Network


Latest external collaboration on country level. Dive into details by clicking on the dots.

Hotspot


Dive into the research topics where S. Jane Henley is active.

Publication


Featured researches published by S. Jane Henley.


Journal of the National Cancer Institute | 2013

Annual Report to the Nation on the Status of Cancer, 1975–2009, Featuring the Burden and Trends in Human Papillomavirus (HPV)–Associated Cancers and HPV Vaccination Coverage Levels

Ahmedin Jemal; Edgar P. Simard; Christina Dorell; Anne-Michelle Noone; Lauri E. Markowitz; Betsy A. Kohler; Christie R. Eheman; Mona Saraiya; Priti Bandi; Kathleen A. Cronin; Meg Watson; Mark Schiffman; S. Jane Henley; Maria J. Schymura; Robert N. Anderson; David Yankey; Brenda K. Edwards

Background The American Cancer Society (ACS), the Centers for Disease Control and Prevention (CDC), the National Cancer Institute (NCI), and the North American Association of Central Cancer Registries (NAACCR) collaborate annually to provide updates on cancer incidence and death rates and trends in these outcomes for the United States. This year’s report includes incidence trends for human papillomavirus (HPV)–associated cancers and HPV vaccination (recommended for adolescents aged 11–12 years). Methods Data on cancer incidence were obtained from the CDC, NCI, and NAACCR, and data on mortality were obtained from the CDC. Long- (1975/1992–2009) and short-term (2000–2009) trends in age-standardized incidence and death rates for all cancers combined and for the leading cancers among men and among women were examined by joinpoint analysis. Prevalence of HPV vaccination coverage during 2008 and 2010 and of Papanicolaou (Pap) testing during 2010 were obtained from national surveys. Results Death rates continued to decline for all cancers combined for men and women of all major racial and ethnic groups and for most major cancer sites; rates for both sexes combined decreased by 1.5% per year from 2000 to 2009. Overall incidence rates decreased in men but stabilized in women. Incidence rates increased for two HPV-associated cancers (oropharynx, anus) and some cancers not associated with HPV (eg, liver, kidney, thyroid). Nationally, 32.0% (95% confidence interval [CI] = 30.3% to 33.6%) of girls aged 13 to 17 years in 2010 had received three doses of the HPV vaccine, and coverage was statistically significantly lower among the uninsured (14.1%, 95% CI = 9.4% to 20.6%) and in some Southern states (eg, 20.0% in Alabama [95% CI = 13.9% to 27.9%] and Mississippi [95% CI = 13.8% to 28.2%]), where cervical cancer rates were highest and recent Pap testing prevalence was the lowest. Conclusions The overall trends in declining cancer death rates continue. However, increases in incidence rates for some HPV-associated cancers and low vaccination coverage among adolescents underscore the need for additional prevention efforts for HPV-associated cancers, including efforts to increase vaccination coverage.


Cancer | 2014

Annual Report to the Nation on the status of cancer, 1975-2010, featuring prevalence of comorbidity and impact on survival among persons with lung, colorectal, breast, or prostate cancer.

Brenda K. Edwards; Anne-Michelle Noone; Angela B. Mariotto; Edgar P. Simard; Francis P. Boscoe; S. Jane Henley; Ahmedin Jemal; Hyunsoon Cho; Robert N. Anderson; Betsy A. Kohler; Christie R. Eheman; Elizabeth Ward

The American Cancer Society (ACS), the Centers for Disease Control and Prevention (CDC), the National Cancer Institute (NCI), and the North American Association of Central Cancer Registries (NAACCR) collaborate annually to provide updates on cancer incidence and death rates and trends in these outcomes for the United States. This years report includes the prevalence of comorbidity at the time of first cancer diagnosis among patients with lung, colorectal, breast, or prostate cancer and survival among cancer patients based on comorbidity level.


