Carlos A. González, Paula Jakszyn, Guillem Pera, Antonio Agudo, Sheila Bingham, Domenico Palli, Pietro Ferrari, Heiner Boeing, Giuseppe del Giudice, Mario Plebani, Fátima Carneiro, Gabriella Nesi, Franco Berrino, Carlotta Sacerdote, Rosario Tumino, Salvatore Panico, Göran Berglund, Henrik Simán, Olof Nyrén, Göran Hallmans, Carmen Martinez, Miren Dorronsoro, Aurelio Barricarte, Carmen Navarro, José R. Quirós, Naomi Allen, Timothy J. Key, Nicholas E. Day, Jakob Linseisen, Gabriele Nagel, Manuela M. Bergmann, Kim Overvad, Majken K. Jensen, Anne Tjonneland, Anja Olsen, H. Bas Bueno-de-Mesquita, Marga Ocke, Petra H. M. Peeters, Mattijs E. Numans, Françoise Clavel-Chapelon, Marie-Christine Boutron-Ruault, Antonia Trichopoulou, Theodora Psaltopoulou, Dimitrios Roukos, Eiliv Lund, Bertrand Hemon, Rudolf Kaaks, Teresa Norat, Elio Riboli

Affiliations of authors: Department of Epidemiology, Catalan Institute of Oncology, Barcelona, Spain (CAG, PJ, GP, AA); Medical Research Council Dunn Human Nutrition Unit, Cambridge, United Kingdom (SB); Molecular and Nutritional Epidemiology Unit, CSPO–Scientific Institute of Tuscany, Florence, Italy (DP, MMB); German Institute of Human Nutrition, Potsdam–Rehbücke, Germany (HB); IRIS Research Center, Chiron-Vaccines, Siena, Italy (GdG); Servizio di Medicina di Laboratorio, Azienda Ospedaliera di Padova, Padua, Italy (MP); Institute of Molecular Pathology and Immunology of the University of Porto and Medical Faculty, Porto, Portugal (FC); Department of Human Pathology and Oncology, University of Florence, Florence, Italy (G. Nesi); Epidemiology Unit, Istituto Tumori, Milan, Italy (FB); University of Torino, Turin, Italy (CS); Cancer Registry, Azienda Ospedaliera “Civile M.P. Arezzo,” Ragusa, Italy (RT); Dipartamento di Medicina Clinica e Sperimentale, Federico II University, Compagnia di San Paolo, Naples, Italy (SP); Department of Medical Epidemiology, Karolinska Instututet, Stockholm, Sweden (GB, HS); Department of Nutritional Research, University of Umeå, Umeå, Sweden (ON, GH); Andalusian School of Public Health, Granada, Spain (CM); Department of Public Health of Guipuzkoa, San Sebastian, Spain (MD); Public Health Institute of Navarra, Pamplona, Spain (AB); Epidemiology Department, Health Council of Murcia, Murcia, Spain (CN); Public Health and Health Planning Directorate, Asturias, Spain (JRQ); Cancer Epidemiology Unit, University of Oxford, Oxford, United Kingdom (NA, TJK); Strangeways Research Laboratory, Cambridge, United Kingdom (NED); Division of Clinical Epidemiology, Deutsches Krebsforschungszentrum, Heidelberg, Germany (JL, G. Nagel); Department of Clinical Epidemiology, Aalborg Hospital, Aarhus University Hospital, Aalborg, Denmark (KO, MJK); Institute of Cancer Epidemiology, Danish Cancer Society, Copenhagen, Denmark (AT, AO); Center for Nutrition and Health, National Institute for Public Health and the Environment, Bilthoven, The Netherlands (HBBdM, MO); Julius Center for Health Sciences and Primary Care, University Medical Center, Utrecht, The Netherlands (PHMP, MEN); INSERM, Institut Gustave Roussy, Villejuif, France (FC-C, M-CB-R); Department of Hygiene and Epidemiology, Medical School, University of Athens, Athens, Greece (AT, TP); University of Ioannina, Medical School, University of Athens, Athens, Greece (DR); Institute of Community Medicine, University of Tromso, Tromso, Norway (EL); Nutrition and Hormones Group, International Agency for Research on Cancer, Lyon, France (PF, BH, RK, TN, ER)

Correspondence to: Carlos A. González, MD, PhD, Department of Epidemiology, Catalan Institute of Oncology, Barcelona, Spain (e-mail: cagonzalez@ico.scs.es

).

