Albert Szent-Györgyi 简历，图片是其得回诺贝尔奖时照得Albert Szent-Györgyi – BiographyAlbert von Szent-Györgyi was born in Budapest on September 16， 1893， the son of Nicolaus von Szent-Györgyi， a great landed proprietor and Josefine， whose father， Joseph Lenhossék， and brother Michael were both Professors of Anatomy in the University of Budapest. He matriculated in 1911 and entered his uncle's laboratory where he studied until the outbreak of World War I when he was mobilized. He served on the Italian and Russian fronts， gaining the Silver Medal for Valour， and he was discharged in 1917 after being wounded in action. He completed his studies in Budapest and then worked successively with the pharmacologist， G. Mansfeld at Pozsony， with Armin von Tschermak at Prague， where he studied electrophysiology， and with L. Michaelis in Berlin， before he went to Hamburg for a two-year course in physical chemistry at the Institute for Tropical Hygiene.In 1920 he became an assistant at the University Institute of Pharmocology in Leiden and from 1922 to 1926 he worked with H. J. Hamburger at the Physiology Institute， Groningen， The Netherlands. In 1927 he went to Cambridge as a Rockefeller Fellow， working under F. G. Hopkins， and spent one year at the Mayo Foundation， Rochester， Minnesota， before returning to Cambridge. In 1930 he obtained the Chair of Medical Chemistry at the University of Szeged and in 1935 he also took the Chair in Organic Chemistry. At the end of World War II， he took the Chair of Medical Chemistry at Budapest and in 1947 he left Hungary to settle in the United States where he is Director of Research， Institute of Muscle Research， Woods Hole， Massachusetts.Szent-Györgyi's early researches at Groningen concerned the chemistry of cell respiration. He described the interdependence of oxygen and hydrogen activation and made his first observations on co-dehydrases and the polyphenol oxidase systems of plants. He also demonstrated the existence of a reducing substance in plant and animal tissues. At Cambridge and during his early spell in the United States， he isolated from adrenals this reducing substance， which is now known as ascorbic acid. Returning to Cambridge in 1929， he later described the pharmacological activity of the nucleotides with Drury.On his return to Hungary， he noted the anti-scorbutic activity of ascorbic acid and discovered that paprika (capsicum annuum) was a rich source of vitamin C. His persistent studies of biological oxidation led to the recognition of the catalytic function of the C4-dicarboxylic acids， the discovery of «cytoflav» (flavin) and a recognition of the biological activity and probable vitamin nature of flavanone (vitamin P).In 1938 he commenced work on muscle research and quickly discovered the proteins actin and myosin and their complex. This led to a reproduction of the fundamental reaction of muscle contraction which formed the foundation of muscle research in the following decades. The preservation of biological material in glycerine， which has had extensive application including agricultural use in the preservation of sperm， has resulted from his more recent work. He has also developed the use of rabbit psoas muscle as an experimental material， published theories on the problems of energetics and investigated the regulation of growth and cell membrane potential， and the hormonal function of the thymus gland.Szent-Györgyi， a member of many scientifc societies， is a Past President of the Academy of Sciences， Budapest， and a Vice-President of the National Academy， Budapest. He was Visiting Professor， Harvard University in 1936 and Franchi Professor， University of Liège， 1938. He received the Cameron Prize (Edinburgh) in 1946 and the Lasker Award in 1954. His many publications include Oxidation， Fermentation， Vitamins， Health and Disease (1939); Muscular Contraction (1947); The Nature of Life (1947); Contraction in Body and Heart Muscle (1953); and Bioenergetics (1957).Szent-Györgyi married Cornelia Demény， daughter of the Hungarian Postmaster-General， in 1917. During the 1930's he was actively anti-Nazi and during World War II he became a Swedish citizen - he was given extensive help by the Swedish Embassy in Budapest. In 1941， he married Màrta Borbiro， a co-worker at Woods Hole: they have one daughter.He is interested in sport of all kinds， his favourites being sailing and alpinism.From Nobel Lectures， Physiology or Medicine 1922-1941， Elsevier Publishing Company， Amsterdam， 1965 This autobiography/biography was written at the time of the award and later published in the book series Les Prix Nobel/Nobel Lectures. The information is sometimes updated with an addendum submitted by the Laureate. To cite this document， always state the source as shown above.Albert Szent-Györgyi died on October 22， 1986. screen.width-333)this.width=screen.width-333" width=140 height=198 title="Click to view full szent-gyorgyi.gif (140 X 198)" border=0 align=absmiddle>磨蹭最大的特色便是将启事弱化，一朝发生有无启事就不紧迫了磨蹭承认无序和不成瞻望，磨蹭要贬责的是创造条目去使无序酿成有序(比如维甲酸率领肿瘤细胞分化.