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1.  Disparities in liver cancer incidence by nativity, acculturation, and socioeconomic status in California Hispanics and Asians 
Background
Asians and Hispanics have the highest incidence rates of liver cancer in the US, but little is known about how incidence patterns in these largely immigrant populations vary by nativity, acculturation, and socioeconomic status (SES). Such variations can identify high-priority subgroups for prevention and monitoring.
Methods
Incidence rates and rate ratios (IRRs) by nativity among 5,400 Hispanics and 5,809 Asians diagnosed with liver cancer in 1988–2004 were calculated in the California Cancer Registry. Neighborhood ethnic enclave status and SES were classified using 2000 US Census data for cases diagnosed in 1998–2002.
Results
Foreign-born Hispanic males had significantly lower liver cancer incidence rates than US-born Hispanic males in 1988–2004 (e.g., IRR=0.54, 95% confidence interval [CI]=0.50–0.59), whereas foreign-born Hispanic females had significantly higher rates in 1988–1996 (IRR=1.42, 95% CI=1.18–1.71), but not 1997–2004. Foreign-born Asian males and females had up to 5-fold higher rates than the US-born. Among Hispanic females, incidence rates were elevated by 21% in higher-enclave versus lower-enclave neighborhoods, and by 24% in lower- versus higher-SES neighborhoods. Among Asian males, incidence rates were elevated by 23% in higher-enclave neighborhoods and by 21% in lower-SES neighborhoods. In both racial/ethnic populations, males and females in higher-enclave, lower-SES neighborhoods had higher incidence rates.
Conclusions
Nativity, residential enclave status, and neighborhood SES characterize Hispanics and Asians with significantly unequal incidence rates of liver cancer, implicating behavioral or environmental risk factors and revealing opportunities for prevention.
Impact
Liver cancer control efforts should especially target foreign-born Asians, US-born Hispanic men, and residents of lower-SES ethnic enclaves.
doi:10.1158/1055-9965.EPI-10-0863
PMCID: PMC3005535  PMID: 20940276
2.  Second Malignancy Risks After Non-Hodgkin's Lymphoma and Chronic Lymphocytic Leukemia: Differences by Lymphoma Subtype 
Journal of Clinical Oncology  2010;28(33):4935-4944.
Purpose
Previous studies have shown increased risks of second malignancies after non-Hodgkin's lymphoma (NHL) and chronic lymphocytic leukemia (CLL); however, no earlier investigation has quantified differences in risk of new malignancy by lymphoma subtype.
Patients and Methods
We evaluated second cancer and leukemia risks among 43,145 1-year survivors of CLL/small lymphocytic lymphoma (SLL), diffuse large B-cell lymphoma (DLBCL), or follicular lymphoma (FL) from 11 Surveillance, Epidemiology, and End Results (SEER) population-based registries during 1992 to 2006.
Results
Among patients without HIV/AIDS–related lymphoma, lung cancer risks were significantly elevated after CLL/SLL and FL but not after DLBCL (standardized incidence ratio [SIR], CLL/SLL = 1.42, FL = 1.28, DLBCL = 1.00; Poisson regression P for difference among subtypes, PDiff = .001). A similar pattern was observed for risk of cutaneous melanoma (SIR: CLL/SLL = 1.92, FL = 1.60, DLBCL = 1.06; PDiff = .004). Acute nonlymphocytic leukemia risks were significantly elevated after FL and DLBCL, particularly among patients receiving initial chemotherapy, but not after CLL/SLL (SIR: CLL/SLL = 1.13, FL = 5.96, DLBCL = 4.96; PDiff < .001). Patients with HIV/AIDS–related lymphoma (n = 932) were predominantly diagnosed with DLBCL and had significantly and substantially elevated risks for second anal cancer (SIR = 120.50) and Kaposi's sarcoma (SIR = 138.90).
Conclusion
Our findings suggest that differing immunologic alterations, treatments (eg, alkylating agent chemotherapy), genetic susceptibilities, and other risk factors (eg, viral infections, tobacco use) among lymphoma subtypes contribute to the patterns of second malignancy risk. Elucidating these patterns may provide etiologic clues to lymphoma as well as to the second malignancies.
doi:10.1200/JCO.2010.29.1112
PMCID: PMC3020697  PMID: 20940199
3.  Long-Term Use of Acetaminophen, Aspirin, and Other Nonsteroidal Anti-Inflammatory Drugs and Risk of Hematologic Malignancies: Results From the Prospective Vitamins and Lifestyle (VITAL) Study 
Journal of Clinical Oncology  2011;29(17):2424-2431.
Purpose
Among previous studies examining the associations of over-the-counter analgesics or nonsteroidal anti-inflammatory drugs (NSAIDs) and incident hematologic malignancies, results were inconsistent for NSAIDs but suggested an increased risk with acetaminophen (paracetamol). Herein, we used a large prospective cohort study to examine these associations.
Patients and Methods
In total, 64,839 men and women age 50 to 76 years were recruited from 2000 to 2002 to the Vitamins and Lifestyle (VITAL) study. Incident hematologic malignancies (n = 577) were identified through December 2008 by linkage to the Surveillance, Epidemiology and End Results cancer registry. Hazard ratios (HRs) associated with use of analgesics for total incident hematologic malignancies and cancer subcategories were estimated by Cox proportional hazards models. Models were adjusted for age, sex, race/ethnicity, education, smoking, self-rated health, arthritis, chronic musculoskeletal pain, migraines, headaches, fatigue, and family history of leukemia/lymphoma.
Results
After adjustment, there was an increased risk of incident hematologic malignancies associated with high use (≥ 4 days/week for ≥ 4 years) of acetaminophen (HR, 1.84; 95% CI, 1.35 to 2.50 for high use; P trend = .004). This association was seen for myeloid neoplasms (HR, 2.26; 95% CI, 1.24 to 4.12), non-Hodgkin's lymphomas (HR, 1.81; 95% CI, 1.12 to 2.93), and plasma cell disorders (HR, 2.42; 95% CI, 1.08 to 5.41), but not chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL; HR, 0.84; 95% CI, 0.31 to 2.28). By comparison, there was no association with risk of incident hematologic malignancies for increasing use of aspirin, nonaspirin NSAIDs, or ibuprofen.
Conclusion
High use of acetaminophen was associated with an almost two-fold increased risk of incident hematologic malignancies other than CLL/SLL. Neither aspirin nor nonaspirin NSAIDs are likely useful for prevention of hematologic malignancies.
doi:10.1200/JCO.2011.34.6346
PMCID: PMC3107756  PMID: 21555699
4.  Epidemiology of non‐Hodgkin lymphomas in Tyrol/Austria from 1991 to 2000 
Journal of Clinical Pathology  2006;59(1):48-55.
