Exploring the Importance of Language Sensitivity in Journalism

Style and Language Sensitivity
Stovall (2015) writes:
Writers must understand that language has the ability to define,
offend, and demean. Readers and viewers of the mass media are
a broad and diverse group, and those who would communicate
with them should be aware of the language sensitivities of that
group…Media writers and organizations should go beyond
simply trying not to offend. They should make efforts to expand
their thinking and news coverage to be inclusive toward groups
that previously have not been part of the news…They should
seek diversity for their work because the world is a diverse
place.
Taking these ideas into consideration, visit theConscious Style
Guide and scan through the articles. Choose one area of
diversity on which to focus.
Ability & Disability
· Age
· Appearance
· Ethnicity & Nationality
· Gender & Sexuality
· Health
· Othering
After reading through the articles listed under your chosen area
of diversity, write a paper that explores the importance of
language sensitivity in journalism. Support your ideas with a
personal experience, an event you witnessed, a current issue
being discussed in the news, or how language sensitivity (or a
lack thereof) may impact an individual or group of individuals.
The paper must be between four and five pages in length and
written according to AP style. You should use sources to
support your claims, and be sure to properly cite all of your
sources within the body of your paper and on the References
page. For APA style guidance and examples, visit Ashford

Writing Center’sAPA Key Elements.
For this Style and Language Sensitivity Assignment, students
must
· Identify one area of diversity on which to focus.
· Explain language sensitivity.
· Relate an area of diversity to a personal experience, current
news story or impacted group of individuals.
· Assess the importance of language sensitivity in news media.
The Style and Language Sensitivity Assignment
· Must be four to five double-spaced pages in length (not
including title and references pages) and formatted according to
APA style as outlined in theAPA Checklist.
· Must include a separatetitle page with the following:
· Title of paper
· Student’s name
· Course name and number
· Instructor’s name
· Date submitted
· Must use at least 1credible source in addition to the course
text.
· Must document all sources in text in APA style as outlined in
the Writing Center’sin-text citation resource.
· Must include a separate references page that is formatted
according to APA style as outlined in the Writing
Center’sreference page resource.
· Check it! Your assignment must be submitted
throughGrammarly and Turnitin prior to submission.
Carefully review theGrading Rubric for the criteria that will be
used to evaluate your assignment.
The new england
journal of medicine

n engl j med 373;22 nejm.org November 26, 2015 2103
established in 1812 November 26, 2015 vol. 373 no. 22
The members of the writing committee
( Jackson T. Wright, Jr., M.D., Ph.D., Jeff
D. Williamson, M.D., M.H.S., Paul K.
Whelton, M.D., Joni K. Snyder, R.N.,
B.S.N., M.A., Kaycee M. Sink, M.D.,
M.A.S., Michael V. Rocco, M.D., M.S.C.E.,
David M. Reboussin, Ph.D., Mahboob
Rahman, M.D., Suzanne Oparil, M.D.,
Cora E. Lewis, M.D., M.S.P.H., Paul L.
Kimmel, M.D., Karen C. Johnson, M.D.,
M.P.H., David C. Goff, Jr., M.D., Ph.D.,
Lawrence J. Fine, M.D., Dr.P.H., Jeffrey A.
Cutler, M.D., M.P.H., William C. Cush-
man, M.D., Alfred K. Cheung, M.D., and
Walter T. Ambrosius, Ph.D.) assume re-
sponsibility for the overall content and
integrity of the article. The affiliations of
the members of the writing group are
listed in the Appendix. Address reprint
requests to Dr. Wright at the Division of
Nephrology and Hypertension, Univer-
sity Hospitals Case Medical Center, Case
Western Reserve University, 1100 Euclid
Ave. Cleveland, OH 44106-6053, or at
jackson . [email protected] case . edu.
* A complete list of the members of the
Systolic Blood Pressure Intervention
Trial (SPRINT) Research Group is pro-
vided in the Supplementary Appendix,
available at NEJM.org.

This article was published on November 9,
2015, at NEJM.org.
N Engl J Med 2015;373:2103-16.
DOI: 10.1056/NEJMoa1511939
Copyright © 2015 Massachusetts Medical Society.
BACKGROUND
The most appropriate targets for systolic blood pressure to
reduce cardiovascular
morbidity and mortality among persons without diabetes remain
uncertain.
METHODS
We randomly assigned 9361 persons with a systolic blood
pressure of 130 mm Hg
or higher and an increased cardiovascular risk, but without
diabetes, to a systolic
blood-pressure target of less than 120 mm Hg (intensive
treatment) or a target of
less than 140 mm Hg (standard treatment). The primary
composite outcome was
myocardial infarction, other acute coronary syndromes, stroke,
heart failure, or
death from cardiovascular causes.
RESULTS
At 1 year, the mean systolic blood pressure was 121.4 mm Hg in
the intensive-
treatment group and 136.2 mm Hg in the standard-treatment
group. The interven-
tion was stopped early after a median follow-up of 3.26 years
owing to a signifi-
cantly lower rate of the primary composite outcome in the
intensive-treatment
group than in the standard-treatment group (1.65% per year vs.

2.19% per year;
hazard ratio with intensive treatment, 0.75; 95% confidence
interval [CI], 0.64 to
0.89; P<0.001). All-cause mortality was also significantly lower
in the intensive-
treatment group (hazard ratio, 0.73; 95% CI, 0.60 to 0.90; P =
0.003). Rates of seri-
ous adverse events of hypotension, syncope, electrolyte
abnormalities, and acute
kidney injury or failure, but not of injurious falls, were higher
in the intensive-
treatment group than in the standard-treatment group.
CONCLUSIONS
Among patients at high risk for cardiovascular events but
without diabetes, target-
ing a systolic blood pressure of less than 120 mm Hg, as
compared with less than
140 mm Hg, resulted in lower rates of fatal and nonfatal major
cardiovascular
events and death from any cause, although significantly higher
rates of some adverse
events were observed in the intensive-treatment group. (Funded
by the National
Institutes of Health; ClinicalTrials.gov number, NCT01206062.)
a b s t r a c t
A Randomized Trial of Intensive versus
Standard Blood-Pressure Control
The SPRINT Research Group*
The New England Journal of Medicine
Downloaded from nejm.org on December 25, 2015. For personal
use only. No other uses without permission.

Copyright © 2015 Massachusetts Medical Society. All rights
reserved.
n engl j med 373;22 nejm.org November 26, 20152104
T h e n e w e n g l a n d j o u r n a l o f m e d i c i n e
Hypertension is highly prevalent in the adult population in the
United States, especially among persons older
than 60 years of age, and affects approximately
1 billion adults worldwide.1,2 Among persons 50
years of age or older, isolated systolic hyperten-
sion is the most common form of hypertension,3,4
and systolic blood pressure becomes more im-
portant than diastolic blood pressure as an inde-
pendent risk predictor for coronary events, stroke,
heart failure, and end-stage renal disease (ESRD).5-13
The Global Burden of Disease Study identified
elevated blood pressure as the leading risk fac-
tor, among 67 studied, for death and disability-
adjusted life-years lost during 2010.14
Clinical trials have shown that treatment of
hypertension reduces the risk of cardiovascular
disease outcomes, including incident stroke (by
35 to 40%), myocardial infarction (by 15 to 25%),
and heart failure (by up to 64%).5,15,16 However,
the target for systolic blood-pressure lowering is
uncertain. Observational studies have shown a
progressive increase in cardiovascular risk as
systolic blood pressure rises above 115 mm Hg,10
but the available evidence from randomized,
controlled trials in the general population of

patients with hypertension only documents the
benefit of treatment to achieve a systolic blood-
pressure target of less than 150 mm Hg, with
limited data concerning lower blood-pressure
targets.11,17-21 In a trial involving patients with
type 2 diabetes mellitus, the rate of major cardio-
vascular events was similar with a systolic blood-
pressure target of less than 120 mm Hg and the
commonly recommended target of less than
140 mm Hg, though the rate of stroke was
lower with the target of less than 120 mm Hg.22
A recent trial involving patients who had had a
stroke compared treatment to lower systolic blood
pressure to less than 130 mm Hg with treatment
to lower it to less than 150 mm Hg and showed
no significant benefit of the lower target with
respect to the overall risk of another stroke but
a significant benefit with respect to the risk of
hemorrhagic stroke.23
The hypothesis that a lower systolic blood-
pressure goal (e.g., <120 mm Hg) would reduce
clinical events more than a standard goal was
designated by a National Heart, Lung, and Blood
Institute (NHLBI) expert panel in 2007 as the
most important hypothesis to test regarding the
prevention of hypertension-related complications
among patients without diabetes.24 The current
article describes the primary results of the Sys-
tolic Blood Pressure Intervention Trial (SPRINT),
which compared the benefit of treatment of
systolic blood pressure to a target of less than
120 mm Hg with treatment to a target of less
than 140 mm Hg.

M e t h o d s
Study Design and Oversight
SPRINT was a randomized, controlled, open-la-
bel trial that was conducted at 102 clinical sites
(organized into 5 clinical center networks) in the
United States, including Puerto Rico (see the
Supplementary Appendix, available with the full
text of this article at NEJM.org). A trial coordi-
nating center served as a data and biostatistical
core center and supervised the central laboratory,
the electrocardiography reading center, the mag-
netic resonance imaging reading center, and the
drug-distribution center. The rationale and pro-
tocol for the trial are publicly available,25,26 and
the protocol is available at NEJM.org.
SPRINT was sponsored by the NHLBI, with
cosponsorship by the National Institute of Dia-
betes and Digestive and Kidney Diseases, the
National Institute of Neurological Disorders and
Stroke, and the National Institute on Aging. An
independent data and safety monitoring board
monitored unblinded trial results and safety
events. The study was approved by the institu-
tional review board at each participating study
site. The steering committee designed the study,
gathered the data (in collaboration with investi-
gators at the clinics and other study units), made
the decision to submit the manuscript for publi-
cation, and vouches for the fidelity of the study
to the protocol. The writing committee wrote
the manuscript and vouches for the complete-
ness and accuracy of the data and analysis. The
coordinating center was responsible for analyz-

ing the data. Scientists at the National Institutes
of Health participated in the design of the study
and as a group had one vote on the steering
committee of the trial.
Study Population
Participants were required to meet all the follow-
ing criteria: an age of at least 50 years, a systolic
blood pressure of 130 to 180 mm Hg (see the
Supplementary Appendix), and an increased risk
A Quick Take
is available at
NEJM.org
reserved.
In tensi v e vs. S ta nda r d Bl ood -Pr essur e Con trol
of cardiovascular events. Increased cardiovascu-
lar risk was defined by one or more of the fol-
lowing: clinical or subclinical cardiovascular dis-
ease other than stroke; chronic kidney disease,
excluding polycystic kidney disease, with an esti-
mated glomerular filtration rate (eGFR) of 20 to

