Tag: Non-Hodgkin Lymphoma

New Findings May Play Role in Development of Future DLBCL Treatments

Researchers from Weill Cornell Medicine led by Dr. Olivier Elemento, recently published results announcing the discovery of thousands of new genes from human samples of lymphoma. Known as IncRNAs these genes produce long non-coding RNAs and are involved in gene regulation. The IncRNAs appear to control whether other genes make proteins. The discovery of these genes could underline the processes of gene regulation that drives lymphomas, while in the future leading to possible targets for new  diffuse large B-cell lymphoma therapies.

“These genes produce long non-coding RNAs, known as lncRNAs. Unlike RNA that produces proteins that enable the body to do its work, the lncRNA appear to switch on — or off — other genes that make proteins, researchers say. They counted 2,632 different forms of these unusual RNA molecules. They also found a substantial number of the same or similar lncRNAs in canine lymphoma.”

The study’s senior author, Dr. Olivier Elemento commented,

“While we don’t know precisely what these molecules are doing, the fact that the majority — about two-thirds — of the long non-coding RNAs we found are expressed exclusively in lymphoma, and that many are found in both human and dog lymphoma, tells us that they are likely playing fundamental roles in this cancer…”

Findings like these exemplify the bench to bedside approach in the Lymphoma Program at Weill Cornell Medicine. Look to this space for future updates on this topic and other advances in the treatment of lymphoma. A full listing of available clinical trials for DLBCL lymphoma can be found on our Joint Clinical Trials website.

REDLAMP 11: Does a Family History of Lymphoma Increase My Risk?

Great strides in the understanding of familial predisposition to common forms of lymphoma including non-Hodgkin lymphoma, Hodgkin lymphoma, and chronic lymphocytic leukemia have been made in the past decade. Many lymphoma patients wonder if their family faces an increased risk. In this video Dr. Peter Martin explains the results from a recent study published in Blood, which sought to quantify these risks, and give a better understanding of how a family history of lymphoma increases the risk for other family members.

Previous #REDLAMP entries can be viewed on our Youtube channel.

We encourage you to follow the Lymphoma Program on Twitter, Youtube, and Facebook where we will highlight new videos are about research publications as they are released. We also welcome your feedback, suggestions and questions about this project. If you have other questions about our lymphoma program or clinical trials or would like to see one of our lymphoma specialists, please contact us at 212-746-2919.

Researchers Discover Role of Mutated Gene in Development of non-Hodgkin Lymphomas

Recently researchers from Weill Cornell Medical College and Memorial Sloan Kettering Cancer Center discovered how a mutation in the KMT2D gene can drive the development of certain non-Hodgkin lymphomas. When properly functioning the gene KMT2D allows B-immune cells to generate antibodies against foreign objects in the blood stream. However, genetic mutations can disrupt normal immune cell growth, and prevent the proper functioning B-immune cells. Researchers found that,

“…normally KMT2D prepares key genes to respond to signals from other immune cells that stop B-cells, also called B-lymphocytes, from dividing and cause them to start making antibodies. However, when KMT2D mutations develop in B-cells, these external signals are no longer able to restrain them from dividing and stimulate their production of antibodies. As a result, there is an accumulation of rapidly dividing B-cells that eventually become malignant lymphomas. Importantly, the group demonstrated that therapies that have been developed to kill lymphoma cells by targeting these same signals are ineffective in the presence of KMT2D mutations.”

“KMT2D turns out to be one of the top 20 most mutated genes across all cancer types. It is really one of the superstars of cancer because it is one of the genes that is most strongly linked to tumors,” said co-senior author Dr. Ari Melnick, chair of the hematologic malignancies program in the Sandra and Edward Meyer Cancer Center and the Gebroe Family Professor of Hematology/Oncology at Weill Cornell Medical College. “Now that we understand how the gene functions in this treatment-resistant lymphoma, we can investigate the role of KMT2D mutations in other cancer types.”

These findings could potentially answer the question as to why certain lymphoma sub-types are treatment-resistant, while allowing for new avenues of therapeutic targeting.