Cancer-Killing Virus Shows Promise as Metastatic Cancer Treatment
The Seneca Valley Virus is a potent cancer killer and can differentiate between normal and cancerous cells. The virus may be a potential treatment for some metastatic cancers, such as small-cell lung cancer.
Cancer-killing viruses have been shown in clinical trials to be promising therapies for localized cancer. But so far their success has been limited in metastatic cancers. This could be due to the viruses targeting normal cells as well as cancer cells or the viruses being inactivated by a patient's blood or immune system.
Paul Hallenbeck, Ph.D., of Neotropix in Malvern, Pa., and colleagues examined the cancer-killing potential of the newly discovered Seneca Valley Virus-001 in normal and tumor cell lines. They also tested the virus in human blood to assess whether it would be suitable for intravenous delivery. The researchers evaluated the safety and efficacy of the virus in mice with tumors derived from human small-cell lung cancer and childhood eye cancer cell lines.
The Seneca Valley Virus was more effective at killing the lung and eye cancer cell lines than the normal cells, and the virus was not inhibited in the blood. Among mice treated with the virus, there was a complete response in all the mice with lung cancer tumors and in the majority of those with eye cancer tumors.
"The data in this report suggest that [the Seneca Valley Virus] may overcome many of the challenges faced by traditional therapies and other [cancer-killing] viruses," the authors write.
Contact: Paul Hallenbeck, (610) 296-8660, email@example.com
Cervical Cancer Survivors Are at Greater Risk of Second Cancers
Cervical cancer patients treated with radiation have an increased risk of second cancers, particularly in areas of the body previously exposed to high levels of radiation. The risk of second cancers increases over time and remains elevated for over 40 years.
The 10-year survival rate for cervical cancer is nearly 70%. But exposure to radiation therapy and the presence of other risk factors among cervical cancer survivors, such as HPV infection, puts this population at high risk for second cancers.
Anil Chaturvedi, Ph.D., of the National Cancer Institute in Bethesda, Md., and colleagues collected data on 104,760 cervical cancer survivors from several Scandinavian countries and the United States. They calculated the incidence of second cancers among these women during a follow-up period of more than 40 years.
About 12,500 women were diagnosed with second cancers. These women were more likely to have HPV-related cancers or smoking-related cancers. Cervical cancer patients treated with radiation were at greater risk for all second cancers, compared with those treated with other methods, and were at particular risk of cancers at sites that were exposed to radiation--the colon, rectum, bladder, ovaries, and genitals. The 40-year risk of a second cancer was greater among women diagnosed with cervical cancer before age 50 than among women diagnosed after age 50.
"The high cumulative risk of second primary cancers in cervical cancer survivors should prompt screening efforts in this group of women," the authors write.
Contact: National Cancer Institute press office, (301) 496-6641, firstname.lastname@example.org
Sequential Randomization in Clinical Trials Points Out Promising Cancer Treatments
A novel trial design offers a way to select which promising drug combinations should be pursued in more advanced clinical trials. Because it is impossible to conduct randomized comparisons of all possible therapies, a new selection method was needed to identify the most promising ones.
Randall Millikan, Ph.D., M.D., of the University of Texas M. D. Anderson Cancer Center in Houston and colleagues conducted a randomized trial to identify promising treatments for androgen-independent prostate cancer. Patients were randomly assigned to one of four different chemotherapy regimens and were evaluated every 8 weeks. Patients who did not respond to their treatment were randomly assigned to one of the other three treatments. The pattern continued until the patient responded to one of the regimens or until the patient failed to respond to two different regimens.
Thirty-five patients responded to their initial treatment and nine more patients to their second treatment. Their median survival was 30 months, compared with 19 months for the patients who did not respond. Weekly treatment with a combination of paclitaxel, estramustine, and carboplatin was the most successful of the four regimens.
"In our view, the results of this trial provide an objective basis for phase III evaluation of [paclitaxel, estramustine, and carboplatin] versus the current standard of single-agent docetaxel," the authors write.
In a commentary, graduate student Oliver Bembom and Mark van der Laan, Ph.D., of the University of California at Berkeley review recent advances in statistical methods for estimating the success rates of different adaptive treatment strategies, such as those employed by Millikan and colleagues.
"By emphasizing the intuitive appeal and straightforward implementation of these methods and by illustrating the striking findings to which these methods can lead, we hope to convince the reader that such trials provide a rich source of information that is made readily accessible though current analytical approaches," they write.
Fighting Brain Cancer May Require Targeting Normal Brain Cells
Glioma, a type of brain cancer, often returns because invasive cells are not killed by standard treatments. In a review, Dominique Hoelzinger, Ph.D., of the Translational Genomics Research Institute in Phoenix and colleagues discuss current therapies for glioma that affect communication between tumor cells and neighboring normal cells. The authors suggest that these neighboring cells in normal brain tissue could be potential targets for therapies because they are less likely to develop resistance than glioma cells.
"A better understanding of the influence of tumors on their microenvironment could lead to therapies that target the more genetically stable normal cells that surround the glioma rather than the genetically unstable tumor cells themselves, which invariably develop resistance to therapy," the authors write.
Contact: Galen Perry, director of communications, Tgen, (602) 343-8423, email@example.com
Also in October 30 JNCI:
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