Cancer surveillance series: interpreting trends in prostate cancer--part II: Cause of death misclassification and the recent rise and fall in prostate cancer mortality.

BACKGROUND: The rise and fall of prostate cancer mortality correspond closely to the rise and fall of newly diagnosed cases. To understand this phenomenon, we explored the role that screening, treatment, iatrogenic (i.e., treatment-induced) deaths, and attribution bias (incorrect labeling of death from other causes as death from prostate cancer) have played in recent mortality trends. METHODS: Join point regression is utilized to assess the recent rise and fall in mortality and the relationship of total U.S. trends to those areas served by the National Cancer Institute's Surveillance, Epidemiology, and End Results (SEER) Cancer Registry Program. Incidence-based mortality (IBM) is estimated with the use of prostate cancer data from the SEER Program to partition (from overall prostate cancer mortality trends) the contribution of cases diagnosed since the widespread use of prostate-specific antigen (PSA) testing starting in 1987. IBM is also used to examine the contribution of stage at diagnosis to the recent prostate cancer mortality trends. RESULTS: IBM for cases diagnosed since 1987 rose above the pre-1987 secular (i.e., background) trend, peaked in the early 1990s, and almost returned to the secular trend by 1994. This rise and fall of IBM track with the pool of prevalent cases diagnosed within the prior 2 years. IBM for cases diagnosed with metastatic disease fell starting in 1991, while IBM for those diagnosed with localized/regional disease was relatively flat. CONCLUSIONS: The rise and fall in prostate cancer mortality observed since the introduction of PSA testing in the general population are consistent with a hypothesis that a fixed percent of the rising and falling pool of recently diagnosed patients who die of other causes may be mislabeled as dying of prostate cancer. The decline in IBM for distant stage disease and flat IBM trends for localized/regional disease provide some evidence of improved prognosis for screen-detected cases, although alternative interpretations are possible.

The lifetime risk of developing breast cancer.

BACKGROUND: The lifetime risk of developing breast cancer in U.S. women, often quoted as one in nine, is a commonly cited cancer statistic. However, many estimates have used cancer rates derived from total rather than the cancer-free population and have not properly accounted for multiple cancers in the same individual. PURPOSE: Our purpose was to provide a revised method for calculating estimates of the lifetime risk of developing breast cancer and to aid in interpretation of the estimates. METHODS: A multiple decrement life table was derived by applying age-specific incidence and mortality rates from cross-sectional data to a hypothetical cohort of women. Incidence, mortality, and population data from 1975-1988 were used, representing the geographic areas of the National Cancer Institute's Surveillance, Epidemiology, and End Results (SEER) Program. The incidence rates reflected only the first breast primary cancer; mortality rates reflected causes other than breast cancer. The population denominator used in calculating incidence rates was adjusted to reflect only those women without previously diagnosed breast cancers in the hypothetical cohort. RESULTS: Our calculations showed an overall lifetime risk for developing invasive breast cancer of approximately one in eight with use of 1987-1988 SEER data, although up to age 85, it was still the commonly quoted one in nine. CONCLUSION: Our estimate was calculated assuming constant age-specific rates derived from 1987-1988 SEER data. Because incidence and mortality rates change over time, conditional risk estimates over the short term (10 or 20 years) may be more reliable. A large portion of the rise in the lifetime risk of breast cancer estimated using 1975-1977 data (one in 10.6) to an estimate using 1987-1988 data (one in eight) may be attributed to 1) early detection of prevalent cases due to increased use of mammographic screening and 2) lower mortality due to causes other than breast cancer. A common misperception is that the lifetime risk estimate assumes that all women live to a particular age (e.g., 85 or 95). In fact, the calculation assumes that women can die from causes other than breast cancer at any possible age. Cutting off the lifetime risk calculation at age 85 assumes that no women develop breast cancer after that age. While the lifetime risk of developing breast cancer rose over the period 1976-1977 to 1987-1988, the lifetime risk of dying of breast cancer increased from one in 30 to one in 28, reflecting generally flat mortality trends.

Cancer surveillance series: interpreting trends in prostate cancer--part III: Quantifying the link between population prostate-specific antigen testing and recent declines in prostate cancer mortality.

