NEW YORK, NY (May 12, 2014) — Two genes work together to drive the most lethal forms of prostate cancer, according to new research from the Herbert Irving Comprehensive Cancer Center at Columbia University Medical Center (CUMC).
Mutated beta-catenin in bone cells may cause up to 40 percent of acute myeloid leukemia cases. In the cells of healthy subjects (left), beta catenin proteins (red dots) sit along the outer edges of the cell. In approximately 40 percent of AML patients (right), abnormal beta-catenin proteins (red dots) move into the cell interior; in mouse models, this movement sets cancer-causing changes into motion.
Credit: Dr. Aruna Kode/Kousteni lab, Columbia University Medical Center.
Alfredo Axtmayer II will have a unique perspective to share with his patients when he becomes a nurse practitioner with a specialty in oncology. In 2008, when he was 27, he was diagnosed with Hodgkin’s lymphoma. It is now in remission.
“Global mapping of cancer gene expression changes to the human metabolic network; increased enzymatic expression across tumors is shown in red and decreased in blue,” said Dr. Vitkup (who provided the image).
Columbia Engineering researchers, led by Dimitris Anastassiou, Charles Batchelor Professor in Electrical Engineering and member of the Columbia Initiative in Systems Biology, have developed a new computational model that is highly predictive of breast cancer survival.
A study by researchers at the Herbert Irving Comprehensive Cancer Center (HICCC) at NewYork-Presbyterian/Columbia University Medical Center, recently e-published ahead of print by the "Journal of Clinical Oncology," suggests that women who have surgery for ovarian cancer at high-
Figure 2: Abnormal accumulation of the FGFR-TACC fusion protein (red) in glioblastoma stem cells isolated from a primary human glioblastoma with fused FGFR- TACC genes. Cellular nuclei are colored blue. Image credit: Anna Lasorella and Antonio Iavarone/Columbia University Medical Center