Aims
To analyse the entity specific incidence and disease specific survival (DSS) of non‐Hodgkin lymphomas (NHLs) in Tyrol/Austria, 1991–2000.
Methods
Data from 1307 NHLs (excluding primary cutaneous lymphomas and monoclonal gammopathies of undetermined significance) were obtained. Current status was available for all patients. Except for 29 cases of small lymphocytic (CLL/SLL), lymphoblastic leukaemia (ALL), and myeloma (MM), which were diagnosed cytologically, diagnoses were reclassified on paraffin wax embedded archival material according to new World Health Organisation criteria. Sex specific age adjusted standardised incidence rates were computed using Segi's population weighting. Annual incidence changes were calculated by weighted least square regression analysis. Survival was estimated by the Kaplan–Meier method and compared by log rank test.
Results
NHL more frequently affected men (male/female ratio, 1.52). Mean age of occurrence was 61 and 66 years for men and women, respectively. The incidence rate of 14.3 remained constant. There was a significant increase in diffuse large B cell lymphoma (DLBCL) and decrease in CLL/SLL in men, and a decrease in MM in women. Overall DSS was 64% during the mean follow up (43 months). Age, T‐NHL, λ light chain restriction in MM, and male sex in CLL/SLL were associated with poor prognosis. In B‐NHL, DSS decreased in the following order: hairy cell leukaemia, marginal zone lymphoma, follicular lymphoma, Burkitt lymphoma, ALL, DLBCL, CLL, MM, and mantle cell lymphoma.
Conclusions
The incidence of NHL in Tyrol has changed in the past decade, with a significant increase in DLBCL, decrease in CLL/SLL in men, and decrease in MM in women.
doi:10.1136/jcp.2005.026815
PMCID: PMC1860250  PMID: 16394280
epidemiology; non‐Hodgkin lymphoma; prognosis
5.  Prevalence of Familial Malignancy in a Prospectively Screened Cohort of Patients with Lymphoproliferative Disorders 
British journal of haematology  2008;143(3):361-368.
Summary
Increasing evidence points to a heritable contribution to the development of lymphoma. The goal of this study was to determine the rate of familial lymphoproliferative malignancy among consecutive lymphoma patients presenting to a tertiary care center and to enroll families with multiple affected first degree relatives on a data and tissue collection study. Beginning in 2004 all new patients presenting to the Dana-Farber Cancer Institute with non-Hodgkin’s or Hodgkin’s lymphoma or chronic lymphocytic leukemia (CLL) were asked to complete a one-page IRB-approved self-administered family history questionnaire. 55.4% of 1948 evaluable patients reported a 1st degree relative with a malignancy, highest among CLL probands. Lymphoid malignancies were particularly common, with 9.4% of all probands reporting a 1st degree relative with a related LPD. This frequency was again highest for CLL, at 13.3% of CLL probands, compared to 8.8% of NHL probands and 5.9% of HL probands (p=0.002). The prevalence of CLL was significantly increased in parents of CLL probands (p < 0.05), and a greater risk of NHL was seen in fathers of NHL probands than in mothers (p=0.026). We conclude that familial aggregation of lymphoproliferative disorders is common among newly diagnosed patients, varies significantly by diagnosis and contributes meaningfully to the population disease burden.
doi:10.1111/j.1365-2141.2008.07355.x
PMCID: PMC2704548  PMID: 18729853
familial lymphoma; familial CLL; heritable; lifetime risk
6.  Incidence of lymphoid neoplasms by subtype among six Asian ethnic groups in the United States, 1996–2004 
Cancer causes & control : CCC  2008;19(10):1171-1181.
Objectives
To establish baseline data for lymphoid neoplasm incidence by subtype for six Asian-American ethnic groups.
Methods
Incident rates were estimated by age and sex for six Asian ethnic groups—Asian Indian/Pakistani, Chinese, Filipino, Japanese, Korean, Vietnamese— in five United States cancer registry areas during 1996–2004. For comparison, rates for non-Hispanic Whites were also estimated.
Results
During 1996–2004, Filipinos had the highest (24.0) and Koreans had the lowest incidence (12.7) of total lymphoid neoplasms. By subtype, Vietnamese and Filipinos had the highest incidence for diffuse large B-cell lymphoma (DLBCL) (8.0 and 7.2); Japanese had the highest incidence of follicular lymphoma (2.3). Although a general male predominance of lymphoid neoplasms was observed, this pattern varied by lymphoid neoplasm subtype. Whites generally had higher rates than all Asian ethnic groups for all lymphoid neoplasms and most lymphoma subtypes, although the magnitude of the difference varied by both ethnicity and lymphoma subtype.
Conclusions
The observed variations in incidence patterns among Asian ethnic groups in the United States suggest that it may be fruitful to pursue studies that compare Asian populations for postulated environmental and genetic risk factors.
doi:10.1007/s10552-008-9184-z
PMCID: PMC2581633  PMID: 18543071
Lymphoid neoplasms; Asians
7.  Breast cancer incidence patterns among California Hispanic women: Differences by nativity and residence in an enclave 
Background
Breast cancer incidence is higher in US-born Hispanic women than foreign-born Hispanics, but no studies have examined how these rates have changed over time. To better inform cancer control efforts, we examined incidence trends by nativity and incidence patterns by neighborhood socioeconomic status (SES) and Hispanic enclave (neighborhoods with high proportions of Hispanics or Hispanic immigrants).
Methods
Information regarding all Hispanic women diagnosed with invasive breast cancer between 1988 and 2004 were obtained from the California Cancer Registry. Nativity was imputed from Social Security number for the 27% of cases with missing birthplace information. Neighborhood variables were developed from Census data.
Results
From 1988 to 2004, incidence rates for US-born Hispanics were parallel, but lower than, those of non-Hispanic whites, showing an annual 6% decline from 2002 to 2004. Foreign-born Hispanics had an annual 4% increase in incidence rates from 1995 to 1998 and a 1.4% decline thereafter. Rates were 38% higher for US- than foreign-born Hispanics, with elevations more pronounced for localized than regional/distant disease, and for women > 50 years of age. Residence in higher SES and lower Hispanic enclave neighborhoods were independently associated with higher incidence, with Hispanic enclave having a stronger association than SES.
Conclusions
Compared to foreign-born, US-born Hispanic women in California had higher prevalence of breast cancer risk factors, suggesting that incidence patterns largely reflects these differences in risk factors.
Impact
Further research is needed to separate the effects of individual- and neighborhood-level factors that impact incidence in this large and growing population.
doi:10.1158/1055-9965.EPI-10-0021
PMCID: PMC2895619  PMID: 20447917
8.  Outcomes for lymphoid malignancies in the Nurses' Health Study (NHS) as compared to the Surveillance, Epidemiology, and End Results (SEER) program 
Hematological oncology  2010;28(3):133-136.