BACKGROUND: The objective of this study was to investigate the circumstances under which dissemination of prostate-specific antigen (PSA) testing, beginning in 1988, could plausibly explain the declines in prostate cancer mortality observed from 1992 through 1994. METHODS: We developed a computer simulation model by use of information on population-based PSA testing patterns, cancer detection rates, average lead time (the time by which diagnosis is advanced by screening), and projected decreased risk of death associated with early diagnosis of prostate cancer through PSA testing. The model provides estimates of the number of deaths prevented by PSA testing for the 7-year period from 1988 through 1994 and projects what prostate cancer mortality for these years would have been in the absence of PSA testing. RESULTS: Results were generated by assuming a level of screening efficacy similar to that hypothesized for the Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer Screening Trial. Under this assumption, the projected mortality in the absence of PSA testing continued the increasing trend observed before 1991 only when it was assumed that the mean lead time was 3 years or less. Projected mortality trends in the absence of PSA screening were not consistent with pre-1991 increasing trends for lead times of 5 years and 7 years. CONCLUSIONS: When screening is assumed to be at least as efficacious as hypothesized in the PLCO trial, it is unlikely that the entire decline in prostate cancer mortality can be explained by PSA testing based on current beliefs concerning lead time. Only very short lead times would produce a decline in mortality of the magnitude that has been observed.

Cancer surveillance series: interpreting trends in prostate cancer--part I: Evidence of the effects of screening in recent prostate cancer incidence, mortality, and survival rates.

BACKGROUND: The prostate-specific antigen test was approved by the U.S. Food and Drug Administration in 1986 to monitor the disease status in patients with prostate cancer and, in 1994, to aid in prostate cancer detection. However, after 1986, the test was performed on many men who had not been previously diagnosed with prostate cancer, apparently resulting in the diagnosis of a substantial number of early tumors. Our purpose is to provide insight into the effect of screening on prostate cancer rates. Detailed data are presented for whites because the size of the population allows for calculating statistically reliable rates; however, similar overall trends are seen for African-Americans and other races. METHODS: Prostate cancer incidence data from the National Cancer Institute's Surveillance, Epidemiology, and End Results Program and mortality data from the National Center for Health Statistics were analyzed. RESULTS/CONCLUSIONS: The following findings are consistent with a screening effect: 1) the recent decrease since 1991 in the incidence of distant stage disease, after not having been perturbed by screening; 2) the decline in the incidence of earlier stage disease beginning the following year (i.e., 1992); 3) the recent increases and decreases in prostate cancer incidence and mortality by age that appear to indicate a calendar period effect; and 4) trends in the incidence of distant stage disease by tumor grade and trends in the survival of patients with distant stage disease by calendar year that provide suggestive evidence of the tendency of screening to detect slower growing tumors. IMPLICATIONS: The decline in the incidence of distant stage disease 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.

Augmentation of activity of cis-diamminedichloroplatinum(II) and mitomycin C by interferon in human malignant mesothelioma xenografts in nude mice.

Two human mesothelioma xenograft lines, BG and ES, serially passaged in athymic mice, were studied to determine the efficacy of alpha-interferon in this type of tumor. Treatment began after progressive tumor growth was established. Recombinant human alpha-interferon-2a (Roferon- A) was given by s.c. injection, at a site distant from the tumor, at a dose of 2 x 10(5) IU 5 days per wk for 5 wk. Mild inhibitory activity was noted in both lines with interferon alone. cis-Diamminedichloroplatinum(II) (CDDP) (4 mg/kg) weekly x 5 was effective in line BG, while mitomycin C (1.5 mg/kg) weekly x 3 was effective in line ES. CDDP was not as effective in line ES. The moderate activity of CDDP in line BG and of mitomycin C in line ES was markedly increased by the addition of alpha-interferon. The combination of mitomycin C and alpha-interferon was as effective as mitomycin C and CDDP. No additional toxicity was noted by the addition of alpha-interferon. The combination of recombinant human alpha-interferon-2a and active chemotherapeutic agents is effective in mesothelioma xenografts.

Etoposide induced blood-brain barrier disruption in rats: duration of opening and histological sequelae.