less than 60 ml per minute per 1.73 m2 of body-
surface area, calculated with the use of the four-
variable Modification of Diet in Renal Disease
equation; a 10-year risk of cardiovascular disease
of 15% or greater on the basis of the Framing-
ham risk score; or an age of 75 years or older.
Patients with diabetes mellitus or prior stroke
were excluded. Detailed inclusion and exclusion
criteria are listed in the Supplementary Appen-
dix. All participants provided written informed
consent.
Randomization and Interventions
Eligible participants were assigned to a sys-
tolic blood-pressure target of either less than
140 mm Hg (the standard-treatment group) or
less than 120 mm Hg (the intensive-treatment
group). Randomization was stratified according
to clinical site. Participants and study personnel
were aware of the study-group assignments, but
outcome adjudicators were not.
After the participants underwent randomiza-
tion, their baseline antihypertensive regimens
were adjusted on the basis of the study-group
assignment. The treatment algorithms were sim-
ilar to those used in the Action to Control Car-
diovascular Risk in Diabetes (ACCORD) trial.22
These algorithms and our formulary are listed in
Figures S1 and S2 and Table S1 in the Supple-
mentary Appendix. All major classes of antihy-
pertensive agents were included in the formulary
and were provided at no cost to the participants.
SPRINT investigators could also prescribe other
antihypertensive medications (not provided by

the study). The protocol encouraged, but did not
mandate, the use of drug classes with the stron-
gest evidence for reduction in cardiovascular
outcomes, including thiazide-type diuretics (en-
couraged as the first-line agent), loop diuretics
(for participants with advanced chronic kidney
disease), and beta-adrenergic blockers (for those
with coronary artery disease).5,27 Chlorthalidone
was encouraged as the primary thiazide-type di-
uretic, and amlodipine as the preferred calcium-
channel blocker.28,29 Azilsartan and azilsartan
combined with chlorthalidone were donated by
Takeda Pharmaceuticals International and Arbor
Pharmaceuticals; neither company had any other
role in the study.
Participants were seen monthly for the first
3 months and every 3 months thereafter. Medi-
cations for participants in the intensive-treat-
ment group were adjusted on a monthly basis
to target a systolic blood pressure of less than
120 mm Hg. For participants in the standard-
treatment group, medications were adjusted
to target a systolic blood pressure of 135 to
139 mm Hg, and the dose was reduced if sys-
tolic blood pressure was less than 130 mm Hg
on a single visit or less than 135 mm Hg on two
consecutive visits. Dose adjustment was based
on a mean of three blood-pressure measure-
ments at an office visit while the patient was
seated and after 5 minutes of quiet rest; the
measurements were made with the use of an
automated measurement system (Model 907,
Omron Healthcare). Lifestyle modification was
encouraged as part of the management strategy.

Retention in the study and adherence to treat-
ment were monitored prospectively and routinely
throughout the trial.26
Study Measurements
Demographic data were collected at baseline.
Clinical and laboratory data were obtained at
baseline and every 3 months thereafter. A struc-
tured interview was used in both groups every
3 months to obtain self-reported cardiovascular
disease outcomes. Although the interviewers
were aware of the study-group assignments, they
used the same format for interviews in the two
groups to minimize ascertainment bias. Medical
records and electrocardiograms were obtained
for documentation of events. Whenever clinical-
site staff became aware of a death, a standard
protocol was used to obtain information on the
event.
Serious adverse events were defined as events
that were fatal or life-threatening, that resulted
in clinically significant or persistent disability,
that required or prolonged a hospitalization, or
that were judged by the investigator to represent
a clinically significant hazard or harm to the
participant that might require medical or surgi-
cal intervention to prevent one of the other
events listed above.30,31 A short list of monitored
conditions were reported as adverse events if
they were evaluated in an emergency department:

reserved.
hypotension, syncope, injurious falls, electrolyte
abnormalities, and bradycardia. We also moni-
tored occurrences of acute kidney injury or acute
renal failure if they were noted on admission or
occurred during a hospitalization and were re-
ported in the hospital discharge summary as a
primary or main secondary diagnosis. The Medi-
cal Dictionary for Regulatory Activities was used to
classify the safety events. Coding was performed
at the coordinating center, and up to three codes
were assigned to each safety event. The relation-
ship of serious adverse events to the intervention
was assessed by the trial safety officer and re-
viewed monthly by the safety committee.
Study Outcomes
Definitions of study outcomes are outlined in
the Supplementary Appendix. A committee whose
members were unaware of the study-group as-
signments adjudicated the clinical outcomes
specified in the protocol. The primary hypothe-
sis was that treatment to reach a systolic blood-
pressure target of less than 120 mm Hg, as
compared with a target of less than 140 mm Hg,
would result in a lower rate of the composite

outcome of myocardial infarction, acute coro-
nary syndrome not resulting in myocardial in-
farction, stroke, acute decompensated heart
failure, or death from cardiovascular causes.
Secondary outcomes included the individual
components of the primary composite outcome,
death from any cause, and the composite of the
primary outcome or death from any cause.
We also assessed renal outcomes, using a dif-
ferent definition for patients with chronic kidney
disease (eGFR <60 ml per minute per 1.73 m2) at
baseline and those without it. The renal outcome
in participants with chronic kidney disease at
baseline was a composite of a decrease in the
eGFR of 50% or more (confirmed by a subse-
quent laboratory test) or the development of
ESRD requiring long-term dialysis or kidney
transplantation. In participants without chronic
kidney disease at baseline, the renal outcome
was defined by a decrease in the eGFR of 30%
or more to a value of less than 60 ml per minute
per 1.73 m2. Incident albuminuria, defined for
all study participants by a doubling of the ratio
of urinary albumin (in milligrams) to creatinine
(in grams) from less than 10 at baseline to
greater than 10 during follow-up, was also a
prespecified renal outcome.
Prespecified subgroups of interest for all out-
comes were defined according to status with re-
spect to cardiovascular disease at baseline (yes vs.
no), status with respect to chronic kidney disease
at baseline (yes vs. no), sex, race (black vs. non-
black), age (<75 vs. ≥75 years), and baseline sys-
tolic blood pressure in three levels (≤132 mm Hg,

>132 to <145 mm Hg, and ≥145 mm Hg). We
also planned a comparison of the effects of
systolic blood-pressure targets on incident de-
mentia, changes in cognitive function, and cere-
bral small-vessel ischemic disease; these results
are not presented here.
Statistical Analysis
We planned a 2-year recruitment period, with a
maximum follow-up of 6 years, and anticipated
a loss to follow-up of 2% per year. With an en-
rollment target of 9250 participants, we estimated
that the trial would have 88.7% power to detect
a 20% effect with respect to the primary out-
come, assuming an event rate of 2.2% per year
in the standard-treatment group.
Our primary analysis compared the time to
the first occurrence of a primary outcome event
between the two study groups with the use of
the intention-to-treat approach for all randomly
assigned participants; for this analysis, we used
Cox proportional-hazards regression with two-
sided tests at the 5% level of significance, with
stratification according to clinic. Follow-up time
was censored on the date of last event ascertain-
ment. Interactions between treatment effect and
prespecified subgroups were assessed with a
likelihood-ratio test for the interaction with the
use of Hommel-adjusted P values.32 Interim
analyses were performed for each meeting of the
data and safety monitoring board, with group-
sequential stopping boundaries defined with the
use of the Lan–DeMets method with an O’Brien–
Fleming–type spending function.33 The Fine–

Gray model for the competing risk of death was
used as a sensitivity analysis.34
R e s u l t s
Study Participants
A total of 9361 participants were enrolled be-
tween November 2010 and March 2013 (Fig. 1).
Descriptive baseline statistics are presented in
Table 1. On August 20, 2015, the NHLBI director
accepted a recommendation from the data and
reserved.
safety monitoring board of the trial to inform
the investigators and participants of the cardio-
vascular-outcome results after analyses of the
primary outcome exceeded the monitoring bound-
ary at two consecutive time points (Fig. S3 in the
Supplementary Appendix), thus initiating the
process to end the blood-pressure intervention
early. The median follow-up on August 20, 2015,
was 3.26 years of the planned average of 5 years.

Blood Pressure
The two treatment strategies resulted in a rapid
and sustained between-group difference in sys-
tolic blood pressure (Fig. 2). At 1 year, the mean
systolic blood pressure was 121.4 mm Hg in the
intensive-treatment group and 136.2 mm Hg in
the standard-treatment group, for an average
difference of 14.8 mm Hg. The mean diastolic
blood pressure at 1 year was 68.7 mm Hg in the
intensive-treatment group and 76.3 mm Hg in the
standard-treatment group (Fig. S4 in the Supple-
mentary Appendix). Throughout the 3.26 years
of follow-up, the mean systolic blood pressure
was 121.5 mm Hg in the intensive-treatment
group and 134.6 mm Hg in the standard-treat-
ment group, and the mean number of blood-
pressure medications was 2.8 and 1.8, respec-
tively. The relative distribution of antihypertensive
medication classes used was similar in the two
groups, though the use of each class was greater
in the intensive-treatment group (Table S2 in the
Supplementary Appendix).
Clinical Outcomes
A primary outcome event was confirmed in 562
participants — 243 (1.65% per year) in the inten-
sive-treatment group and 319 (2.19% per year) in
the standard-treatment group (hazard ratio with
intensive treatment, 0.75; 95% confidence inter-
val [CI], 0.64 to 0.89; P<0.001) (Table 2). Separa-
tion in the primary outcome between the groups
was apparent at 1 year (Fig. 3A). The between-
group differences were consistent across the
components of the primary outcome and other

prespecified secondary outcomes (Table 2).
A total of 365 deaths occurred — 155 in the
intensive-treatment group and 210 in the stan-
dard-treatment group (hazard ratio, 0.73; 95% CI,
0.60 to 0.90; P = 0.003). Separation in mortality
between the groups became apparent at ap-
proximately 2 years (Fig. 3B). Causes of death are
provided in Table S3 in the Supplementary Ap-
pendix. The relative risk of death from cardiovas-
cular causes was 43% lower with the intensive
intervention than with the standard treatment
(P = 0.005) (Table 2).
The numbers needed to treat to prevent a
primary outcome event, death from any cause,
and death from cardiovascular causes during the
median 3.26 years of the trial were 61, 90, and
172, respectively. The effects of the intervention
on the rate of the primary outcome and on the
rate of death from any cause were consistent
across the prespecified subgroups (Fig. 4, and
Fig. S5 in the Supplementary Appendix). There
were no significant interactions between treat-
ment and subgroup with respect to the primary
outcome or death from any cause. When death
Figure 1. Eligibility, Randomization, and Follow-up.
Discontinued intervention refers to participants who
discontinued the study
treatment but did not withdraw consent or become lost to
follow-up.
9361 Underwent randomization