American Journal of Public Health | 2002

Benefits of Smoking Cessation for Longevity

Donald H. Taylor; Vic Hasselblad; S. Jane Henley; Michael J. Thun; Frank A. Sloan

OBJECTIVES This study determined the life extension obtained from stopping smoking at various ages. METHODS We estimated the relation between smoking and mortality among 877,243 respondents to the Cancer Prevention Study II. These estimates were applied to the 1990 US census population to examine the longevity benefits of smoking cessation. RESULTS Life expectancy among smokers who quit at age 35 exceeded that of continuing smokers by 6.9 to 8.5 years for men and 6.1 to 7.7 years for women. Smokers who quit at younger ages realized greater life extensions. However, even those who quit much later in life gained some benefits: among smokers who quit at age 65 years, men gained 1.4 to 2.0 years of life, and women gained 2.7 to 3.7 years. CONCLUSIONS Stopping smoking as early as possible is important, but cessation at any age provides meaningful life extensions.


Cancer | 2012

Annual Report to the Nation on the status of cancer, 1975-2008, featuring cancers associated with excess weight and lack of sufficient physical activity†‡

Christie R. Eheman; S. Jane Henley; Rachel Ballard-Barbash; Eric J. Jacobs; Maria J. Schymura; Anne-Michelle Noone; Liping Pan; Robert N. Anderson; Janet E. Fulton; Betsy A. Kohler; Ahmedin Jemal; Elizabeth Ward; Marcus Plescia; Lynn A. G. Ries; Brenda K. Edwards

Annual updates on cancer occurrence and trends in the United States are provided through collaboration between the American Cancer Society (ACS), the Centers for Disease Control and Prevention (CDC), the National Cancer Institute (NCI), and the North American Association of Central Cancer Registries (NAACCR). This years report highlights the increased cancer risk associated with excess weight (overweight or obesity) and lack of sufficient physical activity (<150 minutes of physical activity per week).


Circulation | 2005

Role of Smoking in Global and Regional Cardiovascular Mortality

Majid Ezzati; S. Jane Henley; Michael J. Thun; Alan D. Lopez

Background—Smoking is a major cause of cardiovascular disease mortality. There is little information on how it contributes to global and regional cause-specific mortality from cardiovascular diseases for which background risk varies because of other risks. Method and Results—We used data from the American Cancer Society’s Cancer Prevention Study II (CPS II) and the World Health Organization Global Burden of Disease mortality database to estimate smoking-attributable deaths from ischemic heart disease, cerebrovascular disease, and a cluster of other cardiovascular diseases for 14 epidemiological subregions of the world by age and sex. We used lung cancer mortality as an indirect marker for accumulated smoking hazard. CPS-II hazards were adjusted for important covariates. In the year 2000, an estimated 1.62 (95% CI, 1.27 to 2.04) million cardiovascular deaths in the world, 11% of total global cardiovascular deaths, were due to smoking. Of these, 1.17 million deaths were among men and 450 000 among women. There were 670 000 (95% CI, 440 000 to 920 000) smoking-attributable cardiovascular deaths in the developing world and 960 000 (95% CI, 770 000 to 1 200 000) in industrialized regions. Ischemic heart disease accounted for 54% of smoking-attributable cardiovascular mortality, followed by cerebrovascular disease (25%). There was variability across regions in the role of smoking as a cause of various cardiovascular diseases. Conclusions—More than 1 in every 10 cardiovascular deaths in the world in the year 2000 were attributable to smoking, demonstrating that it is an important preventable cause of cardiovascular mortality.


Journal of the National Cancer Institute | 2015

Annual Report to the Nation on the Status of Cancer, 1975-2011, Featuring Incidence of Breast Cancer Subtypes by Race/Ethnicity, Poverty, and State

Betsy A. Kohler; Recinda Sherman; Nadia Howlader; Ahmedin Jemal; A. Blythe Ryerson; Kevin A. Henry; Francis P. Boscoe; Kathleen A. Cronin; Andrew J. Lake; Anne-Michelle Noone; S. Jane Henley; Christie R. Eheman; Robert N. Anderson; Lynne Penberthy

