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Biomedical subjects

Otis W Brawley

Publications and source records attributed to Otis W Brawley.

13 recordsLinked to original sources
PubMed2003

Nonmedical factors in treatment selection.

Given that no therapy for localized prostate cancer has been proven superior to any other in well-designed clinical trials, the patient and physician may be influenced toward a particular therapy by a number of nonmedical factors. These factors can be logistic, socioeconomic, or related to the patient's perception of the disease and expectations concerning the disease. These factors, along with the absence of a clearly superior therapy, account, at least in part, for the tremendous variance in patterns of care by age, geography, race and education.

Attitude to Health↗
PubMed2003

Prostate cancer in black and white Americans.

The prostate cancer incidence and mortality of black Americans is among the highest in the world. The reasons have not been adequately explained. Similar disparities have been noted for men of sub-Saharan origin living in Brazil and the Caribbean. Avenues of investigation have assessed racial and ethnic differences in diet as well as possible differences in the prevalence of genetics (both polymorphisms and mutations). There are studies to suggest that there are no racial differences in outcome when there is equal treatment. Several studies show that there are racial differences in patterns of care in the US and it has been hypothesized that this contributes to some of the racial disparity in survival after diagnosis.

Black or African American↗
PubMed2003

Population categorization and cancer statistics.

Racial/ethnic groups as used in data published by the US government are defined by sociopolitical and not scientific criteria. Much can be learned through the study of cancer rates of various populations. This knowledge benefits all who are at risk for the disease. Cancer incidence and mortality rates are influenced by numerous extrinsic factors such as diet, socioeconomic status, and cultural factors that often correlate with race/ethnicity. The prevalence of a gene or genetic mutation is often higher in a particular population compared to another. While a specific gene or series of genes can be conserved within a relatively closed population, genetic variation within a given population or race is significant.

Female↗
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

Myeloma and race: a review of the literature.

Multiple myeloma is an uncommon disease, with approximately 12,000 cases per year diagnosed in America. Blacks have had at least double the risk of being diagnosed with myeloma, and have had twice the mortality rate from the disease compared to whites. Research of the origins of this difference has yielded both insight and controversy. Obesity is likely a risk factor for myeloma, in both blacks and whites. Obesity is more prevalent in the black population, and this may help explain some of the increased incidence of myeloma. Also, genetic factors such as HLA antigens and family history seem to be important in explaining the differential risk of myeloma. Exposure to immunological challenges, especially urinary tract infections in black men, seems important in explaining some of the excess risk in blacks. Factors such as socioeconomic status, dietary preferences, vitamin intake, alcohol and tobacco use, either lack a consensus finding, or may not play a role in explaining the increased myeloma morbidity and mortality in blacks.

Black or African American↗
PubMed2002

Survival of blacks and whites after a cancer diagnosis.

CONTEXT: In recent years a theory that cancer biology is different in blacks and whites has gained prominence in reaction to epidemiologic observations that blacks have poorer survival than whites, even when diagnosed with cancer of similar severity. Yet, few studies have evaluated whether lower-quality treatment and shorter overall life expectancy due to a greater burden of other illnesses may explain the survival discrepancy. OBJECTIVE: To estimate the magnitude of overall and cancer-specific survival differences between blacks and whites who receive comparable treatment for similar-stage cancer. DATA SOURCES: We searched MEDLINE for English-language articles published from 1966 to January 2002 that reported on overall survival for black and white patients treated similarly for cancer. STUDY SELECTION: The abstracts or titles for 891 citations were independently examined by 2 authors. The full text was retrieved if the abstract mentioned both black and white patients, made some comment regarding either similarity of treatment received or presented an analysis based on the treatment received, and commented on survival. Studies were included if they included data for at least 10 black and 10 white patients; specified the cohort ascertainment method and what measures were undertaken to minimize loss to follow-up; summarized survival of both blacks and whites using actuarial measures; presented outcomes within stage, adjusted for stage, or based on cohorts with balanced stage distributions; and specified that blacks and whites in the study received similar treatment. We identified 89 unique cohorts in 54 articles that met our inclusion criteria. DATA EXTRACTION: Overall survival rates and hazard ratios (HRs) for death for blacks relative to whites were calculated. These were subsequently adjusted for rates of death due to causes other than the cancer under study to determine cancer-specific survival and cancer-specific HRs. DATA SYNTHESIS: Results represent 189 877 white and 32 004 black patients with 14 different cancers. Compared with whites, blacks had an overall excess risk of death (HR, 1.16; 95% confidence interval [CI], 1.12-1.20). After correction for deaths due to other causes, the cancer-specific HR was 1.07 (95% CI, 1.02-1.13). Of the 14 cancers, blacks were at a significantly higher risk of cancer-specific death only for cancer of the breast, uterus, or bladder. CONCLUSIONS: Only modest cancer-specific survival differences are evident for blacks and whites treated comparably for similar-stage cancer. Therefore, differences in cancer biology between racial groups are unlikely to be responsible for a substantial portion of the survival discrepancy. Differences in treatment, stage at presentation, and mortality from other diseases should represent the primary targets of research and interventions designed to reduce disparities in cancer outcomes.

