PubMed Health⌕ Search

Biomedical subjects

William F Anderson

Publications and source records attributed to William F Anderson.

At least 19 recordsLinked to original sources

Estimating age-specific breast cancer risks: a descriptive tool to identify age interactions.

OBJECTIVE: Clarifying age-specific female breast cancer risks and interactions may provide important etiologic clues. METHOD: Using a population-based case-control study in Poland (2000-2003) of 2,386 incident breast cancer cases and 2,502 control subjects aged 25-74 years, we estimated age-specific breast cancer incidence rates according to risk factors. RESULTS: Breast cancer risks were elevated among women with positive family history (FH), younger age at menarche, older age at first full-term birth, nulliparity, exogenous hormonal usage, and reduced physical activity (PA). Notwithstanding overall risks, we observed statistically significant quantitative (non-crossover) and qualitative (crossover) age interactions for all risk factors except for FH and PA. For example, nulliparity compared to parity reduced breast cancer risk among women ages 25-39 years then rates crossed or reversed, after which nulliparity increased relative risks among women ages 40-74 years. CONCLUSION: Though quantitative age interactions could be expected, qualitative interactions were somewhat counterintuitive. If confirmed in other populations, qualitative interactions for a continuous covariate such as age will be difficult to reconcile in a sequential (multistep or monolithic) 'stochastic' breast cancer model. Alternatively, the reversal of relative risks among younger and older women suggests subgroup heterogeneity with different etiologic mechanisms for early-onset and late-onset breast cancer types.

Adult↗

A prospective study of adjuvant CMF in males with node positive breast cancer: 20-year follow-up.

PURPOSE: To determine the long-term overall survival of male patients with stage II node positive breast cancer treated with adjuvant chemotherapy. PATIENTS AND METHODS: Between 1974 and 1988, 31 male breast cancer patients were prospectively enrolled on study MB-82 in the National Cancer Institute. Following mastectomy, patients were treated with 12 cycles of cyclophosphamide, methotrexate, and fluorouracil (CMF) chemotherapy. RESULTS: Median patient age was 61 years (38-74 years). Twenty-one patients (68%) had 1-3 positive axillary lymph nodes while ten patients (32%) had four or more positive nodes. Estrogen receptor status was positive in 22 (71%), negative in 1 (3%), and unknown in 8 (26%) tumors. Progesterone receptor status was positive in 18 (58%), negative in 3 (10%), and unknown in 10 (32%) tumors. Median potential follow-up for all patients is 22.5 years with a median survival of 16.3 years. Twenty-one of 31 patients have died; one from a treatment-related complication, nine patients from recurrent breast cancer, five from other cancers, one from non-cancer related causes, and five from unknown causes. Ten patients remain alive at a median of 19.2 years. The overall survival probability at 10 years is 64.5% (95% CI: 46.9-78.9%), at 15 years is 51.6% (95% CI: 34.8-68%), and at 20 years is 42.4% (95% CI: 25.8-60.8%). CONCLUSION: To our knowledge, 20-year prospective data with adjuvant chemotherapy in male breast cancer has never been reported. Adjuvant chemotherapy may benefit male breast cancer patients with positive nodes.

Adult↗

Celecoxib for the prevention of sporadic colorectal adenomas.

