You must reference using one of the three formats and following your major’s designated style: MLA, APA, CS, Kate L. Turabian’s Manual, and the Chicago Manual of Style (CMS). YOU MUST CITE YOUR SOURCES!
Remember that this is a formal essay so your essay will need to include an introduction paragraph (with a thesis statement), body paragraph(s), and the conclusion paragraph.
Essay:
Throughout the course we have examined that the African American communities have changed drastically as more Americans have become aware of the injustices faced by millions of people of color. Analyzing African American history, examine the historical processes that led to Black Lives Matters
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Think about the Hip-Hop culture and how it has gone mainstream. What is its importance for black culture, and how is it another example of sports and the arts breaking down racial barriers? Why is it in sports and the arts that this happens and not in, for example, science or religion?
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What occurred during the presidential campaign of Jesse Jackson? List at least 3 black political leaders that were important prior to Barack Obama’s entrance onto the national stage? *Focus on the 1980s and 1990s, as that is our time frame.
You must use these two sources, outside sources are NOT ALLOWED.
1.* Chapter 5 has been attached.
2. Do not forget to read the documents they provide and watch the videos. Look at the biographies for the key figures. Read about the important organizations and institutions.
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As business professionals and future business managers, you will be expected to make presentations both in person and virtually. This assignment is part 4 of your Team Project. You will learn how to develop and deliver an effective presentation by creating a report to present the key findings from your business report.
Instructions and Submission
Step 1: Review the unit readings.
Step 2: Plan your presentation based on what you have learned from the readings.
Step 3: Build your presentation in a Power Point file. Prepare a 10-15 slide presentation to convey the key findings from your formal report.
a. The submission must include major findings from your research, key conclusions and recommendations, and action plan.
b. Ensure that your presentation is annotated (i.e. that all concepts are fully explained in the Notes section of each slide. These are your speaker’s notes.).
Step 4: Edit and proof-read the presentation.
Step 5: Select a team member to submit the presentation to the assignment page.
Submission Details
Your presentation should include the following slides:
2. Agenda Slide (Lists what will be included in the presentation.)
3. Introduction Slide (Introduce the topic and include a clear purpose statement)
4. Body Slides (3-4 relevant points related to topics, each supported by at least one reference), in-text citations must be used for the slides.
5. Recommendations Slide
6. Conclusion Slide (confirms what was said in body)
7. Action plan
8. References Slide (full references for all work cited in body, use the same references from your report).
Helpful Hints
· Use APA referencing guidelines for citations and references. Click here to review “APA Style”.
· Do not write in first person (I) but rather the third (they, he, she).
· Ensure all references are academic sources. If an article is found in an academic journal in one of the library databases, then you can assume it has been peer reviewed and thus acceptable. Many articles found readily online may not have been exposed to any editorial vetting process, and thus should not be used as a resource
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Read the below article titled “Too Stressed to Learn.” I need you to show me how you will “annotate” or mark-up the text in the article below. Highlighting the text and inserting comments is a common way to annotate using Microsoft Word or Google Docs, but I know students have creative ways to annotate using different software tools. You can also print the articles annotate with handwritten notes, then scan and upload an image of your annotations in Canvas. The skill-set we’ll be practicing this semester is annotating the research articles you are using in your speeches and submitting them within Canvas. Show me in this assignment how you’ll annotate evidence you use in our class.
In this assignment find the data/evidence within the Too Stressed to Learn article to respond to the following 3 questions:
1/ What are the 2 stress hormones listed in the article?
2/ what’s causing the stress?
3/how should you solve the problem of stress?
Submit the marked-up article with your annotations within this Discussion forum to show your classmate’s how you prefer to annotate. Additionally, write at least 1 paragraph (5-7 sentences) describing the steps involved when you annotate. In this discussion show your classmates your best tricks and strategies you have learned to use to closely read a text and document your thoughts on the text for future use. To earn full credit, you need to include your annotated article and your description of your annotation process.
Los Angeles Times
Too stressed out to learn?
New brain research may reveal how emotions make it harder for impoverished students to concentrate.
