Circulating tumour cells--a bona fide cause of metastatic cancer.

Circulating tumour cells (CTCs) are emerging as important prognostic markers and have potential clinical utility as tumour biomarkers for targeted cancer therapy. Although CTCs were proposed more than 100 years ago as potential precursors that may form metastatic lesions, formal evidence that CTCs are indeed capable of initiating metastases is limited. Moreover, the process of CTCs shedding into the circulation, relocating to distant organ sites and initiating metastatic foci is complex and intrinsically inefficient. To partially explain the metastatic process, the concepts of CTCs as metastatic precursors or pre-metastatic conditioners have been proposed; however, it is questionable as to whether these are both variable pathways to metastasis or just markers of metastatic burden. This review explores the evidence for CTCs in the initiation and progression of metastatic cancer and the data supporting these different concepts in an attempt to better understand the role of CTCs in metastasis. A greater understanding of the metastatic potential of CTCs will open new avenues for therapeutic interventions in the future.

HLA DR-DQ associations with cervical carcinoma show papillomavirus-type specificity.

Cervical carcinoma is now known to be associated with human papillomaviruses (HPV), but the evidence for a link with specific HLA loci is controversial. The role of genetic variation at the HLA class II loci and among HPV types in cervical carcinoma was investigated by PCR DNA amplification and oligonucleotide probe typing of paraffin-embedded invasive cervical cancer tissue from Hispanic patients and of cervical swabs from Hispanic controls. Certain HLA class II haplotypes (such as DRB1*1501-DQB1*0602) were associated significantly, while DR13 haplotypes were negatively associated with cervical carcinoma. These associations are HPV16-type specific. These results suggest that specific HLA class II haplotypes may influence the immune response to specific HPV-encoded epitopes and affect the risk of cervical neoplasia.

The predictive and prognostic significance of liquid biopsy in advanced epidermal growth factor receptor-mutated non-small cell lung cancer: A prospective study.

OBJECTIVE: To determine the predictive and prognostic roles of three blood-based biomarkers: circulating tumour DNA (ctDNA), circulating tumour cells (CTC) and carcinoembryonic antigen (CEA), in patients with advanced epidermal growth factor receptor-mutated (EGFR+) lung cancer. MATERIALS AND METHODS: We recruited 28 patients with 103 serial blood samples. We performed mutational analyses for EGFR mutations using droplet digital PCR (ddPCR) on ctDNA. We evaluated the accuracy of EGFR mutation detection in ctDNA compared with tissue biopsy. We also quantified CTCs, ctDNA and CEA in serially collected blood samples, and evaluated the baseline and changes in these blood-based biomarkers with clinical outcomes. RESULTS: EGFR mutation detection in plasma was highly concordant as compared with tissue biopsy. Detectable baseline ctDNA was associated with higher disease burden (p < 0.01). Early disappearance of ctDNA at 4 weeks was associated with radiological response at 12 weeks of treatment (p = 0.01) and improved progression free survival (PFS) (HR 5.47, 95%CI 1.32-22.72, p = 0.02) and overall survival (OS) (HR 5.46, 95%CI 1.28-23.22, p = 0.02). A decrease in CTC count at 4 weeks was associated with improved PFS (HR 3.81, 95%CI 1.13-12.79, p = 0.03) but not OS. 85% of patients with radiological progression had a ctDNA rise compared with 22% of patients with stable disease (p=0.01). ctDNA rise was seen on average 170 days prior to radiological progression. There is a significant association between the rise of CEA level with radiological progression (p=0.001). CONCLUSION: Early change in ctDNA, CTC and CEA levels may be long-term predictors of treatment benefit and failure prior to availability of radiological response data.

Comparison of human leukocyte antigen DR-DQ disease associations found with cervical dysplasia and invasive cervical carcinoma.