Background: The American Cancer Society (ACS), Centers for Disease Control and Prevention (CDC), National Cancer Institute (NCI), and North American Association of Central Cancer Registries (NAACCR) collaborate annually to produce updated, national cancer statistics. This Annual Report includes a focus on breast cancer incidence by subtype using new, national-level data. Methods: Population-based cancer trends and breast cancer incidence by molecular subtype were calculated. Breast cancer subtypes were classified using tumor biomarkers for hormone receptor (HR) and human growth factor-neu receptor (HER2) expression. Results: Overall cancer incidence decreased for men by 1.8% annually from 2007 to 2011. Rates for women were stable from 1998 to 2011. Within these trends there was racial/ethnic variation, and some sites have increasing rates. Among children, incidence rates continued to increase by 0.8% per year over the past decade while, like adults, mortality declined. Overall mortality has been declining for both men and women since the early 1990’s and for children since the 1970’s. HR+/HER2- breast cancers, the subtype with the best prognosis, were the most common for all races/ethnicities with highest rates among non-Hispanic white women, local stage cases, and low poverty areas (92.7, 63.51, and 98.69 per 100000 non-Hispanic white women, respectively). HR+/HER2- breast cancer incidence rates were strongly, positively correlated with mammography use, particularly for non-Hispanic white women (Pearson 0.57, two-sided P < .001). Triple-negative breast cancers, the subtype with the worst prognosis, were highest among non-Hispanic black women (27.2 per 100000 non-Hispanic black women), which is reflected in high rates in southeastern states. Conclusions: Progress continues in reducing the burden of cancer in the United States. There are unique racial/ethnic-specific incidence patterns for breast cancer subtypes; likely because of both biologic and social risk factors, including variation in mammography use. Breast cancer subtype analysis confirms the capacity of cancer registries to adjust national collection standards to produce clinically relevant data based on evolving medical knowledge.


Cancer | 2016

Annual Report to the Nation on the Status of Cancer,1975-2012, Featuring the Increasing Incidence of Liver Cancer

A. Blythe Ryerson; Christie R. Eheman; Sean F. Altekruse; John W. Ward; Ahmedin Jemal; Recinda Sherman; S. Jane Henley; Deborah Holtzman; Andrew J. Lake; Anne-Michelle Noone; Robert N. Anderson; Jiemin Ma; Kathleen N. Ly; Kathleen A. Cronin; Lynne Penberthy; Betsy A. Kohler

Annual updates on cancer occurrence and trends in the United States are provided through an ongoing collaboration among the American Cancer Society (ACS), the Centers for Disease Control and Prevention (CDC), the National Cancer Institute (NCI), and the North American Association of Central Cancer Registries (NAACCR). This annual report highlights the increasing burden of liver and intrahepatic bile duct (liver) cancers.


Morbidity and Mortality Weekly Report | 2016

Human Papillomavirus-Associated Cancers - United States, 2008-2012.

Laura Viens; S. Jane Henley; Meg Watson; Lauri E. Markowitz; Cheryll C. Thomas; Trevor D. Thompson; Hilda Razzaghi; Mona Saraiya

Human papillomavirus (HPV) is a known cause of cervical cancers, as well as some vulvar, vaginal, penile, oropharyngeal, anal, and rectal cancers (1,2). Although most HPV infections are asymptomatic and clear spontaneously, persistent infections with one of 13 oncogenic HPV types can progress to precancer or cancer. To assess the incidence of HPV-associated cancers, CDC analyzed 2008-2012 high-quality data from the CDCs National Program of Cancer Registries and the National Cancer Institutes Surveillance, Epidemiology, and End Results program. During 2008-2012, an average of 38,793 HPV-associated cancers were diagnosed annually, including 23,000 (59%) among females and 15,793 (41%) among males. By multiplying these counts by the percentages attributable to HPV (3), CDC estimated that approximately 30,700 new cancers were attributable to HPV, including 19,200 among females and 11,600 among males. Cervical precancers can be detected through screening, and treatment can prevent progression to cancer; HPV vaccination can prevent infection with HPV types that cause cancer at cervical and other sites (3). Vaccines are available for HPV types 16 and 18, which cause 63% of all HPV-associated cancers in the United States, and for HPV types 31, 33, 45, 52, and 58, which cause an additional 10% (3). Among the oncogenic HPV types, HPV 16 is the most likely to both persist and to progress to cancer (3). The impact of these primary and secondary prevention interventions can be monitored using surveillance data from population-based cancer registries.


