Cancer

http://organic-health.us/cancer/cannabis-hemp-oil.shtml

Are there ALTERNATIVE “treatments” for Cancer ?

The medical and drug industries (in cooperation with the FDA) make too much money FROM cancer “treatments” (and donations to NGOs “not interested” in homeopathic remedies) to ADVERTISE any natural treatments they cannot directly regulate, nor patent and collect revenue from. There are a few ORGANIC compounds (which are NOT patented, nor patentable) that have been proven to reduce tumors (in laboratory animals and terminal cancer patients) by as much as 70% over just a few weeks.

the above web site shows the different alternative methods for treating Cancer.

UROTHERAPY FOR PATIENTS WITH CANCER

Joseph Eldor, MD

Theoretical Medicine Institute
P.O.Box 12142, Jerusalem, 91120,Israel

Abstract

Cancer cells release various antigens, some of which appear

in the urine. Oral auto-urotherapy is suggested as a new

treatment modality for cancer patients. It will provide the

intestinal lymphatic system the many tumor antigens against

which antibodies may be produced. These antibodies may be

transpierced through the blood stream and attack the tumor

and its cells.

The philosophy of cancer

Microbes were known long before the germ theory of disease

was invented. It was not the discovery of germs that

revolutinized medicine, but the invention of a philosophy of

medical explanation that permitted germs to be causative

agents of disease (1).

Burnet and Thomas (2) postulated that specific cell

mediated immunity may have evolved in vertebrates

specially for defense against the “enemy within” rather than

against infecting microorganisms and parasites. Most human

cancers appear to lack truly tumor-specific antigens. The

same neoplastic cell can express several different tumor

antigens. For example, relatively cross-reacting

tumor-specific transplantation antigens have been

demonstrated in many chemically induced tumors (3).

Tumor-associated differentiation antigens are shared by

neoplastic and embryonic cells (4). The extent to which

human patients react immunologically against their cancers

has been a subject of much controversy (5).

Paul Ehrlich, in 1909, said:”I am convinced that during

development and growth malignant cells arise extensively

frequently but that in the majority of people they remain

latent due to the protective action of the host. I am also

convinced that this natural immunity is not due to the

presence of antimicrobial bodies but is determined purely by

cellular factors. These may be weakened in the older age

groups in which cancer is more prevalent” (6).

Tumor antigens in urine

Human melanoma cells express membrane antigens distinct from

those of the normal ectodermal counterparts (7).

Urinary-tumor-associated antigen (U-TAA) is one such

antigen. This high-molecular weight glycoprotein was first

described when melanoma urine was found to react with

autologous antibody (8). The antigen has since been detected

in the urine of 68% of melanoma patients. In addition, high

levels of U-TAA are found to correlate positively with

disease occurrence in surgically treated patients (9).

Prostatic specific antigen (PSA) has become an important

laboratory test in the management of prostate cancer. PSA

levels can be as readily obtained from voided urine as from

serum samples (10).

Quantitative urinary immunocytology with monoclonal antibody

(mab) 486p 3/12 proved to be valuable for diagnostic use in

bladder-cancer patients` urine, especially in the followup

of patients with superficial bladder carcinoma (11).

Quantitative urinary immunocytology is a general tool to

test the diagnostic usefulness of mabs, assuming that normal

and malignant cells differ in their quantitative expression

of a given antigen. Selective criteria for selecting mabs

for diagnostic approaches should ask not for tumor

specificity, but for different quantitative expression of

antigen in the tissues or cells in question.

Gastric juice oncofetal antigen determination, due to direct

shedding of antigens into the fluid around tumor tissues,

appears to accurately indicate the presence and degree of

gastric mucosal damage and to be to a slight extent

influenced by unrelated factors (12). Patients` age, for

example, modifies CEA serum levels (13). A monoclonal

antibody (mab) against a human colorectal adenocarcinoma

cell line has been raised (14), which reacts with

sialosylfucosyllactoteraose (15) corresponding to the

sialylated blood group antigen Lewis (a). The antigen

defined by this antibody, CA50, is elevated in the serum of

many patients with gastrointestinal tumors (16), with a

sensitivity for gastric cancer ranging from 20 (17) to 65%

(18). CA50 (a tumor-associated gangliosidic antigen) levels

have been determined by an RIA test in serum, gastric juice

and urine of patients undergoing upper gastrointestinal

tract endoscopy. Sensitivity and specificity were

respectively 23% and 89% for CA50 determination in urines

(19).