BACKGROUND: Human leukocyte antigen (HLA) molecules, whose biological role is in the regulation of immune responses to foreign antigens and in discrimination of self from non-self antigens, are encoded by a series of closely linked genetic loci found on chromosome 6. Although the evidence for a link between HLA and cervical cancer has been controversial, it has been recently reported that certain HLA class II haplotypes (linked class II alleles) are positively associated with invasive cervical cancer, while other class II haplotypes are negatively associated or protective. Since HLA associations between human papillomavirus type 16 (HPV16)-mediated cancer cases and non-HPV16-mediated cancer cases have been found to be different, this suggests that specific HLA class II haplotypes may influence the immune response to HPV infection and may affect the risk of acquiring invasive cervical carcinoma. PURPOSE: This study was conducted to determine if the same HLA class II haplotypes that are associated with invasive cervical carcinoma are also associated with cervical dysplasia (presumed precursors of invasive cervical cancer). METHODS: We have examined HLA DR-DQ haplotypes among 128 Hispanic women from New Mexico with biopsy-confirmed cervical dysplasia in a case-control study using sensitive DNA-based polymerase chain reaction amplification and sequence-specific oligonucleotide probe hybridization methods to detect the presence and type of HPV and to detect allelic polymorphism in the HLA DRB1 and DQB1 loci. RESULTS: Dysplasia cases were divided into two groups for comparison to controls: severe dysplasia/carcinoma in situ (CIS), and slight/moderate dysplasia. The frequency distribution of HLA class II haplotypes among the HPV16-positive severe dysplasia/CIS cases had a statistically significant (two-tailed P < .005) difference compared with controls, whereas haplotypes among the severe dysplasia/CIS cases containing HPV types other than HPV16 did not show statistically significant frequency differences. DR-DQ haplotypes previously found to be associated with HPV16-invasive cervical carcinomas were also associated with HPV16-positive severe dysplasia/CIS. However, no statistically significant haplotype frequency difference was observed between slight/moderate dysplasia cases and controls. In addition, we noted a DQA1-DQB1 haplotype negatively associated with severe dysplasia/CIS but not with invasive cervical cancers. CONCLUSIONS: Our results strongly suggest that certain HLA haplotypes confer an increased risk for severe cervical dysplasia and invasive cervical carcinoma following HPV16 infection. IMPLICATIONS: Further molecular studies are needed to identify HLA alleles or haplotypes that may provide increased susceptibility to HPV-associated cervical disease.

Cancer mortality among New Mexico's Hispanics, American Indians, and non-Hispanic Whites, 1958-1987.

BACKGROUND: Racial and ethnic differences in cancer incidence and mortality are well documented. New Mexico's ethnically and racially diverse population provides an opportunity to further examine ethnic and racial differences in cancer occurrence. PURPOSE: To address differences in cancer mortality among the state's Hispanics, American Indians, and non-Hispanic Whites, we examined mortality data collected from 1958 through 1987. METHODS: Sex and age-specific and age-adjusted cancer mortality rates were calculated for all sites and specific sites for American Indians, Hispanics, and non-Hispanic Whites. From 1958 through 1987, deaths due to malignant neoplasms were coded according to the International Classification of Diseases. The categories of malignant neoplasms investigated were chosen, in part, to minimize bias due to changes in disease classification. Ethnicity was assigned by the Bureau of Vital Statistics on the basis of information on death certificates. Denominators were derived from the censuses of 1960, 1970, 1980, and 1990. Age-standardized mortality rates were calculated for 5-year periods (1958-1962, 1963-1967, 1968-1972, 1973-1977, 1978-1982, and 1983-1987), with the 1970 U.S. population as the standard. We also examined age-specific rates by time period. RESULTS: Within each of New Mexico's ethnic groups, overall cancer mortality increased over the 30-year time span, and the cancer mortality rates were greater for males than for females. For most major cancer sites, mortality rates for New Mexico's non-Hispanic Whites were comparable with data for U.S. Whites. American Indians had the lowest rates for most sites, whereas cancer mortality rates for most sites among Hispanics were intermediate between the two other groups. However, Hispanics and American Indians had higher mortality rates for cancers of the gallbladder, cervix, and stomach compared with non-Hispanic Whites throughout most of the study period. Several other cancer sites showed major mortality rate differences among these racial and ethnic groups, including cancers of the colon, rectum, breast, bladder, lung, ovary, and uterus. We also observed strong temporal trends of increasing or decreasing mortality rates for several cancer sites. CONCLUSIONS: Race and ethnicity have been strong determinants of cancer mortality in New Mexico. Within the span of one generation, cancer mortality has changed substantially for some cancer sites in each of the population groups studied. IMPLICATIONS: These mortality data underscore the need for appropriately designed etiologic studies of cancer in diverse racial and ethnic groups. Such etiologic studies could provide new insights concerning risk factors for cancer and useful data for developing race- and ethnic-specific cancer control strategies.

