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Thomas L. Vaughan

Bio: Thomas L. Vaughan is an academic researcher from Fred Hutchinson Cancer Research Center. The author has contributed to research in topics: Population & Barrett's esophagus. The author has an hindex of 70, co-authored 227 publications receiving 17549 citations. Previous affiliations of Thomas L. Vaughan include QIMR Berghofer Medical Research Institute & University of Washington.


Papers
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Journal ArticleDOI
TL;DR: A proinflammatory cytokine genetic profile increases the risk of noncardia gastric adenocarcinoma but not other upper gastrointestinal cancers, possibly by inducing a hypochlorhydric and atrophic response to gastric H. pylori infection.

918 citations

Journal ArticleDOI
TL;DR: In this population, a few known risk factors account for a majority of esophageal and gastric cancers, and results suggest that the incidence of these cancers may be decreased by reducing the prevalence of smoking, gastric reflux, and being overweight and by increasing the consumption of fruits and vegetables.
Abstract: Background Several risk factors have been identified for esophageal adenocarcinoma, gastric cardia adenocarcinoma, esophageal squamous cell carcinoma, and noncardia gastric adenocarcinoma, but no study has comprehensively examined their contributions to the cancer burden in the general population. Herein, we estimate the population attributable risks (PARs) for various risk factors observed in a multicenter population-based case-control study. Methods We calculated PARs by using 293 patients with esophageal adenocarcinoma, 261 with gastric cardia adenocarcinoma, 221 with esophageal squamous cell carcinoma, 368 with noncardia gastric adenocarcinoma, and 695 control subjects. We included smoking for all four tumor types and Helicobacter pylori infection for noncardia gastric adenocarcinoma as established causal risk factors as well as several other factors for which causality is under evaluation. Results Ever smoking, body mass index above the lowest quartile, history of gastroesophageal reflux, and low fruit and vegetable consumption accounted for 39.7% (95% confidence interval [CI] = 25.6% to 55.8%), 41.1% (95% CI = 23.8% to 60.9%), 29.7% (95% CI = 19.5% to 42.3%), and 15.3% (95% CI = 5.8% to 34.6%) of esophageal adenocarcinomas, respectively, with a combined PAR of 78.7% (95% CI = 66.5% to 87.3%). Ever smoking and body mass index above the lowest quartile were responsible for 45.2% (95% CI = 31.3% to 59.9%) and 19.2% (95% CI = 4.9% to 52.0%) of gastric cardia adenocarcinomas, respectively, with a combined PAR of 56.2% (95% CI = 38.1% to 72.8%). Ever smoking, alcohol consumption, and low fruit and vegetable consumption accounted for 56.9% (95% CI = 36.6% to 75.1%), 72.4% (95% CI = 53.3% to 85.8%), and 28.7% (95% CI = 11.1% to 56.5%) of esophageal squamous cell carcinomas, respectively, with a combined PAR of 89.4% (95% CI = 79.1% to 95.0%). Ever smoking, history of gastric ulcers, nitrite intake above the lowest quartile, and H. pylori infection were responsible for 18.3% (95% CI = 6.5% to 41.8%), 9.7% (95% CI = 5.4% to 16.8%), 40.7% (95% CI = 23.4% to 60.7%), and 10.4% (95% CI = 0.3% to 79.6%) of noncardia gastric adenocarcinomas, respectively, with a combined PAR of 59.0% (95% CI = 16.2% to 91.4%). Conclusion In this population, a few known risk factors account for a majority of esophageal and gastric cancers. These results suggest that the incidence of these cancers may be decreased by reducing the prevalence of smoking, gastroesophageal reflux, and being overweight and by increasing the consumption of fruits and vegetables.

692 citations

Journal ArticleDOI
TL;DR: Increasing prevalence of obesity in the United States population may have contributed to the upward trends in esophageal and gastric cardia adenocarcinomas.
Abstract: Background Incidence rates have risen rapidly for esophageal adenocarcinoma and moderately for gastric cardia adenocarcinoma, while rates have remained stable for esophageal squamous cell carcinoma and have declined steadily for noncardia gastric adenocarcinoma. We examined anthropometric risk factors in a population-based case-control study of esophageal and gastric cancers in Connecticut, New Jersey, and western Washington. Methods Healthy control subjects (n = 695) and case patients with esophageal squamous cell carcinoma or noncardia gastric adenocarcinoma (n = 589) were frequency-matched to case patients with adenocarcinomas of esophagus or gastric cardia (n = 554) by 5-year age groups, sex, and race (New Jersey only). Classification of cases by tumor site of origin and histology was determined by review of pathology materials and hospital records. Data were collected using in-person structured interviews. Associations with obesity, measured by body mass index (BMI), were estimated by odds ratios (ORs). All ORs were adjusted for geographic location, age, sex, race, cigarette smoking, and proxy response status. Results The ORs for esophageal adenocarcinoma rose with increasing adult BMI. The magnitude of association with BMI was greater among the younger age groups and among nonsmokers. The ORs for gastric cardia adenocarcinoma rose moderately with increasing BMI. Adult BMI was not associated with risk of esophageal squamous cell carcinoma or noncardia gastric adenocarcinoma. Conclusions Increasing prevalence of obesity in the United States population may have contributed to the upward trends in esophageal and gastric cardia adenocarcinomas.

