Lung cancer and race: equal treatment yields equal outcome among equal patients, but there is no equal treatment.
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Biomedical subjects
Publications and source records attributed to Otis W Brawley.
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BACKGROUND: It is widely claimed that racial and ethnic minorities, especially in the US, are less willing than non-minority individuals to participate in health research. Yet, there is a paucity of empirical data to substantiate this claim. METHODS AND FINDINGS: We performed a comprehensive literature search to identify all published health research studies that report consent rates by race or ethnicity. We found 20 health research studies that reported consent rates by race or ethnicity. These 20 studies reported the enrollment decisions of over 70,000 individuals for a broad range of research, from interviews to drug treatment to surgical trials. Eighteen of the twenty studies were single-site studies conducted exclusively in the US or multi-site studies where the majority of sites (i.e., at least 2/3) were in the US. Of the remaining two studies, the Concorde study was conducted at 74 sites in the United Kingdom, Ireland, and France, while the Delta study was conducted at 152 sites in Europe and 23 sites in Australia and New Zealand. For the three interview or non-intervention studies, African-Americans had a nonsignificantly lower overall consent rate than non-Hispanic whites (82.2% versus 83.5%; odds ratio [OR] = 0.92; 95% confidence interval [CI] 0.84-1.02). For these same three studies, Hispanics had a nonsignificantly higher overall consent rate than non-Hispanic whites (86.1% versus 83.5%; OR = 1.37; 95% CI 0.94-1.98). For the ten clinical intervention studies, African-Americans' overall consent rate was nonsignificantly higher than that of non-Hispanic whites (45.3% versus 41.8%; OR = 1.06; 95% CI 0.78-1.45). For these same ten studies, Hispanics had a statistically significant higher overall consent rate than non-Hispanic whites (55.9% versus 41.8%; OR = 1.33; 95% CI 1.08-1.65). For the seven surgery trials, which report all minority groups together, minorities as a group had a nonsignificantly higher overall consent rate than non-Hispanic whites (65.8% versus 47.8%; OR = 1.26; 95% CI 0.89-1.77). Given the preponderance of US sites, the vast majority of these individuals from minority groups were African-Americans or Hispanics from the US. CONCLUSIONS: We found very small differences in the willingness of minorities, most of whom were African-Americans and Hispanics in the US, to participate in health research compared to non-Hispanic whites. These findings, based on the research enrollment decisions of over 70,000 individuals, the vast majority from the US, suggest that racial and ethnic minorities in the US are as willing as non-Hispanic whites to participate in health research. Hence, efforts to increase minority participation in health research should focus on ensuring access to health research for all groups, rather than changing minority attitudes.
Improvements in technology have led to a number of tests that can be used to suggest that a patient has a cancer. Advances in cancer biology and medical imaging have led to a number of cancer screening tests. Cancer screening is commonly advocated, but its complexity is often lost in guidelines that have sound-bite quality. It is commonly viewed as of no harm, when in fact there are harms associated with every known screening test. Indeed, many screening experts believe a screening test should only be used when the potential for benefit clearly outweighs the potential for harm. Cancer screening principles are classically within the realm of the epidemiologist. As more screening tests are developed, these principles have become more relevant to the practicing clinician. What is known and what is unknown about screening is distinctly different from what is believed by the public and many practicing clinicians. Many tests have both screening and diagnostic uses, and it is only the context in which these are used that determines whether they are screening or diagnostic. A screening test is done on asymptomatic individuals who receive the test principally because they are of the age or sex at risk for the cancer. A diagnostic test is done on an individual because of clinical suspicion of disease.
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Cancer screening is a complicated science. Each screening intervention must be carefully assessed before it is widely implemented. A screening test can falsely appear useful as it finds disease at an early stage and leads to intervention and cure. Such a test can be harmful to the population screened if it commonly finds disease that fulfills the pathologic criteria of cancer but behaves indolently (meaning it would never harm the host). Such "pseudo-disease" or "overdiagnosed disease" has been demonstrated in many malignancies including cancers of the lung, breast, and especially the prostate. The nature of each specific screening test and each disease is such that some screened patients may receive unnecessary treatment with all its complications and risk. Alternatively, some screening technologies have been proven useful providing net benefit to the population screened. Often these beneficial technologies are underused. These screening technologies if widely implemented have the potential of saving countless lives. Many available screening tests have tremendous potential in terms of benefit, but have yet to be fully assessed. At the minimum, patients should be informed of what is known, what is not known, and what is believed about these tests.
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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.
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.
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.
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.
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.
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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.
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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.
The dramatic international variation in prostate cancer incidence and mortality rates suggests that changeable environmental factors exert an influence. This has prompted a search for ways to prevent the disease. Epidemiologic studies suggest that dietary factors such as the carotenoid lycopene, selenium, vitamin E, and high intake of fat have roles in prostate cancer risk. Several studies show that impairment of androgen synthesis lowers the risk of prostate cancer. 5-alpha-reductase inhibitors such as finasteride have been shown to decrease prostate size by decreasing androgenic stimulation to the prostate. Other promising, but less developed, interventions include vitamin D supplements and modification of diet. Any manipulation to decrease one's relative risk of prostate cancer will by necessity have to be given to a large proportion of men who would never develop prostate cancer even without the intervention. To be acceptable, a successful preventive intervention should have few or no side effects; some additional benefits would be useful. All potential preventive interventions will need to be rigorously evaluated before they can be advocated for prostate cancer prevention.