A virus-like particle enzyme-linked immunosorbent assay detects serum antibodies in a majority of women infected with human papillomavirus type 16.

BACKGROUND: Previous studies have demonstrated that genital infection with high-risk types of human papillomavirus (HPV), most often HPV16, is the most significant risk factor for the development of cervical cancer. However, serologic assays that have been developed to identify high-risk HPV infection have either failed to associate serum reactivity with other indicators of HPV infection or have identified only a minority of HPV-infected individuals. PURPOSE: Our purpose was to determine whether a specifically developed enzyme-linked immunosorbent assay (ELISA) could detect IgG anti-HPV16 virion antibodies in the sera of women who had tested positive for genital HPV16 infection by DNA-based methods. METHODS: An ELISA was developed using newly developed HPV16 virus-like particles as antigens to detect anti-HPV16 virion IgG antibodies. These particles are comprised of HPV16 structural proteins that are self-assembled in insect cells after expression by recombinant baculoviruses. The sera of 122 women, whose HPV status had been previously evaluated by nucleic acid-based methods, were tested by this ELISA. RESULTS: The sera of 59% of women (32 of 54) positive for genital HPV16 DNA by polymerase chain reaction (PCR) were positive in the ELISA assay compared with sera from women who had tested negative for HPV DNA (P < .0005). In contrast, 6% of HPV DNA-negative women (two of 31) and 9% of women positive for low-risk HPV6/11 DNA (one of 11) were ELISA positive by this criterion. The sera of women who were DNA positive for two additional high-risk HPV types were evaluated; the sera of 31% of HPV18-positive (four of 13) and 38% of HPV31-positive women (five of 13) were positive in the HPV16 particle ELISA. The sera of 75% of HPV16 DNA-positive women with severe dysplasias (12 of 16) gave positive ELISA results. The sera of 67% of women (28 of 42) who tested positive for HPV16 DNA by both PCR and the less sensitive ViraType assay tested positive in the ELISA compared with 33% of women (four of 12) who were positive by PCR but negative by ViraType (P < .05). CONCLUSION: The majority of women with cervical HPV16 infection generate an IgG antibody response to conformationally dependent epitopes of HPV16 L1 that can be detected by ELISA. IMPLICATION: This particular ELISA, or a similar one incorporating virus-like particles of additional HPV types, may be useful in determining the natural history of high-risk HPV infection and perhaps help to identify women at risk for developing cervical cancer.

Stomach cancer among New Mexico's American Indians, Hispanic whites, and non-Hispanic whites.

Stomach cancer incidence rates vary by ethnic group in New Mexico, with American Indians and Hispanic Whites at higher risk than the state's non-Hispanic White population. To further characterize the descriptive epidemiology of this disease in New Mexico, we investigated temporal trends in stomach cancer mortality and incidence rates. Stomach cancer mortality rates declined over a 25-year period (1958-1982) among New Mexico's Hispanic and non-Hispanic Whites. Birth cohort analysis suggests that much of the decline was achieved prior to 1968. Stomach cancer mortality rates did not drop among American Indians during the same period. Stomach cancer incidence rates remained constant for Hispanic Whites, non-Hispanic Whites, and American Indian males over a 13-year period (1969-1982), but more than doubled among American Indian females. Although environmental factors have been implicated in the etiology of stomach cancer, little is currently known about the distribution of such risk factors among the ethnic groups described in this report. The environmental and biological correlates of sex, ethnicity, and socioeconomic status that determine stomach cancer risk merit further investigation in New Mexico.

Differential expression of p16INK4a and p16beta transcripts in B-lymphoblastoid cells from members of hereditary melanoma families without CDKN2A exon mutations.