Soluble forms of membrane proteins such as cytokine

receptors or cellular adhesion molecules (CD14, TNF

receptor, CD25, IL-6 receptor, IFN-ç-receptor and CD54) have

been detected in human body fluids. They may have important

functions in immune regulation by blocking receptor/ligand

interactions. The human adhesion receptor CD58 (LFA-3) is

expressed on most cell types. A soluble form of CD58 (sCD58)

was purified from human urine and partially purified from

supernatant of the Hodgkin-derived cell line L428 (20).

Urinary organ-specific neoantigen from colorectal cancer

patients has been used to make a monoclonal antibody, BAC

18.1 (21). Organ-specific neoantigen originates in the colon

and is excreted into the urine, so the BAC 18.1 binding

levels in the urine may be a diagnostic aid for colorectal

cancer.

The polyamines spermidine, spermine and their diamine

precursor putrescine are ubiquitous constituents of

mammalian cells that are fundamentally involved in normal,

malignant and induced proliferative states. The polyamines

and ornithine decarboxylase (ODC), the rate-limiting enzyme

of the polyamine metabolism, were found to play an important

role in tumor promotion (22). The suggestion that polyamines

play an important role in colorectal cancer was confirmed by

studies that found elevated polyamine concentrations in

blood or urine (23) of patients with colon carcinoma.

Sensitivity of urinary polyamines for colon cancer were

highest for total spermidine (92.1%), acetylated putrescine

(84.5%), total putrescine (84.0%), N1-acetylspermidine

(79.3%) and N8-acetylspermidine (78.6%), but in all these

cases specificity was lower than 65% (24). In patients with

successful curative surgical treatment all preoperatively

elevated urinary polyamine concentrations markedly decreased

and returned to normal, whereas they were elevated and

increased further in patients with proven relapse of the

tumor and/or metastases in different organs (24).

The function of the CD44 gene is severely damaged, beginning

with the very early pre-invasive stages of tumor

development. This can be used as a means of tumor detection

and diagnosis both on solid tissue specimens (25) and on

exfoliated cells in clinically obtained excreta and body

fluids (26). Urine cell lysates obtained from patients with

bladder cancer can be discriminated from normal urine

lysates (27) using Western blotting with a monoclonal

antibody against the standard form of the CD44 protein.

Immunotherapy

Zbar and Tanaka (28) first reported on animal immunotherapy

based on the principle that tumor growth is inhibited at

sites of delayed hypersensitivity reactions provoked by

antigens unrelated to the tumor.They injected living

Mycobacterium bovis (strain BCG) into established

intradermal tumors and caused tumor regression and prevented

the development of metastases. For optimum therapeutic

effect contact between BCG and tumor cells was necessary.

The ability of tumor immune lymphocytes to localize

specifically to tumor offers a possibility for therapy which

has been utilized over the past several years (29).

The rejection of murine tumors expressing tumor-specific

transplantation antigens has been shown to be mediated

primarily by immune cells (30). Some 6 to 7% of transplant

recipients may develop cancer as a consequence of iatrogenic

immunosuppression (31).

Studies on the ability of patient lymphocytes to lyse tumor

cells in short term (2-8 hr) isotope release assays have

shown that lymphocytes from cancer patients can generally

destroy only tumor cells from the same patient (32-34),

unless the effector cells are not cytolytic T cells but, for

example, Natural Killer cells or Lymphokine Activated Killer

cells, in which case neoplastic cells representing many

different types are sensitive.