BACKGROUND: Studies showing that drugs that inhibit cyclooxygenase-2 (COX-2) reduce the number of colorectal adenomas in animals and patients with familial adenomatous polyposis suggest that COX-2 inhibitors may also prevent sporadic colorectal neoplasia. METHODS: We randomly assigned patients who had adenomas removed before study entry to receive placebo (679 patients) or 200 mg (685 patients) or 400 mg (671 patients) of celecoxib twice daily. Randomization was stratified for the use of low-dose aspirin. Follow-up colonoscopies were performed at one and three years after randomization. The occurrence of newly detected colorectal adenomas was compared among the groups with the life-table extension of the Mantel-Haenszel test. RESULTS: Follow-up colonoscopies were completed at year 1 in 89.5 percent of randomized patients, and at year 3 in 75.7 percent. The estimated cumulative incidence of the detection of one or more adenomas by year 3 was 60.7 percent for patients receiving placebo, as compared with 43.2 percent for those receiving 200 mg of celecoxib twice a day (risk ratio, 0.67; 95 percent confidence interval, 0.59 to 0.77; P<0.001) and 37.5 percent for those receiving 400 mg of celecoxib twice a day (risk ratio, 0.55; 95 percent confidence interval, 0.48 to 0.64; P<0.001). Serious adverse events occurred in 18.8 percent of patients in the placebo group, as compared with 20.4 percent of those in the low-dose celecoxib group (risk ratio, 1.1; 95 percent confidence interval, 0.9 to 1.3; P=0.5) and 23.0 percent of those in the high-dose group (risk ratio, 1.2; 95 percent confidence interval, 1.0 to 1.5; P=0.06). As compared with placebo, celecoxib was associated with an increased risk of cardiovascular events (risk ratio for the low dose, 2.6; 95 percent confidence interval, 1.1 to 6.1; and risk ratio for the high dose, 3.4; 95 percent confidence interval, 1.5 to 7.9). CONCLUSIONS: These findings indicate that celecoxib is an effective agent for the prevention of colorectal adenomas but, because of potential cardiovascular events, cannot be routinely recommended for this indication. (ClinicalTrials.gov number, NCT00005094 [ClinicalTrials.gov].).

Adenoma↗

Effects of estrogen receptor expression and histopathology on annual hazard rates of death from breast cancer.

BACKGROUND: Breast cancer incidence rates vary according to estrogen receptor expression (ER) and histopathology. We hypothesized that annual mortality rates from breast cancer after initial diagnosis (hazard rates) might also vary by ER and histopathology. METHODS: We accessioned the National Cancer Institute's Surveillance, Epidemiology, and End Results (SEER, 1992-2002) program to estimate hazard rates according to ER (positive and negative) and histopathology (duct, tubular, lobular, medullary, inflammatory, papillary, and mucinous types). We used spline functions to model hazard rates free of strongly parametric assumptions for ER negative and positive cases overall and by histopathology. RESULTS: Hazard rates for ER negative and ER positive cases were distinct and non-proportional. At 17 months, ER negative hazard rates peaked at 7.5% per year (95% CI, 7.3-7.8% per year) then declined, whereas ER positive hazard rates lacked a sharp early peak and were comparatively constant at 1.5-2% per year. Falling ER negative and constant ER positive hazard rates crossed at 7 years; after which, prognosis was better for ER negative cases. Among ER positive and negative cases, there were proportional and non-proportional hazards according to histopathologic type, but the two basic ER-associated patterns were maintained. CONCLUSIONS: Hazard rates differed quantitatively and qualitatively according to ER and histopathology. These large-scale population-based results seem consistent with genomic studies, demonstrating two main classes of breast cancers with distinct prognoses according to ER expression.

Adenocarcinoma↗

Patterns of cancer incidence, mortality, and prevalence across five continents: defining priorities to reduce cancer disparities in different geographic regions of the world.

Efforts to reduce global cancer disparities begin with an understanding of geographic patterns in cancer incidence, mortality, and prevalence. Using the GLOBOCAN (2002) and Cancer Incidence in Five Continents databases, we describe overall cancer incidence, mortality, and prevalence, age-adjusted temporal trends, and age-specific incidence patterns in selected geographic regions of the world. For the eight most common malignancies-cancers of lung, breast, colon and rectum, stomach, prostate, liver, cervix, and esophagus-the most important risk factors, cancer prevention and control measures are briefly reviewed. In 2002, an estimated 11 million new cancer cases and 7 million cancer deaths were reported worldwide; nearly 25 million persons were living with cancer. Among the eight most common cancers, global disparities in cancer incidence, mortality, and prevalence are evident, likely due to complex interactions of nonmodifiable (ie, genetic susceptibility and aging) and modifiable risk factors (ie, tobacco, infectious agents, diet, and physical activity). Indeed, when risk factors among populations are intertwined with differences in individual behaviors, cultural beliefs and practices, socioeconomic conditions, and health care systems, global cancer disparities are inevitable. For the eight most common cancers, priorities for reducing cancer disparities are discussed.

Cost of Illness↗

Assessing the impact of screening mammography: Breast cancer incidence and mortality rates in Connecticut (1943-2002).