Mutations in the CDKN2A (p16INK4a) tumour suppressor gene on chromosome 9p21 are associated with inherited predisposition to melanoma, yet some 9p-linking hereditary melanoma families show no mutations in this gene. Splicing of CDKN2A exons 2 and 3 to an alternative first exon produces a transcript (p16beta) encoding a protein with cell cycle regulatory properties. We have analysed allele-specific expression levels of both the p16INK4a and p16beta transcripts in B-lymphoblastoid cells from 18 members of hereditary melanoma kindreds including four unrelated control individuals. In 15 of the 18 individuals examined, steady-state levels of each transcript either originated equally from each parental chromosome, or one parental chromosome was dominant for both transcripts. However, in three affected members of two 9p-linking hereditary melanoma kindreds, without exonic CDKN2A mutations, this pattern of coordinate expression was disrupted. In these individuals there was underexpression of the p16beta transcript, relative to the p16INK4a transcript, from the chromosome segregating with disease susceptibility. Loss of coordinate expression of the p16INK4a and p16beta transcripts may be an alternative genetic basis for melanoma susceptibility in certain 9p-linking kindreds.

Analysis of the p16 gene, CDKN2, in 17 Australian melanoma kindreds.

CDKN2 has been implicated as a melanoma susceptibility gene in some kindreds with a family history of this disease. Mutation analysis of CDKN2 in 17 familial melanoma Australian kindreds revealed a paucity of exon mutations and none of the previously described disease-related mutations. One novel germline mutation was found in exon one, Arg24Pro, which segregates with melanoma in 1/17 kindreds. Two previously described polymorphisms, Ala148Thr and a base change at nucleotide 540 were detected and one novel polymorphism in the untranslated region of exon 3 (nucleotide 580) was also found. Together with other recent reports, these findings provide support for CDKN2 as a susceptibility locus for familial melanoma but suggest that other loci are involved in some hereditary melanoma kindreds.

Functional impairment of melanoma-associated p16(INK4a) mutants in melanoma cells despite retention of cyclin-dependent kinase 4 binding.

PURPOSE: Melanoma-associated germ-line mutations affecting the tumor suppressor and cyclin-dependent kinase (CDK) inhibitor, CDKN2A/p16(INK4a) have been identified in >100 melanoma-prone families. To predict the melanoma risk for carriers of specific mutations, it is useful to test the function of the mutant proteins in biochemical assays; however, it is unclear how well these results correlate with their cellular effects. We examined the relationship between loss of CDK binding by mutant proteins and various measures of cellular growth in melanoma cells. EXPERIMENTAL DESIGN: The cellular activities of four melanoma-associated p16(INK4a) mutations (Arg24Pro, Ala36Pro, Met53Ile, and Val126Asp) were compared by use of inducible expression in stably transfected melanoma cells, deficient in expression of the endogenous protein, and compared with their ability to bind CDK4. RESULTS: The cell cycle-inhibitory activity of all of the mutants was profoundly reduced, and partially retained capacity for CDK4 binding in functional assays did not correlate with significant preservation of cell cycle-regulatory function. CONCLUSION: Testing of p16(INK4a) interactions with CDKs in protein-binding assays is an unreliable predictor of mutant p16(INK4a) function in cells. In addition to exhibiting reduced stability, these mutant proteins may also be defective in interaction with cellular targets other than CDKs.

Diabetes mortality among New Mexico's American Indian, Hispanic, and non-Hispanic white populations, 1958-1987.

OBJECTIVE: To determine the diabetes-related mortality rates among New Mexico's American Indians, Hispanics, and non-Hispanic whites over a 30-yr period. RESEARCH DESIGN AND METHODS: Death certificates were used to identify diabetes as an underlying cause of death by ethnic group in New Mexico during each 5-yr period from 1958 through 1987. The age-adjusted rates were calculated by ethnic group and sex, and temporal trends were examined. Comparison was made to U.S. white age-adjusted rates during the same time period. RESULTS: Age-adjusted diabetes mortality rates for American Indians and Hispanics increased throughout the 30-yr period, and far exceeded rates for New Mexico non-Hispanic whites and U.S. whites by the 1983-1987 time period. The rates increased most dramatically among the state's American Indians, increasing 550% among women and 249% among men. Hispanic women and men experienced increases of 112 and 140%, respectively. CONCLUSIONS: New Mexico's American Indian and Hispanic populations have higher diabetes mortality rates than non-Hispanic whites, and American Indian mortality rates have risen dramatically over the 30-yr period included in our study. Although the high prevalence of diabetes in American Indians and Hispanics is a major contributor to these rates, other factors may also influence the reported mortality rates.

