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Beyond the clinic, this analysis touches on the role of supportive
and symptomatic care in persons who have cancer and the use of
cost-effectiveness criteria in determining coverage of supportive care
agents. Given the median age of diagnosis noted by Lathia et al. (1),
about 50% of persons with lymphoma will qualify for Medicare at
diagnosis; thus how insurers make use of cost-effectiveness information has important implications for national health policy (12).
Furthermore, incremental costs per QALY (or other measure of
time) are challenging to estimate and use in clinical practice and policy making, particularly estimates of survival benefits and longer term
benefits as well as inclusion of nonclinical outcomes such as hospital avoidance. Additionally, situations like the one modeled here, in
which the time horizon is very short, complicate the use of outcomes
like the QALY. Despite this understanding, the optimal choice of
an outcome to model in persons with cancer remains incompletely
understood (13). Last, the importance of patient-reported outcomes
is rising. In the current case, the potential to avoid hospitalizations is
likely to be important from the patient’s perspective. Although this
trend does not change the conclusions Lathia et al.pe make regarding prophylactic use of filgastrim and pegfilgrastim, patient satisfaction, ability to function, and time preferences are likely to play an
increasing role in future coverage and clinical use decisions.
References
1. Lathia N, Isogai PK, De Angelis C, et al. Cost-effectiveness of filgrastim
and pegfilgrastim as primary prophylaxis against febrile neutropenia in
lymphoma patients. J Natl Cancer Inst. 2013;105(15):1078–1085.
2. Doorduijn JK, van der Holt B, van Imhoff GW, et al. CHOP compared with
CHOP plus granulocyte colony-stimulating factor in elderly patients with
aggressive non-hodgkin’s lymphoma. J Clin Oncol. 2003;21(16):3041–3050.
3.Zinzani PL, Pavone E, Storti S, et al. Randomized trial with or without
granulocyte colony-stimulating factor as adjunct to induction VNCOP-B
treatment of elderly high-grade non-hodgkin’s lymphoma. Blood.
1997;89(11):3974–3979.
4. Pettengell R, Gurney H, Radford JA, et al. Granulocyte colony-stimulating
factor to prevent dose-limiting neutropenia in non-Hodgkin’s lymphoma:
a randomized controlled trial. Blood. 1992;80(6):1430–1436.
5.Chan KKW, Siu E, Krahn MD, Imrie K, Alibhai SMH. Cost-utility
analysis of primary prophylaxis versus secondary prophylaxis with granulocyte colony- stimulating factor in elderly patients with diffuse aggressive lymphoma receiving curative-intent chemotherapy. J Clin Oncol.
2012;30(10):1064–1071.
6.Lyman G, Lalla A, Barron R, Dubois RW. Cost-effectiveness of pegfilgrastim versus 6-day filgrastim primary prophylaxis in patients with
DOI: 10.1093/jnci/djt196
Advance Access publication July 22, 2013
non-Hodgkin’s lymphoma receiving CHOP-21 in United States. Curr
Med Res Opin. 2009;25(2):401–411.
7.Bohlius J, Herbst C, Reiser M, Schwarzer G, Engert A. Granulopoiesisstimulating factors to prevent adverse effects in the treatment of malignant
lymphoma. Cochrane Database Syst Rev. 2008;4:CD003189.
8. Bennett CL, Djulbegovic B, Norris LB, Armitage JO. Colony-stimulating
factors for febrile neutropenia during cancer therapy. New Engl J Med.
2013;368(12):1131–1139.
9. Potosky AL, Malin JL, Kim B, Chrischilles EA, Makgoeng SB, Howlader
N, Weeks JC. Use of colony stimulating factors with chemotherapy:
opportunities for cost savings and improved outcomes. J Natl Cancer Inst.
2011;103(12):979–982.
10. Weeks JC, Tierney MR, Weinstein MC. Cost effectiveness of prophylactic
intravenous immune globulin in chronic lymphocytic leukemia. New Engl
J Med. 1991;325(2):81–86.
11. Vose JM, Crump M, Lazarus H. Randomized multicenter open-label study
of pegfilgrastim compared with daily filgastrim after chemotherapy for
lymphoma. J Clin Oncol. 2003;21(3):514–519.
12.Chambers JD, Morris S, Neumann PJ, Buxton MJ. Factors predicting Medicare national coverage: an empirical analysis. Med Care.
2012;50(3):249–256.
13.Woodward RM, Menzin J, Neumann PJ. Quality-adjusted life years in
cancer: pros, cons, and alternatives. Eur J Cancer Care. 2013;22(1):12–19.