14,692 Patients were assessed
for eligibility
5331 Were ineligible or declined
to participate
34 Were <50 yr of age
352 Had low systolic blood
pressure at 1 min after
standing
2284 Were taking too many
medications or had systolic
blood pressure that was out
of range
718 Were not at increased
cardiovascular risk
703 Had miscellaneous reasons
587 Did not give consent
653 Did not complete screening
4678 Were assigned to intensive
treatment
4683 Were assigned to standard
treatment
224 Discontinued intervention
111 Were lost to follow-up
154 Withdrew consent
242 Discontinued intervention
134 Were lost to follow-up

121 Withdrew consent
4678 Were included in the analysis 4683 Were included in the
analysis
reserved.
Characteristic
Intensive Treatment
(N = 4678)
Standard Treatment
(N = 4683)
Criterion for increased cardiovascular risk — no. (%)†
Age ≥75 yr 1317 (28.2) 1319 (28.2)
Chronic kidney disease‡ 1330 (28.4) 1316 (28.1)
Cardiovascular disease 940 (20.1) 937 (20.0)
Clinical 779 (16.7) 783 (16.7)

Subclinical 247 (5.3) 246 (5.3)
Framingham 10yr cardiovascular disease risk score ≥15% 2870
(61.4) 2867 (61.2)
Female sex — no. (%) 1684 (36.0) 1648 (35.2)
Age — yr
Overall 67.9±9.4 67.9±9.5
Among those ≥75 yr of age 79.8±3.9 79.9±4.1
Race or ethnic group — no. (%)§
Non-Hispanic black 1379 (29.5) 1423 (30.4)
Hispanic 503 (10.8) 481 (10.3)
Non-Hispanic white 2698 (57.7) 2701 (57.7)
Other 98 (2.1) 78 (1.7)
Black race§¶ 1454 (31.1) 1493 (31.9)
Baseline blood pressure — mm Hg
Systolic 139.7±15.8 139.7±15.4
Diastolic 78.2±11.9 78.0±12.0
Distribution of systolic blood pressure — no. (%)
≤132 mm Hg 1583 (33.8) 1553 (33.2)
>132 mm Hg to <145 mm Hg 1489 (31.8) 1549 (33.1)

≥145 mm Hg 1606 (34.3) 1581 (33.8)
Serum creatinine — mg/dl 1.07±0.34 1.08±0.34
Estimated GFR — ml/min/1.73 m2
Among all participants 71.8±20.7 71.7±20.5
Among those with estimated GFR ≥60 ml/min/1.73 m2
81.3±15.5 81.1±15.5
Among those with estimated GFR <60 ml/min/1.73 m2 47.8±9.5
47.9±9.5
Ratio of urinary albumin (mg) to creatinine (g) 44.1±178.7
41.1±152.9
Fasting total cholesterol — mg/dl 190.2±41.4 190.0±40.9
Fasting HDL cholesterol — mg/dl 52.9±14.3 52.8±14.6
Fasting total triglycerides — mg/dl 124.8±85.8 127.1±95.0
Fasting plasma glucose — mg/dl 98.8±13.7 98.8±13.4
Statin use — no./total no. (%) 1978/4645 (42.6) 2076/4640
(44.7)
Aspirin use — no./total no. (%) 2406/4661 (51.6) 2350/4666
(50.4)
Smoking status — no. (%)
Never smoked 2050 (43.8) 2072 (44.2)

Former smoker 1977 (42.3) 1996 (42.6)
Current smoker 639 (13.7) 601 (12.8)
Missing data 12 (0.3) 14 (0.3)
Framingham 10-yr cardiovascular disease risk score — %
20.1±10.9 20.1±10.8
Table 1. Baseline Characteristics of the Study Participants.*
reserved.
was treated as a competing risk in a Fine–Gray
model, the results with respect to the primary
outcome were virtually unchanged (hazard ratio,
0.76; 95% CI, 0.64 to 0.89).
Among participants who had chronic kidney
disease at baseline, no significant between-group
difference in the composite outcome of a de-
crease in the eGFR of 50% or more or the devel-
opment of ESRD was noted, though the number
of events was small (Table 2). Among partici-
pants who did not have chronic kidney disease at

baseline, the incidence of the outcome defined
by a decrease in the eGFR of 30% or more to a
value of less than 60 ml per minute per 1.73 m2
was higher in the intensive-treatment group than
in the standard-treatment group (1.21% per year
vs. 0.35% per year; hazard ratio, 3.49; 95% CI,
2.44 to 5.10; P<0.001).
Serious Adverse Events
Serious adverse events occurred in 1793 partici-
pants in the intensive-treatment group (38.3%)
and in 1736 participants in the standard-treat-
ment group (37.1%) (hazard ratio with intensive
treatment, 1.04; P = 0.25) (Table 3, and Table S4
in the Supplementary Appendix). Serious adverse
events of hypotension, syncope, electrolyte ab-
normalities, and acute kidney injury or acute
renal failure, but not injurious falls or bradycar-
dia, occurred more frequently in the intensive-
treatment group than in the standard-treatment
group. Orthostatic hypotension as assessed dur-
ing a clinic visit was significantly less common
in the intensive-treatment group. A total of 220
participants in the intensive-treatment group
(4.7%) and 118 participants in the standard-
treatment group (2.5%) had serious adverse
events that were classified as possibly or defi-
nitely related to the intervention (hazard ratio,
1.88; P<0.001) (Table S5 in the Supplementary
Appendix). The magnitude and pattern of differ-
ences in adverse events according to treatment
assignment among participants 75 years of age
or older were similar to those in the overall co-
hort (Table S6 in the Supplementary Appendix).

D i s c u s s i o n
SPRINT showed that among adults with hyperten-
sion but without diabetes, lowering systolic blood
pressure to a target goal of less than 120 mm Hg,
as compared with the standard goal of less than
140 mm Hg, resulted in significantly lower rates
of fatal and nonfatal cardiovascular events and
death from any cause. Trial participants as-
signed to the lower systolic blood-pressure target
(intensive-treatment group), as compared with
those assigned to the higher target (standard-
treatment group), had a 25% lower relative risk
of the primary outcome; in addition, the inten-
sive-treatment group had lower rates of several
other important outcomes, including heart fail-
ure (38% lower relative risk), death from cardio-
vascular causes (43% lower relative risk), and
death from any cause (27% lower relative risk).
During the follow-up period of the trial (median,
3.26 years), the number needed to treat with a
strategy of intensive blood-pressure control to
Characteristic
Intensive Treatment
(N = 4678)
Standard Treatment
(N = 4683)
Bodymass index‖ 29.9±5.8 29.8±5.7
Antihypertensive agents — no./patient 1.8±1.0 1.8±1.0

Not using antihypertensive agents — no. (%) 432 (9.2) 450
(9.6)
* Plus–minus values are means ±SD. There were no significant
differences (P<0.05) between the two groups except for
statin use (P = 0.04). To convert the values for creatinine to
micromoles per liter, multiply by 88.4. To convert the values
for cholesterol to millimoles per liter, multiply by 0.02586. To
convert the values for triglycerides to millimoles per liter,
multiply by 0.01129. To convert the values for glucose to
millimoles per liter, multiply by 0.05551. GFR denotes glomer-
ular filtration rate, and HDL high-density lipoprotein.
† Increased cardiovascular risk was one of the inclusion
criteria.
‡ Chronic kidney disease was defined as an estimated
glomerular filtration rate of less than 60 ml per minute per 1.73
m2
of body-surface area.
§ Race and ethnic group were self-reported.
¶ Black race includes Hispanic black and black as part of a
multiracial identification.
‖ The bodymass index is the weight in kilograms divided by
the square of the height in meters.
Table 1. (Continued.)
reserved.

prevent one primary outcome event was 61, and
the number needed to treat to prevent one death
from any cause was 90. These benefits with re-
spect to both the primary outcome and death
were consistent across all prespecified subgroups,
including participants 75 years of age or older.
Owing in part to a lower-than-expected de-
cline in the eGFR and to the early termination of
the trial, the number of renal events was small.
Among participants who had chronic kidney
disease at baseline, the number of participants
with a decrease in the eGFR of 50% or more or
reaching ESRD over the course of the trial did
not differ significantly between the two interven-
tion groups. Among participants who did not have
chronic kidney disease at baseline, a decrease in
the eGFR of 30% or more to a value of less than
60 ml per minute per 1.73 m2 occurred more
frequently in the intensive-treatment group than
in the standard-treatment group (1.21% per year
vs. 0.35% per year). Among all participants, acute
kidney injury or acute renal failure occurred
more frequently in the intensive-treatment group
than in the standard-treatment group (Table 3,
and Table S5 in the Supplementary Appendix).
The differences in adverse renal outcomes may
be related to a reversible intrarenal hemody-
namic effect of the greater reduction in blood
pressure and greater use of diuretics, angioten-

sin-converting–enzyme inhibitors, and angio-
tensin-receptor blockers in the intensive-treat-
ment group.35,36 With the currently available data,
there is no evidence of substantial permanent
kidney injury associated with the lower systolic
blood-pressure goal; however, the possibility of
a long-term adverse renal outcome cannot be ex-
cluded. These observations and hypotheses need
to be explored further in analyses that incorpo-
rate more clinical outcomes and longer follow-up.
The results of SPRINT add substantially to
the evidence of benefits of lowering systolic
blood pressure, especially in older patients with
hypertension. Trials such as the Systolic Hyper-
tension in the Elderly Program trial,17 the Sys-
Figure 2. Systolic Blood Pressure in the Two Treatment Groups
over the Course of the Trial.
The systolic blood-pressure target in the intensive-treatment
group was less than 120 mm Hg, and the target in the
standard-treatment group was less than 140 mm Hg. The mean
number of medications is the number of blood-
pressure medications administered at the exit of each visit. I
bars represent 95% confidence intervals.
S
ys
to
lic
B
lo

o
d
P
re
ss
u
re
(
m
m
H
g)
150
140
130
110
120
0 1 2 3 4 5
Years
No. with Data
Standard treatment
Intensive treatment

1000
1048
3115
3204
3997
4029
4222
4231
4683
4678
1974
2035
3904
3920
4092
4091
4345
4375
274
286
Mean No. of Medications
Standard treatment
Intensive treatment
1.9
2.3