Trends in prostate cancer incidence and mortality in New Mexico are consistent with an increase in effective screening.

The increasing occurrence of prostate cancer in the United States has led to recommendations for routine prostate cancer screening in men aged 50 years and older. Although present methods of prostate cancer screening have not been shown to reduce mortality, screening using digital rectal examination or prostate-specific antigen does detect tumors at earlier stages. To assess whether trends in incidence and mortality rates are consistent with an increase in effective screening in New Mexico, we examined prostate cancer incidence rates calculated from data collected by the New Mexico Tumor Registry for the years 1969-1991, and mortality rates calculated from data collected by the New Mexico Bureau of Vital Statistics for the years 1958-1991. Population-based measures of prostate cancer screening frequency in New Mexico are not available for the period of this study; however, the proportion of prostate cancers detected by screening, as documented by a review of records from a random sample of prostate cancer cases, increased 3-fold, from 13% during the 1969-1972 period to 41% in the 1988-1991 period. During the period of study, age-adjusted incidence rates increased from 66.3 to 122.3/100,000 men. Stage migration from distant to earlier stages was apparent in the increase in the proportion of early stage cancers from 77.5 to 85.5%, and the decrease of distant stage cancers from 21.2 to 9.8%. Stage-specific incidence rates increased for local (87.3%) and regional stage cancers (283.0%), and decreased for distant stage cancers (16.0%).(ABSTRACT TRUNCATED AT 250 WORDS)

Ovarian cancer incidence and mortality in American Indian, Hispanic, and non-Hispanic white women in New Mexico.

Although ethnic and racial differences in ovarian cancer incidence and mortality have been reported worldwide, few published data have addressed the epidemiology of ovarian cancer among U.S. American Indians and Hispanics. We reviewed ovarian cancer incidence and survival data from New Mexico's population-based cancer registry collected from 1969 to 1992, and examined state vital records data for ovarian cancer deaths collected from 1958 to 1992, focusing on ethnic differences in occurrence and outcomes of ovarian malignancies. Non-Hispanic white women had age-adjusted incidence rates that were slightly higher (13.3/100,000) than rates for American Indians (11.4) and Hispanics (10.7) over the 24-year period. Ovarian cancer mortality rates were also higher for non-Hispanic whites than for minority women. Neither incidence rates nor mortality rates for ovarian cancer improved over the span of the study period. In addition, the stage at diagnosis did not shift substantially over time for any of the ethnic groups studied, nor did the distribution of various histopathological types shift proportionately. Only slight improvement was observed in 5-year survival over the time period of the study, with greater gains among younger (50 years old or less) versus older women. Ethnic differences in ovarian cancer incidence and mortality were apparent in our population-based data. However, our analysis indicated no reduction in ovarian cancer incidence or mortality in our state over the past quarter century and only slight improvement in 5-year survival.

Serum carotenoids and risk of cervical intraepithelial neoplasia in Southwestern American Indian women.

The objective of this research was to evaluate the association between serum carotenoids and cervical intraepithelial neoplasia (CIN) among Southwestern American Indian women. Cases were American Indian women with biopsy-proven CIN II/III cervical lesions (n = 81) diagnosed between November 1994 and October 1997. Controls were American Indian women from the same clinics with normal cervical epithelium (n = 160). All of the subjects underwent interviews and laboratory evaluations. Interviews evaluated demographic information, sexual history, and cigarette smoking. Serum concentrations of alpha-carotene, beta-carotene, beta-cryptoxanthin, lycopene, and lutein/zeaxanthin were measured by high performance liquid chromatography. Cervical human papillomavirus infection was detected using a PCR-based test. Increasing levels of alpha-carotene, beta-cryptoxanthin, and lutein/zeaxanthin were associated with decreasing risk of CIN II/III. In addition, the highest tertiles of beta-cryptoxanthin (odds ratio = 0.39, 95% confidence interval = 0.17-0.91) and lutein/zeaxanthin (odds ratio = 0.40, 95% confidence interval = 0.17-0.95) were associated with the lowest risk of CIN. In conclusion, specially targeted intervention efforts to increase consumption of fruits and vegetables may protect Southwestern American Indian women from developing CIN.

