על הקשר בין וירוסים לסרטן

http://health.nana10.co.il/Article/?ArticleID=605007&TypeID=&sid=220

ידוע מזמן שוירוסים מעורבים בכ 15% מסך כל הגידולים הסרטניים באדם. ידוע גם שגידולים מסויימים עוברים רגרסיה ספונטנית ללא כל טיפול. במחקר הנורבגי לא הוכיחו שבחולות שסבלו מסרטן השד הגידול נעלם. התיאוריה של דר' חנן פולנסקי (דרך אגב הוא כלכלן!) מעניינת אבל אין לה כל הוכחה. על תוסף המזון של דר' פולנסקי, "גן עדן", שאמור לחסל דנ"א זר וכך למנוע מחלות אין כל מידע ואין כל הוכחה מעשית שזה אכן יעיל.

מה זו הוכחה? את המאמר Bonnet et al 1999 אתה מכיר? במחקר מצאו באמצעות “real time PCR” דנ"א של EBV (סוג אחד בלבד של דנ"א זר) ב52% מגידולי סרטן השד! (לא 15% כמו שאתה כותב אלא ב-52%!) בנוסף המחקר הראה שבריקמה הבריאה ליד הגידול לא היה דנ"א של EBV (ב-90% מהדגימות!) איך אתה מסביר את התוצאות האלו? ואת המאמר Perkins 2006 אתה מכיר? במאמר זה החוקרים מצאו דנ"א של EBV ב 46% מהגידולים! בנוסף, המחקר הראה ב-64% מדגימות הדם של החולות הכיל את הדנ"א הזר. מה בדיוק הדנ"א הזר עושה ב- 50% מהגידולים הללו? הוא במקרה שם? יתר על כן, שני מחקרים אלו הם רק קצה הקרחון. מאז הפירסום של התגלית של ד"ר פולנסקי מספר רב של מחקרים דווחו תוצאות דומות, ובסרטנים שונים. מצטער,אבל אתה פשוט לא בעינינים.

1: Cancer Res. 2008 Oct 1;68(19):7693-706. The history of tumor virology. In the century since its inception, the field of tumor virology has provided groundbreaking insights into the causes of human cancer. Peyton Rous founded this scientific field in 1911 by discovering an avian virus that induced tumors in chickens; however, it took 40 years for the scientific community to comprehend the effect of this seminal finding. Later identification of mammalian tumor viruses in the 1930s by Richard Shope AND John Bittner, AND in the 1950s by Ludwik Gross, sparked the first intense interest in tumor virology by suggesting the possibility of a similar causal role for viruses in human cancers. This change in attitude opened the door in the 1960s AND 1970s for the discovery of the first human tumor viruses--EBV, hepatitis B virus, AND the papillomaviruses. Such knowledge proved instrumental to the development of the first cancer vaccines against cancers having an infectious etiology. Tumor virologists additionally recognized that viruses could serve as powerful discovery tools, leading to revolutionary breakthroughs in the 1970s AND 1980s that included the concept of the oncogene, the identification of the p53 tumor suppressor, AND the function of the retinoblastoma tumor suppressor. The subsequent availability of more advanced molecular technologies paved the way in the 1980s AND 1990s for the identification of additional human tumor viruses--human T-cell leukemia virus type 1, hepatitis C virus, AND Kaposi's sarcoma virus. In fact, current estimates suggest that viruses are involved in 15% to 20% of human cancers worldwide. Thus, viruses not only have been shown to represent etiologic agents for many human cancers but have also served as tools to reveal mechanisms that are involved in all human malignancies. This rich history promises that tumor virology will continue to contribute to our understanding of cancer AND to the development of new therapeutic AND preventive measures for this disease in the 21st century. Methods Mol Biol. 2009;471:421-38. Do viruses cause breast cancer? Because mouse mammary tumor virus (MMTV; the Bittner virus) is the proven cause of breast cancer in both field AND experimental mice, similar viruses have long been suspects as a potential cause of human breast cancer. MMTV-like viral genetic material has been identified in human breast tumors, but there is no definitive evidence whether MMTV is causal AND not merely an innocuous infection in humans. High-risk human papilloma viruses (HPVs), Epstein-Barr (EBV), AND other viruses also have been identified in human breast tumors, but again there is no definitive evidence for a causal role. Any viral hypothesis as a cause of breast cancer must take into account the most striking epidemiologic feature of human breast cancer, the three- to sixfold differences in mortality AND up to eightfold differences in incidence between some Asian AND Western populations. These differences dramatically lessen to a two- to threefold difference within one OR two generations of migration of females from low to high risk of breast cancer countries. In this chapter, a plausible explanation for these phenomena is offered; that is, the hypothesis that oncogenic viruses such as MMTV AND high-risk HPVs may initiate some breast cancers in most populations. Furthermore, dietary patterns are suggested to determine circulating sex hormone levels, which in turn promote the replication of the hormone-dependent viruses MMTV AND HPV. In addition, diet AND hormones promote growth of both normal AND malignant cells. Finally, the hypothesis that migrants from low to high risk of breast cancer countries change their food consumption patterns is suggested, which leads to higher circulating hormone levels, which in turn promotes viral replication, which initiates breast oncogenesis, which is enhanced by sex AND growth hormones.