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Biomedical subjects

William F Anderson

Publications and source records attributed to William F Anderson.

At least 37 records · Page 2Linked to original sources
PubMed2005

Distinct breast cancer incidence and prognostic patterns in the NCI's SEER program: suggesting a possible link between etiology and outcome.

BACKGROUND: Breast cancer is a heterogeneous and chronic disease with relapses and death occurring 25 years or more after primary diagnosis. Standard tumor characteristics are used to predict initial relapse or death, but their ability to estimate long-term patterns of failure may be limited. METHODS: To further evaluate the significance of standard tumor features, we compared incidence and prognostic patterns in the National Cancer Institute's (NCI's) large-scale population-based Surveillance, Epidemiology, and End Results (SEER) program for high-risk versus low-risk breast cancers, i.e., size > 2.0 versus < or = 2.0 cm, lymph node positive versus negative, high versus low histologic grade, and hormone receptor negative versus positive expression, respectively. Data were stratified by age 50 years to approximate menopause. RESULTS: High-risk versus low-risk breast cancers demonstrated two very different incidence and prognostic patterns. Age-specific incidence rates among women with high-risk tumors increased until age 50 years then flattened, whereas rates among women with low-risk tumors increased continuously with aging. Hazard rates for breast cancer death spiked sharply two years following primary breast cancer diagnosis among women with high-risk but not with low-risk tumors. Paradoxically, hazard function crossed over 6-8 years following breast cancer diagnosis, with hazard rates lower for high-risk than for low-risk breast cancers. CONCLUSION: Distinct incidence and prognostic patterns among high-risk and low-risk breast cancers suggest a possible link between breast cancer etiology and outcome. These epidemiologic results appear to complement emerging molecular genetic techniques, showing distinct genotypes for high-risk and low-risk breast cancer phenotypes.

Aged↗
PubMed2005

Cancer screening.

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Age Factors↗
PubMed2005

Enzyme pretreatment of grass lignocellulose for potential high-value co-products and an improved fermentable substrate.

Crops such as switchgrass (Panicum virgatum L.), bermudagrass(Cynodon dactylon L.), or napiergrass (Pennisetum purpureum Schumach.)have the capacity to produce large quantities of lignocellulose for biofuel(1). To facilitate use of lignocellulosic material for ethanol, it will be necessaryto determine cost-efficient pretreatments to enhance the conversion tofermentable sugars. The lignified residual products from ethanol productioncould also provide a value-added co-product for industrial feedstocks(e.g., nutritional antioxidants, ultraviolet absorbers, resins).

Cell Culture Techniques↗
PubMed2004

Distinct incidence patterns among in situ and invasive breast carcinomas,with possible etiologic implications.

BACKGROUND: Incidence patterns are well-established for invasive breast carcinoma (InvBC) overall and for InvBC defined by estrogen receptor (ER) expression, but are not as well-defined for breast carcinoma in situ (CIS). METHODS: We, therefore, examined and compared the incidence patterns for CIS and InvBC in the SEER program to define these patterns and to generate etiologic hypotheses. Data were stratified by age < 50 and > or =50 years to approximate menopause. RESULTS: During the years 1973-2000, annual age-adjusted incidence rates rose 660% for CIS and 36% for InvBC, with the most rapid increases occurring in women age > or =50 years. Age-specific incidence rate curves for CIS increased until age 50 years, and then flattened, irrespective of ER expression. On the other hand, rates for InvBC overall and for InvBC defined by ER-positive expression increased continuously with aging, whereas rates for InvBC defined by ER-negative expression flattened after 50 years. Age frequency distribution for CIS and for ER-negative InvBC demonstrated bimodal populations, with a predominant early onset peak incidence at age 50 years. Age frequency distribution for ER-positive InvBC showed bimodal populations with a predominant late-onset mode at age 71 years. CONCLUSION: Over the last three decades, age-adjusted incidence trends differed for CIS and InvBC in the United States, possibly due to screening mammography and/or etiologic diversity. Indeed, age-specific incidence patterns suggested that carcinogenic events operating early in reproductive life had greater impact upon CIS and InvBC defined by ER-negative expression than upon InvBC overall and InvBC defined by ER-positive expression.

Adult↗
PubMed2004

Is male breast cancer similar or different than female breast cancer?

