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Annals of Oncology
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Annals of Oncology 23: 2128–2137, 2012
doi:10.1093/annonc/mdr578
Published online 11 January 2012
Racial disparities in Hodgkin’s lymphoma: a
comprehensive population-based analysis
A. M. Evens1*, M. Antillón2, B. Aschebrook-Kilfoy2 & B. C.-H. Chiu2,3
1
Division of Hematology/Oncology, The University of Massachusetts Medical School and the UMass Memorial Cancer Center, Worcester; 2Department of Health
Studies, The University of Chicago, Chicago; 3The University of Chicago Comprehensive Cancer Center, Chicago, USA
Received 23 August 2011; revised 9 November 2011; accepted 15 November 2011
Background: Racial disparity has been investigated in a number of cancers; however, there remains a comparative
paucity of data in Hodgkin’s lymphoma (HL).
Patients and methods: We examined time-, age-, and gender-specific incidence, disease characteristics, and
survival across and within races for adolescent/adult HL (age 10–79 years) diagnosed during 1992–2007 in the SEER
13 registries.
Results: A total of 15 662 HL cases were identified [11 211 non-Hispanic whites, 2067 Hispanics, 1662 blacks, and
722 Asian/Pacific Islanders (A/PI)]. Similar to whites, A/PIs had bimodal age-specific incidence, while blacks and
Hispanics did not. Further, HL was significantly more common in Hispanics versus whites age >65 years (7.0/1 × 106
versus 4.5/1 × 106, respectively, P <0.01). By place of birth, US-born Hispanics and A/PIs age 20–39 years had higher
incidence of HL versus their foreign-born counterparts (P <0.05), however, rates converged age >40 years.
Interestingly, from 1992–1997 to 2003–2007, A/PI incidence rates increased >50% (P <0.001). Moreover, this increase
was restricted to US-born A/PI. We also identified a number of disease-related differences based on race. Finally, 5-,
10-, and 15-year overall survival rates were inferior for blacks and Hispanics compared with whites (P <0.005 and P
<0.001, respectively) and A/PI (P <0.018 and P <0.001, respectively). These differences persisted on multivariate
analysis.
Conclusion: Collectively, we identified multiple racial disparities, including survival, in adolescent/adult HL.
Key words: cancer, epidemiology, ethnicity, Hodgkin lymphoma, prognosis, race
introduction
Racial disparity has been investigated in a number of cancers
[1–10]. Many studies have noted significant differences in
incidence rates, patient and disease-related characteristics, and/
or survival based on race. However, population-based survival
analyses of racial disparities have been reported mostly in solid
tumors (e.g. breast, colon, prostate, and lung) with recent
reports in non-Hodgkin’s lymphoma (HL) [6] and multiple
myeloma [10]. A comparative paucity of data are available in
adult HL.
*Correspondence to: A. M. Evens, Division of Hematology/Oncology, Lymphoma
Program, UMass Memorial Cancer Center, The University of Massachusetts Medical
School, 55 Lake Avenue North, Worcester, MA 01655, USA. Tel: +1-774-443-7433;
Fax: +1-774-443-2298; E-mail: [email protected]
In pediatric HL, Metzger et al. [11] found that diseaserelated features and clinical characteristics did not differ
between races (white and black children). Furthermore, black
children with HL had lower event-free survival (EFS)
compared with white children, while both populations had
similar 5-year overall survival (OS). Studies examining racial
disparities in adult HL including age-specific HL incidence
patterns have been reported, however they have been smaller
scope (statewide), did not encompass all races (i.e. including
Hispanics and Asian/Pacific Islanders (A/PI)), and/or did not
include analyses by place of birth [12, 13].
The overall incidence of HL varies greatly throughout the
world. Pathogenesis of this geographic discrepancy of HL
incidence is not known; however, environmental and lifestyle
factors have been theorized as potential factors [14]. A British
© The Author 2012. Published by Oxford University Press on behalf of the European Society for Medical Oncology.
