Bench to bedside: What's on the horizon
The Annual Meeting of the American Association for Cancer Research remains the premier destination to showcase the newest and most exciting developments in cancer prevention and treatment. At the AACR 100th Annual Meeting 2009, Pasi A. Janne, M.D., Ph.D., an assistant professor of medicine at Harvard Medical School in Boston, will host a press conference that will highlight cutting-edge research. The press conference will take place on Sunday, April 19 at 1:00 p.m. MST in room 108 of the Colorado Convention Center. Those reporters who cannot attend in person can dial in to the teleconference using the following information:
- U.S./Canada Dial-In: (888) 282-7404
- International Dial-In: (763) 488-9184
- Access Code: 88612689
Each new advancement in cancer research helps to move the research community closer to the ultimate goal of personalized medicine, but challenges remain, according to Janne.
"The most important challenge will be implementation. How can we determine the patients who are most likely to benefit from these new interventions," he said. "And along with implementation, how can we make sure that access is as widespread as possible? We do not want the best therapies to only be available at the top hospitals."
1890. Preclinical Analysis of Combined PI3K and MEK Inhibition as a Strategy for the Treatment of Cancer
Researchers at Genentech believe they may have found a way to attack cancer by simultaneously targeting two of the primary outputs of a known oncogene.
Lori S. Friedman, Ph.D., director of cancer signaling and translational oncology at Genentech, said the ras oncogene is an attractive target due to its known role in many human cancers, but direct targeting has been challenging.
For the current study, Friedman and colleagues used small molecule inhibitors to target PI3K and MEK proteins, which are downstream signaling effectors of ras. The researchers believe that by simultaneously targeting both PI3K and MEK, they may see greater efficacy than they would see by targeting either alone.
"Ras-driven cancer cells are driven to grow via two main pathways. If you block one growth pathway, they will turn to the second and continue to grow. If we block them both simultaneously, we might be able to stop them more effectively," Friedman said.
Findings showed significant anti-tumor activity and tumor cell death in the laboratory models in this study.
Full data will be presented at the AACR 100th Annual Meeting 2009.
LB-261. Combined Inhibition of Histone Deacetylase and mTOR: A Novel Therapeutic Approach for Pancreatic Cancer
Pancreatic cancer is one of the most deadly cancers and the only established clinical treatment for patients who are not surgically resected is gemcitabine.
"The response to gemcitabine is modest at best and new agents are really needed for these patients. If the laboratory studies of this combination are confirmed in clinical trials, we may see a survival benefit with this combination," said Mamta Gupta, Ph.D., a research associate in the Mayo Clinic Cancer Center in Rochester, Minn.
Both mTOR and histone deacetylase play key roles in the biological formation of tumors via different mechanisms.
"We've shown on a cellular level that the combination of a mTOR inhibitor like rapamycin, which is clinically available, with a histone deacetylase inhibitor like LBH589, which is undergoing laboratory tests, appears to kill pancreatic cancer cells and may provide a new therapeutic approach," said Gupta.
For the current study, Gupta and colleagues tested the two agents on pancreatic cancer cell lines in the laboratory. They first treated the lines with rapamycin and found that there was a less than 10 percent reduction in overall cell survival. However, when rapamycin was combined with LBH589 the cell death was between 60 percent and 70 percent depending upon cell lines.
Gupta said the results are clear that the pharmacologic combination of LBH589 and rapamycin somehow interferes with the survival and proliferation pathways of pancreatic cancer cells.
"We still have a long way to go, but this is very exciting data that opens a potential new treatment avenue for these patients," said Gupta. "What we do not know at this point is the molecular mechanism of this combination."
128. 2.5-Dimethyl-Celecoxib Exerts Antiangiogenic Effects on the Tumor Vasculature
Embargo: 8:00 a.m. MST, Sunday, April 19, 2009
The compound 2.5-dimethyl-celecoxib appears to exert strong anti-tumor and anti-angiogenic effects without the side effects normally associated with Cox-2 inhibitors, according to research conducted at the University of Southern California.
"This drug targets both the vasculature and the tumor cells, and it is not a Cox-2 inhibitor, so it could be given as a long-term therapy without side effects," said Florence M. Hofman, Ph.D., professor of pathology at the University of Southern California, Keck School of Medicine.