Immunotherapy is believed to be capable of eliminating only

relatively small amounts of neoplastic cells and, therefore,

the failure to induce a regression in patients with

excessive tumor burden is not unexpected (35,36). One

approach of immunotherapy is to “xenogenize” tumor cells by

virus infection. Another is to culture tumor infiltrating

lymphocytes with interleukin-2 and reinoculate them into the

host with cytokines (37). The introduction of recombinant

vectors expressing cytokine genes into tumor infiltrating

lymphocyte cells (38) or into the tumor cells themselves

(39) may enhance the migration of effector immune cells into

the tumor with consequent immunomediated control. The

considerable heterogeneity in the expression of tumor

associated differentiation antigens by cells within the same

tumor constitutes a problem for any immunotherapy, since it

facilitates the escape of antigen-negative tumor variants.

An alternative approach toward increasing the immune

response to tumor-associated differentiation antigens is to

treat the host to be immunized so as to abolish a

“suppressor” response. Such treatment can be provided in the

form of sublethal whole body x-irradiation (40), injection

of a drug such as cyclophosphamide (41), or by the

administration of certain anti-idiotypic antibodies (42).

Anergy is defined as a state of T lymphocyte

unresponsiveness characterized by absence of

proliferation,IL-2 production and diminished expression of

IL-2R (43,44). Most available data support suppression as a

mechanism of oral tolerance (45,46). Immunological

suppression is classically demonstrated by the suppression

of antigen-specific immune responses by T lymphocytes

(47,48).

Autoantigens

Oral administration of S-antigen (S-Ag), a retinal

autoantigen that induces experimental autoimmune uveitis,

prevented or markedly diminished the clinical appearance of

S-Ag-induced disease as measured by ocular inflammation

(49,50).

Gut associated lymphoid tissue has the capacity to generate

potent immune responses on one hand, and to induce

peripheral tolerance to external antigens on the other

(51-53). Both processes require antigen stimulation (53),

involve cytokine production (51) and might occur at the same

time – the first leading to potent local and systemic immune

responses, while the latter leads to systemic

antigen-specific nonresponsiveness (54). The generation of

acquired immune responses in the small intestine is believed

to occur in Peyer`s patches (51,55).

Orally fed protein antigens are found in the blood within 1

hr of feeding (56). Peripheral tolerance is not induced

locally, but rather is induced systemically upon transfer of

intact antigen, or its peptides, into the circulation

(57-59).Oral tolerance may be induced by a single feeding of

a protein antigen (60,61) or by several intermittent

feedings (46,62). In order to test whether feeding on

autoantigen could suppress an experimental autoimmune

disease, the Lewis rat model of experimental autoimmune

encephalomyelitis was studied (63). With increasing dosages

of GP-MBP, the incidence and severity of disease was

suppressed, as well as proliferative responses of lymph node

cells to MBP. Antibody responses to MBP were decreased but

not as dramatically as proliferative responses. Thus it

appears that oral tolerance to MBP, as to other non-self

antigens (45), preferentially suppress cellular immune

responses. It appears that homologous MBP is a more potent

oral tolerogen for experimental autoimmune encephalomyelitis

than heterologous MBP (64).

Tumor cells may escape immune recognition in immunocompetent

hosts by clonal evolution.Attention could be directed to

activate the resident immune effectors to break the anergy

or tolerance.

Urotherapy

Subcutaneous urine injections was practiced in 1912 by

Duncan (65) from New York under the name of auto-pyotherapy

for urinary infections, and in 1919 by Wildbolz (65) from

Bern for diagnostic purposes. Cimino (66) from Palermo

reported in 1927 on the use of auto uro-therapy for urinary

infections. Rabinowitch (67) in 1931 described this

auto-urine therapy for gonarthritis. Jausion et al. (68)

used this kind of therapy in 1933 for desensitization and

endocrinological problems. They treated with auto urotherapy

injections patients who suffered from migraine, pruritus,

asthma, urticaria, eczema, psoriasis, etc. Day (69)in 1936

treated patients with acute and subacute glomerulonephritis

by injection of an autogenous urinary extract. Sandweiss,

Saltzstein and Farbman (70) reported in 1938 that an extract

from urine of pregnant women has a prophylactic and

therapeutic effect on experimental ulcers in dogs. Shortly

thereafter the same group noted that an extract from urine

of normal women has a similar beneficial effect (71).