1.8
2.7
1.8
2.8
1.8
2.8
1.8
2.8
1.8
2.8
1.8
2.8
1.8
2.8
1.8
2.8
1.9
3.0
Intensive treatment
Standard treatment�
�
�

�
�
� �
� � �
�
� �
�
�
� � �
�
�
� �
reserved.
tolic Hypertension in Europe trial,11 and the

Hypertension in the Very Elderly Trial18 showed
the benefits of lowering systolic blood pressure
below 150 mm Hg. However, trials evaluating
systolic blood-pressure levels lower than those
studied in these trials have been either under-
powered19-21 or performed without specific sys-
tolic blood-pressure targets.37 A major component
of the controversy regarding the selection of the
systolic blood-pressure goal in this population
has resulted from inadequate data on the risks
versus benefits of systolic blood-pressure targets
below 150 mm Hg.11,17-21,37 SPRINT now provides
evidence of benefits for an even lower systolic
blood-pressure target than that currently recom-
mended in most patients with hypertension.
Comparisons between SPRINT and the
ACCORD trial22 are inevitable, because the trials
examined identical systolic blood-pressure tar-
gets (<120 mm Hg vs. <140 mm Hg). In contrast
to the findings of SPRINT, the cardiovascular
and mortality benefits observed in the ACCORD
trial were not statistically significant and were
of a lesser magnitude. Several important differ-
ences between these trials should be noted. The
ACCORD trial enrolled participants with diabe-
tes exclusively, whereas SPRINT excluded par-
ticipants with diabetes; in addition, the sample
Outcome Intensive Treatment Standard Treatment
Hazard Ratio
(95% CI) P Value
no. of patients (%) % per year no. of patients (%) % per year

All participants (N = 4678) (N = 4683)
Primary outcome† 243 (5.2) 1.65 319 (6.8) 2.19 0.75 (0.64–
0.89) <0.001
Secondary outcomes
Myocardial infarction 97 (2.1) 0.65 116 (2.5) 0.78 0.83 (0.64–
1.09) 0.19
Acute coronary syndrome 40 (0.9) 0.27 40 (0.9) 0.27 1.00
(0.64–1.55) 0.99
Stroke 62 (1.3) 0.41 70 (1.5) 0.47 0.89 (0.63–1.25) 0.50
Heart failure 62 (1.3) 0.41 100 (2.1) 0.67 0.62 (0.45–0.84)
0.002
Death from cardiovascular causes 37 (0.8) 0.25 65 (1.4) 0.43
0.57 (0.38–0.85) 0.005
Death from any cause 155 (3.3) 1.03 210 (4.5) 1.40 0.73 (0.60–
0.90) 0.003
Primary outcome or death 332 (7.1) 2.25 423 (9.0) 2.90 0.78
(0.67–0.90) <0.001
Participants with CKD at baseline (N = 1330) (N = 1316)
Composite renal outcome‡ 14 (1.1) 0.33 15 (1.1) 0.36 0.89
(0.42–1.87) 0.76
≥50% reduction in estimated GFR§ 10 (0.8) 0.23 11 (0.8) 0.26
0.87 (0.36–2.07) 0.75

Long-term dialysis 6 (0.5) 0.14 10 (0.8) 0.24 0.57 (0.19–1.54)
0.27
Kidney transplantation 0 0
Incident albuminuria¶ 49/526 (9.3) 3.02 59/500 (11.8) 3.90 0.72
(0.48–1.07) 0.11
Participants without CKD at baseline‖ (N = 3332) (N = 3345)
≥30% reduction in estimated GFR to <60 ml/
min/1.73 m2§
127 (3.8) 1.21 37 (1.1) 0.35 3.49 (2.44–5.10) <0.001
Incident albuminuria¶ 110/1769 (6.2) 2.00 135/1831 (7.4) 2.41
0.81 (0.63–1.04) 0.10
* CI denotes confidence interval, and CKD chronic kidney
disease.
† The primary outcome was the first occurrence of myocardial
infarction, acute coronary syndrome, stroke, heart failure, or
death from cardio-
vascular causes.
‡ The composite renal outcome for participants with CKD at
baseline was the first occurrence of a reduction in the estimated
GFR of 50% or
more, long-term dialysis, or kidney transplantation.
§ Reductions in the estimated GFR were confirmed by a second
laboratory test at least 90 days later.
¶ Incident albuminuria was defined by a doubling of the ratio
of urinary albumin (in milligrams) to creatinine (in grams) from
less than 10 at

baseline to greater than 10 during follow-up. The denominators
for number of patients represent those without albuminuria at
baseline.
‖ No longterm dialysis or kidney transplantation was reported
among participants without CKD at baseline.
Table 2. Primary and Secondary Outcomes and Renal
Outcomes.*
reserved.
size of the ACCORD trial was only half that of
SPRINT (4733 vs. 9361). SPRINT enrolled an
older cohort (mean age, 68 years, vs. 62 years
in the ACCORD trial), with 28% of participants
75 years of age or older, and also included partici-
pants with chronic kidney disease. The ACCORD
trial showed a (nonsignificant) 12% lower risk
of its primary composite cardiovascular out-
come, with a 95% confidence interval that in-
cluded the possibility of a 27% lower risk, which
is consistent with the cardiovascular benefit
observed in SPRINT. The ACCORD trial also
used a factorial design that included compari-

sons of standard and intensive glycemic and
lipid treatment targets in the same trial. A sec-
ondary analysis of the ACCORD results showed
that, as compared with the combined standard
glycemia and blood-pressure treatments, inten-
sive blood-pressure treatment alone reduced ma-
jor cardiovascular outcomes by 26% without
additional benefit from combining the two in-
tensive treatments.38 Thus, the difference in re-
sults between the trials could be due to differ-
ences in study design, treatment interactions, or
the play of chance. An inherent difference in the
cardiovascular benefits of systolic blood-pressure
lowering between the population with diabetes
and the population without diabetes seems un-
likely but cannot be ruled out.
In the Secondary Prevention of Small Sub-
cortical Strokes trial (intensive systolic blood-
pressure goal <130 mm Hg)23 and in the
ACCORD trial (intensive systolic blood-pressure
goal <120 mm Hg), the lower blood-pressure
target was associated with a nonsignificant 19%
lower incidence of stroke (P = 0.08) and a signifi-
cant 41% lower incidence of stroke, respectively,
than the incidence with higher targets. The
intensive-treatment group in SPRINT had a non-
significant 11% lower incidence of stroke, though
SPRINT also excluded persons with prevalent
stroke or transient ischemic attack at baseline.
In SPRINT, significant between-group differ-
ences were noted in some adverse effects that
were attributed to the intervention (Table S5 in
the Supplementary Appendix). Orthostatic hypo-
tension as assessed during a clinic visit (Table 3)

was observed less frequently in the intensive-
treatment group than in the standard-treatment
group (P = 0.01), but syncope was more common
among participants in the intensive-treatment
group than among those in the standard-treat-
ment group (3.5% vs. 2.4%, P = 0.003), as was
hypotension (3.4% vs. 2.0%, P<0.001). There was
no between-group difference in injurious falls
(hazard ratio, 1.00; P = 0.97). There was a higher
rate of acute kidney injury or acute renal failure
in the intensive-treatment group, as noted above.
These adverse events need to be weighed against
the benefits with respect to cardiovascular events
and death that are associated with intensive con-
trol of systolic blood pressure.
Figure 3. Primary Outcome and Death from Any Cause.
Shown are the cumulative hazards for the primary outcome (a
composite
of myocardial infarction, acute coronary syndrome, stroke, heart
failure, or
death from cardiovascular causes) (Panel A) and for death from
any cause
(Panel B). The inset in each panel shows the same data on an
enlarged y axis.
CI denotes confidence interval.
C
u
m
u
la
ti

ve
H
az
ar
d
1.0
0.8
0.6
0.4
0.2
0.0
0 1 2 3 4 5
Years
B Death from Any Cause
A Primary Outcome
No. at Risk
Standard treatment
Intensive treatment
4683
4678
4437
4436

4228
4256
2829
2900
721
779
Standard treatment
0.10
0.08
0.06
0.04
0.02
0.00
0 1 2 3 4 5
Hazard ratio with intensive treatment,
0.75 (95% CI, 0.64–0.89)
Intensive treatment
C
u
m
u

la
ti
ve
H
az
ar
d
1.0
0.8
0.6
0.4
0.2
0.0
0 1 2 3 4 5
Years
No. at Risk
Standard treatment
Intensive treatment
4683
4678
4528
4516

4383
4390
2998
3016
789
807
Standard treatment
0.10
0.08
0.06
0.04
0.02
0.00
0 1 2 3 4 5
Hazard ratio with intensive treatment,
0.73 (95% CI, 0.60–0.90)
Intensive treatment
reserved.

The strengths of SPRINT include a large
sample size, the diversity of the population
(including a large proportion of patients 75 years
of age or older), and its success in achieving the
intended separation in systolic blood pressure
between the two intervention groups throughout
the trial. The lack of generalizability to popula-
tions not included in the study — such as per-
sons with diabetes, those with prior stroke, and
those younger than 50 years of age — is a limi-
tation. It is also worth noting that we did not
enroll older adults residing in nursing homes or
assisted-living facilities. In addition, the effects
of the lower blood pressure on the central ner-
vous system and kidney cannot be reasonably
interpreted until analysis of these end points has
been completed.
The SPRINT results raise important practical
issues. Hypertension control to a blood pressure
of less than 140/90 mm Hg is achieved in only
about 50% of the general population in the
United States, which suggests that control to even
that level is challenging.39 We excluded patients
with more severe hypertension, and control of
systolic blood pressure to less than 120 mm Hg
required, on average, one additional antihyper-
tensive drug. In addition, the median systolic
blood pressure in the intensive-treatment group

was just above 120 mm Hg, which indicates that
more than half the participants had a systolic
blood pressure above the 120 mm Hg target.
These observations suggest that achieving a sys-
tolic blood-pressure goal of less than 120 mm
Hg in the overall population of patients with
hypertension would be more demanding and
time-consuming for both providers and patients
than achieving a goal of 140 mm Hg, and would
necessitate increased medication costs and clin-
ic visits.
In conclusion, targeting a systolic blood pres-
sure of less than 120 mm Hg, as compared with
less than 140 mm Hg, in patients at high risk for
Figure 4. Forest Plot of Primary Outcome According to
Subgroups.
The dashed vertical line represents the hazard ratio for the
overall study population. The box sizes are proportional to the
precision of
the estimates (with larger boxes indicating a greater degree of
precision). The subgroup of no previous chronic kidney disease
(CKD)
includes some participants with unknown CKD status at
baseline. Black race includes Hispanic black and black as part
of a multiracial
identification.
0.75 1.00 1.20
Standard Treatment BetterIntensive Treatment Better
Overall