INTRODUCTION
Vital statistics for the lymphoid malignancies obtained from the Surveillance, Epidemiology and End Results (SEER) Program have seldom been directly compared to data from alternative national databases; while SEER is recognized as the standard, some lymphoid malignancies—especially the chronic ones—may be underreported.
METHODS
We compared the incidence, all-cause, and cause-specific mortality for Hodgkin's lymphoma (HL), non-Hodgkin's lymphoma (NHL), multiple myeloma (MM) and chronic lymphocytic leukemia (CLL) in SEER to that in the Nurses' Health Study (NHS), a national cohort study of 121,700 female registered nurses, matching for age and race.
RESULTS
In over 2.5 million person-years, the incidence of HL was the same as in SEER (SIR= 1.01 [0.75, 1.26]), while the incidence of NHL, CLL and MM were slightly higher. All-cause mortality was lower for the lymphoid malignancies except for MM, which was the same; there were no differences in cause-specific mortality, except for MM (HR= 1.26 [1.07, 1.48]).
CONCLUSION
Our analysis suggests that, at least among white women, SEER is a reliable data source with respect to lymphoid malignancies.
doi:10.1002/hon.930
PMCID: PMC2946462  PMID: 19866451
hematologic malignancy; health services research; lymphoma; leukemia; myeloma
9.  Disparities in Breast Cancer Survival Among Asian Women by Ethnicity and Immigrant Status: A Population-Based Study 
American journal of public health  2010;100(5):861-869.
Objectives
We investigated heterogeneity in ethnic composition and immigrant status among US Asians as an explanation for disparities in breast cancer survival.
Methods
We enhanced data from the California Cancer Registry and the Surveillance, Epidemiology, and End Results program through linkage and imputation to examine the effect of immigrant status, neighborhood socioeconomic status, and ethnic enclave on mortality among Chinese, Japanese, Filipino, Korean, South Asian, and Vietnamese women diagnosed with breast cancer from 1988 to 2005 and followed through 2007.
Results
US-born women had similar mortality rates in all Asian ethnic groups except the Vietnamese, who had lower mortality risk (hazard ratio [HR]=0.3; 95% confidence interval [CI]=0.1, 0.9). Except for Japanese women, all foreign-born women had higher mortality than did US-born Japanese, the reference group. HRs ranged from 1.4 (95% CI=1.2, 1.7) among Koreans to 1.8 (95% CI=1.5, 2.2) among South Asians and Vietnamese. Little of this variation was explained by differences in disease characteristics.
Conclusions
Survival after breast cancer is poorer among foreign- than US-born Asians. Research on underlying factors is needed, along with increased awareness and targeted cancer control.
doi:10.2105/AJPH.2009.176651
PMCID: PMC2853623  PMID: 20299648
10.  Distribution of lymphomas in Poland according to World Health Organization classification: analysis of 11718 cases from National Histopathological Lymphoma Register project - the Polish Lymphoma Research Group study 
Most national lymphoma registers rely on broad classifications which include Hodgkin and non-Hodgkin lymphomas (NHL), multiple myeloma and leukaemia. In Poland the National Histopathological Lymphoma Register project (NHLR) was implemented by hematopathologists in accordance with the 2008 WHO classification into haematopoietic and lymphoid tissues. We present the NHLR data and compare lymphoma distribution in Poland, Europe, as well as in North Central and South America. Records of 11718 patients diagnosed in 24 pathology departments from all over the country were retrieved and reclassified into indolent and aggressive lymphomas according to the 2008 revised WHO classification system. DLBCL (32.9%; 2587), CLL/SLL (31.84%; 2504) and MCL (9.04%; 711) were the three most frequent NHL. The ratio of indolent to aggressive NHL was 1.72; 63.25% (4809) to 36.25% (2794) of cases respectively. Multiple myeloma was less frequent as compared to the data from population-based national cancer register (13.32% vs. 28.94%). Major differences between NHLR and European and American data on NHL subtypes concered: higher incidence of aggressive B-cell lymphomas including DLBCL, lower FL and MALT incidence rate. The percentage of unclassified lymphomas in the study was minimal due to participation of hematopathologists.
PMCID: PMC4097276  PMID: 25031749
Lymphoma; register; histopathology; epidemiology; hematopathology
11.  Dietary factors and risk of chronic lymphocytic leukemia and small lymphocytic lymphoma: a pooled analysis of two prospective studies 
Background
Other than male sex, family history, advanced age, and race, risk factors for chronic lymphocytic leukemia and small lymphocytic lymphoma (CLL/SLL) are unknown. Very few studies have investigated diet in relation to these leukemias, and no consistent associations are known.
Methods
Using two large prospective population-based studies, we evaluated the relationship between diet and CLL/SLL risk. Among 525,982 men and women free of cancer at enrollment, we identified 1,129 incident CLL/SLL cases during 11.2 years of follow-up.
Results
We found no associations between total fat, saturated fat, fiber, red meat, processed meat, fruit or vegetable intake and risk of CLL/SLL. We noted a suggestive positive association between body mass index (BMI) and CLL/SLL (hazard ratio =1.30; 95% confidence interval= 0.99-1.36).
Conclusion
We did not find any associations between foods or nutrients and CLL/SLL.
Impact
Our large prospective study indicates that diet may not play a role in CLL/SLL development.
doi:10.1158/1055-9965.EPI-10-0585
PMCID: PMC3501724  PMID: 20929883
diet; chronic lymphocytic leukemia; body mass index; cohort study
12.  Patient, hospital, and neighborhood factors associated with treatment of early-stage breast cancer among Asian American women in California 
Background
Clinical guidelines recommend breast conserving surgery (BCS) with radiation as a viable alternative to mastectomy for treatment of early-stage breast cancer. Yet, Asian Americans (AA) are more likely than other groups to have mastectomy or omit radiation after BCS.
Methods
We applied polytomous logistic regression and recursive partitioning (RP) to analyze factors associated with mastectomy, or BCS without radiation, among 20,987 California AAs diagnosed with stage 0–II breast cancer from 1990–2007.
Results
The percentage receiving mastectomy ranged from 40% among US-born Chinese to 58% among foreign-born Vietnamese. Factors associated with mastectomy included tumor characteristics such as larger tumor size, patient characteristics such as older age and foreign birthplace among some AA ethnicities, and additional factors including hospital (smaller hospital size, not NCI cancer center, low socioeconomic status (SES) patient composition, and high hospital AA patient composition) and neighborhood characteristics (ethnic enclaves of low SES). These hospital and neighborhood characteristics were also associated with BCS without radiation. Through RP, the highest mastectomy subgroups were defined by tumor characteristics such as size and anatomic location, in combination with diagnosis year and nativity.