The intracarotid infusion of the antineoplastic compound etoposide enhances blood-brain barrier (BBB) permeability. In a rat model system, the functional reversibility and anatomic sequelae of etoposide induced BBB disruption were investigated. Etoposide, in a dose range from 3.0 to 22.5 mg/kg, was infused into the left internal carotid artery of Sprague-Dawley rats. BBB disruption was evaluated by the appearance in the infused hemisphere of systemically administered Evans blue dye and quantitatively by the ratio of counts of the technetium labeled chelate of diethylenetriaminepentaacetic acid in the infused to the noninfused hemisphere. Functional reversibility of altered BBB permeability was investigated at three dose levels of etoposide (3.0, 15.0, and 22.5 mg/kg) by the administration of Evans blue dye at the time of etoposide infusion and the administration of the technetium labeled chelate of diethylenetriamine-pentaacetic acid at varying time intervals after etoposide infusion. Fourteen groups of 12 rats each were studied to define the time course of altered BBB permeability at these three doses. The anatomic sequelae of etoposide induced BBB disruption were investigated at varying time intervals (up to 3 weeks) after intracarotid etoposide infusion. Nineteen rats were examined after sacrifice by intracardiac fixation perfusion with 10% formalin. Each brain was sectioned coronally and examined under light microscopy after hematoxylin and eosin staining. Evidence of BBB disruption was seen at all dose levels of etoposide. The degree of BBB disruption increased with increasing doses of etoposide. The duration of altered BBB permeability increased from less than 1 day at 3.0 mg/kg to between 3 and 4 days at 22.5 mg/kg. Histological studies revealed no evidence of parenchymal damage, although at 4 days postdisruption, a mild perivascular lymphocytic infiltration was noted in the infused hemisphere. Etoposide infusion and subsequent BBB disruption were well tolerated by all test animals. In a rat model system the intracarotid infusion of etoposide is capable of producing prolonged reversible BBB disruption.

Improvement in the prognosis of breast cancer from 1965 to 1984.

PURPOSE: The prognosis of breast cancer has improved over the past three decades. It is uncertain, however, whether this improvement results from an increase in the cure rate, extension of the life span of uncured patients, or some combination. METHODS: From the Connecticut Tumor Registry, we obtained data on 25,091 patients with localized (node-negative) and regionally metastatic (node-positive) breast cancer who were diagnosed over the two decades between 1965 and 1984, with follow-up through 1993. The data for these patients were analyzed using a variety of parametric models to quantitate likelihood of cure and median survival time among uncured patients. These models incorporate the assumption that time to death from breast cancer follows a specific distribution. RESULTS: For patients with node-negative disease, parametric analysis revealed no significant difference in cured-fraction or median survival time over the two decades studied. For patients with node-positive disease, however, a significant increase in median survival time (P < .001) was found during the second decade (1970 to 1979). There was also a trend toward a higher cured-fraction over time, but this was not statistically significant. CONCLUSION: This study confirms that patients with node-positive disease had an improved prognosis over the two decades studied. Parametric analysis suggests that this improvement reflects primarily an increase in the median survival time for uncured patients, although there is a trend toward an increase in the likelihood of cure.

After a treatment breakthrough: a comparison of trial and population-based data for advanced testicular cancer.

PURPOSE: To determine to what extent the benefits of cisplatin-based combination chemotherapy have been disseminated to all American men diagnosed with advanced testicular cancer. PATIENTS AND METHODS: One hundred seventy-two advanced testicular cancer cases from five population-based registries of the Surveillance, Epidemiology, and End Results (SEER) Program diagnosed from 1978 to 1984 were compared with 133 diagnostically comparable cases from the Memorial Sloan-Kettering Cancer Center (MSKCC) vinblastine, dactinomycin, and bleomycin (VAB) regimens 7 through 9. Exclusions were made in both series for cases with elevated markers only, abdominal disease only, or extragonadal tumors. Ratings of extent of disease using the Indiana University system (minimal/moderate or advanced) were available for the MSKCC cases, and were determined retrospectively on the SEER cases based on information abstracted from medical records. RESULTS: Among the SEER cases, 89% reported receiving chemotherapy, and 95% of these received cisplatin-containing regimens. Survival among the MSKCC patients was significantly better than for the SEER cases in the minimal/moderate extent of disease category (95% and 73% 3-year survival rate, respectively); however, the difference for advanced cases was only marginally significant (52% and 40% 3-year survival rates, respectively). Survival did not vary significantly by year of diagnosis in either series. CONCLUSION: Although most of the patients in the SEER series received cisplatin-based chemotherapy, this alone did not produce results equivalent to that in the MSKCC series. Since the patients were selected to be as diagnostically comparable as possible at baseline, remaining differences in survival may be due to adherence to a fixed regimen and level of dose-intensity, adequacy of diagnostic work-up, implementation of salvage therapies and debulking surgery, and unknown factors related to who is willing and able to travel to a tertiary care center for treatment. Whatever the reason for not achieving optimal results in the SEER series, the very modest survival improvements over the time period 1978 to 1984 indicates that the differences in outcome between the two series were basically stable over the study period.