618 citations

Journal ArticleDOI
TL;DR: Because of the long lag time before risk of these tumors is reduced among ex-smokers, smoking may affect early stage carcinogenesis.
Abstract: Background: Incidence rates for adenocarcinomas of the esophagus and gastric cardia have risen steeply over the last few decades. To determine risk factors for these tumors, we conducted a multicenter, population-based, case‐control study. Methods: The study included 554 subjects newly diagnosed with esophageal or gastric cardia adenocarcinomas, 589 subjects newly diagnosed with esophageal squamous cell carcinoma or other gastric adenocarcinomas, and 695 control subjects. Estimates of risk (odds ratios [ORs] and corresponding 95% confidence intervals [CIs]) were calculated for the four tumor types separately and for esophageal and gastric cardia adenocarcinomas combined. Results: Risk of esophageal and gastric cardia adenocarcinomas combined was increased among current cigarette smokers (OR = 2.4; 95% = 1.7‐3.4), with little reduction observed until 30 years after smoking cessation; this risk rose with increasing intensity and duration of smoking. Risk of these tumors was not related to beer (OR = 0.8; 95% CI = 0.6‐1.1) or liquor (OR = 1.1; 95% CI = 0.8‐1.4) consumption, but it was reduced for drinking wine (OR = 0.6; 95% CI = 0.5‐0.8). Similar ORs were obtained for the development of noncardia gastric adenocarcinomas in relation to tobacco and alcohol use, but higher ORs were obtained for the development of esophageal squamous cell carcinomas. For all four tumor types, risks were higher among those with low income or education. Conclusions: Smoking is a major risk factor for esophageal and gastric cardia adenocarcinomas, accounting for approximately 40% of cases. Implications: Because of the long lag time before risk of these tumors is reduced among exsmokers, smoking may affect early stage carcinogenesis. The increase in smoking prevalence during the first two thirds of this century may be reflected in the rising incidence of these tumors in the past few decades among older individuals. The recent decrease in smoking may not yet have had an impact. [J Natl Cancer Inst 1997;89:1277‐84] The incidence rates for adenocarcinomas of the esophagus and gastric cardia have risen steeply in the United States and Europe during the past few decades, whereas the incidence of squamous cell carcinoma of the esophagus and of adenocarci

579 citations

Journal Article
TL;DR: Body mass index was inversely associated with risk, whereas for adenocarcinoma, the highest risk was observed among persons who were in the highest decile of body mass index, Whereas for squamous cell carcinoma, body mass indices were inverselyassociated with risk.
Abstract: Adenocarcinomas of the esophagus and gastric cardia were once rare. However, for unknown reasons, their incidence has been increasing rapidly over the past 15 years in the United States and parts of Western Europe. In contrast, the incidence of esophageal squamous cell carcinomas has remained relatively constant. To investigate possible reasons for these diverging incidence rates we analyzed data from two population-based case-control studies of cancers of the esophagus and gastric cardia that were conducted among male and female residents of western Washington between 1983 and 1990. Information on body mass index, cigarette use, alcohol intake, and other possible risk factors was collected via personal interviews with 404 cases or their next of kin (including 298 adenocarcinomas and 106 squamous cell carcinomas) and 724 controls identified by random digit dialing. Use of alcohol and cigarettes were significant risk factors for both histological types. The increase in risk for current smokers of 80 or more pack-years compared to nonsmokers was substantially higher for squamous cell cancer [odds ratio (OR) = 16.9; 95% confidence interval (CI) = 4.1-69.1] than for adenocarcinoma (OR = 3.4; 95% CI = 1.4-8.0), as was the increase for persons who typically drank 21 or more drinks/week compared to those who drank <7/week (OR = 9.5; 95% CI = 4.1-22.3 versus OR = 1.8; 95% CI = 1.1-3.1). For squamous cell carcinoma, body mass index was inversely associated with risk, whereas for adenocarcinoma, the highest risk was observed among persons who were in the highest decile of body mass index (OR = 1.9; 95% CI = 1.1-3.2).(ABSTRACT TRUNCATED AT 250 WORDS)