使无序分化的细胞都向有序分化达到颐养指标，这个比方不一定正确)，概况是有序变为无序(一队东说念主过桥正步走不错因为共振引起桥垮塌，但闲逸走就不会).究诘的指标便是为了欺诈，肿瘤究诘迟迟没灵验果便是因为她触及到了人命，虚弱的本色，有一句话一直引发着我"肿瘤被治服的时辰 ，也便是东说念主类揭开人命本色奥密的时辰.有一句话一直不念念说出来，其实倭寇在医学基础究诘上比咱们强许多，他们在NATURE SCIENCE 险些期期有著作发表，他们说过21世纪要拿几十个诺贝尔奖，就拿cypress1975的非整倍体学说来讲，倭寇们早就闪耀到染色体辞别极端跟肿瘤的关系了，SGO1(SHUGOSHIN1) SGO2这些跟辞别关系的卵白就发表在NATURE上，SHUGOSHIN带有浓厚的倭寇颜色的名字，中国有吗?莫得基础究诘临床永久跟在东说念主家屁股背面，今天分子靶向颐养，嗡，一窝风:未来RNAI，嗡，又一窝风;后天肿瘤干细胞，哗，又掉头.什么原因?没我方基础，就只消靠东说念主家，东说念主家基因你基因，东说念主家RNA你也RNA，东说念主家卵白了，喔，你就跟不上了.中国有民间医学国际也有，而况这些东说念主物都是很有来头，包括诺贝尔奖得回者望望这些东说念主如何意志和颐养肿瘤>Revised lecture at the meeting of the Nobel-Laureates on June 30， 1966at Lindau， Lake Constance， Germanyby Otto WarburgDirector， Max Planck-Institute for Cell Physiology， Berlin-DahlemEnglish Edition by Dean BurkNational Cancer Institute， Bethesda， Maryland， USAThe Second Revised EditionPublished by Konrad Triltsch， W黵zburg， Germany1969Preface to the Second Revised German Edition of the Lindau Lecture(The way to prevention of cancer) screen.width-333)this.width=screen.width-333" width=171 height=250 title="Click to view full owarbug002p1.jpg (171 X 250)" border=0 align=absmiddle>This graph (based on the work of E. Sinn et al， Cell 49:465，1987) shows the synergistic effect of two oncogenes. The fraction (%) of transgenic mice without tumors is shown as a function of age. Three groups are shown: those mice transgenic for a hyperactive myc alone (blue) those transgenic for ras alone (green) those transgenic for both myc and ras (red) screen.width-333)this.width=screen.width-333" width=399 height=341 title="Click to view full myc_ras_Sinn.gif (399 X 341)" border=0 align=absmiddle>Harvey Ras oncogeneCancer occurs when the growth and differentiation of cells in a body tissue become uncontrolled and deranged. While no two cancers are genetically identical (even in the same tissue type)， there are relatively few ways in which normal cell growth can go wrong. One of these is to make a gene that stimulates cell growth hyperactive; this altered gene is known as an 'oncogene'.Ras is one such oncogene product that is found on chromosome 11. It is found in normal cells， where it helps to relay signals by acting as a switch. When receptors on the cell surface are stimulated (by a hormone， for example)， Ras is switched on and transduces signals that tell the cell to grow. If the cell-surface receptor is not stimulated， Ras is not activated and so the pathway that results in cell growth is not initiated. In about 30% of human cancers， Ras is mutated so that it is permanently switched on， telling the cell to grow regardless of whether receptors on the cell surface are activated or not.Usually， a single oncogene is not enough to turn a normal cell into a cancer cell， and many mutations in a number of different genes may be required to make a cell cancerous. To help unravel the intricate network of events that lead to cancer， mice are being used to model the human disease， which will further our understanding and help to identify possible targets for new drugs and therapies> screen.width-333)this.width=screen.width-333" width=250 height=310 title="Click to view full HRAS.gif (250 X 310)" border=0 align=absmiddle>What is p53 ?> screen.width-333)this.width=screen.width-333" width=492 height=275 title="Click to view full p53_structure.gif (492 X 275)" border=0 align=absmiddle>p53 MUTATIONS IN HUMAN CANCER> （缩略图，点击图片皆集看原图）The p53 tumor suppressor protein> screen.width-333)this.width=screen.width-333" width=234 height=266 title="Click to view full p53.gif (234 X 266)" border=0 align=absmiddle>太好了，这个帖子对生人很有平正！谢谢！！！抗体产生的机制【SOE-209】ギリモザ バコバコ乱交 Ami，Edelman（1972年诺贝尔奖得回者）的极品Gally JA， Edelman GM. The genetic control of immunoglobulin synthesis.Annu Rev Genet. 1972;6:1-46. Review. . Gally JA， Edelman GM. Somatic translocation of antibody genes.Nature. 