“Imagine you’re standing on a bridge over a river, and you throw a message in a bottle out in the middle,” he said. “If the river is moving really slowly…the bottle will drift over to the riverbank and somebody can grab it. But if the river is flowing too quickly, then the bottle is swept downstream without ever approaching the sides.” As cell mixtures flow through Ian’s new device, the fluids are slowed and directed in such a way that target cells come into contact with antibodies that recognize and attach to them.

With Ian’s design in hand, researchers may be able to isolate cancer cells from blood samples. That would mark a major leap forward in diagnosing patients and personalizing medicine.

> Learn more about Ian and his cancer cell research

Quotes adapted from MIT News

Published in: Cancer Discoveries by Todd

Approved by the FDA last year thanks to clinical trials led by Jedd, Yervoy is the first drug to improve overall survival for patients with advanced melanoma. Used alone, it did not stop the slow growth of Valerie’s melanoma. After adding localized radiation, however, tumors all over Valerie’s body began to rapidly regress. “What we think is happening here is that the immune system’s cancer-fighting response is turned up a notch with the addition of focused radiation,” said Jedd.

While these results come from one patient, larger clinical trials are already underway to evaluate the combination’s effects on melanoma and prostate cancers.

> Video: NBC Nightly News interviews Jedd and Valerie about the discovery
> Read a New Yorker article featuring Jedd’s discovery

Quotes adapted from Science Daily 

Published in: Cancer Discoveries by Todd

In 2008, Damon Runyon Scholar Hai Yan, PhD, and his colleagues were the first scientists to link the IDH gene to cancer. Setting out to determine which gene mutations were unique to brain cancer cells, they sequenced nearly 20,000 brain tumor genes. They found dozens of unique mutations, but IDH was notable for its presence in at least 70% of tumors.

Last month, Damon Runyon Clinical Investigator Ralph J. DeBerardinis, MD, PhD, and Damon Runyon-Rachleff Innovator Matthew G. Vander Heiden, MD, PhD, applied this research to patients. Each used magnetic resonance imaging to distinguish—with 100% accuracy—which patients’ brain tumors have the IDH mutation and which do not. It’s a remarkable leap forward that may spare patients painful biopsies and help physicians select treatments based on their patients’ distinct tumors. Moreover, their imaging technique is noninvasive and can be done with MRI scanners that most hospitals already own.

“The most exciting thing about this,” Matt said, “is it opens up the possibility that as drugs against gliomas come online, you could know which patients with brain tumors to put in the clinical trials, and you would know if the drug you’re giving them is actually doing what it’s supposed to do.”

Pharmaceutical and academic researchers are already developing drugs that target the IDH mutation.

> Video: Matthew discusses his research and Damon Runyon’s support
> Learn more about Ralph and his research into cell biology

Quotes adapted from PRNewswire and MIT News

Published in: Cancer Discoveries by Todd

Adding to her accolades, Pardis was named a 2011 PopTech Science Fellow after being nominated by Damon Runyon Chief Scientific Officer Yung Lie, PhD. The PopTech program trains exceptional young scientists to become more effective at communicating their research to the public and to colleagues in other fields. The result is an international community of innovative young researchers better equipped to collaborate and influence public attitudes toward science.

“Pardis is an ideal scientist for the PopTech program,” Yung said. “Not only is she brilliant and highly regarded in her field, but she is an innovative thinker committed to sharing her science with a broader audience.”

In the video below, Pardis discusses how her work is helping cure Lassa fever in Africa.

> Learn more about Pardis and PopTech

Published in: Damon Runyon News by Todd

An international collaboration of researchers, including former Damon Runyon Fellow David E. Lebwohl, MD, enrolled 724 metastatic breast cancer patients, all of whom had hormone receptor-positive tumors.  Some women received a combination treatment of everolimus (Afinitor), which blocks a protein known to affect blood vessel growth in cancer cells, and exemestane (Aromasin), a commonly-used hormone therapy.  Other patients received only exemestane and a placebo. 

Patients who received the combination survived progression-free for 7.4 months compared to 3.2 months for those who only received exemestane. According to lead author Gabriel Hortobagyi, MD, this “highly significant” result marks “the first time in a large Phase III trial [that] we have demonstrated that this dual-attack is more effective than a single [hormone] treatment.” 

> Video: Hear from Suzanne Hebert, a patient who participated in the trial

Quotes adapted from ScienceDaily.com

Published in: Cancer Discoveries by Todd

In 2008, Mark’s colleague Dr. Yaël Mossé found that mutations in the ALK gene can cause a form of neuroblastoma.  They began experimenting with crizotinib, which blocks ALK activity, and found that tumor response varied according to the type of mutation.  “We predicted that…we’d see differences in how the drug binds to the ALK protein,” Yaël said.  “That was completely wrong.” They instead found that certain tumors simply required a much higher dose of the drug. 