International Journal of Cancer | 2005

Role of smoking in global and regional cancer epidemiology: current patterns and data needs

Majid Ezzati; S. Jane Henley; Alan D. Lopez; Michael J. Thun

Although smoking is widely recognized as a major cause of cancer, there is little information on how it contributes to the global and regional burden of cancers in combination with other risk factors that affect background cancer mortality patterns. We used data from the American Cancer Societys Cancer Prevention Study II (CPS‐II) and the WHO and IARC cancer mortality databases to estimate deaths from 8 clusters of site‐specific cancers caused by smoking, for 14 epidemiologic subregions of the world, by age and sex. We used lung cancer mortality as an indirect marker for accumulated smoking hazard. CPS‐II hazards were adjusted for important covariates. In the year 2000, an estimated 1.42 (95% CI 1.27–1.57) million cancer deaths in the world, 21% of total global cancer deaths, were caused by smoking. Of these, 1.18 million deaths were among men and 0.24 million among women; 625,000 (95% CI 485,000–749,000) smoking‐caused cancer deaths occurred in the developing world and 794,000 (95% CI 749,000–840,000) in industrialized regions. Lung cancer accounted for 60% of smoking‐attributable cancer mortality, followed by cancers of the upper aerodigestive tract (20%). Based on available data, more than one in every 5 cancer deaths in the world in the year 2000 were caused by smoking, making it possibly the single largest preventable cause of cancer mortality. There was significant variability across regions in the role of smoking as a cause of the different site‐specific cancers. This variability illustrates the importance of coupling research and surveillance of smoking with that for other risk factors for more effective cancer prevention.


Oncogene | 2002

Tobacco use and cancer: an epidemiologic perspective for geneticists.

Michael J. Thun; S. Jane Henley; Eugenia E. Calle

Much of what is known about the deleterious effects of tobacco use on health was learned from epidemiologic studies over the last half century. These studies establish unequivocally that tobacco use, particularly manufactured cigarette smoking, causes most cancers of the lung, oropharynx, larynx, and esophagus in the USA, and approximately one-third of all cancers of the pancreas, kidney, urinary bladder and uterine cervix. More recent evidence also implicates smoking with cancers of the stomach, liver and colorectum. While over half of the estimated 440 000 smoking-attributable deaths that occur annually in the USA involve non-malignant cardiovascular and respiratory conditions, smoking-attributable cancers are more recognized and feared. Geneticists increasingly study tobacco use as a model for environmental carcinogenicity. Tobacco-exposed populations provide opportunities to characterize the somatic mutations that give rise to specific cancers and to identify the inherited genetic traits that confer susceptibility or resistance. Studies to identify the genetic determinants of addiction may be particularly important. Future research to identify other susceptibility factors, such as genes that modify carcinogen metabolism or DNA repair, will need to be substantially larger and to quantify lifetime tobacco exposure with more precision than have past studies in order to distinguish gradations in risk due to exposure from those caused by genetic susceptibility. This review considers: (a) the epidemiology of tobacco use; (b) cancers presently classified as smoking-attributable by the US Surgeon General; (c) the magnitude of the epidemic of cancers and other diseases caused by tobacco use; (d) selected issues in the epidemiology of lung cancer; and (e) the interface of genetics and epidemiology in understanding, preventing, and treating tobacco-attributable disease.

Collaboration


Dive into the S. Jane Henley's collaboration.

Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar

Robert N. Anderson

Centers for Disease Control and Prevention

View shared research outputs
Top Co-Authors

Avatar

Christie R. Eheman

Centers for Disease Control and Prevention

View shared research outputs
Top Co-Authors

Avatar

Thomas B. Richards

Centers for Disease Control and Prevention

View shared research outputs
Top Co-Authors

Avatar

Anne-Michelle Noone

National Institutes of Health

View shared research outputs
Top Co-Authors

Avatar
Top Co-Authors

Avatar

Kathleen A. Cronin

National Institutes of Health

View shared research outputs
Top Co-Authors

Avatar

Mary C. White

Centers for Disease Control and Prevention

View shared research outputs
Researchain Logo
Decentralizing Knowledge