Previous CKD
No
Yes
Age
<75 yr
≥75 yr
Sex
Female
Male
Race
Black
Nonblack
Previous cardiovascular disease
No
Yes
Systolic blood pressure
≤132 mm Hg
>132 to <145 mm Hg

≥145 mm Hg
Intensive Treatment Hazard Ratio (95% CI)Standard
TreatmentSubgroup
0.77 (0.57–1.03)
0.83 (0.63–1.09)
0.70 (0.51–0.95)
0.71 (0.57–0.88)
0.83 (0.62–1.09)
0.77 (0.55–1.06)
0.74 (0.61–0.90)
0.72 (0.59–0.88)
0.84 (0.62–1.14)
0.80 (0.64–1.00)
0.67 (0.51–0.86)
0.82 (0.63–1.07)
0.75 (0.64–0.89)
0.50
0.70 (0.56–0.87)
P Value for
Interaction
0.36

0.32
0.45
0.83
0.39
0.77
no. of patients with primary outcome/total no. (%)
243/4678 (5.2)
135/3348 (4.0)
108/1330 (8.1)
142/3361 (4.2)
101/1317 (7.7)
77/1684 (4.6)
166/2994 (5.5)
62/1454 (4.3)
181/3224 (5.6)
149/3738 (4.0)
94/940 (10.0)
71/1583 (4.5)

77/1489 (5.2)
95/1606 (5.9)
319/4683 (6.8)
193/3367 (5.7)
126/1316 (9.6)
175/3364 (5.2)
144/1319 (10.9)
89/1648 (5.4)
230/3035 (7.6)
85/1493 (5.7)
234/3190 (7.3)
208/3746 (5.6)
111/937 (11.8)
98/1553 (6.3)
106/1549 (6.8)
115/1581 (7.3)

reserved.
cardiovascular events but without diabetes re-
sulted in lower rates of fatal and nonfatal major
cardiovascular events and death from any cause.
However, some adverse events occurred signifi-
cantly more frequently with the lower target.
The content is solely the responsibility of the authors and
does not necessarily represent the official views of the National
Institutes of Health (NIH), the Department of Veterans Affairs,
or the U.S. Government.
Supported by contracts (HHSN268200900040C,
HHSN268200900046C, HHSN268200900047C,
Variable
Intensive Treatment
(N = 4678)
Standard Treatment
(N = 4683) Hazard Ratio P Value
no. of patients (%)
Serious adverse event* 1793 (38.3) 1736 (37.1) 1.04 0.25

Conditions of interest
Serious adverse event only
Hypotension 110 (2.4) 66 (1.4) 1.67 0.001
Syncope 107 (2.3) 80 (1.7) 1.33 0.05
Bradycardia 87 (1.9) 73 (1.6) 1.19 0.28
Electrolyte abnormality 144 (3.1) 107 (2.3) 1.35 0.02
Injurious fall† 105 (2.2) 110 (2.3) 0.95 0.71
Acute kidney injury or acute renal failure‡ 193 (4.1) 117 (2.5)
1.66 <0.001
Emergency department visit or serious adverse
event
Hypotension 158 (3.4) 93 (2.0) 1.70 <0.001
Syncope 163 (3.5) 113 (2.4) 1.44 0.003
Bradycardia 104 (2.2) 83 (1.8) 1.25 0.13
Electrolyte abnormality 177 (3.8) 129 (2.8) 1.38 0.006
Injurious fall† 334 (7.1) 332 (7.1) 1.00 0.97
Acute kidney injury or acute renal failure‡ 204 (4.4) 120 (2.6)
1.71 <0.001
Monitored clinical events
Adverse laboratory measure§

Serum sodium <130 mmol/liter 180 (3.8) 100 (2.1) 1.76 <0.001
Serum sodium >150 mmol/liter 6 (0.1) 0 0.02
Serum potassium <3.0 mmol/liter 114 (2.4) 74 (1.6) 1.50 0.006
Serum potassium >5.5 mmol/liter 176 (3.8) 171 (3.7) 1.00 0.97
Orthostatic hypotension¶
Alone 777 (16.6) 857 (18.3) 0.88 0.01
With dizziness 62 (1.3) 71 (1.5) 0.85 0.35
* A serious adverse event was defined as an event that was
fatal or life-threatening, that resulted in clinically significant or
persistent disability,
that required or prolonged a hospitalization, or that was judged
by the investigator to represent a clinically significant hazard or
harm to the
participant that might require medical or surgical intervention
to prevent one of the other events listed above.
† An injurious fall was defined as a fall that resulted in
evaluation in an emergency department or that resulted in
hospitalization.
‡ Acute kidney injury or acute renal failure were coded if the
diagnosis was listed in the hospital discharge summary and was
believed by the
safety officer to be one of the top three reasons for admission or
continued hospitalization. A few cases of acute kidney injury
were noted in
an emergency department if the participant presented for one of
the other conditions of interest.

§ Adverse laboratory measures were detected on routine or
unscheduled tests; routine laboratory tests were performed at 1
month, then quar-
terly during the first year, then every 6 months.
¶ Orthostatic hypertension was defined as a drop in systolic
blood pressure of at least 20 mm Hg or in diastolic blood
pressure of at least
10 mm Hg at 1 minute after the participant stood up, as
compared with the value obtained when the participant was
seated. Standing blood
pressures were measured at screening, baseline, 1 month, 6
months, 12 months, and yearly thereafter. Participants were
asked if they felt
dizzy at the time the orthostatic measure was taken.
Table 3. Serious Adverse Events, Conditions of Interest, and
Monitored Clinical Events.
reserved.
HHSN268200900048C, and HHSN268200900049C) and an
inter-
agency agreement (A-HL-13-002-001) from the NIH, including

the National Heart, Lung, and Blood Institute (NHLBI), the Na-
tional Institute of Diabetes and Digestive and Kidney Diseases,
the National Institute on Aging, and the National Institute of
Neurological Disorders and Stroke. Several study sites were
supported by Clinical and Translational Science Awards fund-
ed by the National Center for Advancing Translational Sciences
of the NIH (Case Western Reserve University: UL1TR000439;
Ohio State University: UL1RR025755; University of Pennsyl-
vania: UL1RR024134 and UL1TR000003; Boston University:
UL1RR025771; Stanford University: UL1TR000093; Tufts
Univer-
sity: UL1RR025752, UL1TR000073, and UL1TR001064;
University
of Illinois: UL1TR000050; University of Pittsburgh:
UL1TR000005;
University of Texas Southwestern: 9U54TR000017-06;
University
of Utah: UL1TR000105-05; Vanderbilt University:
UL1TR000445;
George Washington University: UL1TR000075; University of
Cali-
fornia, Davis: UL1TR000002; University of Florida:
UL1TR000064;
University of Michigan: UL1TR000433; and Tulane University:
P30GM103337 COBRE Award NIGMS). The trial was also sup-
ported in part with respect to resources and the use of facilities
by the Department of Veterans Affairs.
Disclosure forms provided by the authors are available with
the full text of this article at NEJM.org.
We thank the study participants, without whom this trial
would not have been possible.
Appendix

The affiliations of the members of the writing group are as
follows: the Division of Nephrology and Hypertension,
University Hospitals
Case Medical Center, Case Western Reserve University (J.T.W.,
M.R.), and Division of Nephrology and Hypertension, Louis
Stokes
Cleveland Veterans Affairs (VA) Medical Center (M.R.),
Cleveland; Sticht Center on Aging (J.D.W., K.M.S.), Section on
Nephrology
(M.V.R.), and Department of Biostatistical Sciences (D.M.R.,
W.T.A.), Wake Forest School of Medicine, Winston-Salem, NC;
Depart-
ment of Epidemiology, Tulane University School of Public
Health and Tropical Medicine, New Orleans (P.K.W.); Clinical
Applications
and Prevention Branch, National Heart, Lung, and Blood
Institute (J.K.S., L.J.F., J.A.C.), and Division of Kidney,
Urologic, and Hema-
tologic Diseases, National Institute of Diabetes and Digestive
and Kidney Diseases (P.L.K.), Bethesda, MD; Divisions of
Cardiovascular
Diseases (S.O.) and Preventive Medicine (C.E.L.), University of
Alabama at Birmingham, Birmingham; Department of
Preventive Medi-
cine, University of Tennessee Health Science Center (K.C.J.),
and the Preventive Medicine Section, VA Medical Center
(W.C.C.), Mem-
phis; School of Public Health, University of Colorado, Aurora
(D.C.G.); and Division of Nephrology and Hypertension,
University of
Utah, Salt Lake City (A.K.C.).
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fects of ACE inhibitors, calcium antago-
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16. Psaty BM, Smith NL, Siscovick DS, et
al. Health outcomes associated with anti-
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20. Ogihara T, Saruta T, Rakugi H, et al.
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reserved.
Cancer incidence and mortality worldwide: Sources, methods
and major patterns in GLOBOCAN 2012
Jacques Ferlay1, Isabelle Soerjomataram1, Rajesh Dikshit2,
Sultan Eser3, Colin Mathers4, Marise Rebelo5,
Donald Maxwell Parkin6, David Forman1 and Freddie Bray1
1 Section of Cancer Surveillance, International Agency for
Research on Cancer, Lyon, France