Funding
Funding was provided in part from the National Cancer Institute (1R01CA
102713-01 to CLB and 1R01CA165609-01A1 to LBN); the South Carolina
Center of Economic Excellence Center for Medication Safety Initiative (to
CLB); the American Cancer Society (IRG 11100-KA00 to CLB and LBN);
the University of South Carolina Advanced Support Programs for Innovative
Research Excellence (to LBN); and the Doris Levkoff Meddin Medication
Safety Program (to CLB and LBN).
Notes
The study sponsors had no role in the writing of the editorial or the decision to
submit it for publication. M. Dickson previously published an article with several
employees of Amgen [Kozma C, Dickson M, Chia V, Legg J, Barron R. Trends
in neutropenia-related inpatient events. J Oncol Pract. 2012;8(3):149–155] and
received a consulting fee from the first author of that article. C.L. Bennett is a
paid consultant for Teva.
Affiliations of authors: Austin, TX (SAS); Department of Clinical Pharmacy
and Outcomes Sciences, South Carolina College of Pharmacy, Columbia, SC
(MD, LBN, CLB); Department of Pharmacy Services, William Jennings Bryan
Dorn VA Medical Center, Columbia, SC (LBN); Hollings Cancer Center of the
Medical University of South Carolina, Charleston, SC (CLB); Arnold School of
Public Health, University of South Carolina, Columbia, SC (CLB).
© The Author 2013. Published by Oxford University Press. All rights reserved.
For Permissions, please e-mail: [email protected].
Cancer Incidence Among Specific Asian and Pacific Islander
Populations in the Unites States
Dee W. West, Paul K. Mills
Correspondence to: Dee W. West, PhD, Public Health Institute, Cancer Registry of Greater California, Sacramento, CA 95825 (e-mail: [email protected]).
To identify disease etiology and its consequences, epidemiologists
compare disease rates in different populations, geographic areas,
and time periods. These statistical comparisons become difficult
jnci.oxfordjournals.org
when diseases are relatively rare (eg, most cancers), and this problem is often resolved by broadening the definition of the groups
(eg, all Asians or Pacific Islanders), geographic areas (eg, many
JNCI | Editorials 1073
Asian or Pacific Island countries), or time of observation (eg, 1990–
2010). Populations may also be grouped when specific groups are
difficult to identify (eg, Chinese vs Vietnamese of Chinese descent)
or when individuals are classified from nonpatient sources such as
medical records, resulting in very general categories such as “Asian”
or “Unknown” race or ethnicity. Yet, disease rates may be different
among consolidated groups of people, geographic areas, or time
periods. The companion articles in this issue of the Journal by
Gomez et al. and Liu et al. (1,2) address many of these difficulties
in calculating cancer incidence rates in specific Asian and Pacific
Islander populations in the United States and, in overcoming many
of these, provide new insights into the roles of immigrant populations in cancer etiology and help elucidate environmental aspects
potentially involved in the induction of cancer. These studies are
the first to publish cancer incidence rates with improved classification methods. They mainly discuss implications of the data for
cancer control, but to more completely understand the patterns
reported, it is useful to examine immigration patterns among these
populations.
Almost 50 years ago, studies of cancer mortality among Japanese
immigrants to Hawaii and the US mainland reported remarkable
reductions in stomach cancer deaths with concomitant increases in
breast and colorectal cancer mortality (3,4). Since then, numerous
studies (5) of immigrants to the United States have reported the
common phenomenon of decreasing incidence rates of cancers of
infectious origin, such as liver (linked to hepatitis B virus), stomach (associated with Helioobacter pylori infection), and cervix (caused
by human papilloma virus), common in the countries of origin,
whereas incidence rates of breast, colon, prostate, and lung cancer
have increased despite remaining relatively low in the host nation.
Those patterns are confirmed in the articles by Gomez et al. and
Liu et al. (1,2). Factors related to changing incidence rates of cancers not related to infections are not well understood but include
age at immigration, place of immigration (such as rural areas), time
in the United States, and socioeconomic status of the immigrants
(6).
People immigrate for many reasons (e.g., famine, war, education, employment, family unification, and health), and immigrants
usually are not representative of the population of their native
country in terms of age, sex, education, occupation, and urban or
rural residence. Ability to immigrate is not the same for all populations and is influenced by multiple factors. One factor is previous
relationships with the United States. For example, Guamanians
are US citizens, American Samoans are US nationals, and Western
Samoans are neither. Immigration is easier for citizens (7,8). A second factor is changing immigration policy. For example, in 1882
the Chinese Exclusion Act halted immigration of the Chinese until
the 1943 Magnuson Act again permitted immigration, and in 1965
separate quotas were maintained for mainland China, Taiwan, and
Hong Kong (9). Japanese citizens began immigrating to Hawaii
and the US west coast after the 1868 Meiji Restoration; in 1907 an
agreement between Japan and the United States ended immigration of unskilled labors, and the Immigration Act of 1924 banned
immigration of almost all Japanese (10). A third factor is wars.