All rights reserved. For permissions, please email: [email protected]
original articles
Annals of Oncology
Columbia study of Chinese immigrants to Canada [15] and a
San Francisco (California) analysis[16] reported that the
incidence of HL among Asian immigrants was lower than
expected from the background populations, although the rates
of Canadian- or California-born Asians were higher than
foreign born. However, minimal recent data are available
regarding age-specific incidence rates for US- versus foreignborn A/PI including any potential differences in disease-related
characteristics or survival.
The goals of the current project were to examine differences
in HL age-specific incidence patterns, patient and diseaserelated characteristics, and survival across all major races
within the United States including whites, Hispanics, blacks,
and A/PIs. Furthermore, we investigated potential differences
within Hispanics and A/PIs based on birthplace (i.e. US versus
foreign born).
patients and methods
data sources
Incidence data and survival data were obtained from the US National
Cancer Institute’s Surveillance, Epidemiology, and End Results (SEER)
program. The 13 registries in SEER-13 account for ∼14% of the US
population, including 12% of the white population, 12% of black
population, 35% of A/PI population, and 22% of the Hispanic population
(see supplemental Methods, available at Annals of Oncology online) [17].
The current report examined the incidence of all HL diagnosed between
1 January 1992 and 31 December 2007. Native American and Alaskan
natives were excluded from this analysis because the number of cases were
too small for meaningful analyses [17]. Our analysis utilized data from the
November 2009 SEER data submission, which was released April 2010
[18].
population estimates
The SEER program also links cases to the vintage 2008 intercensal
population estimates, provided by the US Census Bureau. Population
estimates are matched to cases by county, age group, race group, Hispanic/
non-Hispanic group, gender, and year of diagnosis. While birthplace can
be identified in the SEER registries, the corresponding population estimates
are not readily available. Therefore, we multiplied SEER’s population
estimates by the proportion of the population that were US and foreign
born in the 2000 Census, 5% Public Use Microdata Sample (PUMS) files
[19], while taking into account gender, age, race, and geographic area of
each subpopulation listed in the SEER population files. In addition, while
SEER population files identified population estimates by year, there were
no data sources to provide estimates of the proportion of the population
that were US or foreign born for each year. We used the 5% sample of the
Census 2000 to provide these proportions at the midpoint (year 2000) of
the study period of interest (i.e. 1992–2007).
Census PUMS files provide the population estimates of Public Use
Microdata Areas, which are areas that are not equivalent to a complete
group of counties in the SEER registry areas. Thus, we excluded the Rural
Georgia registry and Grays Harbor, a county in the Seattle-Pudget Sound
registry, from the analysis that examined incidence of HL by birthplace.
statistical analysis
Age-specific incidence rates were computed for 10-year age groups ranging
from age 10 to 79 years for each race group [non-Hispanics whites
(referred to as whites), Hispanic whites (referred to as Hispanics), blacks,
Volume 23 | No. 8 | August 2012
and A/PIs] and rates were all presented in terms of cases per 100 000
population. Characteristics for the patient population were also examined
by Pearson’s χ2 statistic. Incidence rates and 95% confidence intervals (CI)
were calculated according to the algorithms provided by SEER [20]. Agespecific incidence rates were computed for 10-year age groups ranging from
age 10 to 79 years. We also calculated incidence rates for major histological
subtypes including mixed cellularity (MC) and nodular sclerosis (NS). The
‘Other’ group included lymphocyte-rich HL, lymphocyte-depleted HL, and
nodular lymphocyte predominant HL. Incidence rates were compared by
sex for each of four racial groups (non-Hispanics whites, Hispanics, blacks,
and A/PIs). Incidence rates were also examined according to three periods
1992–1997, 1998–2002, and 2003–2007. Furthermore, we investigated
incidence rates for Hispanic and A/PIs according to birthplace (i.e. US and
foreign born).
