Tuesday, October 28, 2003 Forums (held at 7:30 AM) this morning consisted of: “Chemoprevention of Genitourinary Cancers”, Role of Cancer Centers and Cooperative Groups in Cancer Prevention”, and SNP Selection for Association Studies: An Evolutionary Perspective”. Ann Fonfa attended: “Trends in Global Cancer Mortality Revisited”. Donald Maxwell Parkin, Chief, Unit of Descriptive Epidemiology, International Agency for Research on Cancer, Lyon, France told the audience that smoking has been taken up strongly by Spanish women, that Italy has no national mammography screening program but has seen the same decline in mortality as other European nations. Perhaps due to earlier diagnosis, better treatments (hormonal or chemotherapy). He said that since the mortality trend was similar in Europe and the U.S., it was probably due more to changes in treatment than screening success. Ann’s NOTE: reduction of amounts and length of time for chemotherapy are said to have impacted survival. There has been an increase in Europe of young women with squamous cancer of the cervix. This is probably related to HPV (viral) infections. Prostate cancer incidence is showing a blip of growth from the late 80's into the 90's. Mortality is relatively flat but may show a slight decrease (whether a country is screening with PSA tests or not). Asia and Africa are also showing a rise in incidence, in some part due to increased detection but perhaps due to diet, lack of exercise and rising rates of obesity. Esophageal cancer incidence is also on the rise, as is testicular and non Hodgkins lymphoma. Susan S. Devesa, Chief, Descriptive Studies Section, Biostatistics, NCI, Bethesda, MD, discusses lung cancer, the leading cause of cancer deaths worldwide. Mortality and incidence rates vary by country and sex. She suggested that rates may have peaked in Denmark, England, Canada, the U.S. and Australia. But rates are continuing to increase everywhere else and especially among women. Ann’s NOTE: Somehow ‘liberation’ got mixed up with smoking, could it be the pervasive results of advertising and sales promotion? Dr. D. discussed the way cause of death is shown on a death certificate, pointing out there are lines for immediate cause as well as underlying cause. This was in response to a question from Ann Fonfa about how deaths are recorded. The next plenary session (2) was titled “Life Cycle of Cancer Screening Evaluation: Efficacy, Implementation and Quality Performance”, and consisted of talks on “Evaluating the Performance of Breast Cancer Screening in Practice”, “Appropriate Utilization of Colon Cancer Screening and Surveillance: How to Address Underuse and Overuse”, and “Evaluation of Rapidly Evolving Technologies: Imaging Technologies as an Example”. The first speaker, Joann Elmore, Uwashington School of Medicine, Harborview Med Ctr, Seattle, WA discussed the controversies in mammography screening. David F. Ransohoff, Prof of Med & Epidemiology, UNC Chapel Hill, NC and NCI, Bethesda, MD, mentioned that he had been unable to connect to advocacy groups in colon cancer. Ann’s NOTE: His name and connections have been forwarded to several groups by us. Bruce Hillman, UVA Health Sciences Ctr, Charlottesville, VA discussed the “rapidity of technology innovation” in medical imaging. Plenary Session 3 “Targets for Prevention” included a talk by Andrew J. Danneburg, Prof of Med Weill Med College of Cornell U, NY, NY, on “COX-2". Dr. D. stated that COX-2 is one of 3 metabolic pathways for arachidonic acid. When COX-2 is overexpressed, it can be a target for treatment/prevention. This happens in many different types of cancer: Barrett’s Esophagus, bladder recurrence, gastric, pancreatic, prostate second primaries, breast, head & neck, cervical (CIN), and squamous cell. Celecoxib is a COX-2 inhibitor used in many studies. Some people fully respond to it, some not at all. In colorectal cancer, it is approved as adjuvant therapy for treating FAP. COX-2 overexpression is sufficient to induce mammary tumors in mice. There are currently more than 100 clinical trials of celexcoxib, e.g. breast cancer, oral leukoplakia, etc. Symposia 5-7 & 