BACKGROUND: Randomized controlled studies demonstrate that early detection and intervention reduce breast cancer mortality by approximately 25%. Though the ultimate goal of screening is to reduce breast cancer deaths, the immediate goal is to detect and treat early-stage tumors before they pose a threat to life. MATERIALS AND METHODS: To assess the impact of early detection and intervention in the general population, we analyzed breast cancer incidence and mortality rates in the NCI's Historical Connecticut Tumor Registry (1943-2002). RESULTS: Though breast cancer rates increased for the entire study period, overall incidence rates rose faster than previously following the initiation of mammography screening in the early 1980s in the United States. Of note, stage-specific incidence rates increased 152% (53.2-133.9 per 100,000 woman-years) for early-stage tumors and fell 16% (56.1-47.2 per 100,000 woman-years) for late-stage breast cancers. Period- and cohort-age-specific incidence rates rose dramatically for early-stage tumors among women targeted for screening (ages 40-80 years), whereas rates for regional and distant stages declined modestly among women ages >50 years. Breast cancer mortality rates fell 31.6%. CONCLUSIONS: Along with increases in incidence rates for early-stage tumors, rates for late-stage disease and breast cancer mortality declined following widespread screening mammography, consistent with effective early detection and improved treatment over time. However, the disparity between the dramatic rise in early-stage tumors compared to the more modest declines in late-stage disease and mortality suggests that many mammography-derived early-stage lesions may never progress to late-stage cancers and pose a threat to life.

Adult↗

Emerging and widening colorectal carcinoma disparities between Blacks and Whites in the United States (1975-2002).

BACKGROUND: Colorectal carcinoma (CRC) is the fourth most common cancer diagnosed and the second most common cause of cancer death in the U.S. Incidence and mortality rates have decreased since the mid-1980s, although more among Whites than Blacks. METHODS: To determine if these racial differences were changing over time, we examined CRC rates in the National Cancer Institute's Surveillance, Epidemiology, and End Results (SEER) program (1975-2002). Rates were stratified by gender, race, anatomic subsite, historic stage, and grade. RESULTS: CRC rates were higher among men than women and higher among Blacks than Whites, with Black men having the highest rates during the latter years. Prior to the mid-1980s, male CRC rates were actually higher among Whites than Blacks; after which there was ethnic crossover with Black rates higher than White rates, and the gaps are widening. Proximal and transverse CRCs were more common and rectal cancers were less common among Blacks than Whites. Over time, rates for localized and regional stages increased among Blacks and decreased among Whites. Rates for distant stages declined for both racial groups, although less among Blacks. Black-to-White rate ratio for distant stage was approximately 1.30. Notably, Blacks compared with Whites had lower grade tumors, despite higher stages and mortality rates. CONCLUSIONS: CRC racial disparities have emerged and widened for three decades. These temporal trends probably reflect complicated racial differences between screening practice patterns and etiologic factors.

Adult↗

Merkel cell carcinoma and multiple primary cancers.

Merkel cell carcinoma (MCC) is an aggressive neuroendocrine tumor of the skin for which causative factors remain largely unknown. The site-specific risks of multiple primary cancers associated with MCC, which may provide insight into etiologic influences, have not been quantified in large population-based studies. We estimated the long-term risk of subsequent primary tumors after a first primary MCC (1,306 patients) and the risk of second primary MCC following other first primary cancers (2,048,739 patients) within 11 population-based cancer registries which report to the National Cancer Institute's Surveillance, Epidemiology, and End Results Program (1986-2002). Patients with first primary MCC were at significantly increased risk of developing a subsequent cancer [standardized incidence ratio (SIR), 1.22; 95% confidence intervals (95% CI), 1.01-1.45; observed (O = 122)], with significant excesses restricted to the first year after diagnosis (SIR, 1.71; 95% CI, 1.21-2.33; O = 39). Significantly elevated site-specific risks were observed for cancers of salivary gland (SIR, 11.55; 95% CI, 2.32-33.76; O = 3), biliary sites other than liver and gallbladder (SIR, 7.24; 95% CI, 1.46-21.16; O = 3), and non-Hodgkin lymphoma (SIR, 2.56; 95% CI, 1.23-4.71; O = 10). Nonsignificantly increased risks of 2-fold or higher were seen for chronic lymphocytic leukemia, and cancers of the small intestine and brain. A significantly increased 1.36-fold risk (95% CI, 1.19-1.55; O = 221) of MCC as a second primary malignancy was observed among patients with all other first primary cancers taken together. In particular, significant 3- to 7-fold excesses of MCC followed multiple myeloma (SIR, 3.70; 95% CI, 1.01-9.47; O = 4), chronic lymphocytic leukemia (SIR, 6.89; 95% CI, 3.77-11.57; O = 14), non-Hodgkin lymphoma (SIR, 3.37; 95% CI, 1.93-5.47; O = 16), and malignant melanoma (SIR, 3.05; 95% CI, 1.74-4.95; O = 16). Although enhanced medical surveillance may play a role, increased reciprocal risks suggest that MCC may share etiologic influences with other malignancies. Heightened awareness of the associations of lymphohematopoietic malignancies with MCC may facilitate early clinical recognition.