Finally, we constructed life tables to show 5-, 10-, and 15-year survival
rates by actuarial methods. Survival curves were constructed using the
Kaplan–Meier method and compared with the log-rank test. Z-test was
used to test the equivalence of relative survival at a given time.
Furthermore, a multivariate Cox proportional hazards model was
computed to estimate hazard ratios (HRs) and 95% CIs for the association
of race with survival adjusting for age, sex, and stage. All statistics were
computed using the STATA, MP 11.1 (StataCorp LP Copyright 2009) and
National Cancer Institute SEER*Stat software, version 6.6.2.
results
incidence of HL according to race, age, and gender
Between 1992 and 2007, 16 783 cases of HL were reported to
the SEER 13 registries. HL cases between the age of 10–79
years of white, black, Hispanic, or A/PI racial descent were
included resulting in a final study cohort of 15 662 subjects.
Table 1 describes the characteristics of patient populations by
race. Interestingly, the mean age of HL among whites was
significantly older compared with all other races; mean age was
calculated versus median due to the prominent bimodal
pattern of several races. Racial disparity in incidence is further
illustrated through age-specific analyses (Figure 1). Whites
showed a bimodal age-incidence pattern, while blacks had a
much less clear bimodal distribution. A/PIs exhibited a
bimodal pattern, although at all ages, A/PI have the lowest
incidence rates of any race/ethnic group. Notably, incidence of
HL in Hispanics was distinctly not bimodal with a small
increase at age 20–29 years (2.3/100 000) followed by an
exponential-like rise with peak incidence at age 70–79 years
(5.1/1 × 106) (Figure 1D). Overall, whites had the highest
incidence rates at age <65 years, while Hispanics had the
highest incidence >65 years compared with all other races
(P <0.05).
According to gender, there were comparatively more males
diagnosed with HL among Hispanics compared with whites
(P = 0.005), while there was a trend of more females diagnosed
with HL for blacks versus whites (P = 0.075) (Figure 2). Within
all races, women had a significantly lower age-adjusted
incidence rates than men (P <0.001) (Table 2); however, the
male excess did not occur until after age 40–49 years. Within
the white HL cohort, men and women had similar age specific
rates until age 40, while after age 40, the incidence rate
decreased for females compared with males; this difference
persisted for all ages thereafter (P <0.05) (supplemental
doi:10.1093/annonc/mdr578 | 
original articles
Annals of Oncology
Table 1. Subject and disease-related characteristics based on race
Gender
Male
Female
Age
Mean
Interquartile range
Histology
Nodular sclerosis
Mixed cellularity
Other
Site
Extranodal
Stage
I
II
III
IV
NA
B symptoms
No
Yes
NA
White
(n = 11211)
Count
6096
5115
A/PI (n = 722)
%
Black
(n = 1662)
Count
%
Count
54
46
865
797
386
336
40
26–52
52
48
36.9
25–46
%
Hispanic
(n = 2067)
Count
%
53
47
1193
874
58
42
37.7
23–50
P
38.0
23–51
W versus B
W versus A
W versus H
0.075
0.663
0.005
<0.001
0.002
<0.001
7284
1541
2386
65
14
21
919
254
489
55
15
29
461
105
156
64
15
22
1148
402
517
56
19
25
<0.001
0.788
<0.001
290
3
36
2
26
4
43
2
0.308
0.100
0.176
2526
4503
2059
1681
442
23
40
18
15
4
385
548
325
337
67
23
33
20
20
4
128
320
130
119
25
18
44
18
16
3
377
690
398
477
125
18
33
19
23
6
<0.001
0.012
<0.001
4337
3825
3049
39
34
27
533
615
514
32
37
31
323
255
144
45
35
20
714
903
450
35
44
22
<0.001
0.201
<0.001
A/PI, Asian/Pacific Islander; B, black; H, Hispanic; NA, not available; W, white.