Conclusions
Tumor characteristics and, secondarily, patient, hospital and neighborhood factors, are predictors of mastectomy and omission of radiation following BCS among AAs.
Impact
By focusing on interactions among patient, hospital, and neighborhood factors in the differential receipt of breast cancer treatment, our study identifies subgroups of interest for further study, and translation into public health and patient-focused initiatives to ensure that all women are fully informed about treatment options.
doi:10.1158/1055-9965.EPI-11-1143
PMCID: PMC3406750  PMID: 22402290
13.  Farm residence and lymphohematopoietic cancers in the Iowa Women’s Health Study 
Environmental research  2014;133:353-361.
Background
Cancer incidence in male farmers has been studied extensively; however, less is known about risk among women residing on farms or in agricultural areas, who may be exposed to pesticides by their proximity to crop fields. We extended a previous follow-up of the Iowa Women’s Health Study cohort to examine farm residence and the incidence of lymphohematopoietic cancers. Further, we investigated crop acreage within 750 m of residences, which has been associated with higher herbicide levels in Iowa homes.
Methods
We analyzed data for a cohort of 37,099 Iowa women aged 55–69 years who reported their residence location (farm, rural (not a farm), town size based on population) at enrollment in 1986. We identified incident lymphohematopoietic cancers (1986–2009) by linkage with the Iowa Cancer Registry. Using a geographic information system, we geocoded addresses and calculated acreage of pasture and row crops within 750 m of homes using the 1992 National Land Cover Database. Cox regression was used to estimate hazard ratios (HR) and 95% confidence intervals (CI) in multivariate analyses of cancer risk in relation to both residence location and crop acreage.
Results
As found in an earlier analysis of residence location, risk of acute myeloid leukemia (AML) was higher among women living on farms (HR= 2.23, 95%CI: 1.25–3.99) or rural areas (but not on a farm) (HR= 1.95, 95%CI: 0.89–4.29) compared with women living in towns of > 10,000 population. We observed no association between farm or rural residence and non-Hodgkin lymphoma (NHL; overall or for major subtypes) or multiple myeloma. In analyses of crop acreage, we observed no association between pasture or row crop acreage within 750 m of homes and risk of leukemia overall or for the AML subtype. Chronic lymphocytic leukemia (CLL)/small lymphocytic lymphoma (SLL) risk was nonsignificantly elevated among women with pasture acreage within 750 m of their home (HRs for increasing tertiles= 1.8, 1.8 and 1.5) and with row crop acreage within 750 m (HRs for increasing tertiles of acreage= 1.4, 1.5 and 1.6) compared to women with no pasture or row crop acreage, respectively.
Conclusions
Iowa women living on a farm or in a rural area were at increased risk of developing AML, which was not related to crop acreage near the home. Living near pasture or row crops may confer an increased risk of CLL/SLL regardless of residence location. Further investigation of specific farm-related exposures and these cancers among women living on farms and in agricultural areas is warranted.
doi:10.1016/j.envres.2014.05.028
PMCID: PMC4324553  PMID: 25038451
Farm residence; Pesticides; Iowa Women’s Health Study; GIS; Land use
14.  Smoking among Asian Americans: Acculturation and Gender in the Context of Tobacco Control Policies in New York City 
Health promotion practice  2013;14(5 0):18S-28S.
New York City (NYC) has experienced significant decline in smoking prevalence since its antismoking campaign; however, the rates among NYC’s Asian communities have persisted since 2002. Using combined data from the REACH US Risk Factor Survey (2009-2011), this article examined ethnic- and gender-specific smoking behaviors and the effects of acculturation and location of residence on cigarette smoking behavior among Chinese, Korean, Asian Indians, and other Asian Americans. Results indicated that current smoking prevalence was higher for men than women among all four groups. Korean men and women had the highest current smoking rates whereas Indians had the lowest among the four subgroups. Asian American women reporting speaking only English at home had higher current smoking prevalence, but this was not observed for men. Living in Sunset Park, an emerging Asian ethnic enclave, was associated with higher odds of smoking than living in other locations in NYC. In conclusion, smoking prevalence varied across gender and ethnic subgroups among Asian Americans in NYC. A “one-size-fits-all” type of intervention strategy for “pan-Asians” could not be effective. Community-based culturally appropriate and gender-specific interventions for smoking cessation might be an option for Asian Americans residing in linguistically isolated ethnic enclaves.
doi:10.1177/1524839913485757
PMCID: PMC3751989  PMID: 23667057
health promotion; health research; minority health; tobacco prevention and control
15.  Hodgkin lymphoma transformation of chronic lymphocytic leukemia: cases report and discussion 
B-cell chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL) is the most common form of leukemia affecting adults in Europe and North America. Large B-cell lymphoma known as Richter’s syndrome (RS) may develop approximately in 3–15 % patients. Furthermore, other hematological malignancies may also occur as RS variants, among them—Hodgkin lymphoma (HL). CLL/SLL transformation into HL is observed in about 0.5 % of patients, and till now, fewer than 100 cases have been reported in the medical literature. We present two cases of HL transformation of CLL/SLL and review the previously published literature.
doi:10.1007/s12032-013-0800-8
PMCID: PMC3890034  PMID: 24338339
Hodgkin lymphoma; Chronic lymphocytic leukemia; Histological transformation; Trephine biopsy
16.  Ibrutinib versus Ofatumumab in Previously Treated Chronic Lymphoid Leukemia 
The New England journal of medicine  2014;371(3):213-223.
Background
In patients with chronic lymphoid leukemia (CLL) or small lymphocytic lymphoma (SLL), a short duration of response to therapy or adverse cytogenetic abnormalities are associated with a poor outcome. We evaluated the efficacy of ibrutinib, a covalent inhibitor of Bruton’s tyrosine kinase, in patients at risk for a poor outcome.
Methods
In this multicenter, open-label, phase 3 study, we randomly assigned 391 patients with relapsed or refractory CLL or SLL to receive daily ibrutinib or the anti-CD20 antibody ofatumumab. The primary end point was the duration of progression-free survival, with the duration of overall survival and the overall response rate as secondary end points.