535 citations


Cited by
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TL;DR: A substantial proportion of the worldwide burden of cancer could be prevented through the application of existing cancer control knowledge and by implementing programs for tobacco control, vaccination, and early detection and treatment, as well as public health campaigns promoting physical activity and a healthier dietary intake.
Abstract: The global burden of cancer continues to increase largely because of the aging and growth of the world population alongside an increasing adoption of cancer-causing behaviors, particularly smoking, in economically developing countries. Based on the GLOBOCAN 2008 estimates, about 12.7 million cancer cases and 7.6 million cancer deaths are estimated to have occurred in 2008; of these, 56% of the cases and 64% of the deaths occurred in the economically developing world. Breast cancer is the most frequently diagnosed cancer and the leading cause of cancer death among females, accounting for 23% of the total cancer cases and 14% of the cancer deaths. Lung cancer is the leading cancer site in males, comprising 17% of the total new cancer cases and 23% of the total cancer deaths. Breast cancer is now also the leading cause of cancer death among females in economically developing countries, a shift from the previous decade during which the most common cause of cancer death was cervical cancer. Further, the mortality burden for lung cancer among females in developing countries is as high as the burden for cervical cancer, with each accounting for 11% of the total female cancer deaths. Although overall cancer incidence rates in the developing world are half those seen in the developed world in both sexes, the overall cancer mortality rates are generally similar. Cancer survival tends to be poorer in developing countries, most likely because of a combination of a late stage at diagnosis and limited access to timely and standard treatment. A substantial proportion of the worldwide burden of cancer could be prevented through the application of existing cancer control knowledge and by implementing programs for tobacco control, vaccination (for liver and cervical cancers), and early detection and treatment, as well as public health campaigns promoting physical activity and a healthier dietary intake. Clinicians, public health professionals, and policy makers can play an active role in accelerating the application of such interventions globally.

52,293 citations

Journal ArticleDOI
TL;DR: A substantial portion of cancer cases and deaths could be prevented by broadly applying effective prevention measures, such as tobacco control, vaccination, and the use of early detection tests.
Abstract: Cancer constitutes an enormous burden on society in more and less economically developed countries alike. The occurrence of cancer is increasing because of the growth and aging of the population, as well as an increasing prevalence of established risk factors such as smoking, overweight, physical inactivity, and changing reproductive patterns associated with urbanization and economic development. Based on GLOBOCAN estimates, about 14.1 million new cancer cases and 8.2 million deaths occurred in 2012 worldwide. Over the years, the burden has shifted to less developed countries, which currently account for about 57% of cases and 65% of cancer deaths worldwide. Lung cancer is the leading cause of cancer death among males in both more and less developed countries, and has surpassed breast cancer as the leading cause of cancer death among females in more developed countries; breast cancer remains the leading cause of cancer death among females in less developed countries. Other leading causes of cancer death in more developed countries include colorectal cancer among males and females and prostate cancer among males. In less developed countries, liver and stomach cancer among males and cervical cancer among females are also leading causes of cancer death. Although incidence rates for all cancers combined are nearly twice as high in more developed than in less developed countries in both males and females, mortality rates are only 8% to 15% higher in more developed countries. This disparity reflects regional differences in the mix of cancers, which is affected by risk factors and detection practices, and/or the availability of treatment. Risk factors associated with the leading causes of cancer death include tobacco use (lung, colorectal, stomach, and liver cancer), overweight/obesity and physical inactivity (breast and colorectal cancer), and infection (liver, stomach, and cervical cancer). A substantial portion of cancer cases and deaths could be prevented by broadly applying effective prevention measures, such as tobacco control, vaccination, and the use of early detection tests.

23,203 citations

Journal ArticleDOI
TL;DR: There are striking variations in the risk of different cancers by geographic area, most of the international variation is due to exposure to known or suspected risk factors related to lifestyle or environment, and provides a clear challenge to prevention.
Abstract: Estimates of the worldwide incidence, mortality and prevalence of 26 cancers in the year 2002 are now available in the GLOBOCAN series of the International Agency for Research on Cancer. The results are presented here in summary form, including the geographic variation between 20 large "areas" of the world. Overall, there were 10.9 million new cases, 6.7 million deaths, and 24.6 million persons alive with cancer (within three years of diagnosis). The most commonly diagnosed cancers are lung (1.35 million), breast (1.15 million), and colorectal (1 million); the most common causes of cancer death are lung cancer (1.18 million deaths), stomach cancer (700,000 deaths), and liver cancer (598,000 deaths). The most prevalent cancer in the world is breast cancer (4.4 million survivors up to 5 years following diagnosis). There are striking variations in the risk of different cancers by geographic area. Most of the international variation is due to exposure to known or suspected risk factors related to lifestyle or environment, and provides a clear challenge to prevention.