Figure 1. Age-specific incidence of Hodgkin’s lymphoma by race. Data shown are age-specific incidence rates for 10-year age groups ranging from age 10
to 79 years for each race (non-Hispanics whites (referred to as: whites), Hispanic whites (referred to as: Hispanics), blacks, and A/PIs). Rates are presented
in terms of cases per 100 000 population. (A) Whites showed a continued bimodal age-incidence pattern, while (B) blacks had a much less clear bimodal
distribution. (C) A/PIs exhibited a bimodal pattern and have the lowest incidence rates of any race/ethnic group. (D) Age-specific incidence in Hispanics
was distinctly not bimodal with a small increase at age 20–29 followed by an exponential-like rise in incidence. A/PI, Asian/Pacific Islander.
 | Evens et al.
Volume 23 | No. 8 | August 2012
original articles
Annals of Oncology
Figure 2. Age-specific incidence of HL by race and gender. (A) HL in whites was more common in males versus females, while both genders exhibited a
bimodal incidence pattern. (B) Black men had a rise in incidence at age 20--29 years followed by a relatively flat rate through age 70--79 years. (C) A/PIs
had similar male to female ratios as whites as well as an apparent bimodal age distribution, while among (D) Hispanics, incidence rates rose exponentially;
after the age of 40 years, the incidence of HL was significantly higher in Hispanic males versus females (P <0.05). A/PI, Asian/Pacific Islander; HL,
Hodgkin’s lymphoma.
Table 2. Age-adjusted Hodgkin’s lymphoma incidence rates based on race and gender
Female incidence rates
Male incidence rates
Female versus male incidence ratio
P
White (95% CI)
Black (95% CI)
A/PI (95% CI)
Hispanic (95% CI)
3.44 (3.35–3.54)
4.07 (3.97–4.17)
0.85 (0.81–0.88)
<0.001
2.72 (2.54–2.92)
3.49 (3.25–3.73)
0.78 (0.67–0.91)
<0.001
1.15 (1.03–1.28)
1.47 (1.33–1.63)
0.69 (0.63–0.76)
0.001
2.06 (1.92–2.22)
2.99 (2.80–3.19)
0.69 (0.63–0.76)
<0.001
A/PI, Asian/Pacific Islander; CI, confidence interval.
Table S1, available at Annals of Oncology online). Figure 2D
shows that Hispanic females had a slight bimodal age pattern,
although the lowest incidence was experienced at age 40–49
years rather than age 50–59 years compared with other races
(P <0.05). Further, the incidence of HL in Hispanic males rose
exponentially, and after the age of 40, male incidence was
significantly higher than females (P <0.05).
patient and disease characteristics according
to race
Table 1 denotes patient and disease-related characteristics
based on race. Interestingly, early-stage HL (i.e. stage I/II) was
more prevalent among whites (63%) and A/PI (62%) subjects
versus blacks (56%) and Hispanics (52%) (P <0.0001). Overall
(all races), men presented more commonly with advancedstage disease compared with women (40% versus 30%,
respectively, P <0.0001) (Table 3). This may in part explain the
Volume 23 | No. 8 | August 2012
discrepancy in stage for Hispanics given the increased
frequency of male gender compared with whites and A/PIs as
described before. The gender difference would not explain,
however, the early/advanced-stage discrepancy for blacks since
there was a trend of higher prevalence of female HL versus
Whites (Table 3). The gender-specific distribution differences
in stage were most notable for black men versus women (stage
I/II: black men 50% versus black women 62%, P <0.001) and
white men versus women (stage I/II: white men 59% versus
white women 67%, P <0.001).