The researchers observed the effects of dimethyl-celecoxib (DMC) in brain cancer, but Hofman said the agent could work in different solid tumors that are dependent on the blood supply for growth.
"This drug would be particularly useful for metastatic cancer to the brain, including breast cancer, which is a huge problem," she said.
Hofman and colleagues isolated endothelial cells from human nonmalignant brain and glioma tissues and then treated them with DMC to test for functional activity. They found that DMC suppressed endothelial cell proliferation and migration.
Treatment with this drug in animal studies showed smaller tumors and fewer blood vessels in the tumors, with a 35 to 45 percent reduction in microdensity. This is important because tumors need a growing vasculature, or blood supply, in order to grow.
5662. Phase I Trial of Anti-PSMA Designer T Cells in Prostate Cancer
Researchers at Boston University School of Medicine and the Roger Williams Medical Center in Providence, R.I., have developed a way to manipulate T cells in the fight against prostate cancer, which may in turn help cancer therapy enter into a new era of living drugs.
Richard Junghans, M.D., Ph.D., , associate professor of surgery and medicine, will present data on the first prostate cancer patients treated with designer T cells that have been modified by retroviral gene therapy. These are the patients' own T cells that are "educated" to attack tumors in the body.
"This is the brave new world of oncology treatments because these 'drugs' are alive rather than inert chemicals," said Junghans. "These designer T cells will be able to go and attack cancers where hormone therapies and chemotherapies have failed."
In the human tests, a "hematologic space" in the body is first created by chemotherapy in which these designer T cells expand 100-fold in number after infusion to increase their potency, Junghans said. In the first two patients treated, researchers noted prostate-specific antigen reductions of 50 percent to 75 percent.
"With still higher doses of T cells soon to follow in our dose escalation plan, we hope to observe the 100 percent prostate-specific antigen reductions that everyone seeks," he said. "This genetic engineering brings us into a new era of cancer treatment by reprogramming T cells to attack the cancer in the same way that the T cells would normally fight a virus infection. I predict we will see approval of drugs in this category in the next five years."
Junghans will present data on the patients in this phase I trial at the Annual Meeting.
2608. Development of a Membrane Microfilter Device for Capture and Characterization of Circulating Tumor Cells in Blood
A new microfilter device may aid in the diagnosis and therapeutic decisions for patients with cancer, according to a study conducted at the University of Southern California Keck School of Medicine in collaboration with the California Institute of Technology.
"This is a cheaper and faster method of examining the circulating tumor cell (CTC) environment. As we continue to refine it, we can do a better job of characterizing different disease states and evaluating a patient's response to therapy. This will push us further in the direction of personalized patient management," said Anthony Williams, a graduate student at the Keck School of Medicine.
The microfilter device, which he estimates is about three to five years from clinical use, uses 7.5 ml of blood drawn from patients with cancer by standard measures and captures CTC based on size differences between tumor and normal blood cells. The captured CTC are then accessible for downstream on-chip molecular analyses. For the current study, Williams and colleagues compared the success rate of filtration against the current clinical gold standard.
In a model system where cultured tumor cells were seeded into 7.5 ml blood from a normal healthy donor, statistical analyses confirmed that the true chance of recovering at least one tumor cell when five are seeded using the microfilter device is 95 percent or greater. In clinical blood samples collected at the Memorial Sloan-Kettering Cancer Center in New York, the microfilter device successfully captured CTC in 92.9 percent of patients with metastatic cancer. By contrast, the gold standard only captured CTC in 45.6 percent of corresponding samples.
"This has the potential to be a transformative technology," Williams said.
- UPCI, Pitt researchers present findings of cancer studies at AACR 102nd Annual MeetingWed, 6 Apr 2011, 8:37:09 EDT
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- New drug achieves pancreatic cancer tumor remission and prevents recurrenceSun, 19 Apr 2009, 15:29:49 EDT
- GUMC research summaries for AACR Cancer Prevention MeetingTue, 18 Nov 2008, 17:29:08 EST
- The AACR increases focus on clinical trials Sat, 2 Apr 2011, 18:34:34 EDT
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