Treatment options are currently limited to surgery and chemotherapy.  Unlike chemo, crizotinib is a targeted therapy that would inflict less damage on healthy, non-cancerous cells.  According to Mark, “If we can better individualize treatment to a child’s genetic profile by understanding the effects of mutations on protein structure and function, we may achieve better results for patients.”

> Read more about the discovery at CHOP.edu

Quotes adapted from Children’s Hospital of Philadelphia article

Published in: Cancer Discoveries by Todd

Last month, Ramesh and a team of researchers at the Dana-Farber Cancer Institute discovered how some cancer cells evade Erbitux, a commonly-used treatment for colorectal and head and neck cancers.

Known generically as cetuximab, Erbitux successfully halts cancer cell growth in many patients.  Unfortunately, its effectiveness mysteriously diminishes after about one year.  Ramesh and his colleagues found that the protein ERBB2 signaled cancer cells to continue growing, essentially overriding the anti-growth signals from Erbitux.  “Because ERBB2 isn’t affected by cetuximab, this is an easy way for cancers to become resistant to the drug,” said Pasi Janne, MD, PhD, a lead author of the study.  

With up to 40% of colorectal cancers thought to be Erbitux-resistant, the team hopes that future clinical studies will reveal that a combination of Erbitux and ERBB2-blocking therapies can increase the treatment’s long-term potency and, ultimately, save lives.

> Video: Watch Ramesh discuss his work

> See how Erbitux works on YouTube

Quotes adapted from ScienceDaily.com

Published in: Cancer Discoveries by Todd

While progress against prostate cancer has been significant, several forms of the disease remain highly lethal and stubbornly resistant to standard treatment.  “The most interesting finding…was the discovery of three aggressive tumor types that had 10 times the number of mutations compared to the other advanced prostate cancers we studied,” Peter said. “We don’t know the cause of these hypermutated tumors, but the frequency of the mutations suggests these tumors might evolve very rapidly to develop resistance to therapies.”

These results mark the first time scientists have been able to identify the unique genetic mutations that distinguish advanced prostate tumors from each other and their less-lethal cousins.

Equipped with these new insights, scientists can begin the critically-needed research necessary to develop new ways to detect and treat advanced prostate cancer.

Quotes adapted from ScienceDaily.com

Published in: Cancer Discoveries by Todd

In a two-year study, Wu and her colleagues found that the drug NVP-BEZ235 hinders growth by blocking two critical cancer cell signaling pathways.  Remarkably, it also counteracts the resistance developed by many ovarian cancer cells to platinum chemotherapy.  As platinum chemotherapy is a frontline treatment for ovarian cancer, eliminating cells’ resistance and enhancing the impact of the therapy would be a significant step in attacking the disease.

In an effort to develop new therapies for ovarian cancer, which affects about 22,000 American women each year, Dr. Wu and the team hope to test the drug in combination with platinum chemotherapy in a clinical trial soon.

Dr. Wu also led a recent study that shed light on how prostate cancer is able to evade some therapies.

> Learn more about our Fellowship Award

Published in: Cancer Discoveries by Todd

Speaking to the Wall Street Journal on this shift in the world of cancer research, Dr. John Mendelsohn, Damon Runyon alumnus and President of Houston’s MD Anderson Cancer Center, said “A pattern is developing at an accelerated pace where we are able to match genetic information about a tumor to a new agent and get results.”  In short, scientists are better able to match treatments to individual patients.

This trend, researchers say, will accelerate their ability to determine the effectiveness and safety of treatments and the rate at which they are made available to patients.  Currently, it can take up to 14 years for a new treatment to move from development to market. 

Fortunately, the U.S. Food and Drug Administration sees the high-potential value of targeted therapy and is using its priority review process to bring many of these personalized treatments to the front of the line.  The drug Yervoy, tested in a clinical study led by Jedd D. Wolchok, MD, PhD, a former Damon Runyon Clinical Investigator at Memorial Sloan-Kettering Cancer Center, was fast-tracked in 2010 and approved by the FDA earlier this year. 

Two more promising cancer drugs are now on the FDA fast-track: vemurafenib and crizotinib.  Doctors at Memorial Sloan-Kettering Cancer Center found that a subset of skin cancer patients had a 48% response rate to the targeted treatment vemurafenib compared to 5% for the current standard therapy.  Similarly, researchers at Massachusetts General Hospital discovered that 60% of patients with ALK positive lung cancer who received crizotinib were still alive after two years.

> Read the WSJ article featuring John Mendelsohn

Published in: Commentary by Todd