Results
At a median follow-up of 9.4 months, ibrutinib significantly improved progression-free survival; the median duration was not reached in the ibrutinib group (with a rate of progression-free survival of 88% at 6 months), as compared with a median of 8.1 months in the ofatumumab group (hazard ratio for progression or death in the ibrutinib group, 0.22; P<0.001). Ibrutinib also significantly improved overall survival (hazard ratio for death, 0.43; P = 0.005). At 12 months, the overall survival rate was 90% in the ibrutinib group and 81% in the ofatumumab group. The overall response rate was significantly higher in the ibrutinib group than in the ofatumumab group (42.6% vs. 4.1%, P<0.001). An additional 20% of ibrutinib-treated patients had a partial response with lymphocytosis. Similar effects were observed regardless of whether patients had a chromosome 17p13.1 deletion or resistance to purine analogues. The most frequent nonhematologic adverse events were diarrhea, fatigue, pyrexia, and nausea in the ibrutinib group and fatigue, infusion-related reactions, and cough in the ofatumumab group.
Conclusions
Ibrutinib, as compared with ofatumumab, significantly improved progression-free survival, overall survival, and response rate among patients with previously treated CLL or SLL. (Funded by Pharmacyclics and Janssen; RESONATE ClinicalTrials.gov number, NCT01578707.)
doi:10.1056/NEJMoa1400376
PMCID: PMC4134521  PMID: 24881631
17.  Ataxia telangiectasia gene mutations in leukaemia and lymphoma 
Journal of Clinical Pathology  2001;54(7):512-516.
Ataxia telangiectasia (AT) is a rare multisystem, autosomal, recessive disease characterised by neuronal degeneration, genome instability, and an increased risk of cancer. Approximately 10% of AT homozygotes develop cancer, mostly of the lymphoid system. Lymphoid malignancies in patients with AT are of both B cell and T cell origin, and include Hodgkin's lymphoma, non-Hodgkin's lymphoma, and several forms of leukaemia. The AT locus was mapped to the chromosomal region 11q22–23 using genetic linkage analysis in the late 1980s and the causative gene was identified by positional cloning several years later. The ATM gene encodes a large protein that belongs to a family of kinases possessing a highly conserved C-terminal kinase domain related to the phosphatidylinositol 3-kinase domain. Members of this kinase family have been shown to function in DNA repair and cell cycle checkpoint control following DNA damage. Recent studies indicate that ATM is activated primarily in response to double strand breaks and may be considered a caretaker of the genome. Most mutations in ATM result in truncation and destabilisation of the protein, but certain missense and splicing errors have been shown to produce a less severe phenotype. AT heterozygotes have a slightly increased risk of breast cancer. Atm deficient mice exhibit many of the symptoms found in patients with AT and have a high frequency of thymic lymphoma. The association between mutation of the ATM gene and a high incidence of lymphoid malignancy in patients with AT, together with the development of lymphoma in Atm deficient mice, supports the proposal that inactivation of the ATM gene may be of importance in the pathogenesis of sporadic lymphoid malignancy. Loss of heterozygosity at 11q22–23 (the location of the ATM gene) is a common event in lymphoid malignancy. Frequent inactivating mutations of the ATM gene have been reported in patients with rare sporadic T cell prolymphocytic leukaemia (T-PLL), B cell chronic lymphocytic leukaemia (B-CLL), and most recently, mantle cell lymphoma (MCL). In contrast to the ATM mutation pattern in AT, the most frequent nucleotide changes in these sporadic lymphoid malignancies were missense mutations. The presence of inactivating mutations, together with the deletion of the normal copy of the ATM gene in some patients with T-PLL, B-CLL, and MCL, establishes somatic inactivation of the ATM gene in the pathogenesis of lymphoid malignancies, and strongly suggests that ATM functions as a tumour suppressor. The presence of missense mutations in the germline of patients with B-CLL has been reported, suggesting that some patients with B-CLL may be constitutional AT heterozygotes. The putative hereditary predisposition of B-CLL, although intriguing, warrants further investigation.
Key Words: lymphoid malignancy • mutation • ataxia telangiectasia gene
doi:10.1136/jcp.54.7.512
PMCID: PMC1731462  PMID: 11429421
18.  Polymorphisms, Mutations, and Amplification of the EGFR Gene in Non-Small Cell Lung Cancers 
PLoS Medicine  2007;4(4):e125.
Background
The epidermal growth factor receptor (EGFR) gene is the prototype member of the type I receptor tyrosine kinase (TK) family and plays a pivotal role in cell proliferation and differentiation. There are three well described polymorphisms that are associated with increased protein production in experimental systems: a polymorphic dinucleotide repeat (CA simple sequence repeat 1 [CA-SSR1]) in intron one (lower number of repeats) and two single nucleotide polymorphisms (SNPs) in the promoter region, −216 (G/T or T/T) and −191 (C/A or A/A). The objective of this study was to examine distributions of these three polymorphisms and their relationships to each other and to EGFR gene mutations and allelic imbalance (AI) in non-small cell lung cancers.
Methods and Findings
We examined the frequencies of the three polymorphisms of EGFR in 556 resected lung cancers and corresponding non-malignant lung tissues from 336 East Asians, 213 individuals of Northern European descent, and seven of other ethnicities. We also studied the EGFR gene in 93 corresponding non-malignant lung tissue samples from European-descent patients from Italy and in peripheral blood mononuclear cells from 250 normal healthy US individuals enrolled in epidemiological studies including individuals of European descent, African–Americans, and Mexican–Americans. We sequenced the four exons (18–21) of the TK domain known to harbor activating mutations in tumors and examined the status of the CA-SSR1 alleles (presence of heterozygosity, repeat number of the alleles, and relative amplification of one allele) and allele-specific amplification of mutant tumors as determined by a standardized semiautomated method of microsatellite analysis. Variant forms of SNP −216 (G/T or T/T) and SNP −191 (C/A or A/A) (associated with higher protein production in experimental systems) were less frequent in East Asians than in individuals of other ethnicities (p < 0.001). Both alleles of CA-SSR1 were significantly longer in East Asians than in individuals of other ethnicities (p < 0.001). Expression studies using bronchial epithelial cultures demonstrated a trend towards increased mRNA expression in cultures having the variant SNP −216 G/T or T/T genotypes. Monoallelic amplification of the CA-SSR1 locus was present in 30.6% of the informative cases and occurred more often in individuals of East Asian ethnicity. AI was present in 44.4% (95% confidence interval: 34.1%–54.7%) of mutant tumors compared with 25.9% (20.6%–31.2%) of wild-type tumors (p = 0.002). The shorter allele in tumors with AI in East Asian individuals was selectively amplified (shorter allele dominant) more often in mutant tumors (75.0%, 61.6%–88.4%) than in wild-type tumors (43.5%, 31.8%–55.2%, p = 0.003). In addition, there was a strong positive association between AI ratios of CA-SSR1 alleles and AI of mutant alleles.