September 01, 2008|Rosemary Clandos
Students who grow up amid economic insecurity often face many obstacles: overcrowded schools, lack of enrichment activities, violent neighborhoods. Fear and stress can be two more problems. Brain science is showing how these emotions have effects on the brain and how they can directly impede learning. Some scientists and educators are suggesting ways in which kids and college students can combat the long-lasting effects of poverty-related stress.
Taking over thoughts
In response to fear or stress, the brain quickly releases adrenaline and cortisol, activating the heart, blood vessels and brain for life-saving action — fighting or running. The brain gives the threat priority over anything else — including schoolwork — and it creates powerful memories to help prevent future threats. “All families experience stress, but poor families experience a lot of it,” says Martha Farah, psychology professor at the University of Pennsylvania.
For 20 years, David Diamond, a neuroscience professor at the University of South Florida, has studied the effects of stress-related hormones in rats. He found that high cortisol levels affect the hippocampus — a key learning center in the brain — in three ways. They suppress electrical activity, decrease efficiency and reduce new cell growth.
These effects, thought likely to occur in humans as well, might be one reason it’s hard for impoverished students to concentrate and learn — especially if there is extra stress, violence or abuse in the child’s environment, Diamond says.
In a 2006 issue of Brain Research, Farah reported that growing up in poverty affects thinking processes associated with several brain systems. Sixty healthy middle-school students matched for age, gender and ethnicity but of different socioeconomic status took tests that challenged brain areas responsible for specific cognitive abilities. Researchers found that children from low-income homes had significantly lower scores in areas of language, long-term and short-term memory, and attention.
Research, Farah says, suggests that the effect of stress on the brain may be the reason for these detected differences and disadvantages.
Fear also interferes with learning. A study published in the February online journal of Social Cognitive and Affective Neuroscience shows that students raised in low-income homes have stronger fear reactions — with potential consequences for concentration.
In the study, 33 healthy undergraduate students viewed pictures of facial expressions — angry, surprised and neutral — while MRI imaging measured their brain activity. For students raised in low-income homes, the pictures of angry faces triggered a greater response in the amygdala, a brain region that processes fear and anger.
“Growing up in a socially disadvantaged environment often exposes people to threats to their health and well-being,” says Peter Gianaros, an assistant professor of psychiatry and psychology at the University of Pittsburgh, who headed the research.
Changing the brain
There are science-supported ways to mitigate these accentuated fear and stress responses and nurture the brain, researchers and educators say. “Change the experience, and you change the brain,” says San Diego-based educator Eric Jensen, author of a 2006 book “Enriching the Brain: How to Maximize Every Learner’s Potential,” who has developed a teachers’ training program, “Enriching the Brains of Poverty.” “Many good schools have shown they can create experiences that change the brain for the better.”
Among those experiences:
* Targeted preparation. To help children succeed in school, Jensen teaches educators to build students’ brain capacity in areas shown by science to be lagging: attention, long-term effort, memory, processing skills and sequencing skills. He recommends a slate of activities for each — for example, compelling stories, theater arts and fine-motor tasks all build attention skills, he says.
* Foster a mind-set of hope, determination and optimism — and security. There are many ways to foster hope, Jensen says, including asking about and affirming a student’s dreams, bringing successful students back to talk to new ones, giving useful feedback on schoolwork and teaching students how to set and monitor their own goals.
“Behaviors and thoughts that relate to hope, love and happiness can change the brain — just as fear, stress and anxiety can change it,” Kandel says. “It’s completely symmetrical.”
* Meditation. This has been proven in studies to lower stress.
* Social connectedness. According to Diamond’s work at the Veterans Hospital in Tampa, Fla., “When people are experiencing strong stress, they recover much better when they have social support than when they are socially isolated,” he says.
Jensen recommends mentoring programs for children and student groups.
* Take control. “Feeling helpless increases stress hormones,” Diamond says. To offset learned helplessness and develop a sense of control, Jensen advised students to learn time-management skills and goal setting — and reward small accomplishments.