Black or African American↗
PubMed2002

Estrogen receptor breast cancer phenotypes in the Surveillance, Epidemiology, and End Results database.

BACKGROUND: Researchers question whether estrogen receptor alpha-negative (ERN) and -positive (ERP) represent different stages of one disease or different breast cancer types. OBJECTIVE: To further examine ERalpha phenotypes, we stratified incident tumor characteristics in the Surveillance, Epidemiology, and End Results (SEER) Database (n = 82,488) by ERN and ERP. METHODS: Study variables included black-white race, age-at-diagnosis, and standard incident tumor characteristics. These characteristics were arbitrarily dichotomized into good versus poor prognostic factor groups, for example, good (tumor size < or = 2.0 cm, negative axillary lymph nodes, and good histologic grade) versus poor (tumor size > 2.0 cm, positive nodes, and poor grade). Age frequency density plots were generated from the corresponding age-at-diagnosis frequency histograms. Average annual age-specific incidence rates (or risks) were adjusted to the 1970 United States standard female population. RESULTS: Age frequency density plots demonstrated bimodal premenopausal and postmenopausal breast cancer populations. ERN was correlated with premenopausal disease, black race, and poor prognostic factor groups, whereas ERP was associated with postmenopausal disease, white race, and favorable tumor characteristics. ERN rates increased premenopausally and then flattened to a nearly constant level after 50 years of age. ERP risk rose for most of a woman's lifetime with the greatest risk occurring between 75 and 79 years. CONCLUSIONS: ERalpha exhibited bimodal age frequency distribution with a dichotomous pattern for age-specific rates, racial, and prognostic factor profiles. Menopause had a greater effect on ERN than ERP. Possible implications for breast carcinogenesis and cancer prevention are discussed in the text.

Adult↗
PubMedDate not supplied

Hormonal prevention of prostate cancer.

Prostate cancer is disease in which the mortality rate is highly variable among populations. An increasing risk with migratory changes suggests that some environmental factor or factors influence prostate cancer risk. It is well established that the prostate is hormonally influenced. Carcinogenesis is a process of malignant transformation evolving over time, involving cellular growth and division. There is evidence suggesting that androgenic influences over a period time encourages the process of prostate carcinogenesis. Studies of prostate biology support the concept that dihydrotestosterone is the principal androgen responsible for both normal and hyperplastic growth of the prostate gland. It may be that androgen causes prostate carcinogenesis. Suppression of dihydrotestosterone synthesis may inhibit carcinogenic transformation. Some preclinical and clinical observations support this hypothesis. A placebo controlled randomized trial using finasteride, an inhibitor of 5-alpha-reductase, the enzyme that converts testosterone to dihydrotestosterone, is ongoing. The endpoint of this trial is reduction of prostate cancer incidence.

3-Oxo-5-alpha-Steroid 4-Dehydrogenase↗