7A offered “Epigentic Changes in Prevention Targets” (including a discussion on “Tea Polyphenol (-) -Epigallocatechin-3-Gallate Inhibits DNA Methyltransferase and Reactivates Methylation-Silenced Genes in Cell Cancer Lines”), “The Role of Apoptosis in Carcinogenesis and Cancer Prevention” (focusing on colon and gastric cancer), and “Novel Models for Prevention”. Symposium 7A was added and featured talks on prostate cancer issues. Ann attended 7A which featured Chris Logothetis, Chair, Dept of Genitourinary Med Oncology, Prof of Med, Bessie McGoldrick Prof in Clinical Cancer Research, UT M.D. Anderson Cancer Ctr, Houston, TX as moderator. Dr. Logothetis mentioned the recent finasteride trial making note of the fact that more aggressive disease was shown in the treatment arm, though less overall occurrence than in the control arm. He told the audience that the biggest ‘challenge’ was in interpreting biology from needle biopsies. They are working on modifying current methods. He discussed the complex pathology that raised many questions even after a prostate had been removed. He told us that 200,000 cases are diagnosed, 80,000 are in treatment (26%), and 30,000 (11%) will die from the disease each year. Ian M. Thompson, Prof and Chief, Henry B and Edna Smith Dielmann Memorial Fund Chair in Urologic Science Div of Urology, UT Health Sciences Ctr, Austin, TX spoke about a prevention trial looking at men with BPH (benign prostatic hypertrophy) which featured a biopsy every three months for a year, then an end of study biopsy. About 25% of men with BPH go on to develop prostate cancer. Mark A. Rubin, Chief of Pathology, Brigham & Women’s Hospital, Boston, MA discussed the fact that there is no significant difference in the pathology of prostate cells in untreated individuals. He described a study in which pathologists tried to define a range of alterations in tested cases. They seem to have compared central and local pathology readings. Juergen K.V. Reichardt, Assoc Prof of Biochemistry & Molecular Bio and Preventive Med, USC Keck School of Medicine, Los Angeles, CA spoke about “SNPing Away at Prostate Cancer”. He said we need to think about genetic and genomic questions. He wants to look at long-term exposures and SNPs (single nucleotide polymorphisms which occur once every 200-1,000 benign prostates and are slightly more common in African American men. Peter H. Gann, Assoc Prof of Preventive Med, Feinberg School of Med, Northwestern U, Chicago, IL spoke about “Statistical/Epidemiological Considerations” spoke further about the Finasteride versus placebo trial among men with BPH. He said there were twice as many cases as expected in the placebo group. He also said they had predicted 20% deaths but got only 6.1 in the finasteride arm and 5.8 in the placebo arm. From Symposium 5: Conclusion drawn by S. Jill James, UArkansas for Medical Sciences, Little Rock. AR “(insights from in vivo and in vitro models) suggest that while adequate folate status is clearly chemopreventive, flate repletion may be protective or tumor-promoting depending on the pathophysiolic state of the cell.” And Chung Yang, Rutgers Univ, Piscataway, NJ, in a talk discussing green tea EGCG, said “...results demonstrate for the first time the inhibition of DNA methylation by a commonly consumed dietary constituent and suggest the potential use of EGCG for the prevention or reversal of related gene-silencing in the prevention of carcionogenesis.” From Symposium 6: “Recognition of the role of H. pylori as the major cause of non-cardia gastric cancer, ...is improving understanding of the molecular and cellular events occurring in the gastric epithelium after exposure to H. pylori. Such studies indicate that H. pylori contributes to apoptosis-resistance in gastric carcinogenesis.” (Steven F. Moss, Assoc Prof of Med, Div Gastroenterology, Brown Univ, Providence, RI) Remember we are NOT Doctors and have NO medical training. This site is like an Encylopedia - there are many pages, many links on many topics. Support our work with any size DONATION - see left side of any page - for how to donate. You can help raise awareness of CAM.