* Exercise. “Exercise stimulates and energizes the brain to more efficiently process information. Exercise actually makes more brain cells,” Diamond says. Sports, aerobic exercise, yoga, dance, walking and even exercising the smaller muscles used for playing a musical instrument can change the brain. Music is calming, Diamond says. “If you feel better, you learn better.”
* Eat well. Marian Diamond, a neuroscientist and professor at UC Berkeley, has been using dietary changes to improve the learning capabilities of orphans and impoverished children in Cambodia. For students living in poverty in the U.S., she said, “Be sure you’re getting good sources of protein and calcium. Each day, eat an egg — or egg whites — a glass of milk, and take a multivitamin.” Other researchers recommend cutting back on sugar and smoking because they raise cortisol levels.
* Spirituality. In the January 2003 journal Urban Education, researchers reported that African American and Latino high school seniors who reported that they were very religious and were raised in intact families scored as well as white students on most achievement tests. “The achievement gap disappeared,” says William Jeynes, an education professor at Cal State Long Beach
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1,) Craps is an interesting casino game because it is an example of a random experiemtn that takes place in stages; the evolution of the game depends critically on the outcome of the first roll. In particular, the number of rolls is a random variable.
The player (known as the shooter) rolls a pair of fair dice
a. If the sum is 7 or 11 on the first throw, the shooter wins; this event is called a natural.
b. If the sum is 2, 3, or 12 on the first throw, the shooter loses; this event is called craps.
c. If the sum is 4, 5, 6, 8, 9, or 10 on the first throw, this number becomes the shooter’s point. The shooter continues rolling the dice until either she rolls the point again (in which case she wins) or rolls a 7 (in which case she loses).
The sum of the scores on a given roll has the probability density function in the table. The table of bets (not relevant to this problem) is shown in the image.
Setup an experiment to simulate the sum of a single roll of two 6-sided dice.
Run 1000 replications of the experiment.
Analyze the percentage of time the shooter (1) wins on the first roll or (2) loses on the first roll. (Note: we are ignoring item C above for this problem).
Summarize the sample of the SUMS in a frequency distribution, probability distribution, cumulative probability distribution.
Graph the results.
What would the theorectical probability of winning or losing on the first roll based on classical assignment of probabilities? Graph?
2.) Roulette is the oldest casino game still in operation. It’s invention has been variously attributed to Blaise Pascal, the Italian mathematician Don Pasquale, and several others. In any event, the roulette wheel was first introduced into Paris in 1765. Here are the characteristics of the wheel:
The (American) roulette wheel has 38 slots numbered 00, 0, and 1–36.
The wheel is spun and then a small ball is rolled in a groove, in the opposite direction as the motion of the wheel. Eventually the ball falls into one of the slots.
All 38 possible values for a single spin of the wheel are given in the table. Naturally, we assume mathematically that the wheel is fair, so that the random variable X that gives the slot number of the ball is uniformly distributed over the sample space. An image of the roulette wheel and it’s betting table (not relevant to this problem) is shown in the image.
Setup an experiment to simulate the outcome for a single spin of the wheel.
Run 1000 replications of the experiment.
Analyze the percentage of time the a player wins
1) who only bets on the same number for every spin of the wheel
2) who randomly selects a different number every spin
Describe your findings in the management statement.
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Does Socioeconomic Status Account for Racial and Ethnic
Disparities in Childhood Cancer Survival?