Cigarette smoking and other risk factors for cervical dysplasia in southwestern Hispanic and non-Hispanic white women.

To assess smoking-related and other risk factors for high-grade cervical dysplasia in southwestern Hispanic and non-Hispanic white women in New Mexico, we conducted a clinic-based case-control study among attendees at university-affiliated gynecology clinics. We collected data on cigarette use, sexual behavior, past and current sexually transmitted diseases, hygienic practices, contraception, and diet. For both ethnic groups combined, after adjustment for the effects of human papillomavirus, sexual behavior, and other risk factors, cigarette smoking at the time of diagnosis was associated with high-grade dysplasia (odds ratio, 1.7; 95% confidence limits, 1.0-2.8). In contrast, former smoking was not associated with cervical dysplasia (odds ratio 0.9; 95% confidence limits, 0.5-1.5). Analyses showed dose-response relationships for the amount of cigarettes smoked per day and for cumulative exposure (pack-years of use) in association with cervical dysplasia. Although our study lacked the power to show statistically significant ethnic differences in smoking-related risks for dysplasia, smoking at the time of diagnosis, high pack-years of use, and smoking at the time of menarche were associated with dysplasia only for non-Hispanic white versus Hispanic women. Our data support hypotheses that implicate cigarette use as an etiological factor in the development of high-grade cervical dysplasia and suggest ethnic differences in risks for dysplasia among women attending the same clinics.

Treatment of serious infections with moxalactam.

In 93 hospitalized patients, 111 bacterial infections were treated with moxalactam. Eighty-three infections responded well to therapy, nine infections failed to respond to therapy or relapsed, and nine infections showed superinfection with resistant bacteria. The great majority of bacteria isolated had mean inhibitory concentrations below levels readily achieved in plasma, cerebrospinal fluid, bile, abscess fluid, and peritoneal fluid. Among the commonly identified bacteria, only Pseudomonas aeruginosa, enterococci, and Staphylococcus epidermidis had variable sensitivity to moxalactam.

Colorectal cancer incidence and survival among Alaska Natives, 1969-1993.

BACKGROUND: Although colorectal cancer rates are low among most groups of Native Americans in North America, rates for Alaska Natives have been substantially elevated compared with US rates for all races combined. METHODS: To better describe the epidemiology of colorectal cancer incidence and survival among Alaska Natives, stratified by gender and tribal/ethnic affiliation, we examined data collected by the Alaska Native Cancer Registry 1969-1993. We calculated age-adjusted and age-specific incidence as well as actuarial survival rates, and examined histological type, site, stage at diagnosis, and treatment. We compared these data to colorectal cancer data from whites living in western Washington. RESULTS: In all, 587 colorectal cancer cases were identified among Alaska Natives over the 25-year period, for an age-adjusted annual incidence rate of 71.4/100000 in women, and 69.3/100000 in men. Compared to Alaska Indians, colon cancer rates were significantly higher in Aleuts (relative risk [RR] = 1.6, 95% CI: 1.2-2.2) and in Eskimos (RR = 1.5, 95% CI: 1.2-1.8), while rectal cancer rates did not differ by race/ethnicity. Alaska Natives experienced a 50% higher incidence rate of colorectal cancer overall compared to western Washington whites (RR = 1.5, 95% CI: 1.3-1.6), although rectal cancer rates were similar in the two populations. The highest RR were seen among Alaska Native women; Aleuts and Eskimos had colon cancer rates more than twice that of western Washington white women. No unusual qualitative features were found in the cancers occurring in Alaska Natives. Actuarial colorectal cancer survival rates for Alaska Natives overall were 74% at one year and 42% at 5 years; these rates were very similar to those observed for the western Washington population. Both one and 5-year survival rates showed a significant trend towards improvement over time. CONCLUSIONS: Alaska Natives had substantially higher colorectal cancer incidence rates compared to western Washington whites. Rates were particularly high for Aleut and Eskimo women. These data suggest a need for intensified secondary prevention strategies for this high-risk population, while further research is needed to identify modifiable risk factors.