Racial differences were also noted with blacks and Hispanics
having more frequent presence of B symptoms at diagnosis
(Table 1). Interestingly, the presence of B symptoms followed a
similar pattern as stage with men (all races) presenting more
frequently with presence of B symptoms compared with
women (all races) (39% and 32%, respectively, P <0.0001). This
gender-specific disparity was notable within all races
(supplemental Table S2, available at Annals of Oncology
doi:10.1093/annonc/mdr578 | 
original articles
Annals of Oncology
Table 3. Stage based on race and gender
Stage
I
II
III
IV
Not staged
White
Male
(n = 6096)
Count %
Female
(n = 5115)
Count %
1463
2137
1247
1021
228
1063
2366
812
660
214
24
35
20
17
4
P
21
46
16
13
4
<0.001
Black
Male
(n = 865)
Count %
Female
(n = 797)
Count %
192
243
173
223
34
193
305
152
114
33
22
28
20
26
4
P
24
38
19
14
4
<0.001
A/PI
Male
(n = 386)
Count %
Female
(n = 336)
Count %
69
147
76
82
12
59
173
54
37
13
18
38
20
21
3
P
18
51
16
11
4
<0.001
Hispanic
Male
(n = 1193)
Count %
Female
(n = 874)
Count %
218
329
255
319
72
159
361
143
158
53
18
28
21
27
6
P
18
41
16
18
6
<0.001
P values compare differences in stage for male versus female within each race.
A/PI, Asian/Pacific Islander.
Figure 3. Age-specific incidence of HL by histology and race. Within the (A) white HL cohort, the young adult rise was mostly due to NS subtype, while
the decreased incidence of NS in older whites was accompanied by an increased incidence of MC. Similar to whites, the young adult rise in incidence of (B)
black and (C) A/PI populations were predominantly due to NS HL; the incidence of NS fell steadily after age 30 years. (D) Hispanics (and blacks) presented
significantly less frequently with NS HL compared with whites, both presenting more commonly with MC subtype. A/PI, Asian/Pacific Islander; HL,
Hodgkin’s lymphoma; MC, mixed cellularity; NS, nodular sclerosis.
online). Differences in the presence of extranodal disease were
not different across races (data not shown), however, the
overall frequency of extranodal disease was low.
histologic subtype
The HL histologic tumor subtypes (cell type) also differed by
race (Figure 3). Across races, Hispanics and blacks presented
significantly less frequently with NS HL compared with whites
(Table 1, P <0.001). Among Hispanics, the incidence of NS HL
increased only slightly during age 20–29 years, decreased
during age 30–59, and then rose slightly again after age 60. The
incidence of all HL subtypes within the Hispanic population
 | Evens et al.
had an exponential increase after the age of 40 years, primarily
due to the rapid rise in incidence of MC HL as well as an
increased incidence in ‘other’ subtypes [age 20–29 years: 0.4
(95% CI 0.3–0.5), age 50–59 years: 1.0 (95% CI 0.8–1.3), age
70–79 years: 2.5 (95% CI 1.9–3.2)]. Gender-specific histologic
differences are noted in supplemental Table S3 (available at
Annals of Oncology online).
changes in HL incidence patterns from 1992
to 2007
Period-specific patterns of HL incidence based on race
presented in Figure 4. During the 16-year period from 1992 to
Volume 23 | No. 8 | August 2012
original articles
Annals of Oncology
Figure 4. Period changes in age-specific incidence of HL by race. (A–D) During the 16-year period from 1992 through 2007, age-specific incidence patterns
did not vary within races except for A/PI. Within the A/PI HL population, incidence rates successively increased within each period. A/PI, Asian/Pacific
Islander; HL, Hodgkin’s lymphoma.
2007, age-specific incidence patterns did not vary within races,
except for A/PI. Within A/PI’s, the incidence rates of HL
successively increased within each period [1992–1997: 1.0
(95% CI 0.9–1.2), 1998–2002: 1.3 (95% CI 1.1–1.5), and 2003–
2007: 1.6 (95% CI 1.4–1.7)] (supplemental Table S4, available
at Annals of Oncology online). Moreover, among young A/PI
adults aged 20–29 years, the incidence doubled from 1.5/100
000 (95% CI 1.2–2.0) during the years of 1992–1997 to an
incidence of 3.2/100 000 (95% CI 2.6–3.8) in the latter years
2003–2007 (P <0.05).
