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Cancer represents an increasingly important health problem impacting the health status of American Indians and Alaska Natives (AI/ANs). At the turn of the century and as recently as the 1950s, cancer was such an uncommon occurrence among AI/ANs that they were thought,to be immune. Today, malignant disease represents a leading cause of death among these peoples. This relatively sudden increase has left communities and health agencies unprepared. This paper presents the framework for approaching cancer control research among AI/ANs, including the development of accurate surveillance systems; enhanced public and professional education; research focused on risk-factor prevalence and etiology; improved communication between Native communities and researchers; comprehensive evaluation of cancer control programs; dissemination of successful intervention programs; and research to examine factors responsible for the low risk of specific cancers among Native populations. Moreover, results from a series of national surveys providing a comprehensive overview of the limited cancer control programs directed toward AI/AN populations are highlighted. Efforts to maximize the health status of American Indians and Alaska Natives through cancer control efforts will rely upon a cooperative approach between individual tribal groups along with the proactive involvement of federal and state public health agencies, as well as the support of appropriate private and nonprofit organizations.

Purpose: This manuscript examines shifts in patterns of cancer incidence among the Seneca Nation of Indians (SNI) for the interval 1955-1969 compared to 1990-2004. Methods: A retrospective cohort design was used to examine cancer incidence among the SNI during 2 time intervals: 1955-1969 and 1990-2004. Person-years at risk were multiplied by cancer incidence rates for New York State, exclusive of New York City, over 5-year intervals. A computer-aided match with the New York State Cancer Registry was used to identify incident cancers. Overall and site-specific standardized incidence ratios (SIRs = observed/expected x 100), and 95% confidence intervals (CIs), were calculated for both time periods. Results: During the earlier interval, deficits in overall cancer incidence were noted among males (SIR = 56, CI 36-82) and females (SIR = 71, CI 50-98), and for female breast cancers (SIR = 21, CI 4-62). During the more recent intervals, deficits in overall cancer incidence persisted among both genders (males SIR = 63, CI 52-77; females SIR = 67, CI 55-80). Deficits were also noted among males for cancers of the lung (SIR = 60, CI 33-98), prostate (SIR = 51, CI = 33-76) and bladder (SIR = 17, CI = 2-61) and among females for breast (SIR = 33, CI = 20-53) and uterus (SIR = 36, CI = 10-92). No cancer sites demonstrated increased incidence. Persons ages 60-69 years, 70-79 years, and ages 80+ years tended to exhibit deficits in overall incidence. Conclusions: Despite marked changes over time, deficits in overall cancer incidence have persisted between the time intervals studied. Tribal-specific cancer data are important for the development and implementation of comprehensive cancer control plans which align with local needs.

Women who smoke and can not metabolize carcinogenic chemicals quickly may have a greater risk of breast cancer. Toxic chemicals typically found in cigarette smoke are metabolized by several enzymes, including one called N-acetyltransferase 2 (NAT2). Researchers used DNA analysis on 631 women to detect gene mutations in NAT2 that would cause women to detoxify carcinogens slowly or rapidly. Of the total group, 304 women had breast cancer. Slow metabolizers who were current or former smokers had a greater risk of breast cancer, but this result was only seen in postmenopausal women., Objective.--To determine if N-acetyltransferase 2(NAT2) polymorphisms result in decreased capacity to detoxify carcinogenic aromatic amines in cigarette smoke, thus making some women who smoke more susceptible to breast cancer. Design.--Case-control study with genetic analyses. DNA analyses were performed for 3 polymorphisms accounting for 90% to 95% of the slow acetylation phenotype among whites. Setting and Participants.--White women with incident primary breast cancer (n=304) and community controls (n=327). Results.--Neither smoking nor NAT2 status was independently associated with breast cancer risk. There were no clear patterns of increased risk associated with smoking by NAT2 status among premenopausal women. In postmenopausal women, NAT2 strongly modified the association of smoking with risk. For slow acetylators, current smoking and smoking in the distant past increased breast cancer risk in a dose-dependent manner (odds ratios [95% confidence intervals] for the highest quartile of cigarettes smoked 2 and 20 years previously, 4.4 [1.3-14.8] and 3.9 [1.4-10.8], respectively). Among rapid acetylators, smoking was not associated with increased breast cancer risk. Conclusions.--Our results suggest that smoking may be an important risk factor for breast cancer among postmenopausal women who are slow acetylators, demonstrate heterogeneity in response to carcinogenic exposures, and may explain previous inconsistent findings for cigarette smoking as a breast cancer risk factor. JAMA. 1996;276:1494-1501

Abstract Many challenges emerged during completion of a study to examine radiation dose and acute leukemia among children in areas of the former Soviet Union. In an era of globalization, our experiences might benefit others involved in multinational investigations.

After the publication of this work 1, we noted that we inadvertently failed to acknowledge funding support for this project.