Background: Dietary factors are thought to have an important role in gastric and esophageal carcinogenesis, but evidence from cohort studies for such a role is lacking. We examined the risks of gastric cancer and esophageal adenocarcinoma associated with meat consumption within the European Prospective Investigation Into Cancer and Nutrition (EPIC) cohort. Methods: A total of 521 457 men and women aged 35–70 years in 10 European countries participated in the EPIC cohort. Dietary and lifestyle information was collected at recruitment. Cox proportional hazard models were used to examine associations between meat intake and risks of cardia and gastric noncardia cancers and esophageal adenocarcinoma. Data from a calibration substudy were used to correct hazard ratios (HRs) and 95% confidence intervals (CIs) for diet measurement errors. In a nested case–control study, we examined interactions between Helicobacter pylori infection status (i.e., plasma H. pylori antibodies) and meat intakes. All statistical tests were two-sided. Results: During a mean follow-up of 6.5 years, 330 gastric adenocarcinoma and 65 esophageal adenocarcinomas were diagnosed. Gastric noncardia cancer risk was statistically significantly associated with intakes of total meat (calibrated HR per 100-g/day increase = 3.52; 95% CI = 1.96 to 6.34), red meat (calibrated HR per 50-g/day increase = 1.73; 95% CI = 1.03 to 2.88), and processed meat (calibrated HR per 50-g/day increase = 2.45; 95% CI = 1.43 to 4.21). The association between the risk of gastric noncardia cancer and total meat intake was especially large in H. pylori-infected subjects (odds ratio per 100-g/day increase = 5.32; 95% CI = 2.10 to 13.4). Intakes of total, red, or processed meat were not associated with the risk of gastric cardia cancer. A positive but non–statistically significant association was observed between esophageal adenocarcinoma cancer risk and total and processed meat intake in the calibrated model. In this study population, the absolute risk of development of gastric adenocarcinoma within 10 years for a study subject aged 60 years was 0.26% for the lowest quartile of total meat intake and 0.33% for the highest quartile of total meat intake. Conclusion: Total, red, and processed meat intakes were associated with an increased risk of gastric noncardia cancer, especially in H. pylori antibody-positive subjects, but not with cardia gastric cancer.

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Susanna C. Larsson, Nicola Orsini, Alicja Wolk

Affiliation of authors: Division of Nutritional Epidemiology, The National Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden

Correspondence to: Susanna C. Larsson, MSc, Division of Nutritional Epidemiology, The National Institute of Environmental Medicine, Karolinska Institutet, Box 210, SE-171 77, Stockholm, Sweden

Background: The relationship between processed meat consumption and the risk of stomach cancer is controversial. We conducted a meta-analysis to summarize available evidence from cohort and case–control studies on this issue. Methods: We searched Medline for studies of processed meat consumption and stomach cancer published from January 1966 through March 2006. Random-effects models were used to pool the relative risks from individual studies. All statistical tests were two-sided. Results: Six prospective cohort studies (involving 2209 stomach cancer patients) and nine case–control studies (2495 case patients) were eligible for inclusion in the dose–response meta-analysis of processed meat consumption. The estimated summary relative risks of stomach cancer for an increase in processed meat consumption of 30 g/day, approximately half of an average serving, were 1.15 (95% confidence interval [CI] = 1.04 to 1.27) for the cohort studies and 1.38 (95% CI = 1.19 to 1.60) for the case–control studies. There was no statistically significant heterogeneity among the cohort studies (P = .42) or among the case–control studies (P = .19). In three cohort and four case–control studies that examined the association between bacon consumption and stomach cancer, the summary relative risk was 1.37 (95% CI = 1.17 to 1.61) for the highest versus lowest intake categories of bacon, without heterogeneity among these studies (P = .66). Conclusion: Increased consumption of processed meat is associated with an increased risk of stomach cancer. However, the possibility that the association may be confounded or modified by other factors cannot be ruled out.

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Theories that Napoleon was betrayed, poisoned, or a victim of inappropriate medical treatment have been undermined by new research based on the emperor’s trouser collection. The research has shown that his weight loss in his final year is consistent with a severe progressive illness. It lends credence to the idea that Napoleon died of stomach cancer, which was the cause of death specified in the original autopsy.

Napoleon died in exile on the island of St Helena and almost since the day of his death in 1821 there have been conspiracy theories about the cause. There have also been suggestions that chronic exposure to arsenic and medication errors were involved, while the theories that he had been poisoned was given a considerable boost in 1961, when a raised arsenic concentration was found in his hair.