incidence and HL characteristics by place of birth
Within Hispanic and A/PI populations, place of birth (i.e. US
born versus foreign born) was a significant predictor in
age-specific incidence. US-born A/PI age 20–49 years had a
higher incidence of HL than foreign-born A/PIs (Figure 5A,
P <0.05) with incidence of both populations converging after
age 50 years. Similarly, US-born Hispanic population age 20–
39 years had a significantly higher incidence of HL than
foreign-born Hispanics of the same age (Figure 5B, P <0.05);
and the incidences of both races converged after age 40 years.
Interestingly, the relative increased incidence of HL in younger
US-born Hispanics and A/PI populations consisted
predominantly of NS subtype (supplemental Figure S1,
available at Annals of Oncology online). In terms of periodspecific HL incidence patterns based on birthplace, there was a
trend toward significance for increased incidence of US-born
A/PI aged 20–29 years [1992–1997: 1.9/100 000 (95% CI 1.2–
2.8), 1998–2002: 2.2/100 000 (95% CI 1.4–3.3), and 2003–2007:
Volume 23 | No. 8 | August 2012
3.6/100 000 (95% CI 2.6–5.0)], while there were no differences
among other age groups. Among Hispanics, there were no
changes in HL incidence for both US- and foreign-born
populations (Figure 5E and F).
We analyzed disease characteristics and incidence patterns
for A/PI’s and Hispanics according to birthplace (Table 4).
Significantly, more foreign-born Hispanics with HL were
male compared with US-born Hispanics (64% versus 55%,
respectively, P <0.003). Foreign-born Hispanics had
significantly less frequent incidence of NS compared with
US-born Hispanics (47% versus 60%, respectively, P <0.001);
this was in part due to significantly more frequent MC
subtype for foreign-born versus US-born Hispanics (25%
versus 15%, respectively, P <0.0001). Foreign-born A/PI had
less frequent NS and more common MC compared with
US-born A/PI, however, these differences were not
significant.
survival
We analyzed OS according to race. Kaplan–Meier analysis
showed that Hispanics and blacks had significantly inferior OS
compared with whites and A/PIs (Figure 6). The 5-, 10-, and
15-year OS for whites were 82%, 75%, and 69%, respectively;
for A/PIs 81%, 72%, and 69%, respectively; for Blacks 76%,
68%, and 62%, respectively; and for Hispanics 75%, 65%, and
61%, respectively. On multivariate Cox regression adjusting for
age, gender, and stage, blacks and Hispanics had a persistent
increased risk of death (inferior OS) compared with whites
[Asians versus whites: HR 1.05 (95% CI 0.89–1.23); blacks
doi:10.1093/annonc/mdr578 | 
original articles
Annals of Oncology
Figure 5. Age-specific incidence and period changes by race and birthplace. (A) US-born A/PIs age 20–49 years had a higher incidence of HL than foreignborn A/PI of the same age (P <0.05) with incidence converging after age 50 years. (B) US-born Hispanics age 20–39 years also had a significantly higher
incidence of HL than foreign-born Hispanics of the same age (P <0.05). (C–D) In terms of period-specific HL incidence patterns, there was a trend toward
increased incidence of US-born A/PI age 20–29 years, while there were no differences among other age groups. (E–F) Among Hispanics, there were no
differences in HL incidence for either US- and foreign-born populations. A/PI, Asian/Pacific Islander; HL, Hodgkin’s lymphoma.
versus whites: HR 1.23 (95% CI 1.02–1.47); Hispanics versus
whites: HR 1.69 (95% CI 1.28–2.17)]. When analyzing place of
birth, there were no OS differences comparing US- versus
foreign-born A/PIs (P = 0.96) or Hispanics (P = 0.40).
discussion
To our knowledge, this report represents the largest and most
comprehensive analysis examining the impact of race (white,
black, Hispanic, and A/PI) on age- and gender-specific HL
incidence as well as patient/disease-related characteristics,
place-of-birth, and survival.