OBJECTIVE: To determine if male breast carcinogenesis was similar to its more common female counterpart, we compared incidence patterns among men and women with breast cancer. METHODS: Breast cancer records were obtained from the SEER database. Women were stratified by age < 50 and > or = 50 years to simulate premenopausal and postmenopausal breast cancer. RESULTS: Age-adjusted incidence trends were stable among men but increased among women. Male to female breast cancer ratio was higher for blacks than for whites. Favorable prognostic factors reflective of tumor biology (nuclear grade and hormone receptor expression) were more common for men and postmenopausal women than for premenopausal women. For example, low nuclear grade, estrogen and progesterone receptor-positive expression were more common among men and postmenopausal women than among premenopausal women. The age-specific incidence rate curve for men increased steadily for all ages with a constant slope. On the other hand, age-specific rates for women increased rapidly until age 50 years then rose at a slower rate for postmenopausal women. Age-frequency distribution for male breast cancer was unimodal, with peak incidence at age 71 years. Age-frequency distribution for women was bimodal with early-onset and late-onset incidence at 52 and 71 years, respectively. CONCLUSIONS: Gender-specific incidence trends differed, most likely reflective of female-related changes in surveillance and/or reproductive risk factors. On the other hand, similar prognostic factor profiles reflective of tumor biology, age-specific incidence rate patterns, and age-frequency distributions suggested that male breast cancer was more like postmenopausal than premenopausal female breast cancer.

Age Factors↗
PubMed2004

Comparison of age-specific incidence rate patterns for different histopathologic types of breast carcinoma.

OBJECTIVE: The age-specific incidence rate curve for breast carcinoma overall increases rapidly until age 50 years, and then continues to increase at a slower rate for older women. In this analysis, our objective was to compare age-specific incidence rate patterns for different morphologic types of breast carcinoma. MATERIALS AND METHODS: We analyzed age-specific incidence rate curves by histopathologic subclassification using records from 11 standard National Cancer Institute's Surveillance, Epidemiology, and End Results (SEER) registries, diagnosed during the years 1992 to 1999. Data were examined by age <50 and > or /=50 years to simulate menopause. RESULTS: Age-specific incidence rate curves showed three dominant patterns: (1) Rates for infiltrating duct carcinoma of no special type (duct NST), tubular, and lobular carcinomas increased rapidly until age 50 years then rose more slowly. (2) Rates for medullary and inflammatory breast carcinomas increased rapidly until age 50 years then failed to increase. (3) Rates for papillary and mucinous carcinomas increased steadily at all ages. Rate patterns varied by estrogen receptor expression but were unaffected by SEER registry, race, nodal status, or grade. CONCLUSION: Age-specific incidence rates for breast carcinomas differed by histopathologic type. Rates that failed to increase after 50 years suggested that menopause had greater impact on medullary and inflammatory carcinomas than on duct NST, tubular, and lobular carcinomas. Menopause did not seem to have any effect on papillary or mucinous carcinomas as evidenced by steadily rising rates at all ages. Future etiologic and/or prevention studies should consider the impact of age-specific risk factors and/or exposures on different histopathologic types of breast carcinomas.

Adult↗
PubMed2003

Inflammatory breast carcinoma and noninflammatory locally advanced breast carcinoma: distinct clinicopathologic entities?

PURPOSE: Inflammatory breast carcinoma (IBC) and noninflammatory locally advanced breast carcinoma (LABC) are both associated with poor prognosis; however, whether they are distinct clinicopathologic entities remains controversial. MATERIALS AND METHODS: To determine whether IBC and LABC were different, we compared tumor characteristics, prognosis, and age-specific incidence rate patterns in the Surveillance, Epidemiology, and End-Results program. An age of 50 years served as a surrogate marker for menopause. RESULTS: Younger age at diagnosis, poorer tumor grade, and negative estrogen receptors (ERs) were more predictive of IBC (n = 2,237) than of LABC (n = 7,985). Breast carcinoma survival was worse for patients with IBC than for those with LABC (log-rank test, P <.0001). Age-specific incidence rates for IBC increased until 50 years and then flattened, whereas rates for LABC increased for all ages. When rates for LABC were stratified by estrogen receptor-positive (ERP) and -negative (ERN) expression, rates for ERP and ERN diverged; that is, rates for ERP increased with advancing age, whereas rates for ERN flattened after 50 years. When rates for IBC were stratified by ER expression, rates for both ERP and ERN flattened after 50 years of age. CONCLUSION: IBC and LABC seemed to be distinct biologic entities, as indicated by different prognostic factor profiles and age-specific incidence rate patterns. Rates that increased before 50 years and then stabilized, possibly indicated that premenopausal exposures had a greater effect on maintaining rates for IBC than for LABC.

Adult↗
PubMed2003

Colorectal carcinoma in black and white race.

Worldwide, colorectal carcinoma (CRC) varies by race-ethnicity. The highest incidence occurs in whites of European descent. Rates in blacks of South Africa are much lower, but rise with migration to westernized countries, i.e. African Americans (blacks) in the US. In the US, CRC age-specific incidence rates increased dramatically with biologic aging for black and white men and women. For all ages, rates were slightly higher for black than for whites. Among whites, overall annual rates peaked in the 1980s then declined. Stage- and subsite-specific rate shifts suggested earlier detection of cancers through screening, particularly in the distal colon. Blacks have not experienced the same stage- and subsite temporal shifts, which were observed in whites. CRC racial differences have been attributed to biologic and/or non-biologic factors as well as to routine screening patterns. Racial variations demonstrate the need for a more comprehensive understanding of colorectal carcinogenesis, epidemiology, and colorectal screening patterns for low- and high-risk populations.

