NCI Cancer Bulletin: A Trusted Source for Cancer Research NewsNCI Cancer Bulletin: A Trusted Source for Cancer Research News
July 19, 2005 • Volume 2 / Number 29 E-Mail This Document  |  Download PDF  |  Bulletin Archive/Search  |  Subscribe

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Cancer Research HighlightsCancer Research Highlights

Prostate Cancer PSA Testing Limitations Demonstrated

A large-scale study of prostate-specific antigen (PSA) screening for prostate cancer concluded that, contrary to current clinical practice, there is no definitive "cutpoint" PSA level to determine the level of risk for the disease, according to an article in the July 6 Journal of the American Medical Association.

The study is based on an analysis of 8,575 healthy men who participated in the placebo arm of the Prostate Cancer Prevention trial; the men in the other study arm received finasteride. Researchers examined the receiver operating characteristic (ROC) curves of various PSA levels, which measures the relative sensitivity (percentage of true disease "positives" detected) and specificity (percentage of true disease "negatives" detected) of the screening method. They found that for detecting any prostate cancer, PSA cutoff values of 1.1, 2.1, 3.1, and 4.1 ng/mL yielded sensitivities of 83.4 percent, 52.6 percent, 32.2 percent, and 20.5 percent, and specificities of 38.9 percent, 72.5 percent, 86.7 percent, and 93.8 percent, respectively.

Study co-author Dr. Howard L. Parnes, chief of NCI's Prostate and Urologic Cancer Research Group, commented, "In the past, many clinicians felt that if the PSA value was below 4, men were essentially free of risk from prostate cancer. That is clearly not the case. Conversely, there was the belief if a man's PSA value was over 4, then a biopsy must be performed. That has also now come into question."

Dr. Parnes added, "It's good to remind people that at every level of PSA, the decision whether to have biopsy needs to be a thoughtful one that takes into account all of a man's risk factors."

High-Risk HPVs Confirmed as Clinical Markers for Cervical Precancer and Cancer

Detection of the two common types of human papillomavirus (HPV) may be useful markers for identifying women who are likely to have or develop cervical cancer and precancerous conditions, according to two related studies published in the July 20 Journal of the National Cancer Institute.

HPV infections cause virtually all cervical cancer. HPV16 infections are implicated in 50 to 60 percent of all women who develop cervical cancer or the precancerous condition cervical intraepithelial neoplasia grade 3 (CIN3). HPV18 is associated with an additional 15 to 20 percent of cervical cancers.

The first study was a randomized, multicenter clinical trial in 5,060 women with mildly abnormal or equivocal Pap smears. Dr. Philip E. Castle of NCI's Division of Cancer Epidemiology and Genetics and colleagues found that women infected with HPV16 were 38 times more likely to develop CIN3 or cervical cancer in the succeeding 2 years than were those with no detectable HPV infection, and 5 times more likely to develop CIN3 or cervical cancer than were women who had other oncogenic HPV types.

In the second study, Dr. Castle and colleagues followed a cohort of 20,512 women for 10 years to see who developed cervical cancer or CIN3. Women with normal Pap smears who were infected with HPV16 or HPV18 at the beginning were 10 times more likely to be diagnosed with cervical cancer or CIN3 than those with any other oncogenic HPV type. Women infected with HPV16 or HPV18 were also more likely to be diagnosed with cervical cancer or CIN3 than women with an abnormal Pap smear.

These results suggest that "identifying HPV16-infected women with normal, equivocal, or mildly abnormal cervical cytology, as well as identifying HPV18-infected women with normal cervical cytology, may be useful for determining those women at high risk of having or developing cervical cancer or CIN3 and therefore their optimal clinical management," said Dr. Castle.

Youth Smoking Behaviors Reduced by State-Sponsored TV Ads

Children aged 10 to 17 smoked less and displayed more favorable antismoking attitudes and beliefs when they had been recently exposed to antismoking TV advertisements sponsored by state public health departments, according to a study published in the July 2005 Archives of Pediatrics and Adolescent Medicine.

The cross-sectional study used nationally representative survey data from 1999-2000. "It is important to maintain a minimal mean exposure of at least one cumulative state-sponsored antitobacco ad per 4-month period for the general teen viewing audience," wrote study lead author Dr. Sherry Emery of the Institute for Health Research and Policy at the University of Illinois at Chicago. The research was funded in part by NCI under the Tobacco Research Initiative on State and Community Interventions.

Survey respondents who had seen at least one such ad within 4 months were less likely to be smokers and more committed to not smoking in the future, the researchers concluded. The study also found that teens were less likely to perceive their friends as smokers and more likely to view smoking as harmful. These results indicate that state-sponsored advertising - while much less frequent than "antitobacco" advertising sponsored by the tobacco industry - is significantly more effective, commented Dr. David Nelson of the Centers for Disease Control and Prevention.

Study investigators used Nielsen commercial ratings to determine broadcast and cable TV audience exposure to the antitobacco ads. This information was merged with data from the University of Michigan's Monitoring the Future study, which measured student characteristics, smoking-related attitudes and beliefs, and self-reported tobacco use by 8th, 10th, and 12th graders.

New Clues in Regulation of DNA Duplication

When a cell divides, it generates an identical copy of the three billion letters of the nuclear genome - or at least it tries to. Sometimes mistakes occur, which can lead to cancer. Researchers are now one step closer to understanding how the DNA duplication process works, according to a report in the July 10 online edition of Nature Cell Biology.

"It's a significant result that will allow us to rethink strategies for designing drugs" that prevent errors in DNA duplication, said Dr. Philipp Kaldis of the Mouse Cancer Genetics Program in NCI's Center for Cancer Research.

Much of the cell-division process is regulated by a group of proteins called cyclin-dependent kinases. The proteins have drawn much attention from basic biologists because mutations in them can trigger cancer.

Dr. Kaldis and his colleagues made genetically modified mice that lacked a particular cyclin-dependent kinase. They expected the mice to develop rampant tumors and were surprised when they did not. "It turns out there are two parallel pathways and [more severe cancers] occur only if both are inhibited," said Dr. Kaldis. He added that scientists have been trying to prove a role of a cellular protein called mammalian Cdc2 in DNA duplication for 20 years. "We can change the textbooks now," he said.