In 1926 Seiffert first described the construction of ileal

loop conduits for urinary diversion (72). Bricker in the

1950s popularized the use of the ileal loop as a means of

supravesical urinary diversion following exenteration for

pelvic malignancy in adults (73). Ureterosigmoidostomy as a

means of urinary diversion was used widely from 1920 to

1955. It was this type of implant which Hammer first

reported in 1929 associated with tumor (74).

Peyer`s patches are immunocompetent lymphoid organs which

participate in intestinal immune responses (75). Epithelial

cells within the crypts of the small bowel are one of the

fastest dividing cells in the body and yet they show one of

the lowest rate of malignant transformation (76). Stem cells

in the mucosa of the small bowel can divide every 8 to 12

hours (77). Tapper and Folkman (78) demonstrated that

exposure of intestinal segments to urine causes marked

lymphoid depletion in the segments. These studies give

additional support to the idea that a lymphocyte suppressive

factor exist in urine (79). The continued presence of urine

bathing the intestinal mucosa appears to locally inhibit

regeneration of the Peyer`s patches.

Starkey et al. (80) detected in human urine a material that

is biologically and immunologically similar to epidermal

growth factor that causes proliferation and keratinization

of epidermal tissues.

The increased susceptibility of the colon to cancer

associated with the existence of an implanted ureter has

been theorized to relate to 3 factore: 1. The role of the

urine in the colon (81,82). 2. The mechanical effect of the

fecal stream on the stoma (83). 3. The age of the

anastomosis (84). Adenocarcinoma of the colon mucosa is a

recognized complication of ureterosigmoidostomy. The tumor,

which develops adjacent to the junction of the ureter with

the bowel, occurs 500 times as often as in the population at

large and, in children so operated , 7,000 times as often as

in all persons under age 25. The latency period is 5 to 50

years (81,85-87).

It is common knowledge that malignant tumors may disappear

spontaneously although very infrequently (88-90). Usually it

is accepted that this could be due at least partly to an

immunological reaction (91,92). Renal adenocarcinoma is one

of the cancer types in which such spontaneous regressions

have been described most frequently (88,90).

Urinary extracts from patients with aplastic anemia (93) and

idiopathic thrombocytopenic purpura (94) are capable of

stimulating megakaryocyte colony growth in culture, and when

injected into rats could also induce thrombocytosis in

peripheral blood and megakaryocytosis in the spleens of

these animals. Stanley et al. (95) demonstrated that rabbits

immunized with human urine concentrates from leukemic

patients developed antibody which neutralized the mouse bone

marrow colony stimulating factor in human urine and human

serum.

Preconclusion

Henry Sigerist said, more than 50 years ago:”I personally

have the feeling that the problem of cancer is not merely a

biological and laboratory problem, but it belongs to a

certain extent to the realm of philosophy… All experiments

require certain philosophical preparation. And I have the

feeling that in the case of cancer many experiments were

undertaken without the necessary philosophical background,

and therefore proved useless” (96).

Conclusion

Urotherapy is suggested as a new kind of immunotherapy for

cancer patients. Unlike the clonal immunotherapy the urine

of the cancer patients contain the many tumor antigens which

constitute the tumor. Oral auto-urotherapy will provide the

intestinal lymphatic system the tumor antigens against which

they may produce antibodies due to non-self recognition.

These antibodies may be transpierced through the blood

stream and attack the tumor and its cells.