Examples include immigration of mostly laborers from Korea in
the 1950s after the Korean War and of Vietnamese, Laotians, and
Cambodians in the 1970s after the Vietnamese war (9). A fourth
1074 Editorials | JNCI
factor is US economic needs. For example, immigration of highly
educated people from India to work in high technology industries
has increased in recent years (9).
The cancer incidence rates reported by Gomez et al. may be
explained by these immigration policies. The recent immigrants
to the United States during the last 30 years, from Southeast
Asia, display the continued and increasing high incidence rates of
liver cancer, whereas the more established immigrant groups, the
Japanese and Chinese, have higher incidence rates of prostate and
lung cancer than found in Japan or China.
As seen in the Gomez paper, liver cancer incidence rates are
increasing in recent immigrants, including Filipinos, Laotians,
Vietnamese, and Kampuchean (1). The continuing role of
infections such as perinatal transmission of hepatitis B virus is still
of concern in contributing to the increasing incidence rates of
liver cancer and because two-thirds of Asian Americans are born
abroad. These trends take on urgency because, as noted by Gomez
et al., Asian Americans constitute a rapidly growing segment of the
US population, currently accounting for 5.6% of the population
and projected to increase to 9.2% by 2050 (40.6 million) (11).
Liver cancer is associated with hepatitis B infection, and in 2008,
Asian American/Pacific islanders aged 19 to 24 years had an acute
hepatitis B incidence of 3.1 per 100 000 population, which was 1.6
times greater than the incidence in non-Hispanic whites of the
same age (12).
Early published studies of gastric and colorectal cancer mortality in Japanese immigrants to Hawaii and the mainland United
States were based upon death certificate review in limited geographic areas (13). The studies by Gomez et al. and Lui et al. have
used the resources of the Surveillance Epidemiology and End
Results (SEER) program of the National Cancer Institute, which
allows calculation of population-based incidence rates rather than
relying upon mortality rates. However, the studies have some
limitations. Gomez et al. studied a number of ethnic groups that
are essentially based on the California experience, which may or
may not reflect Asian immigrant experiences to other areas of the
United States, such as New York, Chicago, and Houston. The
specific groups evaluated by the authors are quite heterogeneous,
both genetically and culturally. For example, among the Indian/
Pakistani population, there is a great degree of genetic and cultural heterogeneity, which includes admixture of non-Asian blood
in that the Indo/Aryan population of India (in contrast with the
Dravidian population) is essentially derived from a white population. This might explain the relatively high incidence of ovarian
cancer in the Indian/Pakistani populations. Even within the Indian/
Pakistani populations, there is great heterogeneity in the time since
immigration and duration of US residence variables, with the Sikh
population in California originating from the rural Punjab area
arriving in California nearly 100 years ago (primarily as farmers
and merchants) whereas more recent immigrants from India are
more highly educated professionals originating from urban areas.
In summary, the articles by Gomez et al. and Liu et al. have
carefully classified subgroups among Asian and Pacific Islander
populations in the United States and present cancer incidences
rates from 1990 to 2008 for these groups. This information
is important for control efforts for somewhat preventable cancers such as cervical and liver cancer and for cancers that can be
Vol. 105, Issue 15 | August 7, 2013
detected early through screening such as breast and colon cancers. In these papers by Gomez and Liu, the authors’ discussions of cancer etiology are limited and can be more completely
understood as the immigration patterns of these populations are
investigated.
References
1. Gomez SL, Noone A-M, Lichtensztajn, DY, et al. Cancer incidence trends
among Asian-American populations in the United States, 1990-2008 J
Natl Cancer Inst. 2013;105(15):1096–1110.
2.Liu L, Noone A-M, Gomez SL, et al. Cancer incidence trends among
Native Hawaiians and other Pacific Islanders in the United States, 19902008 J Natl Cancer Inst. 2013;105(15):1086–1095.
3.Buell P, Dunn JE. Cancer mortality among Japanese Issei and Nisei of
California. Cancer. 1965;18(5):656–664.
4.Kolonel L, Hinds MW and Hankin JH. 1980. Cancer patterns among
migrant and native-born Japanese in Hawaii in relation to smoking drinking and dietary habits. In: Gelboin HV, MacMahon B, Matsushima T,
Sugimura T, Takayama S, Takebe H, ed. Genetic and Environmental Factors in
Experimental and Human Cancer. Tokyo: Japan Scientific Societies Press; 1980:
327–340.
