Roswell Park Comprehensive Cancer Center experts from a variety of specialties will share practice-changing discoveries and research advances in hematology and hematologic cancers at the 64th annual meeting of the American Society of Hematology (ASH), held December 10-13 in New Orleans, Louisiana. Roswell Park researchers and physician-scientists in leukemia, lymphoma, and myelodysplastic syndromes were invited to give podium presentations or lead educational sessions during the meeting.

Roswell Park Comprehensive Cancer Center will be well-represented at this week’s 45th annual San Antonio Breast Cancer Symposium (SABCS), running Tuesday through Saturday, December 6-10, at the Henry B. Gonzalez Convention Center in San Antonio, Texas.

Metastasis, or the spread of cancer cells from a primary tumor to distant organs, lacks effective treatment options and remains a major cause of cancer-related deaths. To better understand how metastasis works — and how it might be controlled — scientists at Roswell Park Comprehensive Cancer Center have zeroed in on the role of the metabolic enzyme 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase-4 (PFKFB4) in the spread of triple-negative breast cancer (TNBC). Their study, “Hypoxic activation of PFKFB4 in breast tumor microenvironment shapes metabolic and cellular plasticity to accentuate metastatic competence,” appears today in Cell Reports.

A multi-institutional team led by researchers from Roswell Park Comprehensive Cancer Center has identified a novel approach that could potentially improve the efficacy of immune checkpoint inhibitors — a type of immunotherapy — among cancer patients with solid tumors. Findings from this preclinical study demonstrated that the differentiation agent brequinar effectively targeted myeloid-derived suppressor cells (MDSCs) and significantly improved immune checkpoint inhibitor response.

Researchers at Roswell Park Comprehensive Cancer Center, working in collaboration with Genome Protection, Inc. and Children’s Cancer Institute in Sydney, Australia, have discovered a novel way by which highly repetitive genetic components belonging to the LINE-1 family of retrotransposons enable tumors to escape treatment. The study demonstrates that LINE-1 activation can promote treatment resistance by inducing inflammatory pathways. Importantly, existing antiviral drugs overcame this resistance in preclinical cancer models.