Conclusions
The three polymorphisms associated with increased EGFR protein production (shorter CA-SSR1 length and variant forms of SNPs −216 and −191) were found to be rare in East Asians as compared to other ethnicities, suggesting that the cells of East Asians may make relatively less intrinsic EGFR protein. Interestingly, especially in tumors from patients of East Asian ethnicity, EGFR mutations were found to favor the shorter allele of CA-SSR1, and selective amplification of the shorter allele of CA-SSR1 occurred frequently in tumors harboring a mutation. These distinct molecular events targeting the same allele would both be predicted to result in greater EGFR protein production and/or activity. Our findings may help explain to some of the ethnic differences observed in mutational frequencies and responses to TK inhibitors.
Masaharu Nomura and colleagues examine the distribution ofEGFR polymorphisms in different populations and find differences that might explain different responses to tyrosine kinase inhibitors in lung cancer patients.
Editors' Summary
Background.
Most cases of lung cancer—the leading cause of cancer deaths worldwide—are “non-small cell lung cancer” (NSCLC), which has a very low cure rate. Recently, however, “targeted” therapies have brought new hope to patients with NSCLC. Like all cancers, NSCLC occurs when cells begin to divide uncontrollably because of changes (mutations) in their genetic material. Chemotherapy drugs treat cancer by killing these rapidly dividing cells, but, because some normal tissues are sensitive to these agents, it is hard to kill the cancer completely without causing serious side effects. Targeted therapies specifically attack the changes in cancer cells that allow them to divide uncontrollably, so it might be possible to kill the cancer cells selectively without damaging normal tissues. Epidermal growth factor receptor (EGRF) was one of the first molecules for which a targeted therapy was developed. In normal cells, messenger proteins bind to EGFR and activate its “tyrosine kinase,” an enzyme that sticks phosphate groups on tyrosine (an amino acid) in other proteins. These proteins then tell the cell to divide. Alterations to this signaling system drive the uncontrolled growth of some cancers, including NSCLC.
Why Was This Study Done?
Molecules that inhibit the tyrosine kinase activity of EGFR (for example, gefitinib) dramatically shrink some NSCLCs, particularly those in East Asian patients. Tumors shrunk by tyrosine kinase inhibitors (TKIs) often (but not always) have mutations in EGFR's tyrosine kinase. However, not all tumors with these mutations respond to TKIs, and other genetic changes—for example, amplification (multiple copies) of the EGFR gene—also affect tumor responses to TKIs. It would be useful to know which genetic changes predict these responses when planning treatments for NSCLC and to understand why the frequency of these changes varies between ethnic groups. In this study, the researchers have examined three polymorphisms—differences in DNA sequences that occur between individuals—in the EGFR gene in people with and without NSCLC. In addition, they have looked for associations between these polymorphisms, which are present in every cell of the body, and the EGFR gene mutations and allelic imbalances (genes occur in pairs but amplification or loss of one copy, or allele, often causes allelic imbalance in tumors) that occur in NSCLCs.
What Did the Researchers Do and Find?
The researchers measured how often three EGFR polymorphisms (the length of a repeat sequence called CA-SSR1, and two single nucleotide variations [SNPs])—all of which probably affect how much protein is made from the EGFR gene—occurred in normal tissue and NSCLC tissue from East Asians and individuals of European descent. They also looked for mutations in the EGFR tyrosine kinase and allelic imbalance in the tumors, and then determined which genetic variations and alterations tended to occur together in people with the same ethnicity. Among many associations, the researchers found that shorter alleles of CA-SSR1 and the minor forms of the two SNPs occurred less often in East Asians than in individuals of European descent. They also confirmed that EGFR kinase mutations were more common in NSCLCs in East Asians than in European-descent individuals. Furthermore, mutations occurred more often in tumors with allelic imbalance, and in tumors where there was allelic imbalance and an EGFR mutation, the mutant allele was amplified more often than the wild-type allele.
What Do These Findings Mean?
The researchers use these associations between gene variants and tumor-associated alterations to propose a model to explain the ethnic differences in mutational frequencies and responses to TKIs seen in NSCLC. They suggest that because of the polymorphisms in the EGFR gene commonly seen in East Asians, people from this ethnic group make less EGFR protein than people from other ethnic groups. This would explain why, if a threshold level of EGFR is needed to drive cells towards malignancy, East Asians have a high frequency of amplified EGFR tyrosine kinase mutations in their tumors—mutation followed by amplification would be needed to activate EGFR signaling. This model, though speculative, helps to explain some clinical findings, such as the frequency of EGFR mutations and of TKI sensitivity in NSCLCs in East Asians. Further studies of this type in different ethnic groups and in different tumors, as well as with other genes for which targeted therapies are available, should help oncologists provide personalized cancer therapies for their patients.
Additional Information.
Please access these Web sites via the online version of this summary at http://dx.doi.org/10.1371/journal.pmed.0040125.
US National Cancer Institute information on lung cancer and on cancer treatment for patients and professionals
MedlinePlus encyclopedia entries on NSCLC
Cancer Research UK information for patients about all aspects of lung cancer, including treatment with TKIs
Wikipedia pages on lung cancer, EGFR, and gefitinib (note that Wikipedia is a free online encyclopedia that anyone can edit)
doi:10.1371/journal.pmed.0040125
PMCID: PMC1876407  PMID: 17455987
19.  Epidemiologic overview of malignant lymphoma 
The Korean Journal of Hematology  2012;47(2):92-104.
Malignant lymphoma encompasses a wide variety of distinct disease entities. It is generally more common in developed countries and less common in developing countries. The East Asia region has one of the lowest incidence rates of malignant lymphoma. The incidence of malignant lymphoma around the world has been increasing at a rate of 3-4% over the last 4 decades, while some stabilization has been observed in developed countries in recent years. The reasons behind this lymphoma epidemic are poorly understood, although improving diagnostic accuracy, the recent AIDS epidemic, an aging world population and the increasing adoption of cancer-causing behaviors are suggested as contributing factors. Etiologies of malignant lymphoma include infectious agents, immunodeficiency, autoimmune disease, exposure to certain organic chemicals, and pharmaceuticals. The distribution of many subtypes exhibit marked geographic variations. Compared to the West, T/natural killer (NK) cell lymphomas (T/NK-cell lymphoma) and extranodal marginal zone lymphoma of mucosa-associated lymphoid tissue (MALT lymphoma) are relatively more common, whereas other B-cell lymphomas, particularly follicular lymphoma and chronic lymphocytic leukemia/small lymphocytic lymphoma, are less common in Asia. Some subtypes of T/NK-cell lymphomas defined by Epstein-Barr virus association are predominantly Asian diseases, if not exclusively so. Both ethnic and environmental factors play roles in such diversity. In this review, we discuss the geographic distribution and etiology of malignant lymphoma, as well as the trend.
doi:10.5045/kjh.2012.47.2.92
PMCID: PMC3389073  PMID: 22783355
Malignant lymphoma; Epidemiology; Asia
20.  Epigenetic inactivation of the MIR129-2 in hematological malignancies 
Background
MIR129-2 has been shown to be a tumor suppressor microRNA hypermethylated in epithelial cancers.