Rebecca D. Kehm, PhD 1; Logan G. Spector, PhD 2; Jenny N. Poynter, PhD 2; David M. Vock, PhD 3;
Sean F. Altekruse, PhD 4,5; and Theresa L. Osypuk, SD 1
BACKGROUND: For many childhood cancers, survival is lower among non-Hispanic blacks and Hispanics in comparison with non- Hispanic whites, and this may be attributed to underlying socioeconomic factors. However, prior childhood cancer survival studies
have not formally tested for mediation by socioeconomic status (SES). This study applied mediation methods to quantify the role of SES in racial/ethnic differences in childhood cancer survival. METHODS: This study used population-based cancer survival data from
the Surveillance, Epidemiology, and End Results 18 database for black, white, and Hispanic children who had been diagnosed at the ages of 0 to 19 years in 2000-2011 (n 531,866). Black-white and Hispanic-white mortality hazard ratios and 95% confidence intervals, adjusted for age, sex, and stage at diagnosis, were estimated. The inverse odds weighting method was used to test for mediation by
SES, which was measured with a validated census-tract composite index. RESULTS: Whites had a significant survival advantage over blacks and Hispanics for several childhood cancers. SES significantly mediated the race/ethnicity–survival association for acute lym-phoblastic leukemia, acute myeloid leukemia, neuroblastoma, and non-Hodgkin lymphoma; SES reduced the original association
between race/ethnicity and survival by 44%, 28%, 49%, and 34%, respectively, for blacks versus whites and by 31%, 73%, 48%, and 28%, respectively, for Hispanics versus whites ((log hazard ratio total effect – log hazard ratio direct effect)/log hazard ratio total
effect). CONCLUSIONS: SES significantly mediates racial/ethnic childhood cancer survival disparities for several cancers. However, the proportion of the total race/ethnicity–survival association explained by SES varies between black-white and Hispanic-white com- parisons for some cancers, and this suggests that mediation by other factors differs across groups.
2018 American Cancer Society .
KEYWORDS: cancer survival, childhood cancer, mediation, racial and ethnic disparities, socioeconomic status.
INTRODUCTION
Despite improvements over the last 4 decades in cancer survival in the US pediatric population, marked racial and ethnic
disparities persist. 1Compared with non-Hispanic white (white) children, non-Hispanic black (black) and Hispanic chil-
dren experience lower survival from many cancers, including leukemias, 2,3 lymphomas, 4,5 central nervous system (CNS)
tumors, 6and extracranial solid tumors. 7-9 The underlying causes of racial/ethnic survival differences are not well under-
stood and may vary by cancer type. As outlined in Figure 1,bothbiologicalandsocioeconomicpathwayshavebeenpro-
posed in the literature. 10,11 Underlying genetic variations associated with ancestry may lead to differences in tumor
biology and pharmacogenetics for some childhood cancers. 10 However, race/ethnicity is a socially constructed taxonomy
that is not synonymous with ancestry. 12 Race/ethnicity is highly correlated with socioeconomic status (SES), especially in
the United States, where embedded, institutionalized racism continues to place racial and ethnic minorities at high risk for
low SES. 13 Because of emerging evidence for a positive association between SES and survival from some childhood can-
cers, 11racial/ethnic survival disparities may also be explained by socioeconomic differences.
Quantifying the relative role of SES in explaining racial/ethnic survival disparities will help to inform practice and
intervention efforts. If SES accounts for racial/ethnic survival differences, then interventions addressing social and eco-
nomic barriers to treatment and care are warranted. However, if SES does not fully account for survival differences by
race/ethnicity, then other social factors (eg, immigration) and biological mechanisms (eg, tumor biology) must be consid-
ered. To date, formal mediation methods have not been used to disentangle racial/ethnic disparities in childhood cancer
Corresponding author: Rebecca D. Kehm, PhD, Division of Epidemiology and Community Health, University of Minnesota School of Public Health, 13,000 South Second Street, West Bank Office Building, Minneapolis, MN 55455; kehmx003@umn.edu
1Division of Epidemiology and Community Health, University of Minnesota School of Public Health, Minneapolis, Minnesota; 2Division of Epidemiology and Clini- cal Research, Department of Pediatrics, University of Minnesota, Minneapolis, Minnesota; 3Division of Biostatistics, University of Minnesota School of Public Health, Minneapolis, Minnesota; 4National Cancer Institute, Bethesda, Maryland; 5Epidemiology Branch, Prevention and Population Sciences Program, Division of Cardio- vascular Sciences, National Heart, Lung, and Blood Institute, Bethesda, Maryland.
Seeeditorialonpages thisissue. Additional supporting information may be found in the online version of this article.
DOI: 10.1002/cncr.31560, Received: December 8, 2017; Revised: January 11, 2018; Accepted: February 2, 2018, Published online Online Library (wileyonlinelibrary.com)
Original Article
Cancer 2018;124:40 –
Cancer October 15, 2018 4090
August 20, 2018 in Wiley
90
4097.