1970 Jul 25;227(5256):341-8. Review. . Edelman GM， Gall WE. The antibody problem.Annu Rev Biochem. 1969;38:415-66. screen.width-333)this.width=screen.width-333" width=140 height=198 title="Click to view full edelman.gif (140 X 198)" border=0 align=absmiddle>Jerne的抗私有型表面：镜像表面Immunol Rev. 1984 Jun;79:5-24.Idiotypic networks and other preconceived ideas.Jerne NK.The preceding section implies that the immune system (like the brain) reflects first ourselves， then produces a reflection of this reflection， and that subsequently it reflects the outside world: a hall of mirrors. The second mirror images (i.e.， stable anti-idiotypic elements) may well be more complex than the first images (i.e.， anti-self). Both give rise to distortions (e.g.， mutations， gene rearrangements) permitting the recognition of nonself. The mirror images of the outside world， however， do not have permanency in the genome. Every individual must start with self. Paraphrasing Nicolas Schoffer (Schoffer 1982): those who always seek exterior pressures (e.g.， microbes) to account for the evolution of the sets of V genes， would do well to turn their vision towards the interiors of themselves， and there discover the mystery， perhaps never completely revealable， of the immune system. screen.width-333)this.width=screen.width-333" width=100 height=141 title="Click to view full jerne.jpg (100 X 141)" border=0 align=absmiddle>宇宙好【SOE-209】ギリモザ バコバコ乱交 Ami，我是生人，刚加入肿瘤行业，最念念先知说念一些临床实用的决议，以及关系的学问，有莫得什么保举啊？你们讲的都是作念试验的东西，对我来说，现时还太难了。最近，客岁得回好意思国科学院院士名称的 Jaenisch R发表著作：平庸的基因钤记丢失可导致小鼠发生多种肿瘤，该试验初度诠释不需要基因突变，仅仅基因钤记的改革就足以引起癌症。Cancer Cell. 2005 Oct;8(4):275-85. Global loss of imprinting leads to widespread tumorigenesis in adult mice.Holm TM， Jackson-Grusby L， Brambrink T， Yamada Y， Rideout WM 3rd， Jaenisch R.Whitehead Institute for Biomedical Research， Cambridge， Massachusetts 02142， Boston， USA.Loss of imprinting (LOI)， commonly observed in human tumors， refers to loss of monoallelic gene regulation normally conferred by parent-of-origin-specific DNA methylation. To test the function of LOI in tumorigenesis， we developed a model by using transient demethylation to generate imprint-free mouse embryonic stem cells (IF-ES cells). Embryonic fibroblasts derived from IF-ES cells (IF-MEFs) display TGFbeta resistance and reduced p19 and p53 expression and form tumors in SCID mice. IF-MEFs exhibit spontaneous immortalization and cooperate with H-Ras in cellular transformation. Chimeric animals derived from IF-ES cells develop multiple tumors arising from the injected IF-ES cells within 12 months. These data demonstrate that LOI alone can predispose cells to tumorigenesis and identify a pathway through which immortality conferred by LOI lowers the threshold for transformation.跟踪冷泉试验室的杂志，不错明晰的看到癌症的历史究诘进度：Cold Spring Harb Symp Quant Biol.cypress1975兄。细胞癌基因的发现者，1989年诺贝尔奖得回者J. Michael Bishop 合计：癌基因的究诘需要究诘两个方面：癌基因在癌变的运行历程中的作用；癌基因在保管癌细胞表型中的作用，后者更为紧迫。> （缩略图，点击图片皆集看原图）太好了， 向楼主问候， 我要好顺眼看这些文件.太好了太好了：）有东说念主要p53的著作，以下是对于p53和apoptosis的 1: Int J Mol Med. 2002 Jan;9(1):19-24.A potential role of p53 and WOX1 in mitochondrial apoptosis (review) 2: Biochem Soc Trans. 2001 Nov;29(Pt 6):684-8.Mechanisms of p53-dependent apoptosis((review))3.Journal of Cell Science 116， 4077-4085 (2003)Apoptosis - the p53 network(cypress1975)全文求援，很是感谢篇号：1 作家：Garraway LA， Weir BA， Zhao X， Widlund H， Beroukhim R， Berger A， Rimm D， Rubin MA， Fisher DE， Meyerson ML， Sellers WR..文题： "Lineage Addiction" in Human Cancer: Lessons from Integrated Genomics.杂志全名(或缩写)： Cold Spring Harb Symp Quant Biol. 年份，卷（期）: 起止页码： 2005;70:1-10. 全文皆集： > （缩略图，点击图片皆集看原图）Biography of Rudolf JaenischCancer Surv. 1990;9(3):487-503. Genomics. 2002 Jan;79(1):58-62. Paternal origins of complete hydatidiform moles proven by whole genome single-nucleotide polymorphism haplotyping.Fan JB， Surti U， Taillon-Miller P， Hsie L， Kennedy GC， Hoffner L， Ryder T， Mutch DG， Kwok PY.Affymetrix， 3380 Central Expressway， Santa Clara， CA 95051， USA.Complete hydatidiform moles (CHMs) are diploid tumors that result from fertilization of an empty ovum by a haploid 23，X sperm. In most cases， the resulting duplication of the genome gives rise to a 46，XX genotype and is thought to be androgenetic in origin. If this hypothesis is correct， then the genotypes of all polymorphic markers in CHMs should be homozygous. We used a dense set of single-nucleotide polymorphism (SNP) markers， evenly spaced throughout the genome， to