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We assessed the trends in the proportion of articles on gastric cancer published in major cancer journals, the research fields of interest, and the first author’s affiliation. Articles in PubMed, addressing cancer in general and stomach cancer in particular, were quantified. Abstracts of gastric cancer articles were hand-searched. The British Journal of Cancer, Cancer, Cancer Research, the International Journal of Cancer, and the Journal of the National Cancer Institute were included in the journal survey. Stomach cancer was addressed in 2.9% of the articles in 1982–1984 and 3.3% in 2000–2002. The proportion of articles from Asia increased (32.2% vs 50.2%) and that for the United States decreased (34.4% vs 15.1%) in 2000–2002. Articles addressing etiologic genetic factors were more frequent in 2000–2002 (11.5% vs 61.6%). The proportion of stomach cancer articles was largely below the expected share considering the frequency of malignancies, and did not reflect the geography of biomedical publications. A trend was observed favoring the evaluation of genetic factors.

Keywords: Stomach neoplasms; Research; Trends

Document Type: Research article

DOI: 10.1007/s10120-004-0284-5

Affiliations: 1: Department of Hygiene and Epidemiology, University of Porto Medical School, Al. Prof. Hernâni Monteiro, 4200-319, Porto, Portugal,

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Dopamine Treatment Retards Growth of Gastric Cancer by Inhibiting Angiogenesis

Debanjan Chakroborty¹, Chandrani Sarkar¹, Rita Basu Mitra⁴, Samir Banerjee¹, Partha Sarathi Dasgupta¹ and Sujit Basu^2,3

¹ Signal Transduction and Biogenic Amines Laboratory and ² Department of Medical Oncology, Chittaranjan National Cancer Institute, Calcutta, ³ Mayo Clinic Cancer Center and Department of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, Minnesota, and ⁴ Department of Pathology, Institute of Postgraduate Medical Education and Research, Calcutta, India

ABSTRACT

Purpose: It has been recently shown that the catecholamine neurotransmitter dopamine (DA) strongly and selectively inhibits vascular permeability factor/vascular endothelial growth factor (VPF/VEGF)-induced angiogenesis. Gastric cancer is highly angiogenic and is dependent on VEGF for its growth and progression. Because substantial amounts of DA present in normal stomach tissues has been implicated in several gastric functions, we therefore investigated the role, if any, of this neurotransmitter in the growth and progression of gastric cancer.

Experimental Design: Initially, the status of DA and tyrosine hydroxylase, the rate-limiting enzyme required for DA synthesis, were determined in human gastric cancer tissues and in N-methyl-N‘-nitro-N-nitrosoguanidine (MNNG)-induced gastric cancer tissues of rats. On the basis of our observation of inverse correlation between stomach DA and gastric cancer growth, we determined the effect of pharmacological dose of DA on the angiogenesis and growth of MNNG induced gastric cancer in rats and Hs746T human gastric cancer in nude mice.

Results: DA and tyrosine hydroxylase were absent in both human and rat gastric cancer tissues. On the contrary, a low nontoxic pharmacological dose of DA significantly retarded tumor angiogenesis by inhibiting VEGFR-2 phosphorylation in tumor endothelial cells, which expressed DA D₂ receptors. This action of DA was associated with the growth inhibition of both MNNG-induced rat malignant gastric tumors and xenotransplanted human gastric cancer in nude mice.

Conclusions: Our study demonstrates that there is an inverse correlation between endogenous stomach DA and gastric cancer and indicates that DA already in clinical use for other purposes might have a role as an antiangiogenic agent in the treatment of gastric cancer.

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At one time, stomach cancer was the most common type of cancer known in the United States. As the years progressed, the disease became less common among patients. While there are no definitive answers as to why, it’s thought to be related to the decline in salted or smoked food intake. Even with the decline in cases, this disease still presents a serious problem throughout the nation and the rest of the world.

While studies are unclear, some experts recommend a balanced diet to fighting against cancer development. In addition, researchers believe that damaged DNA in the stomach cells may lead to cancer. A large majority of individuals are infected by a bacteria known as H. pylori, which resides in the stomach. It is unknown how this bacteria is transmitted, but it is believed to be spread from individuals or through drinking water. H. pylori causes ulcers and may also be a leading cause of stomach cancer.

Foods, which include nitrates, are also of concern among cancer researchers. Foods such as hot dogs, certain deli meats, bacon and ham contain substances known to cause stomach cancer, as does red meat, and smoked or salted foods. Certain foods are believed to protect against stomach cancer, including fruits or vegetables. Items such as tomatoes, sweet potatoes and carrots are especially helpful in the prevention of this disease.