VC
3975-8, survival. Therefore, we conducted a mediation analysis
using population-based data, representative of the US
pediatric cancer population, to measure the role of SES in
racial and ethnic childhood cancer survival disparities. We
assessed survival from several childhood cancers to deter-
mine whether mediation by SES differs across cancer
types.
MATERIALS AND METHODS
Study Population
We obtained population-based cancer registry data from
the Surveillance, Epidemiology, and End Results (SEER)
18 database; the Alaska Native Tumor Registry was
excluded. We restricted the analysis to black, Hispanic,
and white cases aged 0 to 19 years with microscopically
confirmed first primary malignancies. Race was assigned
in SEER through medical record abstraction. 14,15 His-
panic ethnicity was assigned in SEER on the basis of self-
report/guardian report of Spanish origin in the medical
record or by a computer algorithm that searches surnames
and maiden names to determine Spanish origin. 14,16 We
assessed race/ethnicity with mutually exclusive categories
(non-Hispanic white, non-Hispanic black, and Hispanic);
individuals of Spanish origin were categorized as His-
panic, regardless of racial background. SES data were
available in SEER for diagnostic years 2000-2012. There-
fore, we restricted our sample to cases diagnosed in 2000-
2011 and followed through December 31, 2012, to allow
for at least 1 year of follow-up. We excluded 45 cases with
in situ tumors, 707 cases with missing/zero months of
follow-up, and 725 cases missing SES data. We assessed
cancers with 200 cases for each racial/ethnic group; they
were classified with the International Classification of
Childhood Cancer, third edition. 17 Our final analytic
sample consisted of 31,866 cases. This study was
approved by the Surveillance Research Program in the
National Cancer Institute’s Division of Cancer Control
and Population Sciences.
Measures
Overall survival was calculated in SEER as months from
the date of the cancer diagnosis to the date of death from
any cause or was censored at the date of last contact.
SES was measured at the neighborhood level (based
on the residential address at the date of the cancer diagno-
sis) with a validated census-tract composite index. 18 As
described in the prior literature, 19 the index was con-
structed through a factor analysis of nationwide 2000
decennial census data and 2005-2009 American Commu-
nity Survey data. 18 Seven indicators of neighborhood
SES, previously specified by Yost et al, 20 were included in
the index: proportion employed in working-class occupa-
tions, proportion aged 16 years or older and unemployed,
aThe stage at diagnosis is N/A for leukemias.bHigher quintiles represent higher SES (ie, Q1 is the lowest SES quintile, and Q5 is the highest SES quintile).
4093 Cancer October 15, 2018
Mediation of Childhood Cancer Survival/Kehm et al race-survival association if the indirect effect of race on
survival operating through SES was statistically signifi-
cant. SES significantly mediated the black-white survival
disparity for acute lymphoblastic leukemia (ALL;
indirect-effect hazard ratio [iHR], 1.17; 95% confidence
interval [CI], 1.07-1.28; P<.01; 44% reduction from
the total effect to the direct effect of the racial disparity in
mortality), AML (iHR, 1.15; 95% CI, 1.03-1.29;
P 5 .01; 28% reduction), and neuroblastoma (iHR, 1.17;
95% CI, 1.03-1.33; P5 .02; 49% reduction). SES was a
marginally significant mediator of the black-white sur-
vival disparity for non-Hodgkin lymphoma (NHL; iHR,
bly, SES significantly mediated both the racial and ethnic
disparities in survival for the same 4 cancers.
Secondary Analyses
Except for NHL, the mediating effect of tract-level SES
was greater than the mediating effect of health insurance
status among black-white and Hispanic-white compari-
sons (Supporting Table 3). For example, the indirect
effect of tract SES on the black-white mortality disparity
for ALL was 1.22 (95% CI, 1.01-1.48; P5 .04; 44%
reduction), whereas the indirect effect of health insurance
was 1.09 (95% CI, 0.94-1.27; P5 .24; 19% reduction).