References

1. Root-Bernstein RS. Causality, complementarity, evolution,

and emergent properties. In Iversen OH (ed.):New Frontiers

in Cancer Causation. Taylor & Francis 1993, p.1-14

2. Burnet FM. The concept of immunological surveillance.

Prog Exp Tumor Res 1970;13:1-27

3. Hellstrom I, Hellstrom KE, Zeidman L, Bernstein ID, Brown

JP. Cell-mediated reactivity to antigens shared by Moloney

virus induced lymphoma cells (LSTRA) and cells from certain

3-methylcholanthrene induced mouse sarcomas. Int J Cancer

1979;23:555-64

4. Hellstrom I, Hellstrom KE, Shepard TH. Cell-mediated

immunity against antigens common to tumor colonic carcinomas

and fetal gut epithelium. Int J Cancer 1970;6:346-51

5. Hellstrom KE, Hellstrom I. Immunological approach to

tumor therapy: Monoclonal antibodies, tumor vaccines, and

anti-idiotypes. In Covalently Modified Antigens and

Antibodies in Diagnosis and Therapy. Vol.2. Edited by Quash

GA, Rodwell JD. Marcel Dekker, Inc., New York 1989, p.1

6. Ehrlich P. In Himmelweit S., ed. The Collected Papers of

Paul Ehrlich (translated by P. Alexander). Pergamon Press,

Oxford, 1957

7. Watanabe T, Punkel CS, Takeyama H, Lloyd KO, Shiku H, Li

LTC, Travassos LR, Oettgen HF, Old LJ. Human melanoma

antigen AH is an autologous ganglioside related to GD2. J

Exp Med 1982;156:1884-9

8. Rote NS, Gupta RK, Morton DL. Tumor-associated antigens

detected by autologous sera in urine of patients with solid

neoplasms. J Surg Res 1980;29:18-22

9. Gupta RK, Huth JF, Korn EL, Morton DL. Prognostic

significance of urinary antigen analysis by enzyme-linked

immunosorbant assay in melanoma patients. Diag Immunol

1983;1:303-309

10. DeVere White RW, Meyers FJ, Soares SE, Miller OG,

Soriano TF. Urinary prostate specific antigen levels: Role

in monitoring the response of prostate cancer to therapy. J

Urol 1992;147:947-951

11. Huland E, Huland H, Meier T, Baricordi O, Fradet Y,

Grossman HB, Hodges GM, Messing EM, Schmitz-Draeger BJ.

Comparison of 15 monoclonal antibodies against

tumor-associated antigens of transitional cell carcinoma of

the human bladder. J Urol 1991;146:1631-6

12. Farinati F, Cardin F, Costa F, Nitti D, Di Mario F,

Naccarato R. Gastric juice CEA levels: importance of age and

gastric mucosal damage. Europ J Cancer Clin Oncol

1986;22:527-9

13. Touitou Y, Proust J, Klinger E, Nakache JP, Huard D,

Sachet A. Cumulative effects of age and pathology on plasma

carcinoembryonic antigen in an unselected elderly

population. Europ J Cancer Clin Oncol 1984;20:369-374

14. Lindholm L, Holmgren J, Svennerholm L, Fredman P,

Nillson O, Persson P, Myrvold H, Lagergard T. Monoclonal

antibodies against gastro-intestinal tumor-associated

antigens isolated as monosialogangliosides. Int Arch Allergy

appl Immun 1983;71:178-181

15. Mansson JE, Fredman P, Nilsson O, Lindholm L, Holmgren

J, Svennerholm C. Chemical structure of carcinoma

ganglioside antigens defined by monoclonal antibody CA50 and

some allied gangliosides of human pancreatic adenocarcinoma.