Patients and methods
Epigenetic inactivation of MIR129-2 was studied by methylation-specific PCR (MSP) in 13 cell lines (eight myeloma and five lymphoma), 15 normal controls and 344 primary samples including acute myeloid leukemia (AML), acute lymphoblastic leukemia (ALL), chronic myeloid leukemia (CML), chronic lymphocytic leukemia (CLL), non-Hodgkin’s lymphoma (NHL), multiple myeloma (MM) at diagnosis, MM at relapse/progression, and monoclonal gammopathy of undetermined significance (MGUS). Expression of MIR129 and its target, SOX4, in cell lines was measured before and after hypomethylating treatment and MIR129 overexpression. MIR129 expression was correlated with MIR129-2 methylation status in primary lymphoma samples. Tumor suppressor function of MIR129 was demonstrated by MTT and trypan blue exclusion assay after MIR129 overexpression.
Results
The sensitivity of the methylated-MSP was one in 103. Different MSP statuses, including complete methylation, partial methylation, and complete unmethylation, were verified by quantitative bisulfite pyrosequencing. All five lymphoma and seven of eight myeloma cell lines showed complete and partial MIR129-2 methylation. In primary samples, MIR129-2 methylation was absent in AML and CML, but detected in 5% ALL, 45.9% CLL, 49.5% MM at diagnosis, and 59.1% NHL. In CLL, MIR129-2 methylation adversely impacted on survival (p=0.004). In MM, MIR129-2 methylation increased from 27.5% MGUS to 49.5% MM at diagnosis and 41.5% at relapse/progression (p=0.023). In NHL, MIR129-2 methylation was associated with MIR124-1 and MIR203 methylation (p<0.001), and lower MIR129 expression (p=0.009). Hypomethylation treatment of JEKO-1, homozygously methylated for MIR129-2, led to MIR129-2 demethylation and MIR129 re-expression, with downregulation of SOX4 mRNA. Moreover, MIR129 overexpression in both mantle cell lines, JEKO-1 and GRANTA-519, inhibited cellular proliferation and enhanced cell death, with concomitant SOX4 mRNA downregulation.
Conclusions
MIR129-2 is a tumor suppressive microRNA frequently methylated in lymphoid but not myeloid malignancies, leading to reversible MIR129-2 silencing. In CLL, MIR129-2 methylation was associated with an inferior survival. In MM, MIR129-2 methylation might be acquired during progression from MGUS to symptomatic MM. In NHL, MIR129-2 methylation might collaborate with MIR124-1 and MIR203 methylation in lymphomagenesis.
doi:10.1186/1756-8722-6-16
PMCID: PMC3576298  PMID: 23406679
microRNA; Tumor suppressor; Hypermethylation; MIR129; Hematological cancers
21.  The spectrum of coincident entities with small lymphocytic lymphoma/chronic lymphocytic leukemia (SLL/CLL) diagnosed by cytology 
CytoJournal  2010;7:20.
Background:
The cytologic diagnosis of Small lymphocytic lymphoma/chronic lymphocytic leukemia (SLL/CLL) often relies on finding a small lymphoid population with the characteristic immunoprofile by ancillary testing. There are only a few reports of other processes identified with SLL/CLL. The aim of this study was to review the fine needle aspiration (FNA) and touch prep (TP) diagnoses of SLL/CLL in order to identify any coincident entities.
Materials and Methods:
We retrospectively reviewed all FNA and TP cytology cases between January 2005 and May 2009 with a diagnosis of SLL/CLL to determine the presence of any coincident process.
Results:
We identified 29 cases, including 23 FNAs and six TPs, from 23 patients. Ancillary studies were utilized in 97% of the cases, including flow cytometry (FC, 79%), immunohistochemistry (IHC, 55%), fluorescent in situ hybridization studies (24%) and special stains (7%). Coincident entities were identified in nine cases (31%) and included seven (28%) neoplastic entities (Hodgkin lymphoma [HL], adenocarcinoma, squamous cell carcinoma, seminoma) and two (7%) non-neoplastic entities (infection and immunoglobulin containing cells). Six cases (21%) suspicious for large cell transformation were also identified.
Conclusion:
In our review of SLL/CLL, coincident entities were present in 31% of the cases and included a spectrum of non-neoplastic and neoplastic processes. FC was the most frequently utilized ancillary test, but IHC provided important information by excluding a mantle cell lymphoma or confirming a coincident process. Thus, cytomorphologic evaluation in these patients is important due to the high risk of a coincident process that may not be apparent by FC alone and may require clinical management.
doi:10.4103/1742-6413.70966
PMCID: PMC2955352  PMID: 20976208
Chronic lymphocytic leukemia; cytopathology; SLL/CLL; small lymphocytic lymphoma
22.  Personal Use of Hair Dye and the Risk of Certain Subtypes of Non-Hodgkin Lymphoma 
American journal of epidemiology  2008;167(11):1321-1331.
Personal use of hair dye has been inconsistently linked to risk of non-Hodgkin lymphoma (NHL), perhaps because of small samples or a lack of detailed information on personal hair-dye use in previous studies. This study included 4,461 NHL cases and 5,799 controls from the International Lymphoma Epidemiology Consortium 1988–2003. Increased risk of NHL (odds ratio (OR) = 1.3, 95% confidence interval (CI): 1.1, 1.4) associated with hair-dye use was observed among women who began using hair dye before 1980. Analyses by NHL subtype showed increased risk for follicular lymphoma (FL) and chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL) but not for other NHL subtypes. The increased risks of FL (OR = 1.4, 95% CI: 1.1, 1.9) and CLL/SLL (OR = 1.5, 95% CI: 1.1, 2.0) were mainly observed among women who started using hair dyes before 1980. For women who began using hair dye in 1980 or afterward, increased FL risk was limited to users of dark-colored dyes (OR = 1.5, 95% CI: 1.1, 2.0). These results indicate that personal hair-dye use may play a role in risks of FL and CLL/SLL in women who started use before 1980 and that increased risk of FL among women who started use during or after 1980 cannot be excluded.
doi:10.1093/aje/kwn058
PMCID: PMC4025953  PMID: 18408225
case-control studies; hair dyes; lymphoma; non-Hodgkin
23.  Herpes zoster is associated with an increased risk of subsequent lymphoid malignancies - A nationwide population-based matched-control study in Taiwan 
BMC Cancer  2012;12:503.
