February 2013 Archives

New approach helps more smokers connect to tobacco treatment

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144020_Irvin_Vidrine_J web.jpgSmoking remains the leading cause of preventable illness and death in the United States, so the health benefits of quitting are substantial. The majority of smokers are motivated to quit and more than half of all smokers attempt to quit each year. Sadly, only a small minority succeeds.

 

Researchers at MD Anderson are working to change this by changing the culture of how they reach self-admitted smokers with a new approach aimed at connecting through family practice clinics.

 

A collaboration involving MD Anderson researchers, the Texas Quitline and Kelsey-Seybold Clinics targeted smokers and their enrollment in tobacco treatment programs by directly connecting smokers with cessation quit lines.

 

Ask-Advise-Connect

 

Ask-Advise-Connect, a new approach designed to efficiently link smokers with cessation treatment, showed a significant increase in tobacco treatment enrollment by smokers who were directly contacted by quit line staff, according to results published online today in JAMA Internal Medicine

 

JAMA published a video interview Feb. 27 with study principal investigator Jennifer Irvin Vidrine, Ph.D., associate professor in the Department of Health Disparities Research at MD Anderson.

 

New initiatives drive personalized cancer care via genetic analysis of tumors

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102621_Mills_G.jpg 124068_Meric_F.jpgBy William Fitzgerald

Gordon Mills, M.D., Ph.D., recalls a proposal he wrote 18 years ago detailing the concept of personalized cancer therapy and its potential impact. Today, that idea is no longer a proposal, but a reality, and it's about to get a boost.

Under a new and innovative institutional protocol called Clearing House, which started in March 2012, scientists are delving deeper into the biology of patients' tumors, with hopes of identifying specific genetic markers and prescribing therapies to attack those markers directly.

Funda Meric-Bernstam, M.D., professor in MD Anderson's Department of Surgical Oncology, and Mills, professor and chair of the institution's Department of Systems Biology, are leading the effort that will test up to 200 genes known to influence cancer in patients with aggressive or recurring disease.

"In the first year, we'll have sequenced the genes of far more than 1,000 MD Anderson patients and are targeting to have more than 3,000 by the second year," Meric-Bernstam says. "This will accelerate our discovery approaches, and we can develop new clinical trials, in which we already have patients pre-identified to enroll."

While the research began with solid tumors, the Clearing House protocol has expanded to all diseases that have ongoing genomically selected trials, Meric-Bernstam says.

Mills is co-director of MD Anderson's Sheikh Khalifa Bin Zayed Al Nahyan Institute for Personalized Cancer Therapy and Meric-Bernstam is medical director of the institute.

Drug is first to control recurrent low-grade ovarian cancer

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 A phase 2 clinical trial of a targeted therapy provides evidence that there might, at last, be a treatment that shrinks or stifles the growth of recurrent low-grade serous ovarian cancer.

Women who have low-grade disease tend to be younger and survive longer than those with high-grade ovarian cancer, but when their cancer persists or comes back, it almost always thwarts treatment. Between 2% and 4% of patients respond to chemotherapy.  Hormonal therapies do modestly better, with a 9% response rate.

Elliott 2 sized.JPGIn the clinical trial of the drug selumetinib published in the February edition of The Lancet Oncology, eight of 52 (15 percent) patients had a complete or objective partial response (tumor shrinkage) and 34 (65 percent) had no disease progression during the two-year course of the study.

"These are remarkably encouraging results for what can ultimately be a devastating disease," says David Gershenson, M.D., professor in MD Anderson's Department of Gynecologic Oncology and Reproductive medicine, the paper's senior author.

Selumetinib hasn't made Doris Elliott's recurrent low-grade ovarian cancer disappear. But it shrank all of her tumors and has arrested their development for five years running. 

For Dotsy Elliott, cancer under control for five years and counting

After her diagnosis in 1997, six rounds of chemotherapy kept  cancer at bay until 2005. Surgery and nine rounds of chemotherapy did little to slow progression. Another clinical trial helped for about 18 months.

A key to the perils of endless injury repair, the molecular path from stress through a cancer-promoting gene to ovarian cancer progression, and signals by endothelial cells that strengthen  colorectal cancer are among recent discoveries by MD Anderson researchers.

By uncovering these new connections, scientists expose new potential targets for fibrosis, the lethal scarring of organs, and cancer.

100454_Ellis_L.jpgEndothelial cells make cancer cells tougher, more dangerous 

Blood vessels feeding colorectal cancer tumors are delivering more than oxygen and nutrients. They also flip a molecular switch that sends a signal to nearby cancer cells telling them to convert to colorectal cancer stem cells.

"Cancer stem cells initiate and sustain tumor growth, promote metastasis and resistance to chemotherapy and have a variety of other attributes," says Lee Ellis, M.D., of MD Anderson's Department of Surgical Oncology. The blood vessels cells activate Notch signaling.  Drugs in  clinical trials attack Notch. 

News release and Cancer Cell paper

136191_Sood_Ani_k(1).jpgStress hormone breaks dam, cancer-promoting flood follows

The hormone noradrenaline turns on the oncogene Src, which promotes ovarian cancer growth and spread through beta-adrenergic (ADRB) receptors expressed on tumor cells.

"When Src is triggered by stress, it works like a dam letting out water that causes a flood downstream. Src, like the dam, is a master regulator switch that causes a chain reaction in the cells," says Anil Sood, M.D., of the departments of gynecological medical oncology and cancer biology. One implication: beta blockers might work against ovarian cancer.

News release and Nature Communications paper

195156_Kalluri_R.jpgProtein plays pivotal role in scarring that destroys organs

When the body's wound-healing process gets endlessly turned on, the tissues that provide a scaffold for injury repair can destroy the kidneys, liver and lungs. This process, known as fibrosis, also is tightly tied to cancer.

"Fibrosis is wound-healing that never stops. The body thinks an injury exists when it doesn't, so it just keeps going, producing scars that clog an organ's system and destroy its functional tissue until it fails," says Raghu Kalluri, Ph.D., M.D., chair of the Department of Cancer Biology. Kalluri and colleagues identified the role of HE4 in promoting fibrosis. A test already approved for ovarian cancer detects HE4 levels in the blood.

News release and Nature Medicine paper

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