2 Tata Memorial Hospital, Mumbai, India
3 Izmir Cancer Registry, Izmir Hub, Izmir & Hacettepe
University Institute of Public Health, Ankara, Turkey
4 Department of Measurement and Health Information Systems,
WHO, Geneva, Switzerland
5 Department of Surveillance and Cancer Information, Brazilian
National Cancer Institute, Ministry of Health, Rio de Janeiro,
Brazil
6 Clinical Trial Service Unit & Epidemiological Studies Unit,
University of Oxford, Oxford, United Kingdom
Estimates of the worldwide incidence and mortality from 27
major cancers and for all cancers combined for 2012 are now
available in the GLOBOCAN series of the International Agency
for Research on Cancer. We review the sources and methods
used in compiling the national cancer incidence and mortality
estimates, and briefly describe the key results by cancer site
and in 20 large “areas” of the world. Overall, there were 14.1
million new cases and 8.2 million deaths in 2012. The most
commonly diagnosed cancers were lung (1.82 million), breast
(1.67 million), and colorectal (1.36 million); the most common
causes of cancer death were lung cancer (1.6 million deaths),
liver cancer (745,000 deaths), and stomach cancer (723,000
deaths).
According to WHO estimates for 2011, cancer now causes
more deaths than all coronary heart disease or all stroke.1 The
continuing global demographic and epidemiologic transitions
signal an ever-increasing cancer burden over the next decades,
particularly in low and middle income countries (LMIC), with

over 20 million new cancer cases expected annually as early as
2025.2 The GLOBOCAN estimates for 20123 aim to provide
the evidence and impetus for developing resource-contingent
strategies to reduce the cancer burden worldwide.
We review here the fifth version of GLOBOCAN, the
sources and methods used in compiling cancer incidence and
mortality estimates for 2012 in 184 countries worldwide, and
briefly describe the key results by cancer site. The basic units
for estimation are countries, although we present the results
globally, by level of development and for aggregated regions,
as defined by the United Nations.4 Such estimates have been
prepared for 27 major cancers and for all cancers combined
and by sex. While the methods of estimation have been
refined over time, they still rely upon the best available data
on cancer incidence and mortality at the national level in
assembling regional and global profiles. Facilities for the tab-
ulation and graphical visualisation of the full dataset of 184
countries and 30 world regions by sex can be accessed via
the GLOBOCAN homepage (http://globocan.iarc.fr).
To document the methods used in compiling the esti-
mates and guide users as to their validity, we introduce an
alphanumeric scoring system that provides information on
the availability and quality of the incidence and mortality
sources at the country level.
Data
Incidence data derive from population-based cancer registries
(PBCR). Although PBCR may cover national populations,
more often they cover smaller, subnational areas, and, partic-
ularly in countries undergoing development, only selected
urban areas. In 2006, about 21% of the world population was
covered by PBCR, with sparse registration in Asia (8% of the

total population) and in Africa (11%).5 In terms of what is
considered data of high quality (for example, those included
in the latest volume (X) of the IARC Cancer Incidence in
Five Continents (CI5) series6), these percentages are even
lower: only 14% of the world population is covered by PBCR
that match the CI5 inclusion criteria, with the figures 5% and
2% in Asia and Africa, respectively. While cancer registries in
lower resource settings may find it difficult to match the
strict criteria of data quality set for inclusion in CI5, the
information generated by such PBCR remains of critical
importance to cancer control as a unique and relatively
unbiased source of information on the profile of cancer.
Population-based cancer registries can produce survival
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Key words: Incidence, mortality, cancer, global estimates,
GLOBOCAN
Additional Supporting Information may be found in the online
version of this article.
DOI: 10.1002/ijc.29210
History: Received 11 June 2014; Accepted 12 Aug 2014; Online
13
Sep 2014

Correspondence to: Jacques Ferlay, Section of Cancer
Information
International Agency for Research on Cancer, 150 Cours Albert
Thomas, 69372 Lyon Cedex 08, France, Tel.: 133-(0)4-72-73-
84-90,
Fax: +33-(0)4-72-73-86-96, E-mail: [email protected]
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Int. J. Cancer: 136, E359–E386 (2015) VC 2014 UICC
International Journal of Cancer
IJC
http://globocan.iarc.fr
statistics by following up the vital status of cancer patients. In
the absence of information on national mortality, it can be esti-
mated using incidence and survival probabilities7 and vice
versa.
Mortality statistics are collected and made available by the
WHO.8 Their great advantage is national coverage and long-
term availability in higher income settings, although not all
datasets are of the same quality. For some countries, coverage

of the population is incomplete, so that the mortality rates
produced are implausibly low, and in others, the quality of
cause of death information is poor. By 2005, around one-
third of the world population was covered by mortality statis-
tics.9 While almost all the European and American countries
have comprehensive death registration systems, most African
and Asian countries (including the populous countries of
Nigeria, India and Indonesia) do not. The mortality data
used to estimate the burden of cancer in China was obtained
from a sample survey based on the “disease surveillance
points” (DSP) project for the period 2004 to 2010 covering
around 6% of the total Chinese population.10 These statistics
are considered nationally representative given the samples
include both urban and rural areas. As the figures were avail-
able for a limited number of cancers, they were supplemented
by cancer registry mortality files for certain sites.
National population estimates for 2012 were extracted
from the United Nations website.4 The geographical defini-
tion of the regions follows the rules as defined by the UN,
except for Cyprus, which is included in Southern Europe
instead of Western Asia (Fig. 1).
An alphanumeric scoring system has been introduced
with the release of GLOBOCAN 2012 that independently
classifies the source availability and estimation methods for
incidence and mortality by country. These scores are pro-
vided together with the results online, and the classification
of sources and methods is described below.
Sources
Incidence data. Depending on the availability and quality of
the information, the countries have been classified as follows
(Fig. 2a):

A. High quality* national data or high quality regional (cov-
erage greater than 50% of the population): 37 countries
B. High quality* regional data (coverage between 10% and
50%): 11 countries.
C. High quality* regional data (coverage lower than 10%): 19
countries.
D. National data (PBCR): 24 countries.
E. Regional data (PBCR): 18 countries.
F. Frequency data (hospital-based or pathological –based
series): 13 countries.
G. No data: 62 countries.
*Data included in Cancer Incidence in Five Continents
(CI5) volume IX11 and/or X.6
Mortality data. Similar to incidence data, the following
schema has been defined (Fig. 2b):
1. High quality complete vital registration**: 23 countries.
2. Medium quality complete vital registration**: 48 countries.
3. Low quality complete vital registration**: 24 countries.
4. Incomplete or sample vital registration: 2 countries.
5. Other sources (cancer registries, verbal autopsy surveys
etc.): 7 countries.
6. No data: 80 countries.

**The criteria defined in points 1–3 are taken from Math-
ers et al.9
Methods of estimation
Cancer incidence and mortality rates for 2012 by sex and for
10 age groups (0–14, 15–39, 40–44, 45–49,. . ., 75 and over)
are estimated for the 184 countries or territories of the world
having a total population greater than 200,000.4 Results are
presented for the following cancer sites or cancer types as
defined by the 10th edition of the International Classification
of Diseases (ICD-10):12 lip, oral cavity (ICD-10 C00-08),
nasopharynx (C11), other pharynx (C09-10, C12-14), oeso-
phagus (C15), stomach (C16), colon and rectum (including
anus C18-21), liver (C22), gallbladder (C23-24), pancreas
(C25), larynx (C32), lung (including trachea, C33-34), mela-
noma of skin (C43), Kaposi sarcoma (C46), female breast
(C50), cervix uteri (C53), corpus uteri (C54), ovary (C56),
prostate (C61), testis (C62), kidney (including renal pelvis
and ureter, C64-66), bladder (C67), brain and central nervous
system (C70-72), thyroid (C73), Hodgkin lymphoma (C81),
non-Hodgkin lymphoma (C82-85, C96), multiple myeloma
(C88 1 C90), leukaemia (C91-95) and all cancers combined,
excluding non-melanoma skin cancer (C00-97, except C44).
This last category was calculated by summing the estimated
counts for each individual cancer site, and the residual
What’s new?
In this report, we present the most recent cancer incidence and
mortality statistics (for 2012) for the major cancers in 20
regions of the world. Details of the data sources and methods
used in GLOBOCAN to compile the estimates at the national

level are provided, and we introduce a novel alphanumeric
scoring system to give a broad indication of the robustness of
the
estimation within each country. A global snapshot of the
patterns by cancer site brings focus to the need for regional
prioriti-
sation of cancer control efforts, as well as the ongoing efforts to
improve the limited surveillance systems in many low and
middle income countries.
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E360 Globocan 2012
category “other and unspecified cancers”. Further details of
the criteria for inclusion are provided in Appendix A.
The methods of incidence and mortality estimation
described below are undertaken at the national level and
hence their validity depends upon the representativeness and
quality of the source information from the country itself. The
methods are largely those developed previously,13 although
one improvement in the 2012 estimation of both incidence

and mortality is the utilisation of the Human Development
Index (HDI)14 to predict survival in countries lacking the
requisite data, as described in detail in Appendix B. The
methods are summarized below, ranked in descending order
of the probable accuracy of the derived estimates.
Estimates of cancer incidence by country.
1. When incidence data were available historically with suffi-
cient numbers of cases, recorded incidence rates were pro-
jected to 2012 using models and the 2012 national
population applied to the fitted rates (38 countries)
2. When recent incidence data were available from a national
registry, the 2012 national population was applied to the
most recently recorded incidence rates (20 countries)
3. When registries were regional and where national mortality
data were available, national incidence was estimated from
national mortality using statistical models, with the fitted
mortality to incidence (M:I) ratios derived from recorded
data from one or more cancer registries within the country
(13 countries)
4. For Europe, when registries were regional rather than
national, and where national mortality data were available,
method (3) was used but with the fitted M:I ratios derived
from recorded data in cancer registries in neighbouring
countries (nine European countries)15
5. When national or regional registries were not available, but
where national mortality data were available, national inci-
dence was estimated from national mortality estimates and
modelled survival (32 countries, see Appendix B for
method)

6. When national or regional registries were available, but
where national mortality data was not available, national
incidence was estimated as the weighted average of the
recorded incidence rates obtained from multiple cancer
registries within the country (16 countries)
7. When incidence data were available from a single registry,
but
national mortality data were not available, national incidence
was estimated from the recorded incidence rates obtained from
one cancer registry within the country (11 countries)
8. When neither national or regional registries, nor national
mortality data were available, and the within-country
source information was considered to lack the necessary
level of accuracy, a set of age- and sex-specific national
incidence rates for all cancers combined were obtained
averaging overall rates from selected neighbouring coun-
tries. These rates were then partitioned to obtain the
national incidence for specific sites using available cancer-
specific relative frequency data (by age and sex, 12 countries).
9. When neither national or regional registries, nor national
mortality data were available, and the within-country
source information was either unavailable or useable, aver-
age incidence rates from selected neighbouring countries in
the same region were used to derive national incidence
within the country (33 countries).
Figure 1. Map showing the 20 world regions.
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Ferlay et al. E361
Kaposi sarcoma (KS) incidence estimation in Sub-Saharan
Africa. Estimates of the incidence of KS were derived using
one of the methods described above, with the exception of
Sub-Saharan Africa, where in certain regions the rates are
correlated with the HIV epidemic and the prevalence of
HIV/AIDS:
� We first estimated the number of endemic (pre-AIDS) KS
cases using the percentage frequency of the disease, by sex
and age, based on data from Uganda, Kampala (1961–
1980) and Nigeria, Ibadan (1971–1990). These percentages
were applied to countries in Eastern and Western Africa
respectively. For countries in Middle and Southern Africa,
we applied a simple average of these frequencies.
� We calculated the number of epidemic (AIDS-related) KS
cases, both sexes, for the year 2011, using estimates of
AIDS deaths by country in 2011 (source UNAIDS, http://
www.unaids.org/), and an estimate of the ratio of deaths
from AIDS to incident cases of KS. This ratio was based
on observed KS rates in several countries (from the senti-
nel registries listed below, minus the endemic KS), and was
Figure 2. (a) Map showing the availability of incidence data. (b)