Background
Infectious agents have been shown to contribute to the development of lymphoid malignancies. The different distribution of lymphoid malignancies in Asian and Western populations suggests possibly different etiologies in Asian populations. Herpes zoster infection, commonly seen in immunocompromised persons, has been reported to be associated with lymphoid malignancies in retrospective case–control studies from Western populations, but the results are controversial and large-scale prospective studies from Asian populations are lacking.
Methods
A nationwide population-based matched-controlled prospective study on Taiwanese patients was performed using the National Health Insurance Research Database from 1996 to 2007. Herpes zoster and malignancies were defined by compatible ICD-9-CM (International Classification of Disease, 9th Revision, Clinical Modification) codes. Patients who had been diagnosed with any malignancies before herpes zoster, with known viral infections including human immunodeficiency virus, and duration from herpes zoster to diagnosis of malignancies less than 6 months were excluded.
Results
Of 42,498 patients with herpes zoster prior to the diagnosis of any malignancies, the cumulative incidence for lymphoid malignancies was 0.11% (n = 48), compared with 0.06% (n = 106) in 169,983 age- and gender-matched controls (univariate hazard ratio (HR): 1.82, 95%CI: 1.29-2.55). The most common lymphoid malignancy was non-Hodgkin’s lymphoma (60.4%, n = 29), followed by multiple myeloma (27.1%, n = 13). Risk for developing lymphoid malignancies is significantly higher in herpes zoster patients (log rank P = 0.005). After adjusting for presence of any comorbidities in Charlson comorbidity index, time-dependent covariate for herpes group, and income category using Cox proportional hazard regressions, herpes zoster patients had an increased risk of developing lymphoid malignancies (adjusted HR: 1.68, 95%CI: 1.35-2.42, P = 0.0026), but did not have an increased risk of developing non-lymphoid malignancies (adjusted HR: 1.00, 95%CI: 0.91-1.05, P = 0.872).
Conclusion
Preceding herpes zoster infection is an independent risk marker for subsequent lymphoid malignancies in Taiwanese subjects. Further studies are warranted for pathogenesis exploration and preventive strategies in Asian populations.
doi:10.1186/1471-2407-12-503
PMCID: PMC3531246  PMID: 23114019
Herpes zoster; Lymphoma; Leukemia; Epidemiology; Taiwan
24.  Papillary thyroid cancer incidence rates vary significantly by birthplace in Asian American women 
Cancer causes & control : CCC  2011;22(3):479-485.
Objective
To investigate how birthplace influences the incidence of papillary thyroid cancer among Asian American women.
Methods
Birthplace- and ethnic-specific age-adjusted and age-specific incidence rates were calculated using data from the California Cancer Registry for the period 1988–2004. Birthplace was statistically imputed for 30% of cases using a validated imputation method based on age at Social Security number issuance. Population estimates were obtained from the US Census. Incidence rate ratios (IRR) and 95% confidence intervals (CI) were estimated for foreign-born vs. US-born women.
Results
Age-adjusted incidence rates of papillary thyroid cancer among Filipina (13.7 per 100,000) and Vietnamese (12.7) women were more than double those of Japanese women (6.2). US-born Chinese (IRR=0.48, 95% CI: 0.40–0.59) and Filipina women (IRR=0.74, 95% CI: 0.58–0.96) had significantly higher rates than those who were foreign-born; the opposite was observed for Japanese women (IRR=1.55, 95% CI: 1.17–2.08). The age-specific patterns among all foreign-born Asian women and US-born Japanese women showed a slow steady increase in incidence until age 70. However, among US-born Asian women (except Japanese), substantially elevated incidence rates during the reproductive and menopausal years were evident.
Conclusions
Ethnic- and birthplace-variation in papillary thyroid cancer incidence can provide insight into the etiology of this increasingly common and understudied cancer.
doi:10.1007/s10552-010-9720-5
PMCID: PMC3291661  PMID: 21207130
papillary thyroid cancer; incidence rates; birthplace; Asian American women; cancer surveillance
25.  Menstrual and reproductive factors and risk of breast cancer in Asian-Americans. 
British Journal of Cancer  1996;73(5):680-686.
We conducted a population-based case-control study of breast cancer among Chinese-, Japanese- and Filipino-American women in Los Angeles County Metropolitan Statistical Area (MSA), San Francisco-Oakland MSA and Oahu, Hawaii. One objective of the study was to quantify breast cancer risks in relation to menstrual and reproductive histories in migrant and US-born Asian-Americans and to establish whether the gradient of risk in Asian-Americans can be explained by these factors. Using a common study design and questionnaire in the three study areas, we successfully conducted in-person interviews with 597 Asian-American women diagnosed with incident, primary breast cancer during the period 1983-87 (70% of those eligible) and 966 population-based controls (75% of those eligible). Controls were matched to cases on age, ethnicity and area of residence. In the present analysis, which included 492 cases and 768 controls, we observed a statistically non-significant 4% reduction in risk of breast cancer with each year delay in onset of menstruation. Independent of age at menarche risk of breast cancer was lower (odds ratio; OR=0.77) among women with menstrual cycles greater than 29 days. Parous Asian-American women showed a significantly lower risk of breast cancer then nulliparous women (OR=0.54). An increasing number of livebirths and a decreasing age at first livebirth were both associated with a lower risk of breast cancer, although the effect of number of livebirths was no longer significant after adjustment for age at first livebirth. Women with a pregnancy (spontaneous or induced abortions) but no livebirth had a statistically non-significant increased risk (OR=1.84), but there was no evidence that one type of abortion was particularly harmful. A positive history of breastfeeding was associated with non-significantly lower risk of breast cancer (OR=.78). There are several notable differences in the menstrual and reproductive factors between Asian-Americans in this study and published data on US whites. US-born Asian Americans had an average age at menarche of 12.12 years-no older than has been found in comparable studies of US whites, but 1.4 years earlier than Asian women who migrated to the US. Asian-American women, particularly those born in the US and those who migrated before age 36, also had a later age at first birth and fewer livebirths than US whites. A slightly higher proportion of Asian-American women breastfed, compared with US whites. The duration of breastfeeding was similar in US-born Asians and US whites, but was longer in Asian migrants, especially those who migrated at a later age. Menstrual and reproductive factors in Asian-American women are consistent with their breast cancer rates being at least as high as in US whites, and they are. However, the effects of these menstrual and reproductive factors were small and the ORs for migration variables changed only slightly after adjustment for these menstrual and reproductive factors. These results suggest that the lower rates of breast cancer in Asians must be largely as a result of other environmental/lifestyle factors.
PMCID: PMC2074339  PMID: 8605107

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