New Weapons Against Aggressive Tumors
Combination oncology therapy may treat neurofibromatosis type 1 and KRAS mutant lung cancer

Many aggressive tumors simply don't respond to a single therapy. That's why there's a major push to develop combination therapies. And scientists have landed on one that has great potential.
Researchers at Brigham and Women's Hospital (BWH) have uncovered a combination of targeted therapies that may treat two rapidly spreading cancers that don't currently have effective treatments.
Two drugs may treat lung cancer and nervous system tumors.
The new approach combined one targeted agent that suppresses growth of the tumor (the mTOR inhibitor rapamycin) with another drug that puts stress on the cancer cells (HSP90 inhibitor IPI-504) . It's sort of a double whammy blow.
This combination was successful in treating two mouse models of 1) a nervous system tumor that's seen in neurofibromatosis type 1 and 2) KRAS-mutant lung cancer which accounts for a quarter of all lung cancers.
These tumors are currently being treated with chemotherapy, but with only limited success, according to lead author, Dr. Karen Cichowski, Associate Professor in Genetics at BWH.
Cichowski says that this type of therapy could offer dramatically improved outcomes and survival for patients with these tumors.
This work has lead to a Phase I clinical trial evaluating the combination on KRAS-mutant lung cancer.
Findings from this study are published in the September 13, 2011 issue of Cancer Cell.
All information on this site is provided “as-is” for informational purposes only and is not a substitute for medical advice or treatment. You should consult with a medical professional if you have any questions about your health.
More health news
Health NewsDealing with KRAS Genes
KRAS mutated colon cancer pathway may become new target
Health NewsSingle Punches Don't Knock Out Advanced Cancers
Advanced colorectal cancers become resistant to single therapies
Health NewsWithout Kras, Pancreatic Cancer Crashes
Pancreatic cancer survival dependent upon Kras oncogene