Map showing the availability of mortality data.
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E362 Globocan 2012
http://www.unaids.org/
http://www.unaids.org/
specific by region (varying from 0.7% in Western Africa to
6% in Eastern Africa). This total number of AIDS-related
KS was partitioned by sex and age using sex- and age-
specific proportions in sentinel registries of Malawi, Blan-
tyre, Uganda, Kampala and Zimbabwe, Harare (Eastern
Africa), Congo, Brazzaville (Middle Africa), Botswana and
Namibia (Southern Africa), Mali, Bamako and Niger, Nia-
mey (Western Africa).
Estimates of cancer mortality by country. National statistics
from vital registration sources are known to be of variable
quality and some corrections were made before they were
used for estimation purposes:
� Where necessary, the overall number of deaths was cor-
rected for under-reporting or incompleteness using the
percentages provided by the WHO.8

� The category “ill-defined cause of deaths” (ICD-9 codes
780-799 and ICD-10 codes R00-R99) was partitioned, by
sex and age into “cancer deaths” and “other” specific
causes of death. The corrected “cancer deaths” category
was then partitioned into cancer-specific categories using
proportions from the uncorrected data.
� Given the large variations in the accuracy of death certifi-
cates related to cancer of the uterus, with many deaths
recorded as “uterus cancer, not otherwise specified” (ICD-
10 C55), these proportions were relocated to specified sites.
By default, the number of cancer deaths coded as “uterus
unspecified” was reallocated to either cervix (C53) or cor-
pus (C54) uterine cancer according to age-specific propor-
tions in the same population.16 For the countries for which
country-specific incidence and survival data were available,
mortality for cervix uteri (C53) and corpus uteri (C54)
cancers was estimated from incidence and 5-year relative
survival probabilities.
Depending on the coverage, completeness and degree of
detail of the mortality data available, six methods were uti-
lised, ranked in descending order of the probable accuracy of
the derived estimates:
1. When mortality data were available historically from
national sources and a sufficient number of recorded can-
cer deaths were available, mortality rates were projected to
2012 using models and applied to 2012 national population
(69 countries)
2. When recent mortality data were available from national
sources, the most recent mortality rates were applied to
2012 national population (26 countries)
3. When recent mortality data were available from regional

sources, national mortality was estimated as the weighted
average of the local mortality rates (one country)
4. When recent mortality data were not available from
national sources but country-specific survival estimates
were available, national mortality was estimated from
national incidence estimates and country-specific survival
(two countries)
national sources, national mortality was estimated from
national incidence estimates using modelled survival as
described in Appendix B (83 countries)
national sources, and survival estimates could not be
derived using the previous method, the country-specific
rates represent simply those of neighbouring countries in
the same region (three countries).
Random fluctuations in the predicted age-specific inci-
dence and mortality rates were smoothed using a loess func-
tion, a locally weighted regression, by country, sex and
cancer site. Estimates for the 20 world regions (Fig. 1) were
obtained by the population-weighted average of the incidence
and mortality rates of the component countries. These rates
were applied to the corresponding population for the region
for 2012 to obtain the estimated numbers of new cancer
cases and deaths in 2012. The rates were age-standardized
(ASRs per 100,000 person-years) using the direct method and
the World standard population as proposed by Segi17 and
modified by Doll et al.18 The cumulative risk of developing
or dying from cancer before the age of 75 in the absence of
competing causes of death was also calculated using the age-
specific rates and expressed as a percentage. Both of these

indicators allow comparisons between populations that are
not influenced by differences in their age structures.
The list of the 184 countries or territories together with
their corresponding indicators of data availability and meth-
ods of estimation is given in Appendix C. The full descrip-
tion of GLOBOCAN 2012 in terms of the data sources and
methods used for each country and further details of the esti-
mations are available online (http://globocan.iarc.fr). Similar
information for Europe has also been described for 40 coun-
tries15 and the results are available online at the European
Cancer Observatory (ECO) (http://eco.iarc.fr). The overall
and cancer-specific results are described and presented here
by world region, and for historical reference, according to the
dichotomy of ‘developed’ and ‘developing’ regions: the former
comprising Northern America, Europe, Australia/New Zea-
land and Japan, the latter, the remaining regions and
countries.
Results
Global burden of cancer
We estimated that 14.1 million new cancer cases and 8.2 mil-
lion cancer deaths occurred in 2012 worldwide. Tables 1
and 2 show the estimated number of cases and deaths (in
thousands) for all cancers combined (excluding non-
melanoma skin cancers) and for 27 specific cancers in men,
women and both sexes, together with the corresponding
ASRs and the cumulative risk. Lung cancer remains the most
common cancer in the world, both in term of new cases (1.8
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Ferlay et al. E363
http://globocan.iarc.fr
http://eco.iarc.fr
million cases, 12.9% of total) and deaths (1.6 million deaths,
19.4%) because of the high case fatality. Breast cancer is the
second most common cancer overall (1.7 million cases,
11.9%) but ranks 5th as cause of death (522,000, 6.4%)
because of the relatively favourable prognosis; these are fol-
lowed, in terms of incidence, by colorectal cancer (1.4 million
cases, 694,000 deaths), prostate cancer (1.1 million cases,
307,000 deaths), stomach cancer (951,000 cases, 723,000
deaths) and liver cancer (782,000 cases and 745,000 deaths).
These six cancers represent 55% of the global incidence bur-
den in 2012; in more developed regions, just four cancers—
female breast, prostate, lung and colorectum (Fig. 3a)—com-
prise half of the total incidence, whereas lung, female breast,
stomach and colorectal cancers combined with liver and cer-
vical cancers explain over half the incidence burden (54%) in
less developed regions (Fig. 3b).
The ranking of the 15 most common cancers are shown
for men (Fig. 4a) and women (Fig. 4b), as numbers of new
cases and deaths in more and less developed regions of the
world. Although lung cancer is the most common cancer
worldwide among men, it ranks second in more developed
regions (490,000 cases) after prostate cancer (759,000 cases).
Cancers of the lung (751,000 cases, 682,000 deaths), liver

(462,000 cases, 441,000 deaths) and stomach (456,000 cases,
362,000 deaths) predominate among males in less developed
regions, representing 40% of the new cancer cases and 48%
of the total cancer deaths. In women, breast cancer is the
most common cancer diagnosed in more and less developed
Table 1. Estimated new cancer cases (thousands), ASRs (per
100,000) and cumulative risks to age 75 (percent) by sex and
cancer site world-
wide, 2012
Both sexes Male Female
Cancer site Cases (%)
ASR
(World)
Cum. risk
(0–74) Cases (%)
ASR
(World)
Cum. risk
(0–74) Cases (%)
ASR
(World)
Cum.risk
(0–74)
Lip, oral cavity 300 2.1 4.0 0.5 199 2.7 5.5 0.6 101 1.5 2.5 0.3
Nasopharynx 87 0.6 1.2 0.1 61 0.8 1.7 0.2 26 0.4 0.7 0.1

Other pharynx 142 1.0 1.9 0.2 115 1.5 3.2 0.4 27 0.4 0.7 0.1
Oesophagus 456 3.2 5.9 0.7 323 4.3 9.0 1.1 133 2.0 3.1 0.4
Stomach 951 6.8 12.1 1.4 631 8.5 17.4 2.0 320 4.8 7.5 0.8
Colorectum 1360 9.7 17.2 2.0 746 10.0 20.6 2.4 614 9.2 14.3
1.6
Liver 782 5.6 10.1 1.1 554 7.5 15.3 1.7 228 3.4 5.4 0.6
Gallbladder 178 1.3 2.2 0.2 77 1.0 2.1 0.2 101 1.5 2.3 0.3
Pancreas 338 2.4 4.2 0.5 178 2.4 4.9 0.6 160 2.4 3.6 0.4
Larynx 157 1.1 2.1 0.3 138 1.9 3.9 0.5 19 0.3 0.5 0.1
Lung 1825 12.9 23.1 2.7 1242 16.7 34.2 3.9 583 8.7 13.6 1.6
Melanoma of skin 232 1.6 3.0 0.3 121 1.6 3.3 0.4 111 1.7 2.8
0.3
Kaposi sarcoma 44 0.3 0.6 0.1 29 0.4 0.8 0.1 15 0.2 0.4 0.0
Breast 1677 11.9 43.3 4.6 1677 25.2 43.3 4.6
Cervix uteri 528 3.7 14.0 1.4 528 7.9 14.0 1.4
Corpus uteri 320 2.3 8.3 1.0 320 4.8 8.3 1.0
Ovary 239 1.7 6.1 0.7 239 3.6 6.1 0.7
Prostate 1112 7.9 31.1 3.8 1112 15.0 31.1 3.8
Testis 55 0.4 1.5 0.1 55 0.7 1.5 0.1

Kidney 338 2.4 4.4 0.5 214 2.9 6.0 0.7 124 1.9 3.1 0.3
Bladder 429 3.1 5.3 0.6 330 4.4 9.0 1.0 99 1.5 2.2 0.2
Brain, nervous system 257 1.8 3.4 0.3 140 1.9 3.9 0.4 117 1.8
3.0 0.3
Thyroid 298 2.1 4.0 0.4 68 0.9 1.9 0.2 230 3.5 6.1 0.6
Hodgkin lymphoma 66 0.5 0.9 0.1 39 0.5 1.1 0.1 27 0.4 0.7 0.1
Non-Hodgkin lymphoma 386 2.7 5.1 0.5 218 2.9 6.0 0.6 168 2.5
4.1 0.4
Multiple myeloma 114 0.8 1.5 0.2 62 0.8 1.7 0.2 52 0.8 1.2 0.2
Leukaemia 352 2.5 4.7 0.4 201 2.7 5.6 0.5 151 2.3 3.9 0.4
All cancers excl.
non-melanoma
skin cancer
14090 100.0 182.3 18.5 7427 100.0 205.4 21.0 6663 100.0 165.3
16.4
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regions, with more cases occurring in less developed (883,000
cases) than more developed regions (794,000). Cervical can-
cer, the second most common cancer in less developed
regions (445,000 cases), ranks only 11th in more developed
regions (83,000 cases). Lung cancer is now the leading cause
of cancer death among women in more developed regions
(210,000 deaths) followed by breast cancer (198,000 deaths)
which ranks as the most frequent in women in less developed
regions (324,000 deaths) followed by cancers of the lung
(281,000 deaths) and cervix (230,000 deaths).
Figure 5 shows the distribution of the global cancer cases
and deaths (all types of cancer, both sexes combined) by world
region. Most cases (4.1 million, 29.4% of the total) and deaths
(2.75 million, 33.6%) occurred in Eastern Asia with its vast
population (1.6 billion, 22% of the global population in 2012).
Northern America ranks second in terms of number of new
cases (1.78 million, 12.7%) but third (691,000, 6.4%) in terms
of cancer deaths after South-Central Asia (1.0 million deaths,
12.5%). Almost a quarter of the new cases (3.44 million) and
one fifth of the deaths (1.75 million) occurred in the four Euro-
pean regions, despite containing 10% of the global population.
Tables 3 and 4 show the estimated incidence and mortality
ASRs (world standard), respectively, by sex and cancer site for
the
20 regions of the world, and for more developed and less devel-
oped regions. Tables 5 and 6 portray the estimates of the
numbers
of cancer cases and deaths, and Tables 7 and 8 the estimates of
cumulative risk (ages 0–74, percent) for the same categories. A
brief description of the patterns for each cancer site follows.

