Hematology/Medical Oncology

An international phase 3 clinical trial, done in participation with Weill Cornell Medicine and NewYork-Presbyterian, found that a new targeted treatment called zolbetuximab, given in combination with a standard chemotherapy, extended survival for patients with advanced gastric or gastroesophageal junction cancer that overexpressed a specific biomarker.

A technique that enables scientists to record gene mutations and patterns of gene activity in individual cells has been extended to cover RNA splicing as well, in a study led by researchers at Weill Cornell Medicine, the New York Genome Center and the Princess Margaret Cancer Centre in Toronto.

 A new, very precise gene-editing tool created by Weill Cornell Medicine investigators will enable scientists to study the impact of these specific genetic changes in preclinical models rather than being limited to more broadly targeted tactics, such as deleting the entire gene.

Cancers often release molecules into the bloodstream that pathologically alter the liver, shifting it to an inflammatory state, causing fat buildup and impairing its normal detoxifying functions.

Dr. David Simon, the Fernholz Foundation Research Scholar in Neuroscience and an assistant professor of biochemistry at Weill Cornell Medicine, was awarded the 2023 Pershing Square Sohn Prize for Young Investigators in Cancer Research on May 16.

Weill Cornell Medicine has received a grant from the National Institutes of Health (NIH) as part of a new $140 million Common Fund program to study somatic mosaicism, a phenomenon in which organs and tissues develop significant genetic differences across their cell populations.

Nearly 90 percent of patients with an aggressive subtype of non-Hodgkin lymphoma had their cancer go into remission in a small phase 2 clinical trial testing a treatment aimed at making chemotherapy more effective, according to Weill Cornell Medicine and NewYork-Presbyterian investigators.

White blood cells called neutrophils have an unappreciated role in eradicating solid tumors.

Dr. Ekta Khurana, an associate professor of physiology and biophysics at Weill Cornell Medicine, has received a 3-year, $1.2 million grant from the United States Department of Defense to investigate how prostate cancer cells evolve to become resistant to hormone-blocking therapy. 

Obesity may spur DNA damage in the breast tissue of women who carry BRCA1 or BRCA2 mutations, possibly contributing to breast cancer development in this already high-risk group.

A small but significant metabolic difference between human and mouse lung tumor cells, has been discovered by Weill Cornell Medicine researchers, explaining a discrepancy in previous study results, and pointing toward new strategies for developing cancer treatments.

The key to understanding how the most aggressive lymphomas arise and resist current therapies may lie in mutations that disrupt a critical natural selection process among antibody-producing B cells.

A new method can illuminate the identities and activities of cells throughout an organ or a tumor at unprecedented resolution.

An enzyme that defends human cells against viruses can help drive cancer evolution towards greater malignancy by causing myriad mutations in cancer cells.

Endothelial cells—the cells that line blood vessels—grown alongside leukemia cells become corrupted and rescue the cancer cells from many chemotherapy drugs, a study by Weill Cornell Medicine investigators found.

A common, spontaneous mutation in blood stem cells, which has been linked to higher risks of blood cancer and cardiovascular disease, may promote these diseases by altering the stem cells’ programming of gene activity and the mix of blood cells they produce.

A new preclinical model for thymic cancer developed by Weill Cornell Medicine investigators has revealed insights into how a common mutation found in thymic epithelial tumors sparks their formation.

There is considerable variation in the management of mantle cell lymphoma across different clinical settings, and some strategies do not always conform with what might be expected, according to an analysis by investigators from Weill Cornell Medicine and other leading health institutions.

Genetically engineered immune cells successfully target the specific cancer cells that may be responsible for relapse of acute myeloid leukemia, a type of blood cancer, and proved effective in animal models of the disease.

DNA mutations are essential to the rapid development of an array of antibody-producing immune cells called B cells that collectively can recognize a vast number of specific targets. But this process can go awry in people with a mutation in a gene called SETD2, leading to a type of aggressive blood cancer.