definitively test this hypothesis. We genotyped genomic DNA samples from five CHMs and their corresponding maternal samples with 1494 SNP markers using high-density microarrays (HuSNP). As predicted， the maternal samples were heterozygous at >25% of the markers， which is consistent with the expected average heterozygosity of this panel of SNPs. In contrast， the five CHM samples were heterozygous at <0.75% of the SNP markers， which shows that these diploid tumors consist of a duplicated set of chromosomes. Because the CHM genotypes represent the haplotypes of their genomes， our results show that long-range haplotypes can be obtained easily with this resource and that a collection of such samples is a simple way to obtain reference haplotypes for association studies in various populations.Genomic imprinting and cancer.Ferguson-Smith AC， Reik W， Surani MA.Department of Molecular Embryology， AFRC Institute of Animal Physiology and Genetics Research， Babraham， Cambridge.Genomic imprinting results in a functional non-equivalence of parental chromosomes， presumably by epigenetic modification of the genome， and is required for normal mammalian development. In general， reciprocal phenotypes are observed in embryos containing alterations in the dosage of parental chromosomes， for example where both copies of chromosomes or chromosomal regions are derived from one parent. These phenotypes indicate that duplications of maternal chromosomes inhibit embryonic growth and proliferation whereas duplications of the paternal genome result in enhanced cell growth and proliferation. Alterations in the dosage of parental chromosomes have recently been observed in some forms of recessive tumour in man. Here we discuss the role and possible mechanisms of genomic imprinting during embryogenesis and attempt to draw parallels between the parental origin of the loss of heterozygosity observed in some human tumours and the developmental phenotypes that arise in mice with similar distortions of parental origin. These observations strongly implicate genomic imprinting in the genesis of some forms of tumour and， more generally， in the genetic predisposition to cancer.Nature. 1985 Jun 6-12;315(6019):496-8. Differential activity of maternally and paternally derived chromosome regions in mice.Cattanach BM， Kirk M.Although both parental sexes contribute equivalent genetic information to the zygote， in mammals this information is not necessarily functionally equivalent. Diploid parthenotes possessing two maternal genomes are generally inviable， embryos possessing two paternal genomes in man may form hydatidiform moles， and nuclear transplantation experiments in mice have shown that both parental genomes are necessary for complete embryogenesis. Not all of the genome is involved in these parental effects， however， because zygotes with maternal or paternal disomy for chromosomes 1， 4， 5， 9， 13， 14 and 15 of the mouse survive normally. On the other hand， only the maternal X chromosome is active in mouse extraembryonic membranes， maternal disomy 6 is lethal， while non-complementation of maternal duplication/paternal deficiency or its reciprocal for regions of chromosome 2， 8 and 17 has been recognized. We report that animals with maternal duplication/paternal deficiency and its reciprocal for each of two particular chromosome regions show anomalous phenotypes which depart from normal in opposite directions， suggesting a differential functioning of gene loci within these regions. A further example of non-complementation lethality is also reported.Adv Anat Pathol. 2004 Jan;11(1):10-23. Gonadal teratomas: a review and speculation.Ulbright TM.Department of Pathology， Indiana University School of Medicine， Indianapolis， Indiana 46202-5280， USA.Teratomas of the ovary and testis are confusing because， despite histologic similarities， they exhibit different biologic behaviors， depending mostly on the site of occurrence and the age of the patient. Thus， most ovarian teratomas are benign， and most testicular teratomas are malignant， with the exception of those occurring in children. These general statements， however， do not hold true for ovarian teratomas that are "immature" or exhibit "malignant transformation" and for dermoid and epidermoid cysts of the testis， categories of ovarian and testicular teratomas that are malignant and benign， respectively. This review concentrates on some of the "newer" observations concerning these interesting and confusing neoplasms， including diagnostically deceptive patterns. It is the author's opinion that much of the confusion regarding gonadal teratomas can be clarified by the concept that the usual ovarian teratoma derives from a benign germ cell in a parthenogenetic-like fashion， whereas the typical postpubertal testicular example derives from a malignant germ cell， mostly after evolution of that originally malignant cell to an invasive germ cell tumor (ie， embryonal carcinoma， yolk sac tumor， etc). The postpubertal testicular teratomas can therefore be thought of as an end-stage pattern of differentiation of a malignant germ cell tumor. The pediatric testicular teratomas， as well as dermoid and epidermoid cysts of the testis， however， must derive from benign germ cells， in a fashion similar to most ovarian teratomas. The teratomatous components of mixed germ cell tumors of the ovary， on the other hand， likely have a pathogenesis similar to that of postpubertal testicular teratomas. Med Hypotheses. 1993 Jul;41(1):37-41. Genomic imprinting: a proposed explanation for the different behaviours of testicular and ovarian germ cell tumors.Porter S， Gilks CB.Department of Pathology， University Hospital， University of British Columbia， Vancouver， Canada.Gonadal germ cell tumors in males are malignant in greater than 98% of cases while their ovarian counterparts are benign in 97% of cases. It has recently become clear that the maternal and paternal genomic contributions to the fertilized egg， provided by the haploid germ cells， have different and， to some extent， complementary effects on the developing embryo. This phenomenon， termed genomic imprinting， is a result of epigenetic modification of the genomes of male and female germ cells that has occurred in a sex-specific way during gametogenesis. There is a balance between the paternal and maternal effects in a normal embryo; results to date suggest that the paternal imprint promotes growth while the maternal imprint acts to limit potentially harmful overgrowth. It is proposed that differences in clinical behaviour between ovarian and testicular germ cell tumors can be explained by differences in the normal pattern of genomic imprinting of female and male germ cells.DURYEE WR， LONG ME， TAYLOR HC Jr， McKELWAY WP， EHRMANN RL. Human and amphibian neoplasms compared.Science. 1960 Jan 29;131:276-80. Wolsky A. Regeneration and cancer.Growth. 1978 Dec;42(4):425-6. Elder D. Why is regenerative capacity restricted in higher organisms?J Theor Biol. 1979 Dec 7;81(3):563-8. Warburton D， Wuenschell C， Flores-Delgado G， Anderson K. Commitment and differentiation of lung cell lineages.Biochem Cell Biol. 1998;76:971-95. van Bekkum DW. Phylogenetic aspects of tissue regeneration: role of stem cells. A concise overview.Blood Cells Mol Dis. 2004 Jan-Feb;32(1):11-6. Sanchez Alvarado A. Regeneration and the need for simpler model organisms.Philos Trans R Soc Lond B Biol Sci. 2004 May 29;359(1445):759-63. Echeverri K， Tanaka EM. Mechanisms of muscle dedifferentiation during regeneration.Semin Cell Dev Biol. 2002 Oct;13(5):353-60. Korystov YN. Tissue regeneration as the basic oncogenic factor.Med Hypotheses. 1996 Sep;47(3):183-90. 1.pdf (237.41k)The history of deciphering the genetic code> The history of deciphering the genetic code.pdf (42.87k)Professor Bryan D YoungBSc， PhD Fellow of Royal College of PathologistsFellow of Academy of Medical SciencesPrincipal ScientistHead of Medical Oncology Laboratory Contact: bryan.young@cancer.org.uk > screen.width-333)this.width=screen.width-333" width=110 height=150 title="Click to view full young.jpg (110 X 150)" border=0 align=absmiddle>Oncology. 1975;31(5-6):310-33.The trophoblast theory of cancer (John Beard， 1857-1924) revisited.Gurchot C.Bread's theory can be restated in a modified form in modern terms in the following way. Cancer represents primarily trophoblastic tissue derived either from an aberrant germ cell or from a somatic cell whose normally repressed 'asexual generation' genes are abnormally reactivated ('derepressed'). The variety of tumors， other than teratomas， may be due to a parallel chance derepression of some genes of somatic ('sexual gneration') characters. This would be a defensive reaction against intramural parasitization by trophoblast and would result in the differentiation and hyperplasia of normally present