5.Kolonel L, Wilkens LR. Migrant Studies. In: Schottenfeld D, Fraumeni
JF Jr, eds. Cancer Epidemiology and Prevention. 3rd ed. New York: Oxford
University Press; 2006:189–201.
6.Ziegler RG, Hoover RN, Pike MC, et al. 1993. Migration patterns
and breast cancer risk in Asian-American women. J Natl Cancer Inst.
1993;85(22):1819–1827.
DOI:10.1093/jnci/djt189
Advance Access publication July 22, 2013
7.Center for Immigration Studies. Immigration Policy at the Edges:
International Migration to and Through the U.S. Island Territories, 2003.
http:www.cis.org/USIslandTerratories-IntrnationalMigration.html.
Accessed June 10, 2013.
8.Countries and their Cultures. Polynesians - History and Cultural Relations.
http://www.everyculture.com/North-America/Polynesians-History-andCulture-Relations.html. Accessed June 10, 2013.
9.Wikipedia. History of Asian American Immigration. http://en.wikipedia.org/
wiki/History_of_Asian_American_immigration. Accessed June 10, 2013.
10.Wikipedia. Japanese American. http://www.en.wikipedia.org/wiki/Japanese_
American. Acccessed June 10, 2013.
11. US Census Bureau. An Older and More Diverse Nation by Midcentury. http://
www.census.gov/newsroom/releases/archives/population/cb08-123.html.
Accessed June 27, 2013.
12.US Department of Health and Human Services. Hepatitis and Asian
Americans. http://minorityhealth.hhs.gov/templates/content.aspx?lvl=3&
lvlid=541&ID=6495. Accessed June 27, 2013.
13. Haenszel W, Kurihara M. Studies of Japanese migrants. I. Mortality from
cancer and other diseases among Japanese in the United States. J Natl
Cancer Inst. 1968;40(1):43–68.
Notes
The authors declare no conflicts of interest.
Affiliations of authors: Public Health Institute, Cancer Registry of Greater
California, Sacramento, CA (DWW); Fresno Medical Education and Research
Program, Department of Medicine, University of California, San Francisco, CA
University of California at San Francisco, Fresno, CA (PKM).
© The Author 2013. Published by Oxford University Press. All rights reserved.
For Permissions, please e-mail: [email protected].
BRAF Mutation and Microsatellite Instability Status in Colonic
and Rectal Carcinoma: Context Really Does Matter
Stanley R. Hamilton
Correspondence to: Stanley R. Hamilton, MD, University of Texas MD Anderson Cancer Center, Division of Pathology and Laboratory Medicine, 1515
Holcombe Blvd, Box 85, G1.3540, Houston, TX 77030 (e-mail: [email protected])
The molecular characteristics of colorectal cancer (CRC) have been
studied extensively since the 1980s, but translation of the remarkable increase in genomic knowledge into clinically used biomarkers
has been distressingly slow. The Cancer Genome Atlas for CRC
was published in mid-2012 (1), and molecular and pathologic findings including genetic and epigenetic abnormalities have now been
incorporated into classification systems that have been reported to
have implications for the clinical management of patients (2–4).
Numerous individual molecular biomarkers with potential applications have been published, but few have achieved levels and breadth
of evidence to become standard of care. Difficulty in convincing payers of the value of biomarkers and fiscal constraints have
impeded adequate reimbursement for testing and disincentivized
their clinical use.
In this issue of the Journal, Lochhead and colleagues (5) provide important additional evidence supporting the routine clinical use in CRC patients of two extensively investigated molecular
alterations: microsatellite instability and BRAF mutation. Both of
these characteristics of CRC are in use as biomarkers (6), but they
jnci.oxfordjournals.org
have been uncommonly addressed together in the four microsatellite instability (MSI)/BRAF subgroups for clinical usage in
prognostication.
High levels of MSI (MSI-H) occur in about 15% of CRC,
and the presence of this feature is a hallmark of Lynch syndrome
(hereditary nonpolyposis colorectal cancer syndrome). Although
most MSI-H CRC are sporadic because of acquired hypermethylation of the MLH1 mismatch repair gene promoter region, germline
mutation in one of several mismatch repair genes, most frequently
MLH1 or MSH2, results in MSI-H tumors in Lynch syndrome
patients. At least three professional organizations (7–9) have issued
recommendations for routine testing for MSI status in CRC to
identify tumors in patients who should be evaluated further for
Lynch syndrome because of the implications for family members
as well as the affected patient with an MSI-H tumor. In addition,
abundant evidence supports MSI-H as a favorable biomarker for
improved stage-specific survival, and testing for MSI status has
therefore demonstrated value as a prognostic marker, also contributing to its frequent routine evaluation in CRC.
JNCI | Editorials 1075