Platelet monoamine oxidase activity and the classification of depression.

An attempt was made to compare platelet monoamine oxidase (MAO) activity in descriptively based types of nonbipolar depression. Platelet MAO activity was significantly higher in depression secondary to chronic anxiety, compared with primary unipolar depression and depression secondary to borderline personality, and in women compared with men. No significant differences were observed between endogenous-nonendogenous, delusional-nondelusional, psychomotor states, or different age groups.

Catechol-O-methyltransferase activity and classification of depression.

Red blood cell catechol-O-methyltransferase (COMT) activity was compared across different depressive diagnoses. In a sample of 88 depressed inpatients, using defined criteria, no difference was found in respect of enzyme activity and the following categories: primary, secondary, delusional, nondelusional, endogenous, nonendogenous (neurotic), characterological depressions. COMT did not vary with age or sex. A significant increase in COMT activity was noted in agitated, depressed males, as compared to other groups.

The lifetime risk of developing prostate cancer in white and black men.

Two factors help explain increases in the lifetime risk of developing cancer: (a) decreasing overall mortality rates such that people are now living to older ages when cancer rates rise rapidly; and (b) increasing numbers of cancer cases discovered by new medical procedures, screening tests, and changes in the population risk factors. Prostate cancer lifetime risk estimates are particularly influenced by improved mortality rates and increased detection of asymptomatic disease. In this study, we report trends in lifetime risk estimates of developing prostate cancer in white and black men in the United States, from 1975 to 1993, and focus on the effects of changing mortality and screening. For the study period 1975-1977 to 1991-1993, the lifetime risk of developing invasive prostate cancer increased from 7.3 to 19.6% for whites and from 8.5 to 18.6% for blacks. When we recalculated these estimates using age-specific incidence trends from 1975 through 1989 (thereby controlling for the effect of prostate-specific antigen serum testing on prostate cancer incidence rates), the lifetime risk estimates in 1991-1993 fell to 13.8% for whites and 12.5% for blacks. When we made an additional assumption, basing lifetime risk estimates on higher 1975-1977 mortality rates, the lifetime risk estimates in 1991-1993 became 11.3% for whites and 11.8% for blacks. It is also shown that although mortality rates have improved for white and black men over the study period, they are much larger for blacks than whites in younger age groups, when the prevalence of prostate cancer is relatively low. As a result, fewer blacks survive to older ages when age-specific prostate cancer rates are large. It is of note that blacks have higher incidence rates for prostate cancer than do whites at every age-specific interval. Hence, increasing trends in lifetime risk of prostate cancer suggest, in large part, longer life expectancy and better detection methods.

The impact of breakthrough clinical trials on survival in population based tumor registries.

Three statistical models are developed to study the impact that two breakthrough clinical trials (MOPP for Hodgkin's disease and PVB for disseminated testicular cancer) had on survival in the Connecticut tumor registry and the National Cancer Institute's Surveillance, Epidemiology, and End Results (SEER) registry program. A segmented regression model is used in conjunction with the Cox semi-parametric proportional hazards model, as well as the parametric Weibull and exponential cure models. These models allow us to determine approximately when survival first began to improve dramatically, indicating that improved treatments had become available, and how long it took for survival to level off again indicating that the full population survival impact had been realized. In addition, the degree to which the parametric models fit allows us to determine if the survival improvements occur within a parametric family. Results of the modelling indicate that dissemination took approximately 11 years in Hodgkin's disease while only 3 years in disseminated testicular cancer. In both disease sites survival first broke with prior trends between the time that the breakthrough trial started and its publication, indicating that earlier moderately successful 'precursor' trials with combination chemotherapy may have initiated the improved population survival trends. Reasons for the difference in dissemination time in the two cancer sites are examined in order to understand what factors may be responsible for the speed of dissemination and effective utilization of new therapies.

A method for partitioning cancer mortality trends by factors associated with diagnosis: an application to female breast cancer.

U.S. cancer mortality data derived from information recorded on death certificates are frequently relied upon as an indicator of progress against cancer. A limitation of this measure is the lack of information pertaining to the onset of disease, such as year-of-diagnosis, age-at-diagnosis, stage of disease at diagnosis and histology of lesions. However, population-based cancer registries collect these types of data and allow the calculation of an incidence-file based mortality rate. This incidence-based mortality rate allows a partitioning of mortality by variables associated with the cancer onset. Breast cancer incidence-based mortality measures are created and compared to mortality rates based on death certificates over a comparable time period. Novel mortality measures, such as mortality rates by stage-at-diagnosis, age-at-diagnosis and year-of-diagnosis, are used to illustrate the value of this approach.