more primative somatic cells.The Trophoblastic Nature of Cancer and Pregnancy Cycle as the Basis for the Enzyme Treatment of Cancerby Roger Cathey This paper is written for the lay person. If you are a doctor， there is a more technical article on page one of our Science Papers page. Part One The primary basis of the enzyme treatment of cancer emanates from a recognition that cancer cells share properties with placental cells found in pregnancy. These placental cells are completely rejected by both fetus and mother by the time of delivery. Therefore it was reasoned that whatever factor or factors which underlay the rejection of the placenta could play a similar role in the body's rejection or remission of cancer cells. Other observations lead the earliest thinker along these lines， Embryologist John Beard (1857-1924)， to believe that the pancreatic enzymes of fetus and mother combine to bring about this event. Thus the basis of enzyme therapy for cancer was first derived from the idea that enzymes play a role in causing birth. These placental cells are called trophoblasts and are the first cells to differentiate from the fertilized egg. In this creation of trophoblasts it is important to note that they are a fully parasitic and a distinct feature surrounding the fetal cells that will form the living individual. In their role， trophoblasts mediate the implantation of the individual， but they are never incorporated into the body of the individual or fetus. Thus it is incorrect to call them "fetal" cells. They will eventually be either destroyed or rendered completely inert as far as the mother and fetus are concerned. These cells are often seen as a thin membrane covering the fetus at birth， the so-called "caul." Again， they never form an integral part of the formative individual. This fact is important to keep in mind， psychologically， because the same holds true of the cancer cell which does not in its incursion form an integral part of the individual. It has been observed that after some time of enzyme treatment tumors often "shell out，" and they can be more readily removed surgically， or they may extrude and drop out by themselves if partially exposed on the outside of the body. Somatic "tumors" or lumps or calluses consist of normal cells that sometimes grow up around the cancer growth in an attempt to mechanically limit their incursion. These types of growths are not affected by enzyme treatment， but are reduced by a morphogenic process of apoptosis or programmed cell death， or they may need to be removed surgically. It is believed that in many cases of radiation therapy， it is these normal cells that are destroyed leaving the hardier cancerous cells with a higher concentration in mass. In enzyme therapy， the cancer cells alone are attacked. The source cells of these trophoblasts in pregnancy are the most potent cells in the life cycle， i.e.， the united sperm and egg result in the original "stem cell，" or cell capable of becoming any and every cell in the completed form. Other tissues formed or differentiated from this primal cell may have various powers of expression， but they do not possess the power to become any other cell in the whole system. Most cells of the body are therefore "derived" cells and they are all observed to be of limited potential. As noted above， in the course of gestation these trophoblasts are rendered completely inert and finally rejected from the host representing the event of birth and probably is also a major cause of birth. This happens despite the fact that the cells seem not to induce any immunological reaction. A prime reason for this was discovered in this century by Currie and Bhagshawe who showed that the trophoblast was surrounded by a coating (sialo-glycoprotein) including a molecule that gave it a negative charge. The molecule can be likened to mucilage and has been termed the sialo-mucinous coat. A negative charge is also found on the white blood cells responsible for immune reactivity. Since two like charges repell we have delineated the primary reason for lack of rejection based on immune responses. This same type of coating is found on the cancer cell. And in fact， it is one of the chief reasons for classifying all cancer cells as "trophoblastic." It bears repeating that although the first trophoblast cell in the life cycle goes on to become the entire placenta， it does not become any part of the