Perhaps one of the most troubling facts about the disease is that stomach cancer is difficult to diagnose. A cancerous tumor may be quite large by the time that it is diagnosed due to the lack of symptoms associated with stomach cancer. When present, the most common signs include upper abdominal pain, especially after eating. Other symptoms include bleeding, weight loss and general weakness. Patients who experience early fullness when eating should also be on alert as this may be a symptom of the stomach’s inability to expand due to the presence of a tumor. If left untreated, the cancer cells can spread quickly to other parts of the body and cause even further damage. Part of the problem is that, like many other illnesses, the symptoms sound very similar to those of other ailments. The presence of one or more of these does not necessarily confirm the presence of cancer, but it should cause the individual to be alert to the possibility.

Studies show that men are twice as likely to develop stomach cancer and is most common in individuals from age 40 to 80. This disease is rarely present in individuals 40 years of ago or younger. In addition, the use of tobacco and alcohol are perhaps the most obvious cancer causing agents. Studies have shown that both men and woman are more likely to develop stomach cancer if they smoke. Other factors, including family history and obesity, can encourage the development of stomach cancer.

This article should not be construed as professional medical advice. If you, or someone that you know, is concerned about the possibility of cancer, you should seek medical attention immediately. A medical doctor can discuss various options, prevention and treatment possibilities should the presence of cancer be detected. A series of tests may be conducted in order to confirm, or rule out, any such diagnosis and can only be done by a medical doctor.

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JeanMarie Houghton,^1* Calin Stoicov,¹ Sachiyo Nomura,^2,3 Arlin B. Rogers,⁴ Jane Carlson,¹ Hanchen Li,¹ Xun Cai,¹ James G. Fox,⁴ James R. Goldenring,^2,5 Timothy C. Wang^1*

Epithelial cancers are believed to originate from transformation of tissue stem cells. However, bone marrow–derived cells (BMDCs), which are frequently recruited to sites of tissue injury and inflammation, might also represent a potential source of malignancy. We show that although acute injury, acute inflammation, or transient parietal cell loss within the stomach do not lead to BMDC recruitment, chronic infection of C57BL/6 mice with Helicobacter, a known carcinogen, induces repopulation of the stomach with BMDCs. Subsequently, these cells progress through metaplasia and dysplasia to intraepithelial cancer. These findings suggest that epithelial cancers can originate from marrow-derived sources and thus have broad implications for the multistep model of cancer progression.

¹ Department of Medicine and Cancer Biology, University of Massachusetts Medical School, Worcester, MA 01605, USA.

² Epithelial Biology Program, Department of Surgery and Vanderbilt-Ingram Cancer Center, Vanderbilt University School of Medicine, Nashville, TN 37232, USA.

³ Department of Gastrointestinal Surgery, Graduate School of Medicine, University of Tokyo, Bunkyo-ku, Tokyo, 113-8655, Japan.

⁴ Division of Comparative Medicine, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.

⁵ The Veterans Administration Medical Center, Nashville, TN 37232, USA.

Present address: Department of Medicine and Cancer Center, Columbia College of Physicians and Surgeons, New York, NY 10032, USA.

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Cancer, stomach: Cancer of the stomach, the main organ that holds food for digestion. Worldwide, stomach cancer is the second most frequent cancer and the second leading cause of death from cancer. It can develop in any part of the stomach and spread to other organs. It is also known as gastric cancer.

Duodenal ulcers (peptic ulcers) are not associated with stomach cancer. However, infection with a bacterium called Helicobacter pylori is associated with gastric cancer. In one study, gastric cancer developed in about 3% of the infected patients and none of the uninfected patients. Eradication of the bacterium prevents or delays the development of gastric cancer. The risk of gastric cancer is also increased in Down syndrome.

Symptoms of stomach cancer are often vague, such as loss of appetite and weight, so diagnosis is often delayed. The cancer is diagnosed definitively with a biopsy of stomach tissue.

Cancer of the stomach is difficult to cure unless it is found early. Treatment may include surgery, chemotherapy and radiotherapy. Surgery is the most common treatment. It involves removal of part (subtotal or partial gastrectomy) or all (total gastrectomy) of the stomach.