Table 2. Estimated cancer deaths (thousands), ASRs (per
100,000) and cumulative risks to age 75 (percent) by sex and
cancer site world-
wide, 2012
Both sexes Male Female
Cancer site Deaths (%)
ASR
(World)
Cum.risk
(0–74) Deaths (%)
ASR
(World)
Cum.risk
(0–74) Deaths (%)
ASR
(World)
Cum.risk
(0–74)
Lip, oral cavity 145 1.8 1.9 0.2 98 2.1 2.7 0.3 47 1.3 1.2 0.1
Nasopharynx 51 0.6 0.7 0.1 36 0.8 1.0 0.1 15 0.4 0.4 0.0
Other pharynx 97 1.2 1.3 0.2 78 1.7 2.2 0.3 19 0.5 0.5 0.1
Oesophagus 400 4.9 5.0 0.6 281 6.0 7.7 0.9 119 3.4 2.7 0.3
Stomach 723 8.8 8.9 1.0 469 10.1 12.8 1.4 254 7.2 5.7 0.6

Colorectum 694 8.5 8.4 0.9 374 8.0 10.0 1.0 320 9.0 6.9 0.7
Liver 745 9.1 9.5 1.0 521 11.2 14.3 1.6 224 6.3 5.1 0.6
Gallbladder 142 1.7 1.7 0.2 60 1.3 1.6 0.2 82 2.3 1.8 0.2
Pancreas 331 4.0 4.1 0.4 174 3.7 4.8 0.5 157 4.4 3.4 0.4
Larynx 83 1.0 1.1 0.1 73 1.6 2.0 0.2 10 0.3 0.2 0.0
Lung 1590 19.4 19.7 2.2 1099 23.6 30.0 3.3 491 13.8 11.1 1.2
Melanoma of skin 55 0.7 0.7 0.1 31 0.7 0.9 0.1 24 0.7 0.6 0.1
Kaposi sarcoma 27 0.3 0.4 0.0 17 0.4 0.5 0.1 10 0.3 0.3 0.0
Breast 522 6.4 12.9 1.4 522 14.7 12.9 1.4
Cervix uteri 266 3.2 6.8 0.8 266 7.5 6.8 0.8
Corpus uteri 76 0.9 1.8 0.2 76 2.1 1.8 0.2
Ovary 152 1.9 3.8 0.4 152 4.3 3.8 0.4
Prostate 307 3.7 7.8 0.6 307 6.6 7.8 0.6
Testis 10 0.1 0.3 0.0 10 0.2 0.3 0.0
Kidney 144 1.7 1.8 0.2 91 2.0 2.5 0.3 53 1.5 1.2 0.1
Bladder 165 2.0 1.9 0.2 123 2.6 3.2 0.3 42 1.2 0.9 0.1
Brain, nervous system 189 2.3 2.5 0.3 106 2.3 3.0 0.3 83 2.3 2.1
0.2

Thyroid 40 0.5 0.5 0.1 13 0.3 0.4 0.0 27 0.8 0.6 0.1
Hodgkin lymphoma 25 0.3 0.3 0.0 15 0.3 0.4 0.0 10 0.3 0.3 0.0
Non-Hodgkin lymphoma 200 2.4 2.5 0.3 115 2.5 3.2 0.3 84 2.4
2.0 0.2
Multiple myeloma 80 1.0 1.0 0.1 43 0.9 1.2 0.1 37 1.0 0.8 0.1
Leukaemia 265 3.2 3.4 0.3 151 3.2 4.2 0.4 114 3.2 2.8 0.3
All cancers excl.
non-melanoma
skin cancer
8201 100.0 102.4 10.5 4653 100.0 126.3 12.7 3548 100.0 82.9
8.4
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Ferlay et al. E365
All sites combined (excluding non-melanoma skin cancer).
Overall incidence rates are almost 25% higher in men (ASR
205 per 100,000) than in women (165 per 100,000), with

male incidence rates varying almost fivefold across the differ-
ent regions of the world, from 79 per 100,000 in Western
Africa to 365 per 100,000 in Australia/New Zealand, with
high rates of prostate cancer making a significant contribu-
tion to the latter (Table 3). There is less variation in female
incidence, rates ranging from 103 per 100,000 in South-
Central Asia to 295 per 100,000 in Northern America (Table
3). In terms of mortality, the cumulative risk of dying from
cancer is 20% higher in more developed than less developed
regions in men, and 10% higher in women (Table 4). The
risk of dying from cancer among men is highest in Central
and Eastern Europe (19%) and lowest in Western Africa
(7%) (Table 8). In contrast, the highest risk of cancer death
in women is in Melanesia and Eastern Africa (both 12%),
and the lowest in Eastern Asia (8%) and South-Central Asia
(7%).
Lung cancer. Lung cancer emerged as the most common
cancer worldwide several decades ago: with 660,000 new
cases estimated in 1980, it had risen to equal stomach can-
cer.19 Of the estimated 1.8 million new cases in 2012 (12.9%
of the total) (Table 1), 58% occurred in less developed
regions. It is the most common cancer in men worldwide
Figure 3. Estimated global numbers of new cases (thousands)
with proportions for (a) more developed and (b) less developed
regions,
both sexes combined, 2012. The area of the pie is proportional
to the number of new cases.
E
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E366 Globocan 2012
(1.2 million, 16.7% of the total), with the highest rates in
Central and Eastern Europe (53.5 per 100,000) and Eastern
Asia (50.4 per 100,000). Incidence rates are very low in Mid-
dle and Western Africa (2.0 and 1.7 per 100,000, respectively)
(Table 3). In women, the incidence rates are generally lower
and the geographical pattern somewhat different, reflecting in
part variations in the uptake and consumption of tobacco.
The highest estimated rates are in Northern America (33.8)
and Northern Europe (23.7) compared with low rates in
Western and Middle Africa (1.1 and 0.8 respectively) (Table
3). The relatively high rate in women in Eastern Asia (19.2)
has been of particular interest, since tobacco smoking is
Figure 4. (a) Estimated numbers (thousands) of new cancer
cases (incidence) and deaths (mortality) in men in more
developed and less developed
regions of the world in 2012. (b) Estimated numbers (thousands)
of new cancer cases (incidence) and deaths (mortality) in
women in more devel-
oped and less developed regions of the world in 2012.
E
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Ferlay et al. E367
generally very rare in these populations. The disease is the
most common cause of death from cancer worldwide,
responsible for nearly one cancer death in five (1.59 million
deaths, 19.4% of the total). Because of the high fatality associ-
ated with the disease, the geographical patterns in mortality
closely follow those of incidence.
Breast cancer. Breast cancer is the second most common
cancer in the world and, by far the most frequent cancer
among women with an estimated 1.67 million new cancer
cases diagnosed in 2012 (25% of all cancers) (Table 1). A
slight majority of cases occur in women in less developed
regions (Table 5). Incidence rates vary nearly fourfold across
the world regions, with rates ranging from 27 per 100,000 in
Middle Africa and Eastern Asia to 96 in Western Europe
(Table 3).
Breast cancer ranks as the fifth cause of death from cancer
overall (522,000 deaths) and while it is the most frequent
cause of cancer death in women in less developed regions
(324,000 deaths, 14.3% of total), it is now the second cause
of cancer death in more developed regions (198,000 deaths,
15.4%) after lung cancer (Table 6). The range in mortality
rates between world regions is less than that for incidence
because of the more favourable survival from breast cancer in
(high-incidence) developed regions.

Colorectal cancer. Colorectal cancer is the third most com-
mon cancer in men (746,000 cases, 10.0% of the total) and
the second in women (614,000 cases, 9.2% of the total)
worldwide (Table 1). Almost 55% of the cases occur in more
developed regions (Table 5). There is a 10-fold variation in
incidence across the world and the patterns are very similar
in men and women, with the highest rates in Australia/New
Zealand (ASR 44.8 and 32.2 per 100,000 in men and women,
respectively), and lowest in Western Africa (4.5 and 3.8 per
100,000) (Table 3).
Mortality is considerably lower (694,000 deaths in both
sexes, 8.5% of the total) with more deaths (52%) in less
developed regions of the world, reflecting poorer prognosis in
these regions (Table 6). There is less variability in mortality
rates worldwide (sixfold in men, fourfold in women), with
rates highest in Central and Eastern Europe (20.3 per
100,000 for men, 11.7 per 100,000 for women), and lowest in
Western Africa (3.5 and 3.0, respectively) (Table 4).
Prostate cancer. Prostate cancer is the fourth most common
cancer in both sexes combined and the second most common
cancer in men. An estimated 1.1 million cases were diag-
nosed worldwide with prostate cancer in 2012, accounting
for 15% of the cancers diagnosed in men, with almost 70%
of them (759,000) occurring in more developed regions
(Table 5). Prostate cancer incidence varies more than 25-fold
worldwide; the rates are highest in Australia/New Zealand
and Northern America (ASR 111.6 and 97.2 per 100,000,
respectively), and in Western and Northern Europe (ASR
94.9 and 85 per 100,000), largely because the widespread
practice of prostate specific antigen (PSA) testing and subse-
quent biopsy in those regions (Table 3). Incidence rates are
also relatively high in certain less developed regions such as
the Caribbean (79.8), Southern Africa (61.7) and South

America (60.1), but remain low in Asian populations, with
Figure 5. Estimated global numbers of new cases and deaths
with proportions by world regions, both sexes combined, 2012.
The area of the pie is
proportional to the number of new cases or deaths.
E
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E368 Globocan 2012
Ta
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Exploring the Importance of Language Sensitivity in Journalism

Exploring the Importance of Language Sensitivity in Journalism

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