Black People↗
PubMed2003

Development of COX inhibitors in cancer prevention and therapy.

On the strength of in vitro, in vivo, observational, and clinical data, nonsteroidal antiinflammatory drugs (NSAIDs)-also referred to as COX inhibitors-have emerged as lead compounds for cancer prevention, and possible adjuncts to cancer therapy. Thus far, the routine use of NSAIDs for these indications is limited, largely owing to toxicity concerns, the paucity of efficacy data for any specific target organ, and uncertainties with regard to the most appropriate regimen (i.e., the best agent, formulation, dose, route of administration, and duration). Strategies to address these concerns primarily aim to improve the therapeutic index (i.e., benefit:risk ratio) of COX inhibitors by 1) minimizing systemic exposures whenever feasible, 2) achieving greater mechanistic specificity, 3) coadministering agents that provide prophylaxis against common toxicities, and 4) coadministering other effective anticancer agents. Clinical trials testing most of these strategies have been completed or are under way. The National Cancer Institute has a substantial research portfolio dedicated to the identification, testing, and development of NSAIDs as preventive and therapeutic anticancer agents. Discovering how to apply NSAIDs in persons with-or at risk for-cancer, although challenging, has the potential for considerable clinical and public health benefits.

Animals↗
PubMed2003

Cyclooxygenase inhibition in cancer prevention and treatment.

Several lines of evidence suggest that the cyclooxygenase enzymes (specifically COX-2) might be an important molecular target for the intervention of cancer at both early and late stages of some cancers, providing an opportunity for both cancer prevention and therapy. COX-2 is overexpressed during carcinogenesis, and appears to have a role in both tumour initiation and promotion and is amenable to intervention. This review discusses the importance of COX modulation via non-specific, as well as COX-2 specific COX inhibitors (NSAIDs and COX-2 selective inhibitors [COXIB]). A brief discussion on the pharmacoeconomic considerations of NSAID and COXIB use and safety issues that have recently been the focus of debate, will be presented.

Anticarcinogenic Agents↗
PubMed2002

Chemoprevention of colorectal carcinogenesis.

The field of cancer prevention is advancing rapidly, largely owing to post-genomic technology that has revolutionized our ability to identify and characterize molecular profiles for cancer. Advances in colorectal cancer screening (e.g., endoscopy, fecal occult blood testing, and mutational analysis) have made the detection and eradication of preinvasive neoplastic lesions the standard of care. Basic and translational sciences are building on these advances, and continue to expose molecular hallmarks of carcinogenesis that can be exploited as targets for molecularly targeted preventive interventions (i.e., chemoprevention). These targets will help identify more effective and better tolerated preventive agents. Carcinogenesis is now recognized as a disease in itself and has become the target of an ever-expanding array of preventive interventions.

Adenomatous Polyposis Coli↗
PubMed2002

Rates for breast cancer characteristics by estrogen and progesterone receptor status in the major racial/ethnic groups.

It has been reported that age-specific breast cancer rates vary by estrogen receptor and progesterone receptor status. We report breast cancer rates for age-at-diagnosis, stage-at-diagnosis, histological grade and type by estrogen (ER) and progesterone (PgR) receptor status in six major racial/ethnic groups. The average annual age-adjusted rates for breast cancers with estrogen receptor positive (ER+), ER-, progesterone receptor positive (PgR+), PgR-, ER+PgR+, ER+PgR-, ER-PgR+ and ER-PgR- are determined from 123,732 breast cancers with known ER status, diagnosed from 1992 to 1998 from 11 Surveillance, Epidemiology, and End Results (SEER) cancer registries. For each racial/ethnic group, their ER+ (ER+PgR+ and ER+PgR-) age-specific rates increased with age (but at a slower pace after ages 50-54) while their ER- (ER- PgR+ and ER-PgR-) age-specific rates did not increase after ages 50-54. The rank orders of the rates among the racial/ethnic groups varied by ER/PgR status. The stage I rates were greater than the stage II rates for the ER/PgR groups except for ER- and ER- PgR- cancers. The grade 2 (moderately differentiated) rates were greater than the grades 3 and 4 (poorly differentiated and undifferentiated cancers) rates for ER+ cancers, but not for ER- cancers. These results suggest that although breast cancer is a disease with enormous heterogeneity, the multiple types of breast cancer can be separated into distinct subgroups by their ER status, and perhaps by their ER/PgR status, and their cancer characteristics may be important in understanding the multiple nature of breast cancer.

Adult↗