Aged↗

Comparison of age distribution patterns for different histopathologic types of breast carcinoma.

BACKGROUND: Historically, female breast carcinoma has been viewed as an etiologically homogeneous disease associated with rapidly increasing incidence rates until age 50 years, followed by a slower rate of increase among older women. More recent studies, however, have shown distinct age incidence patterns for female breast cancer when stratified by estrogen receptor (ER) expression and/or histopathologic subtypes, suggesting etiologic heterogeneity. MATERIALS AND METHODS: To determine if different age incidence patterns reflect etiologic heterogeneity (more than one breast cancer type within the general breast carcinoma), we applied "smoothed" age histograms at diagnosis (density plots) and a two-component statistical mixture model to all breast carcinoma cases (n = 270,124) in the Surveillance, Epidemiology, and End Results Program of the National Cancer Institute. These overall patterns were then reevaluated according to histopathologic type, race, and ER expression. RESULTS: A bimodal age distribution at diagnosis provided a better fit to the data than a single density for all breast carcinoma populations, except for medullary carcinoma. Medullary carcinomas showed a single age distribution at diagnosis irrespective of race and/or ER expression. CONCLUSIONS: Distinct age-specific incidence patterns reflected bimodal breast cancer populations for breast carcinoma overall as well as for histopathologic subtypes, race, and ER expression. The one exception was medullary carcinoma. Of note, medullary carcinomas are rare tumors, which are associated with germ-line mutations in the BRCA1 gene. These descriptive and model-based results support emerging molecular data, suggesting two main types of breast carcinoma in the overall breast cancer population.

Adenocarcinoma↗

Inter- and intra-ethnic differences for female breast carcinoma incidence in the continental United States and in the state of Hawaii.

BACKGROUND: Ethnic diversity is well-documented for female breast carcinoma incidence in the continental US but is not so well-established in the state of Hawaii. METHODS: Using the Surveillance, Epidemiology, and End Results (SEER) program, we analyzed n=323,607 in situ and invasive female breast cancer cases for major ethnic groups in the continental US and in Hawaii, diagnosed during the years 1992-2002. RESULTS: In the continental US, age-specific incidence rate patterns and prognostic factor profiles were good-risk for Asian or Pacific Islanders (API), intermediate for Whites, and poor-risk for Blacks. For example, early age-at-onset, high nuclear grade, aggressive histopathologic subtypes, and hormone receptor negative expression was associated with Black race in the continental US. In Hawaii, age-specific rate and prognostic profiles were more favorable for API than for White women, albeit not so striking as in the continental US. CONCLUSION: We observed inter- and intra-ethnic differences for female breast carcinoma in the continental US and in the state of Hawaii. While inter-racial disparities were expected, intra-racial differences were somewhat unexpected and possibly due to variations in racial subgroup mixing and/or cultural assimilation. For example, API women with breast carcinoma in the continental US included 96.03% Asians and 2.4% Pacific Islanders. In contrast, API women with breast carcinoma in Hawaii included 76.52% Asians and 23.46% Pacific Islanders. Moreover, APIs were more likely to be first-generation migrants in the continental US ( approximately 92%) than in Hawaii ( approximately 34%). Future studies should attempt to disaggregate racial data to separately characterize epidemiological patterns for individual ethnic groups.

