists?

My research is at the interface of two major fields. I aim to assess how persistent damage to the human genome leads to diseases and how a lack of balance in our antioxidant system makes things worse by further damaging our genome. This interplay between genomic instability and redox biology [meaning reduction-oxidation reactions, including cellular respiration] plays a role in many human diseases such as cancer and neurological disorders. My initial training as a Ph.D. student in France was in redox biology, but as a postdoc at the National Cancer Institute and Johns Hopkins School of Medicine, I expanded my work and expertise into genome stability and human diseases.

What kinds of questions does this field of research ask?

As we age, our body accumulates damage to the genome, and we lose the ability to generate healthy levels of antioxidants. These phenomena combine into a dangerous cocktail that is highly detrimental to the human body – and may lead to diseases like cancer or neurological disorders. But there is a gap in our understanding of how deficient repair of the genome alters the balance in the antioxidant system, and vice versa. As a CPRIT Scholar studying cancer biology, I aim to focus on cancer models in which this interaction is known to be important but remains poorly understood.

What possibilities drew you to The University of Texas at Austin in particular?

For my research field (DNA repair and redox biology), the Department of Molecular Biosciences is a unique place where you have a wide diversity of perspectives under one roof. This is the place where you have folks like Tanya Paull, an HHMI Investigator and an authority in the fields of DNA repair and redox biology, or like Kyle Miller who is also a CPRIT Scholar and a rising star in the DNA-repair field. Part of my research includes work on cell metabolism, and you have someone like Lulu Cambronne who is using a cutting-edge technology to monitor important metabolites in the cell. I can go on and on listing great scientists in the department who are potential collaborators. This is really a unique place to foster productive interactions and succeed. Another layer of excitement is the CPRIT recruitment award that I received, and I believe it provides unique resources and opportunity for young PIs to emerge. Lastly, having UT Austin's new Dell Medical School around will definitely enrich my work, especially when it comes time to translating findings from disease models to patients in clinics.

What do you hope to accomplish at UT Austin?

At UT Austin, I will have a mission and a strategy. The mission is to decode the dialogue between genomic instability and redox homeostasis in diseases like cancer, and my strategy is to build a creative, dynamic and inclusive research team to fulfill that mission. I will welcome students and postdocs of every talent, especially those who are excited to explore things beyond their comfort zone. I hope to establish a research group that will last for decades and publish cutting-edge findings. I know The University of Texas at Austin has a culture that values teaching, so I hope to rise to the level of someone who will be regarded as a leading figure in cell biology teaching. 

Why is it important to study cancer at the molecular level?

In cancer research, there is a therapeutic approach that we call precision medicine. These words stem from the simple idea that the same type of cancer may evolve differently from one patient to another, because the molecular and genetic driving forces may differ between individuals. Therefore, you have to approach each type of cancer at a molecular level to assess genes and pathways that are specifically affected, and ultimately define a targeted therapy for patients.

You published a paperregarded as a 'major publication of the National Cancer Institute in 2016,' on a protein (histone H2AX) that is involved in the mechanisms of cancer. Explain what this study uncovered, why it was important and what it might mean for other researchers.

The histone H2AX was discovered in the 80s by my postdoc mentor, Dr. William Bonner at the National Cancer Institute (NCI) [histones are a type of protein involved in the packaging of DNA]. For about two decades, this protein has been primarily seen as involved in genome maintenance and repair. For the first time in 2016, I discovered that H2AX controls regulation of key genes essential for cancer cells to become more aggressive, and especially to expand from their primary site to establish tumors at distant sites. That is what is called metastasis. We discovered a new function for a key protein that was seen for decades as only an actor of genome maintenance and repair.

Quickly after our paper was released, several papers were published showing that other DNA-repair proteins, like BRCA1, a gene that is mutated in breast and ovarian cancer, or even some histone variants are involved in dedifferentiation [change in nature and shape to become aggressive] of cancer cells. 

Having moved to the United States from France, you once observed: "America is a country where everything is possible. That's why I came here after my Ph.D." What did you mean by that?

Most research institutions in France are funded by the government, and there are really very few private endowment funds, at least until recently. To give you an idea, the French government's spending on research stays flat around €7 billion, which is the equivalent of the budget of Harvard and Yale combined. You can hardly find institutions where a postdoc can have continuous funding for 3-5 years. Therefore, many postdocs don't have substantial time to produce consequential publications, except in a few outstanding institutions. Here, there is support that means one can rise to a level to establish one's own research lab and succeed as an investigator.

France just won the men's World Cup in 2018. Any message to U.S. soccer fans?

[North America] will be hosting the 2026 FIFA World Cup …. I would say to the soccer fans that we have to win in 2026!