Two recent studies, one from New York City-based NYU Langone's Perlmutter Cancer Center and one from Tampa, Fla.-based Moffitt Cancer Center, have released findings regarding the behavior of cancer cells, laying the groundwork for future oncology research and treatment development.
NYU Langone researchers analyzed how cancer cells adapt to low-glucose environments, paving the way for therapies to target tumor metabolism, according to a study published Nov. 26 in Nature Metabolism.
Here are five things to know from the NYU Langone study:
- Cancer cells are able to adapt their metabolism to resist chemotherapy treatment.
- Some chemotherapy drugs are designed to block cancer cells from producing the essential molecules needed for reproduction.
- Starving cancer cells of those molecules in a low-glucose environment disrupts cancer cell growth but also slows the process, making the chemotherapy drugs less effective.
- Researchers discovered more about the metabolic changes cancer cells make to avoid death when adjusting to low-glucose environments, according to a Nov. 26 news release from NYU Langone.
- The discoveries could lead to the development of treatments that target those metabolic changes as well as diagnostic tests that predict how cancer cells will respond to specific chemotherapy drugs.
Moffitt researchers identified how a molecule released during cancer cell death could enhance immune response and treatment effectiveness, according to a study published Nov. 26 in Cancer Cell.
Here are five things to know from the Moffitt study:
- During necroptosis, a type of cell death, cancer cells release a molecule called interleukin-1α.
- Moffitt researchers discovered that this molecule suppresses immune system response and, in turn, promotes tumor growth even after cancer cell death.
- Researchers also found that interleukin-1α is released by cancer cells in response to chemotherapy. Uncovering this process may explain why some chemotherapy treatments are less effective, according to a Nov. 26 news release from Moffitt.
- Blocking interleukin-1α in animal models improved immune responses and boosted the effectiveness of chemotherapy and immunotherapy, offering a potential pathway for developing therapies that target interleukin-1α.
- Lower interleukin-1α levels were also linked to better patient outcomes, suggesting those levels could serve as an effective marker for treatment strategy.