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Smoking has recently been recognised as causally associated with the development of gastric cancer (GC). However, evidence on the effect by sex, duration and intensity of smoking, anatomic subsite and cessation of smoking is limited. Our objective was to assess the relation between tobacco use and GC incidence in the European Prospective Investigation into Cancer and Nutrition (EPIC). We studied data from 521,468 individuals recruited from 10 European countries taking part in the EPIC study. Participants completed lifestyle questionnaires that included questions on lifetime consumption of tobacco and diet in 1991-1998. Participants were followed until September 2002, and during that period 305 cases of stomach cancer were identified. After exclusions, 274 were eligible for the analysis, using the Cox proportional hazard model. After adjustment for educational level, consumption of fresh fruit, vegetables and preserved meat, alcohol intake and body mass index (BMI), there was a significant association between cigarette smoking and gastric cancer risk: the hazard ratio (HR) for ever smokers was 1.45 (95% confidence interval [CI] = 1.08-1.94). The HR of current cigarette smoking was 1.73 (95% CI = 1.06-2.83) in males and 1.87 (95% CI = 1.12-3.12) in females. Hazard ratios increased with intensity and duration of cigarette smoked. A significant decrease of risk was observed after 10 years of quitting smoking. A preliminary analysis of 121 cases with identified anatomic site showed that current cigarette smokers had a higher HR of GC in the cardia (HR = 4.10) than in the distal part of the stomach (HR = 1.94). In this cohort, 17.6 % (95% CI = 10.5-29.5 %) of GC cases may be attributable to smoking. Findings from this large study support the causal relation between smoking and gastric cancer in this European population. Stomach cancer should be added to the burden of diseases caused by smoking. Copyright 2003 Wiley-Liss, Inc.

PMID: 14520702 [PubMed - indexed for MEDLINE]

Related Links

—      Meat intake and risk of stomach and esophageal adenocarcinoma within the European Prospective Investigation Into Cancer and Nutrition (EPIC). [J Natl Cancer Inst. 2006]

—      Socioeconomic position and the risk of gastric and oesophageal cancer in the European Prospective Investigation into Cancer and Nutrition (EPIC-EURGAST). [Int J Epidemiol. 2007]

—      Fruits and vegetables and lung cancer: Findings from the European Prospective Investigation into Cancer and Nutrition. [Int J Cancer. 2004]

—      Smoking and alcohol drinking in relation to risk of gastric cancer: a population-based, prospective cohort study. [Int J Cancer. 2007]

—      Fruit and vegetable intake and the risk of stomach and oesophagus adenocarcinoma in the European Prospective Investigation into Cancer and Nutrition (EPIC-EURGAST). [Int J Cancer. 2006]

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In the United States, more than 20,000 individuals are diagnosed with gastric (stomach) cancer each year. Men are more likely to have stomach cancer than women are. Stomach cancer usually affects persons who are older than 55 years, although it may occur at younger ages. Individuals from Asia have the highest rates of stomach cancer. Because stomach cancer may occur without symptoms, it may be in advanced stages by the time the diagnosis is made. Treatment is then directed at making the patient more comfortable and improving quality of life. Stomach cancer can metastasize (spread) to other organs of the body. The January 14, 2004, issue of JAMA includes an article about gastric cancer.http://jama.ama-assn.org/cgi/content/full/291/2/266 - FIGJPG0114F1#FIGJPG0114F1

SYMPTOMS OF STOMACH CANCER

—      Loss of appetite

—      Weight loss without dieting

—      Abdominal pain, with or without swelling

—      Feeling full after small amounts of food

—      Indigestion

—      Nausea or vomiting

—      Vomiting blood

TESTING FOR STOMACH CANCER

If your doctor suspects that you may have stomach cancer, you will have basic tests such as a blood test to look for anemia (low red blood cell count). Other tests may include a computed tomography (CT) scan (computerized x-ray) of the abdomen or an upper GI series (a special x-ray test using a barium-containing liquid). A doctor can examine the inside of the stomach using an endoscope, a lighted tube that is placed through the mouth into the esophagus (the tube that connects the mouth to the stomach) and then into the stomach. This test is done by a gastroenterologist, a doctor who specializes in the diagnosis and management of digestive diseases.

TREATING STOMACH CANCER

Surgery is often the main treatment for stomach cancer. Several different operations are used based on the location of the cancer in the stomach. Because these operations are all considered major surgery, patients will need medical preparation before surgery and time for recovery from the operation. Risks and benefits of these operations may vary with specific medical conditions. Chemotherapy (use of anticancer drugs) and radiation therapy (use of high-energy rays to kill cancer cells) may be used in addition to surgery to help in treating stomach cancer. Because each patient is different, treatment is individualized for each patient’s particular situation. Both chemotherapy and radiation therapy can be used to improve quality of life and decrease symptoms from stomach cancer, even if curative surgery is not possible. Scientists are trying to learn more about what causes this type of cancer and how it can be detected earlier. Finding stomach cancer in the early stages improves chances of living longer if proper treatment is received.

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