Adenocarcinoma↗

Breast cancer trends among black and white women in the United States.

PURPOSE: Overall US breast cancer mortality rates are higher among black women than white women, and the disparity is widening. To investigate this disparity, we examined incidence data and changes in mortality trends according to age, year of death (calendar period), and date of birth (birth cohort). Calendar period mortality trends reflect the effects of new medical interventions, whereas birth cohort mortality trends reflect alterations in risk factors. PATIENTS AND METHODS: Incidence data were obtained from the Connecticut and National Cancer Institute Surveillance, Epidemiology, and End Results registries and mortality data were obtained from the National Center for Health Statistics. Changes in age, period, and cohort mortality trends were analyzed with Poisson regression. RESULTS: For both races, breast cancer incidence rates for localized and regional disease diverged in the late 1970s. Almost concurrently, overall mortality rates diverged among blacks and whites. For both races, mortality increases with age, but blacks have higher mortality at age younger than 57. The calendar period curves revealed declining mortality for whites over the entire study period. For blacks, calendar period mortality declined until the late 1970s, and then sharply increased. After 1994, calendar period mortality declined for both. For women born between 1872 and 1950, trends in mortality were similar for blacks and whites. For women born after 1950, mortality decreased more rapidly for blacks. CONCLUSION: The widening racial disparity in breast cancer mortality seems attributable to calendar period rather than birth cohort effects. Thus, differences in response or access to newer medical interventions may largely account for these trends.

Adult↗

In situ male breast carcinoma in the Surveillance, Epidemiology, and End Results database of the National Cancer Institute.

BACKGROUND: In situ breast carcinoma is not so well characterized for men as for women. METHODS: Therefore, the authors of the current study compared male and female in situ and invasive breast carcinomas in the Surveillance, Epidemiology, and End Results (SEER) database of the National Cancer Institute to document these patterns. RESULTS: In situ breast carcinomas composed 9.4% of all male (n = 280 of 2984) and 11.9% of all female breast carcinomas (n = 53,928 of 454,405) during the years 1973-2001. In situ rates rose 123% for men and 555% for women over this time period; whereas distant disease rates fell for both genders. Median ages at diagnosis were 62 years for in situ and 68 years for invasive breast carcinoma among men, compared with 58 years for in situ and 62 years for invasive breast carcinoma among women. Papillary in situ and invasive architectural types were more common among men than women. In contrast, lobular tumors were more common among women than men. Breast cancer-specific survival was similar among men and women, whereas overall survival was worse for men than women. CONCLUSION: In situ male breast carcinoma is a rare disease, occurring at older ages and with different architectural types than its more common female counterpart. Gender-specific histopathologic differences probably reflect anatomic differences among the normal female and vestigial male breast. Rising in situ male breast carcinoma incidence rates over the past three decades suggest earlier detection over time, irrespective of mammography, because men do not participate in routine screening mammography. Worse overall survival for men than women possibly results from age-dependent comorbid illnesses.

Adenocarcinoma, Mucinous↗

Trends in inflammatory breast carcinoma incidence and survival: the surveillance, epidemiology, and end results program at the National Cancer Institute.

BACKGROUND: Inflammatory breast carcinoma (IBC) appears to be a clinicopathologic entity distinct from noninflammatory locally advanced breast cancer (LABC). We examined incidence and survival trends for IBC in Surveillance, Epidemiology, and End Results (SEER) Program data with a case definition designed to capture many of its unique clinical and pathologic characteristics. METHODS: We analyzed breast cancer cases diagnosed in the SEER 9 Registries (n = 180,224), between 1988 and 2000. Breast cancer cases were categorized using SEER's "Extent of Disease" codes in combination with International Classification of Diseases for Oncology morphology code 8530/3 and classified as IBC (n = 3648), LABC (n = 3636), and non-T4 breast cancer (n = 172,940). We compared changes in incidence rates over 3-year intervals by breast cancer subtype and race using SEER*Stat. Survival differences by breast cancer subtype and race were assessed using Kaplan-Meier curves and log-rank statistics. All statistical tests were two-sided. RESULTS: Between 1988 and 1990 and 1997 and 1999, IBC incidence rates (per 100,000 woman-years) increased from 2.0 to 2.5 (P < .001), whereas those for LABC declined (2.5 to 2.0, P = .0025), as did those for non-T4 breast cancer (108 to 101, P = .0084). IBC incidence rates were statistically significantly higher in black women (3.1) than in white women (2.2) during the study period (P < .001). Women diagnosed with IBC had statistically significantly poorer survival than women with either LABC or non-T4 breast cancer (log-rank test, P < .001). Median survival of women with IBC (2.9 years) was statistically significantly shorter than that of women with LABC (6.4 years; P < .0001) or non-T4 breast cancer (> 10 years, P < .0001). Black women with IBC or LABC had poorer survival than white women with IBC or LABC, respectively (log-rank test, P < .001). CONCLUSIONS: Throughout the 1990s, IBC incidence rose, and survival improved modestly. Substantial racial differences were noted in age at diagnosis, age-specific incidence rates, and survival outcomes.