Cancer prevalence estimates based on tumour registry data in the Surveillance, Epidemiology, and End Results (SEER) Program.

BACKGROUND: The Connecticut Tumor Registry (CTR) has collected cancer data for a sufficiently long period of time to capture essentially all prevalent cases of cancer, and to provide unbiased estimates of cancer prevalence. However, prevalence proportions estimated from Connecticut data may not be representative of the total US, particularly for racial/ethnic subgroups. The purpose of this study is to apply the modelling approach developed by Capocaccia and De Angelis to cancer data from the Surveillance, Epidemiology, and End Results (SEER) Program of the National Cancer Institute to obtain more representative US site-specific cancer prevalence proportion estimates for white and black patients. METHODS: Incidence and relative survival were modelled and used to obtain estimated completeness indices of SEER prevalence proportions for all cancer sites combined, stomach, cervix uteri, skin melanomas, non-Hodgkin's lymphomas, lung and bronchus, colon/rectum, female breast, and prostate. For validation purposes, modelled completeness indices were computed for Connecticut and compared with empirical completeness indices (the ratio of Connecticut based prevalence proportion estimates using 1973-1993 data to 1940-1993 data). The SEER-based modelled completeness indices were used to adjust SEER prevalence proportion estimates for white and black patients. RESULTS: Model validation showed that the adjusted SEER cancer prevalence proportions provided reasonably unbiased prevalence proportion estimates in general, although more complex modelling of the completeness indices is necessary for female cancers of the colon, melanoma, breast, cervix, and all cancers combined. The SEER-based cancer prevalence proportions are incomplete for most cancer sites, more so for women, whites, and at older ages. For all cancers combined, prevalence proportions tended to be higher for whites than blacks. For the site-specific cancers this was true for stomach, prostate, cervix uteri, and lung and bronchus (men only). For colon/rectal cancers the prevalence proportions were higher for blacks through ages 59 (men) and 64 (women), and then for the remaining ages they were higher for whites. Prevalence proportions were lowest for stomach cancer and highest for prostate and female breast cancers. Men experienced higher prevalence proportions than women for skin melanomas, non-Hodgkin's lymphomas, lung and bronchus, and colon/rectal cancers. CONCLUSION: The modelling approach applied to SEER data generally provided reasonable estimates of cancer prevalence. These estimates are useful because they are more representative of cancer prevalence than previously obtained and reported in the US.

Impact of changes in catheter management on infectious complications among children with central venous catheters.

OBJECTIVES: To characterize and enumerate central venous catheter (CVC)-related complications among children with chronic illnesses, and to reduce the complication rate through changes in CVC management and education. DESIGN: A prospective observational study followed by an educational program and a nonrandomized interventional trial. SETTING: The Children's Hospital of Philadelphia, a tertiary, pediatric facility. PATIENTS: 268 children with Broviac, Hickman, or Infusaport catheters in place during 58,290 catheter days. INTERVENTIONS: Development and implementation of protocols for cleaning insertion site and hub, use of nonocclusive dressings, and manipulation of access; formal staff and parental education about protocols. RESULTS: CVC-related infections fell from 4.58/1,000 catheter-days preintervention to 3.83 postintervention (risk ratio [RR], 0.20; 95% confidence interval [CI95], 0.89-1.622; P = .25); exit-site infections fell from 0.58 to 0.11 (CI95, 1.22-45.64; P = .02); rates among infants on the surgical service fell from 15.46 to 6.67 (RR, 2.31; CI95, 1.10-4.30; P = .02). CONCLUSIONS: Education and changes in management protocols reduced the incidence of exit-site infections among all patients and reduced the overall infectious complication rate among the infants receiving parenteral nutrition on the surgical service. Other interventions are needed to decrease further the infectious complications in these children.

On the use of survival analysis techniques to estimate medical care costs.

Measurement of treatment costs is important in the evaluation of medical interventions. Accurate cost estimation is problematic, when cost records are incomplete. Methods from the survival analysis literature have been proposed for estimating costs using available data. In this article, we clarify assumptions necessary for validity of these techniques. We demonstrate how assumptions needed for valid survival analysis may be violated when these methods are applied to cost estimation. Our observations are confirmed through simulations and empirical data analysis. We conclude that survival analysis approaches are not generally appropriate for the analysis of medical costs and review several valid alternatives.