The age-specific bimodal incidence of HL is well
documented; however, most of these reports consisted of a
vast majority white population [21, 22]. We confirmed a
bimodal distribution for whites, as well as A/PIs, in this
 | Evens et al.
analysis, although this was more prominent for men
compared with women. Interestingly, after the age of 30
years, black men had a rather constant incidence rate, while
black women had the suggestion of a bimodal pattern.
Hispanics on the other hand had a small incidence peak at
age 20–29 years followed by an exponential rise in HL
incidence thereafter. Furthermore, after age 65 years, the
incidence of HL was highest in Hispanics compared with all
other races. Clinicopathologic racial differences included less
common frequency of NS histology, more frequent presence
of B symptoms, and more common advanced-stage disease
for Hispanics and blacks compared with whites. The etiology
of these differences is not known, although several factors
have been hypothesized.
Socioeconomic status (SES) has been shown to impact
incidence with individuals living in higher SES having higher
Volume 23 | No. 8 | August 2012
original articles
Annals of Oncology
Table 4. Hispanic and A/PI disease-related characteristics based on birthplace
Gender
Male
Female
Age
Mean
Interquartile range
Histology
Nodular sclerosis
Mixed cellularity
Other HL
Site
Extranodal
Stage at dx
I
II
III
IV
NA
B symptoms
No
Yes
NA
A/PI
US born
Count
120
121
%
Foreign born
Count
%
Unknown
Count
%
50
50
148
105
118
110
34.7
21–44
58
42
43.0
28–57
34.9
23–44
PUS versus
foreign born
52
48
0.052
0
0
<0.001
Hispanic
US born
Count
%
Foreign born
Count
%
Unknown
Count
%
412
341
401
222
380
311
35.7
21–50
55
45
0
0
41.2
27–55
64
36
0
0
37.6
23–50
P US versus
foreign born
55
45
<0.001
0
0
<0.001
161
30
50
67
12
21
154
44
55
61
17
22
146
31
51
64
14
22
0.253
454
130
169
60
17
22
292
156
175
47
25
28
402
116
173
58
17
25
0.001
8
3
8
3
10
4
0.921
19
3
8
1
16
2
0.099
44
100
44
50
3
18
41
18
21
1
47
101
48
41
16
19
40
19
16
6
37
119
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28
6
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129
269
145
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92
189
119
184
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30
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30
6
156
232
134
128
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19
6
0.007
115
87
39
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97
95
61
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24
111
73
44
49
32
19
0.202
247
342
164
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195
317
111
31
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272
244
175
39
35
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0.194
A/PI, Asian/Pacific Islander; dx, diagnosis; HL, Hodgkin’s lymphoma; NA, not available.
Figure 6. Survival of Hodgkin’s lymphoma according to race. Overall
survival (OS) by Kaplan–Meier analysis for whites, Hispanics, A/PI’s, and
Hispanics. Associated inlet compares OS across races.
risk of HL. Several California state-based studies showed that
SES predicted HL incidence [12, 23, 24]. Underscoring the
etiologic complexity of HL, Clarke et al. [23] showed that SES
differences varied by age, race, histology, and gender. Other
groups have shown that Epstein–Barr virus (EBV)-related HL
Volume 23 | No. 8 | August 2012
is most commonly associated with MC histology subtype [25,
26]. The significant rise in HL incidence noted here in USborn A/PI and Hispanics is unlikely related to EBV since the
increase consisted primarily of subjects aged 15–45 years and
with NS histology.
We also identified significant racial disparities in survival.
In a California statewide database study of EBV+ HL,
Keegan et al. [24] showed that blacks and Hispanics had
increased risk of HL-related death for patients age 15–44
years as well as for patients age >44 years compared with
whites. Moreover, the survival disparity persisted for
blacks and Hispanics after adjustment for SES. In another
study, blacks had an increased risk of death (HR 1.54)
compared with whites (Hispanics were not included in this
analysis) [13].