Among cancers with significant SES indirect effects, SES
was not associated with the stage at diagnosis (Supporting
Table 4). The exclusion of the stage at diagnosis from
IOW models did not lead to notably stronger indirect
SES effects (Supporting Tables 5 and 6).
DISCUSSION
This is the first study to use formal mediation methods to
unpack childhood cancer survival disparities by race/eth-
nicity, and it generated several findings. We replicated
TABLE 2. Mediation by SES of Racial (Black vs White) Survival Disparities Among Childhood Cancer Cases
Aged 0 to 19 Years and Diagnosed in 2000-2011 in the SEER 18 Registries
Cancer Type
Total Effect of Race on Survival Through All Medi- ating Pathways
Direct Effect of Race on Survival After Blocking SES Pathway
Indirect Effect of Race on Survival OperatingThrough SES Pathway Reduction From Total Effect to Direct Effect, % b MortalityHR a 95% CI P Mortality HR a 95% CI P Mortality HR a 95% CI P
Germ cell tumors 0.98 0.57-1.69 .94 Not applicable c
Abbreviations: b, log hazard ratio; CI, confidence interval; CNS, central nervous system; HR, hazard ratio; SEER, Surveillance, Epidemiology, and End Results; SES, socioeconomic status; STS, soft-tissue sarcomas.aAdjusted for age, sex, and stage at diagnosis (stage not applicable for leukemias). Bootstrapping was used for standard errors.b( btotal –bdirect )/btotal). cDirect and indirect effects were not estimated for cancers with a statistically nonsignificant total effect ( P>.05); bootstrapping was not used.
4094 Cancer October 15, 2018
Original Article results from prior studies showing that whites have a sig-
nificant survival advantage over blacks and Hispanics for
several childhood cancers, including leukemias, 2,3 lym-
rhabdomyosarcoma soft-tissue sarcomas. 9In no instance
was survival among whites significantly worse than that of
either black or Hispanic children. Racial and ethnic sur-
vival differences were not uniform across cancers, and
some variability between black-white and Hispanic-white
comparisons was observed.
We demonstrated that SES significantly mediates
racial/ethnic survival disparities for several childhood can-
cers, including ALL, AML, neuroblastoma, and NHL.
For these cancers, indirect hazard ratios fell within a nar-
row range (1.13-1.17) for both black-white and Hispanic-
white comparisons. This suggests that the association
between SES and survival is not modified by, and may be
shared across, race/ethnicity. Conversely, the proportion
of the overall survival disparity explained by SES (ie, the
percent reduction) did vary by race/ethnicity for some
cancers. For example, among AML cases, SES explained
only 28% of the black-white survival disparity but 73% of
the Hispanic-white disparity. This may suggest a differen-
tial role of other mediating factors across racial/ethnic
groups for some cancers. For example, prior evidence sug-
gests that, among AML cases, a significantly lower pro-
portion of black children have matched family donors
available in comparison with white and Hispanic chil-
dren. 29Among other cancers with significant racial/ethnic
survival disparities (eg, CNS tumors and soft-tissue sarco-
mas), we found no significant evidence of mediation by
SES. Thus, for these cancers in particular, we cannot rule
out mediation by other factors such as differences in
tumor biology, pharmacogenomics, health care quality,
and other social factors not captured by the SES index (eg,
racism). 30
Because SES did not uniformly influence survival
across different types of childhood cancer, the mecha-
nisms through which SES influences survival may be
cancer-specific. For example, the strong association
between SES and ALL survival may be explained by differ-
ences in treatment adherence. 10 Unlike treatments for
other childhood cancers, the treatment of ALL requires a
prolonged maintenance phase composed of the oral
administration of antimetabolites, which may be difficult
for low-SES families to adhere to because of social and
economic constraints. 10 This is supported by prior evi-
dence of lower treatment adherence among children with
ALL living in a single-mother household versus a 2-parent
household. 31 Other cancer-specific mechanisms through
which SES may influence survival are less understood.