Ethnic differences in uterine corpus cancer incidence and mortality in New Mexico's American Indians, hispanics and non-Hispanic whites.

BACKGROUND: Although ethnic and radical differences in uterine corpus cancer incidence and mortality have been reported worldwide, few published data have addressed the epidemiology of uterine cancer among US American Indians and Hispanics. METHODS: We reviewed uterine corpus cancer incidence and survival data from New Mexico's population-based cancer registry collected from 1969 to 1992, and examined State vital records data for uterine cancer deaths collected from 1958 to 1992, focusing on ethnic differences in occurrence and outcomes of uterine malignancies. RESULTS: Non-Hispanic white women had age-adjusted incidence rates that were substantially higher (20.8 per 100,000) than rates for Hispanics (10.3) and American Indians (6.0) over the 24-year period. Uterine cancer mortality rates were also higher for non-Hispanic whites and Hispanics than for American Indian women, although mortality rates were substantially lower than incidence rates. Five-year survival for uterine cancer was comparable among all groups for all stages combined (87.3% for non-Hispanic whites, 81.4% for Hispanics, and 84.6% for American Indians). CONCLUSIONS: Our population-based data show ethnic differences in uterine corpus cancer incidence rates for non-Hispanic white women that were double those for Hispanics, and triple those for American Indian women. Ethnic differences in survival were comparable. Aetiologic studies are warranted to investigate the dramatic ethnic differences in occurrence of uterine cancer.

Breast cancer among Hispanics, American Indians and non-Hispanic whites in New Mexico.

Variation in breast cancer occurrence among women in New Mexico's three major ethnic groups has not previously been assessed. The address the descriptive epidemiology of breast cancer in New Mexico Hispanics, American Indians, and non-Hispanic whites, we calculated incidence rates from population-based registry data covering 1969-1987 and mortality data collected from 1958 to 1987. Breast cancer incidence and mortality rates for New Mexico's non-Hispanic white women were comparable to those for white women nationwide. In contrast, American Indian women had extremely low incidence and mortality rates for breast cancer; rates for Hispanics were intermediate, but well below those for non-Hispanic white women throughout the study period. Pronounced temporal trends in breast cancer occurrence were evident among Hispanic women, with the incidence rate increasing by 56% over the 19 years of available data and the mortality rate increasing by nearly 100% over 30 years. Age-specific incidence and mortality rates increased at all ages for successive birth cohorts of Hispanic women. For non-Hispanic whites, increasing incidence and mortality rates were also observed, but the increments were much smaller, approximately 15% for incidence and 30% for mortality. Our data show substantial ethnic differences in breast cancer incidence and mortality in New Mexico, suggesting the need for aetiological investigations to assist in controlling this disease.

Changing trends in mortality among New Mexico's American Indians, 1958-1987.

Health care availability and living conditions have improved substantially for American Indians in New Mexico over the past quarter century. To investigate the impact of these changes on health statistics, we examined mortality data collected from 1958 to 1987 for American Indians in the state. We analysed the data for all causes of death combined and for specific causes, and compared these data with figures for nonHispanic whites in the state. Age-adjusted mortality rates were calculated for 5-year periods for each ethnic-gender group, using denominators from US Census reports. Mortality rates for all causes combined did not improve significantly for American Indian males from 1958 to 1987, although the rates for American Indian females showed an 8% decline. Infectious disease-related mortality rates for American Indians decreased dramatically over the 30-year study period; however, mortality rates for cancer and diabetes increased over the 30-year period. Mortality rates for injuries and alcoholism among American Indians increased greatly from 1958 to 1977 and then declined later in the study period, but they were consistently higher than rates for whites. The study indicates that several chronic diseases remain of major public health importance for New Mexico's American Indian population.