Biochim Biophys Acta 1985;834:110-117

16. Holmgren J, Lindholm L, Persson B, Lagergard T, Nilsson

O, Svennerholm L, Rudenstam CM, Unsgaard B, Yngvason F,

Pettersson S, Killander AF. Detection by monoclonal antibody

of carbohydrate antigen CA50 in serum of patients with

carcinoma. Brit Med J 1984;288:1479-1482

17. Dienst C, Clodius T, Oldorp T, Uhlenbruch G, Diehl V. CA

19-9, CA50 und CEA bei Pankreas und gastrointestinal

Tumoren. Medizin Klin 1987;82:45-50

18. Bruhn HD, Broers H, Euler H, Everding A, Feller AC,

Hedderich J, Jostarndt L, Joob B, Zurborn KH, Loffler H. CA

50 im serum von Karzinom-Patienten. Deutsch Med Wochensch

1986;34:1267-1272

19. Farinati F, Holmgren J, Di Mario F, Cardin F, Valliante

F, Fanton MC, Della Libera G, Nitti D, Plebani M, Crestani

B, Naccarato R. CA 50 determination in body fluids: Can we

screen patients at risk for gastric cancer? Int J Cancer

1991;47:7-11

20. Hoffmann JC, Dengler TJ, Knolle PA, Albert-Wolf M, Roux

M, Wallich R, Meuer SC. A soluble form of the adhesion

receptor CD58 (LFA-3) is present in human body fluids. Eur J

Immunol 1993;23:3003-3010

21. Tobi M, Darmon E, Rozen P, Harpaz N, Fink A, Maliakkal

B, Halline A, Mobarhan S, Bentwich Z. Urinary organ specific

neoantigen. A potentially diagnostic test for colorectal

cancer. Dig Dis Sci 1995;40:1531-7

22. Boutwell RK. Evidence that an elevated level of

ornithine decarboxylase activity is an essential component

of tumor promotion. Adv Polyamine Res 1983;4:127-133

23. lipton A, Sheehan L, Harvey HA. Urinary polyamine levels

in patients with gastrointestinal malignancy. Cancer

1975;36:2351-4

24. Loser C, Folsch UR, Paprotny C, Creutzfeldt W.

Polyamines in colorectal cancer. Evaluation of polyamine

concentrations in the colon tissue, serum and urine of 50

patients with colorectal cancer. Cancer 1990;65:958-966

25. Matsumura Y, Tarin D. Significance of CD44 gene products

for cancer diagnosis and disease evaluation. Lancet

1992;340:1053-8

26. Matsumura Y, Hanbury D, Smith JC, Tarin D. Non-invasive

detection of malignancy by identification of unusual CD44

gene activity in exfoliated cancer cells. Br Med J

1994;308:619-624

27. Matsumura Y, Sugiyama M, Matsumura S, Hayle AJ, Robinson

P, Smith JC, Tarin D. Unusual retention of introns in CD44

gene transcripts in bladder cancer provides new diagnostic

and clinical oncological opportunities. J Pathol

1995;177:11-20

28. Zbar B, Tanaka T. Immunotherapy of cancer: regression of

tumors after intralesional injection of living Mycobacterium

bovis. Science 1971;172:271-273

29. Rosenberg SA, Packard BS, Aebersold PM et al. Use of

tumor-infiltrating lymphocytes and interleukin-2 in the

immunotherapy of patients with metastatic melanoma. A

preliminary report. N Engl J Med 1988;319:1676-80

30. Hellstrom KE, Hellstrom I. Cellular immunity against

tumor specific antigens. Adv Cancer Res 1969;12:167-223

31. Penn I. Tumors of the immunocompromised patient. Ann Rev

Med 1988;39:63-73

32. Vanky F, Klein E, Willems J et al. Lysis of autologous

tumor cells by blood lymphocytes activated in autologous

mixed lymphocyte tumor cell culture – no correlation with

the postsurgical clinical course. Cancer Immunol Immunother

1987;24:180

33. Vanky F, Klein E. Specificity of auto-tumor cytotoxicity

exerted by fresh, activated and propagated human T

lymphocytes. Int J Cancer 1982;29:547

34. Knuth A, Wolfel T, Klehmann E, Boon T, Meyer zum

Buschenfelde KH. Cytolytic T cell clones against an

autologous human melanoma: Specificity study and definition

of three antigens by immunoselection. Proc Natl Acad Sci

(USA) 1989;86:2804-8

35. LoBuglio AF, Neidhart JA. A review of transfer factor

immunotherapy in cancer. Cancer 1974;34:1563-70

36. Levin AS, Byers VS, Fudenberg HH, Wybran J, Hackett AJ,

Johnston JO, Spitler LE. Osteogenic sarcoma. Immunologic

parameters before and during immunotherapy with

tumor-specific transfer factor. J Clin Invest 1975;55:487-99

37. Rosenberg SA, Schearz SL, Speiss PJ. Combination

immunotherapy for cancer: synergistic antitumor interactions

of interleukin-2, alpha interferon and tumor-infiltrating

lymphocytes. JNCI 1988;80:1393-1397

38. Rosenberg SA, Aebersold P, Cornetta K et al. Gene

transfer into humans: immunotherapy of melanoma using

tumor-infiltrating lymphocytes modified by retroviral gene

transduction. N Engl J Med 1990;323:570-578

39. Russell SJ, Eccles SA, Fleming CL, Johnson CA, Collins

MKL. Decreased tumorigenicity of a transplantable rat

sarcoma following transfer and expression of an IL-2 cDNA.