Physiological and electrophysiological consequences of etoposide-induced blood-brain barrier disruption.

The present study investigates the effects of etoposide-induced blood-brain barrier (BBB) disruption on systemic blood pressure (SBP), intracranial pressure (ICP), and electroencephalographic (EEG) activity. A total of 29 rats were divided into two groups. In Group 1, 8 control animals received intracarotid normal saline; in Group 2, 21 animals received intracarotid etoposide. SBP, ICP, and EEG were monitored continuously under general anesthesia and controlled ventilation after tracheostomy. Intravenous Evans blue dye was used for determination of BBB disruption. Although none of the Group 1 animals showed BBB disruption, 57% of the animals in Group 2 showed marked BBB disruption (3+). A slight but statistically significant increase in ICP was noted in the Group 2 animals with 3+ BBB disruption, although lesser degrees of barrier disruption (1+ or 2+) resulted in no significant alteration in ICP. The amplitude and frequency of the EEG decreased significantly ipsilateral to the side of intracarotid infusion in all animals with 3+ barrier disruption with a tendency to return toward normal within 2 hours. The degree of transient EEG change observed correlates well with the degree of barrier disruption, potentially allowing clinical determination of BBB disruption by this method.

Prognostic factors in breast cancer--a pathological and immunological study of patients with stage 1 breast cancer.

In order to analyze which features determine a poorer prognosis we undertook a study of 91 consecutive patients with pathological Stage I breast cancer operated on at Beth Israel Medical Center (1968-71). Tumor tissue slides were reviewed and features such as: tumor size, histologic type, nuclear grade, lymphocytic and perivenular lymphocytic infiltration, as well as sinus histiocytosis in the lymph nodes removed. Records were reviewed and classified according to age and ethnic background. Survival and recurrence data were recorded up to 14 years post-mastectomy. Also determined was the presence of an antigen, previously detected in certain human breast cancer tumor tissues, which has been found to cross-react immunologically with the 52,000 dalton major envelope protein of the mouse mammary tumor virus (MMTV--gp52). Ten-year cumulative disease-free survival was 0.65. Univariate analysis of survival within various factors revealed that the only statistically significant influencing factor was the presence or absence of the antigen. Factors such as perivenous lymphocytic infiltration, diffuse lymphoid infiltration and sinus histiocytosis in regional lymph nodes also showed trends in favor of improved survival but the sample may be too small for statistical significance. The presence or absence of the antigen was independent of the host immunological reaction. There was no relationship between localization of tumor, whether medial or lateral and survival, nor with presence or absence of antigen.

The effect of Medicare reimbursement for screening mammography on utilization and payment. National Cancer Institute Breast Cancer Screening Consortium.

OBJECTIVE: In January 1991, Medicare extended its mammography benefit to reimburse for breast cancer screening mammograms. In 1991 and again in 1993, the National Cancer Institute Breast Cancer Screening Consortium (BCSC) conducted a survey to test the hypothesis that this benefit would increase mammography use among women over the age of 65. METHODS: The authors analyzed data on non-Hispanic white women ages 65 to 74 living in 11 geographic areas targeted by the BCSC for an earlier study--six that had received cancer screening educational interventions and five control subsites--to measure the impact of the newly adopted Medicare benefit on the use of mammography and use of Medicare to reimburse mammography costs. RESULTS: The data show little overall increase between 1991 and 1993 in reported mammography use among respondents to the survey. However, in six intervention and five control subsites there was an increase in the percentage of women who reported using public payment sources to at least partially reimburse the cost of mammograms. In three intervention subsites, the increase from 1991 to 1993 in the percentage of women using public sources of payment was greater than in the corresponding control subsites. CONCLUSIONS: These findings suggest that public health interventions are more likely to succeed when educational promotion accompanies a financial benefit.

Parametric cure models of relative and cause-specific survival for grouped survival times.

With parametric cure models, we can express survival parameters (e.g. cured fraction, location and scale parameters) as functions of covariates. These models can measure survival from a specific disease process, either by examining deaths due to the cause under study (cause-specific survival), or by comparing all deaths to those in a matched control population (relative survival). We present a binomial maximum likelihood algorithm to be used for actuarial data, where follow-up times are grouped into specific intervals. Our algorithm provides simultaneous maximum likelihood estimates for all the parameters of a cure model and can be used for cause-specific or relative survival analysis with a variety of survival distributions. Current software does not provide the flexibility of this unified approach.