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Although survival improvements in leukemia clinical trials are often attributed to increased remission rates or decreased relapse, remission and relapse rates did not differ significantly between SNP+ and SNP- patients in this study. The investigators examined whether the SNP had any association with TRM and found that TRM rates did not differ by SNP rs16754 genotype when all ethnicities were considered together. However, TRM rates in SNP+ African-American and Asian patients, when taken together, were significantly lower than in SNP- patients of those two ethnicities. African-American and Asian patients without SNP rs16754 had significantly higher rates of treatment-related toxic death compared to SNP+ patients (African-American: 25% vs. 0%; Asian: 43% vs. 0%). These results suggest that the protective effect of the presence of SNP rs16754 in reducing chemotherapy-related toxicity in pediatric AML patients is more pronounced in those of African-American and Asian descent.

"Identifying the patient-specific factors that can affect responses to treatment in different patients with the same disease brings us closer to our goal of designing personalized treatments that provide the most therapeutic benefit with the least amount of toxicity to these children," said Phoenix Ho, MD, lead author and Attending Physician at Seattle Children's Hospital in the Division of Pediatric Hematology/Oncology at the University of Washington School of Medicine and Research Associate at the Fred Hutchinson Cancer Research Center in Seattle. "Our analysis was conducted on a trial completed in 2002, and treatment protocols for pediatric AML have evolved since that time. Our next step is to validate our findings by studying this same association in contemporary trials. We are also designing studies to uncover the mechanism behind the association between the SNP and reduced toxicity, with the hope of translating these findings into improved treatments for pediatric AML."

Dr. Ho will present this study in a poster presentation on Saturday, December 8, at 5:30 p.m. EST at the Georgia World Congress Center in Hall B1-B2, Level 1, Building B.

Genetic Susceptibility to Anthracycline-Related Congestive Heart Failure (CHF) in Survivors of Hematopoietic Cell Transplantation (HCT) [Abstract 589]

Researchers have identified specific genetic factors that are associated with heart failure in patients who have undergone hematopoietic stem cell transplantation (HCT) for blood cancer.

The transplantation of blood-forming stem cells from the bone marrow, circulating blood, or umbilical cord blood is the primary treatment option for many patients with blood cancer who relapse after receiving standard front-line therapies. During the transplant, healthy stem cells replace damaged cells that caused the illness, effectively curing patients of their disease. Advances in transplant strategies have led to a growing number of long-term survivors of HCT. However, this growing population of survivors is at risk for developing life-threatening complications such as congestive heart failure, due in large part to their exposure to pre-HCT treatments with a class of chemotherapy drugs called anthracyclines. Transplant survivors tend to develop heart failure earlier than the general population, and the overall survival rate following diagnosis is less than 50 percent.

By analyzing transplant patient demographics such as age and gender, treatment strategy (i.e., pre-HCT chemotherapy and chest radiation), and presence of cardiovascular risk factors such as high blood pressure, diabetes, and high cholesterol, researchers have been able to create a clinical profile to determine which patients are likely to develop heart failure after transplant. However, this current profile is limiting, as it fails to accurately explain the wide variability in the risk of heart failure between individual patients. Importantly, it does not account for how individuals' genetic makeup can exacerbate their risk of developing heart failure.