© 1999 by Oxford University Press
Journal of the National Cancer Institute, Vol. 91, No. 12, 987,
June 16, 1999
© 1999 Oxford University Press
IN THIS ISSUE |
Retinoic acid and its analogues possess anticancer activity and have been reported to play a
beneficial role in the prevention and treatment of different neoplastic conditions. The effects of
retinoids are mediated by a variety of nuclear receptors. Picard et al. (p. 1059)
studied the expression patterns of these receptors in non-small-cell lung carcinoma and found
that all of the studied receptors were expressed in normal lung cells and in high-risk
non-neoplastic lesions. In tumor cells, the expression of some receptors (i.e., retinoic acid
receptor [RAR] 
and retinoid X receptor [RXR] ) is either
normal or elevated, whereas the expression of some receptors (i.e., RARß, RAR
, and
RXRß) is markedly decreased. The authors conclude that altered retinoid receptor
expression may play a role in lung carcinogenesis, and receptor analysis will help in identifying
individuals who may benefit most from retinoic acid treatment.
In an accompanying editorial (p. 989), Lotan notes that the novelty of the report by Picard et al. is in the demonstration of receptor modulation in lung cancer at the protein level. Because monitoring protein expression by immunohistochemistry is easier to perform than monitoring messenger RNA by in situ hybridization, the former may be the method of choice once it becomes reproducible in different laboratories.
Screening and Trends in Prostate Cancer Statistics
To provide insight into the effect of screening on prostate cancer incidence and mortality rates, Hankey et al. (p. 1017) have analyzed incidence data from the National Cancer Institute's Surveillance, Epidemiology, and End Results Program and mortality data from the National Center for Health Statistics. They report findings consistent with a screening effect and conclude that the decline in the incidence of distant stage prostate cancer since 1991 holds the promise that testing for prostate-specific antigen may lead to a sustained decline in prostate cancer mortality. However, population data are complex, and it is difficult to confidently attribute relatively small changes in mortality to any one cause.
Rise and Fall in Prostate Cancer Mortality
The recent rise and fall in prostate cancer mortality correspond closely with the rise and fall in newly diagnosed cases. Feuer et al. (p. 1025) have explored the role of prostate-specific antigen (PSA) screening and of possible incorrect labeling of death from other causes as death from prostate cancer (attribution bias) in these mortality trends. With the introduction of widespread PSA testing starting in 1987, mortality rates rose above the pre-1987 background level, peaked in the early 1990s, and returned to the background rate in 1994. The authors conclude that these mortality trends are consistent with the hypothesis that a certain proportion of deaths in the rising and falling pool of newly diagnosed patients was incorrectly attributed to prostate cancer.
PSA Testing and Prostate Cancer Mortality
By use of a computer simulation model, Etzioni et al. (p. 1033) have investigated whether prostate-specific antigen (PSA) testing conducted in the late 1980s and early 1990s could plausibly explain the decline in prostate cancer mortality observed from 1991 through 1994. The model provided estimates of the number of deaths prevented by PSA testing for the 7-year period from 1988 through 1994. The authors report that it is unlikely that the entire decline in prostate cancer mortality can be explained by PSA testing.
Childhood Cancer Incidence and Mortality
Linet et al. (p. 1051) have examined incidence and mortality patterns for childhood cancer over a two-decade period to address public concern about possible increases in cancer rates in children. Cancers diagnosed from 1975 through 1995 in 14,540 children under the age of 15 years and reported to nine population-based registries in the National Cancer Institute's Surveillance, Epidemiology, and End Results Program were investigated. The authors found no substantial change in the incidence of major pediatric cancers, and the rates have remained relatively stable since the mid-1980s. The modest increases that were observed for brain and central nervous system cancers, leukemia, and infant neuroblastoma were confined to the mid-1980s. These increases likely reflect diagnostic improvements or reporting changes. Observed dramatic declines in childhood cancer mortality likely reflect treatment-related improvements in survival.
Geography of Lung Cancer Deaths
"The changing patterns of smoking prevalence and subsequent lung cancer rates should help identify target populations where anti-tobacco research and control programs are especially needed. . . ."
—Devesa et al.
From 1950 through 1994, the geographic patterns of lung cancer mortality by race and sex have changed substantially. In this issue, Devesa et al. (p. 1040), using mortality data from the National Center for Health Statistics for the 3,055 counties in the United States, report that the once-high rates of lung cancer deaths among white males in urban areas of the northeast and north central states observed in the 1950s and 1960s began to fade in the 1970s, while deaths in the south increased. By the 1980s to mid-1990s, elevated lung cancer death rates for white males clustered in the south and south central states, with relatively low rates in much of the northeast. The observed trends in lung cancer mortality for this group, as well as those for white women and blacks of both sexes, generally coincided with regional trends in cigarette smoking for each group, underlining the importance of tobacco control efforts.
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