Adult↗

Global trends in breast cancer incidence and mortality 1973-1997.

BACKGROUND: Worldwide, breast cancer is the most common cancer and is the leading cause of cancer death among women. METHODS: To describe global trends, we compared age-adjusted incidence and mortality rates over three decades (from 1973-77 to 1993-97) and across several continents. RESULTS: Both breast cancer incidence and mortality rates varied 4-fold by geographic location between countries with the highest and lowest rates. Recent (1993-1997) incidence rates ranged from 27/100,000 in Asian countries to 97/100,000 among US white women. Overall, North American and northern European countries had the highest incidence rates of breast cancer; intermediate levels were reported in Western Europe, Oceania, Scandinavia, and Israel; and Eastern Europe, South and Latin America, and Asia had the lowest levels. Breast cancer incidence rose 30-40% from the 1970s to the 1990s in most countries, with the most marked increases among women aged > or =50 years. Mortality from breast cancer paralleled incidence: it was highest in the countries with the highest incidence rates (between 17/100,000 and 27/100,000), lowest in Latin America and Asia (7-14/100,000), and rose most rapidly in countries with the lowest rates. CONCLUSIONS: Breast cancer incidence and mortality rates remain highest in developed countries compared with developing countries, as a result of differential use of screening mammograms and disparities in lifestyle and hereditary factors. Future studies assessing the combined contributions of both environmental and hereditary factors may provide explanations for worldwide differences in incidence and mortality rates.

Adult↗

Cardiovascular risk associated with celecoxib in a clinical trial for colorectal adenoma prevention.

BACKGROUND: Selective cyclooxygenase-2 (COX-2) inhibitors have come under scrutiny because of reports suggesting an increased cardiovascular risk associated with their use. Experimental research suggesting that these drugs may contribute to a prothrombotic state provides support for this concern. METHODS: We reviewed all potentially serious cardiovascular events among 2035 patients with a history of colorectal neoplasia who were enrolled in a trial comparing two doses of celecoxib (200 mg or 400 mg twice daily) with placebo for the prevention of colorectal adenomas. All deaths were categorized as cardiovascular or noncardiovascular, and nonfatal cardiovascular events were categorized in a blinded fashion according to a prespecified scheme. RESULTS: For all patients except those who died, 2.8 to 3.1 years of follow-up data were available. A composite cardiovascular end point of death from cardiovascular causes, myocardial infarction, stroke, or heart failure was reached in 7 of 679 patients in the placebo group (1.0 percent), as compared with 16 of 685 patients receiving 200 mg of celecoxib twice daily (2.3 percent; hazard ratio, 2.3; 95 percent confidence interval, 0.9 to 5.5) and with 23 of 671 patients receiving 400 mg of celecoxib twice daily (3.4 percent; hazard ratio, 3.4; 95 percent confidence interval, 1.4 to 7.8). Similar trends were observed for other composite end points. On the basis of these observations, the data and safety monitoring board recommended early discontinuation of the study drug. CONCLUSIONS: Celecoxib use was associated with a dose-related increase in the composite end point of death from cardiovascular causes, myocardial infarction, stroke, or heart failure. In light of recent reports of cardiovascular harm associated with treatment with other agents in this class, these data provide further evidence that the use of COX-2 inhibitors may increase the risk of serious cardiovascular events.

Adenomatous Polyps↗