There are several potential explanations of why cancerrelated survival may differ based on race. This includes
disease biology, host pharmacogenetics [27], delay in therapy
[28], hospital factors [29], access to health care [30], and/or
differences in SES as noted before [31–34]. In a SWOG
study, Hershman et al. [5] showed that in part due to lower
white blood cell counts, black women were more likely to
experience treatment delay or early discontinuation of breast
cancer therapy compared with white women. However, after
adjustment of these and other factors, inferior survival for
black women persisted. In a pediatric cancer study,
Armstrong et al. [2] reported that blacks had an inferior
doi:10.1093/annonc/mdr578 | 
original articles
survival compared with whites, Hispanics, and A/PI’s and
that this was primarily due to significantly higher mortality
from nonrecurrence/nonexternal causes [2]. The survival
difference emerged mainly >20 to 25 years of follow-up
indicating that racial disparities in long-term utilization of
health care may have been a factor. However, this would not
explain the survival rates noted herein as the inferior
survival for blacks and Hispanics emerged within the first
few years of follow-up. The increased incidence of advancedstage HL for blacks and Hispanics compared with whites
and A/PI may be a factor in the survival disparity. Keegan
et al. [24] showed that younger and older California blacks
and Hispanics with HL stage III/IV disease had inferior
survival rates compared with California whites with stage
III/IV HL.
The current analysis consisted of US HL subjects and the
findings may not be applicable to other countries, especially
ones with less prominent racial diversity. However, we believe
the findings herein are applicable to the overall epidemiology
of HL especially given the differences in incidence and disease
characteristics within Hispanics and A/PI’s based on
birthplace. While genetic influences may in part explain the
global differences in HL incidence, differences in US versus
foreign born support acculturation with an impact of lifestyle
and environmental factors.
A shortcoming of the current analysis is the lack of tumor
(or serum)-specific analyses as well as the absence of
information on access to care and therapy received. In
addition, birthplace information was missing for a significant
minority of cases, especially for young adults. While studies
have linked a number of patient factors to incompleteness of
registry birthplace data [35, 36], these studies also found
that registry birthplace data were highly accurate when they
were recorded. Similar to the current report, numerous
studies have used birthplace data from the SEER registries to
identify disparities in cancer occurrence and for exploring
cancer etiology [37–39]. Furthermore, similar to other
analyses [40], our study uniquely linked the rich SEER
database to estimates of the population that are immigrant
in order to elucidate incidence patterns of US- and foreignborn individuals. Our study provides evidence that
predictors of incidence and survival, such as race, as well as
birthplace, are important factors that should be included in
future studies especially when analyzing potential
environmental/lifestyle and biological differences in disease.
An additional strength of our study includes the large
sample size and the population-based design that included
broad geographic and racial diversity.
In summary, we identified a number of prominent racial
disparities among a large population-based HL SEER
database analysis. This included marked differences in agespecific incidence rates as well as varying clinical
characteristics and disease-related factors (e.g. tumor
histology, B symptoms, and stage) based on race.
Furthermore, we identified a recent increase in the incidence
of HL among young adult, US-born A/PIs, while divergent
OS rates were noted based on race. Continued examination
of racial disparities in adolescent/adult HL, especially the
impact on survival, is needed.
 | Evens et al.
Annals of Oncology
acknowledgements
Author contributions: AME designed research, carried out
research, analyzed data, and wrote the paper. MA carried out
research, analyzed data, and wrote the paper. BA analyzed data
and wrote the paper. BCHC designed research, carried out
research, analyzed data, and wrote the paper.
Presented at the 11th International Conference on
Malignant Lymphoma; June 2011, Lugano, Switzerland (oral
presentation).
disclosure
The authors declare no conflict of interest.
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doi:10.1093/annonc/mdr578 | 