17,730 citations

Book
17 Sep 2013
TL;DR: Purposes and Principles of Cancer Staging and End-Results Reporting are explained.
Abstract: General Information on Cancer Staging and End-Results Reporting.- Purposes and Principles of Cancer Staging.- Cancer Survival Analysis.- Head and Neck.- Lip and Oral Cavity.- Pharynx.- Larynx.- Nasal Cavity and Paranasal Sinuses.- Major Salivary Glands.- Thyroid.- Mucosal Melanoma of the Head and Neck.- Digestive System.- Esophagus and Esophagogastric Junction.- Stomach.- Small Intestine.- Colon and Rectum.- Anus.- Gastrointestinal Stromal Tumor.- Neuroendocrine Tumors.- Liver.- Intrahepatic Bile Ducts.- Gallbladder.- Perihilar Bile Ducts.- Distal Bile Duct.- Ampulla of Vater.- Exocrine and Endocrine Pancreas.- Thorax.- Lung.- Pleural Mesothelioma.- Musculoskeletal Sites.- Bone.- Soft Tissue Sarcoma.- Skin.- Cutaneous Squamous Cell Carcinoma and Other Cutaneous Carcinomas.- Merkel Cell Carcinoma.- Melanoma of the Skin.- Breast.- Breast.- Gynecologic Sites.- Vulva.- Vagina.- Cervix Uteri.- Corpus Uteri.- Ovary and Primary Peritoneal Carcinoma.- Fallopian Tube.- Gestational Trophoblastic Tumors.- Genitourinary Sites.- Penis.- Prostate.- Testis.- Kidney.- Renal Pelvis and Ureter.- Urinary Bladder.- Urethra.- Adrenal.- Ophthalmic Sites.- Carcinoma of the Eyelid.- Carcinoma of the Conjunctiva.- Malignant Melanoma of the Conjunctiva.- Malignant Melanoma of the Uvea.- Retinoblastoma.- Carcinoma of the Lacrimal Gland.- Sarcoma of the Orbit.- Ocular Adnexal Lymphoma.- Central Nervous System.- Brain and Spinal Cord.- Lymphoid Neoplasms.- Lymphoid Neoplasms.

16,806 citations

Journal ArticleDOI
TL;DR: This timely monograph is a distillation of knowledge of hepatitis B, C and D, based on a review of 1000 studies by a small group of scientists, and it is concluded that hepatitis D virus cannot be classified as a human carcinogen.
Abstract: Viral hepatitis in all its forms is a major public health problem throughout the world, affecting several hundreds of millions of people. Viral hepatitis is a cause of considerable morbidity and mortality both from acute infection and chronic sequelae which include, in the case of hepatitis B, C and D, chronic active hepatitis and cirrhosis. Hepatocellular carcinoma, which is one of the 10 commonest cancers worldwide, is closely associated with hepatitis B and, at least in some regions of the world, with hepatitis C virus. This timely monograph is a distillation of knowledge of hepatitis B, C and D, based on a review of 1000 studies by a small group of scientists. (It is interesting to note in passing that some 5000 papers on viral hepatitis are published annually in the world literature.) The epidemiological, clinical and experimental data on the association between infection with hepatitis B virus and primary liver cancer in humans are reviewed in a readable and succinct format. The available information on hepatitis C and progression to chronic infection is also evaluated and it is concluded (perhaps a little prematurely) that hepatitis C virus is carcinogenic. However, it is concluded that hepatitis D virus, an unusual virus with a number of similarities to certain plant viral satellites and viroids, cannot be classified as a human carcinogen. There are some minor criticisms: there are few illustrations and some complex tabulations (for example, Table 6) and no subject index. A cumulative cross index to IARC Monographs is of little value and occupies nearly 30 pages. This small volume is a useful addition to the overwhelming literature on viral hepatitis, and the presentation is similar to the excellent World Health Organisation Technical Reports series on the subject published in the past. It is strongly recommended as a readable up-to-date summary of a complex subject; and at a cost of 65 Sw.fr (approximately £34) is excellent value. A J ZUCKERMAN

11,533 citations