Secondary findings from this study suggest that factors
beyond health insurance status and stage at diagnosis con-
tribute to the SES-survival association, at least for some
TABLE 3. Mediation by SES of Ethnic (Hispanic vs White) Survival Disparities Among Childhood Cancer
Cases Aged 0 to 19 Years and Diagnosed in 2000-2011 in the SEER 18 Registries
Cancer Type
Total Effect of Ethnicity on Survival Through All Medi- ating Pathways
Direct Effect of Ethnicity on Survival After Blocking SES Pathway
Indirect Effect of Ethnicity on Survival OperatingThrough SES Pathway Reduction From Total Effect to Direct Effect, % b MortalityHR a 95% CI P Mortality HR a 95% CI P Mortality HR a 95% CI P
Abbreviations: b, log hazard ratio; CI, confidence interval; CNS, central nervous system; HR, hazard ratio; SEER, Surveillance, Epidemiology, and End Results; SES, socioeconomic status; STS, soft-tissue sarcoma.aAdjusted for age, sex, and stage at diagnosis (stage not applicable for leukemias).b( btotal –bdirect )/btotal). cDirect and indirect effects were not estimated for cancers with a statistically nonsignificant total effect ( P>.05); bootstrapping was not used.
4095 Cancer October 15, 2018
Mediation of Childhood Cancer Survival/Kehm et al childhood cancers. Additional research is needed to fur-
ther unpack the association between SES and childhood
cancer survival.
Limitations
We relied on an area-based variable as our primary measure
of SES because of the lack of individual-level SES measures
in SEER data; moreover, we selected an SES index to oper-
ationalize the SES construct over a meaningful period of
time. Although this improves upon many prior
population-based cancer studies that lacked any measures
of SES or relied on county-level measures, tract-level SES is
still a proxy for individual-level SES in this study because
we could not comprehensively control for SES at the indi-
vidual level. 32,33 Furthermore, we used a fairly crude mea-
sure of individual-level health insurance status (private vs
otherwise) in our secondary analysis. Because the tract-level
SES index was available in SEER only for the years 2000-
2012, the sample size and the follow-up time were limited.
This prevented us from testing more homogenized cancer
and racial/ethnic subgroups or stratifying by age. Addi-
tional research is thus needed for other smaller populations
of racial and ethnic groups not considered in this analysis
because of the rarity of childhood cancer, which limited
power. We also lacked geographic variables to explore
potential spatial variations in survival. Furthermore, the
lack of clinical data in SEER limited our ability to account
for diagnostic, therapeutic, and biological factors, such as
cytogenetic or molecular features. Finally, there is the
potential for differential loss to follow-up by race and SES.
In conclusion, through the application of formal
mediation methods, we have demonstrated that SES signif-
icantly contributes to racial and ethnic survival disparities
for several childhood cancers, including ALL, AML, neuro-
blastoma, and NHL. Thus, for these cancers in particular,
racial/ethnic survival disparities could theoretically be
addressed through initiatives that reduce social and eco-
nomic barriers to effective care. Such efforts may include
expanded health insurance coverage, improved patient care
coordination, increased health literacy, and supplementa-
tion of transportation and childcare costs during treatment.
However, because SES did not fully account for survival
disparities, we cannot rule out the potential role of other
mediating pathways, including tumor biology, pharmaco-
multipronged intervention approach that both addresses
socioeconomic barriers to care and invests in personalized
treatment regimens may ultimately be needed to fully elim-
inate childhood cancer survival disparities.
FUNDING SUPPORT
This work was supported by a National Institutes of Health
Translational Pediatric Cancer Epidemiology Training Grant
(T32CA099936).
CONFLICT OF INTEREST DISCLOSURES
The authors made no disclosures.
AUTHOR CONTRIBUTIONS
Rebecca D. Kehm : Conceptualization, data curation, formal anal-
ysis, methodology, writing–original draft, and writing–review and
editing. Logan G. Spector : Conceptualization, methodology, and
writing–review and editing. Jenny N. Poynter : Conceptualization,
methodology, and writing–review and editing. David M. Vock :
Conceptualization, methodology, and writing–review and editing.
Sean F. Altekruse : Conceptualization, methodology, and writing–
review and editing. Theresa L. Osypuk : Conceptualization, meth-
odology, and writing–review and editing.
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