oncoming fetus， but is strictly a parasitic mediating and terminal cell or tissue type. Because the cellular trophoblast (cytotrophoblast) can differentiate further， it is said to be pleuripotent， but it is still of limited potential compared to the stem or totipotent cell. John Beard was the first to organize a theory around the cause of birth and the destruction of cancer cells. First he observed that the invading and eroding trophoblast component of the fertilized unit was remarkably similar to metastatic cancer cells， and other observations lead him to believe there was some intimate relationship between these trophoblasts and cancer cells. Another observation was that the placental trophoblasts seem to take a downturn in activity around the time of the activation of the fetal pancreas， which occurs around the 56th day. Modern research has shown that these trophoblast cells secrete a hormone called human chorionic gonadotropin (hCG)， and the quantities of this hormone rise until around the 56th day and then begin to taper off. It is this very hormone that coats the trophoblast and cancer cell to make them both immulogically inert. This hormone of pregnancy is expressed in all types of cancers. Seeing this change in trophoblast behavior and the onset of activity of the fetal pancreas has more than mere coincidence， Beard began to speculate in his correspondence with physicians about the possibility that the function of both the mother's and the fetus' pancreases were somehow involved in the resolution or destruction of the trophoblast. If that is so， he asked， then might the same be said of cancer cells in the cancer patient? In time Beard's speculations were put to the test by several physicians using pancreatic enzymes. At first they used only the proteolytic enzyme trypsin， but when the reactions of patients to this tended to be severe they then turned to combining trypsin with amylase， the carbohydrate digesting enzyme， and found that the reactions of the patients were much better. (For details on this historic finding go to: > This accentuation of the protein digesting enzymes in many versions of this therapy explains the oft reported periods of nausea and other symptoms resembling pre-eclampsia or morning sickness. Beard and his associates' final form of therapy always accentuated amylase， sometimes completely eliminating trypsin and other protein digesting enzymes after a certain length of application or during so-called "rest periods" of treatment. This is logical， because the glycoprotein surrounding the cancer cell， and the circulating hormone form of this glycoprotein (often mistakenly called a "protein" or "fibrin" coat)， are fundamentally presenting to the system as carbohydrate complexes. That is， the body sees the carbohydrate side of the molecule， not the protein side， and amylase attacks this before the proteinases can do a thing. There is then the question of how the cancer/trophoblast comes into being in the non-pregnant individual. Since all stem cells have all potentialities within them， it has been assumed by some researchers that cancer must arise from a residual complement of stem cells in the body. There are a number of observations recorded in the medical literature attesting to the presence of these stem or totipotent cells in the adult body. Others contend that since all cells have the complete genome within them， if they can divide at all， there is the possibility of them re-acquiring totipotency， or simply to directly express the trophoblastic suite of characteristics. That is something for research to definitely establish， and we need not concern ourselves too much on this point. It would appear that anything that can disturb the genome sufficiently， presumably factors not normal to the animal economy， whether parasitic， cytotoxins， or carcinogenic or chronic injury of any kind， is sufficient to bring these properties into expression. After all， the trophoblast has proven to be the hardiest of expressions of the differentiating zygote as it goes through a gamut of harsh environs of low oxygen， then establishing a place in the uterus and a reliable blood supply. In injury， something of the same harshness exists. In the next and continuing parts， we will discuss further the means being used today to help control the disease and the adjunctive protocols that may form a part of the overall immuno-enzyme therapy.rio柚木提娜