Int J Cancer 1991;47:244-252

40. Hellstrom KE, Hellstrom I, Kant JA, Tamerius JD.

Regression and inhibition of sarcoma growth by interference

with a radiosensitive T cell population. J Exp Med

1978;148:799-804

41. Estin CD, Stevenson US, Hellstrom I, Hellstrom KE.

Cyclophosphamide potentiates the antitumor activity of

v-p97NY. Cell Immunol 1989;120:126-31

42. Nepom GT, Hellstrom KE. Anti-idiotypic antibodies and

the induction of specific tumor immunity. Cancer Metast Rev

1987;6:489-502

43. Schwartz RH. A cell culture model for T lymphocyte

clonal anergy. Science 1990;248:1349-1356

44. Jenkins MK, Schwartz RH. Antigen presentation by

chemically modified splenocytes induces antigen-specific T

cell unresponsiveness in vitro and in vivo. J Exp Med

1987;165:302-319

45. Mowat AM. The regulation of immune responses to dietary

protein antigens. Immunol Today 1987;8:93-98

46. Weiner HL, Zhang ZJ, Khoury SJ, Miller A, Al-Sabbagh A,

Brod SA, Lider O, Higgins P, Sobel R, Nussenblatt RB, Hafler

DA. Antigen-driven peripheral immune tolerance. Suppression

of organ-specific autoimmune diseases by oral administration

of autoantigens. Ann NY Acad Sci 1991;636:227-232

47. Sercarz E, Krzych U. The distinctive specificity of

antigen-specific suppressor T cells. Immunol Today

1991;12:111-118

48. Green DR, Flood PM, Gershon RK. Immunoregulatory T-cell

pathways. Annu Rev Immunol 1983;1:439-463

49. Thurau SR, Caspi RR, Chan CC, Weiner HL, Nussenblatt RB.

Immunological suppression of experimental autoimmune

uveitis. Fortschr Ophthalmol 1991;88:404-407

50. Nussenblatt RB, Caspi RR, Mahdi R, Chan CC, Roberge F,

Lider O, Weiner HL. Inhibition of S-antigen induced

experimental autoimmune uveoretinitis by oral induction of

tolerance with S-antigen. J immunol 1990;144:1689-1695

51. Brandtzaeg P. Overview of the mucosal immune system.

Curr top Microbiol Immunol 1989;146:13-28

52. MesteckyJ, McGhee JR. Oral immunization: Past and

present. Curr Top Microbiol Immunol 1989;146:3-12

53. Stokes CR. Induction and control of intestinal immune

responses. In Newby TJ, Stokes CR (eds.): Local immune

responses of the gut. Boca Raton, CRC Press, 1984,pp.97-142

54. Hanson DG, Vaz NM, Rawlings LA, Lynch JM. Inhibition of

specific immune responses by feeding protein antigens. II.

Effects of prior passive and active immunization. J Immunol

1979;122:2261-2266

55. Brandtzaeg P, Baklien K, Bjerke K, Rognum TO, Scott H,

Valnes K. Nature and properties of the human

gastrointestinal immune system. In Miller K, Nicklin S

(eds.):Immunology of the Gastrointestinal Tract. Boca Raton,

CRC Press, 1987, pp.1-88

56. Peng HJ, Turner MW, Strobel S. The generation of a

“tolerogen” after the ingestion of ovalbumin is

time-dependent and unrelated to serum levels of

immunoreactive antigen.Clin Exp Immunol 1990;81:510-515

57. Stokes CR, Swarbrick ET, Soothill JF. Genetic

differences in immune exclusion and partial tolerance to

ingested antigens. Clin Exp Immunol 1983;52:678-684

58. Swarbrick ET, Stokes CR, Soothill JF. Absorption of

antigens after oral immunization and the simultaneous

induction of specific systemic tolerance. Gut

1979;20:121-125

59. Miller A, Zhang AJ, Prabdu-Das M, Sobel A, Weiner HL.

Active suppression vs. clonal anergy following oral or IV

administration of MBP in actively and passively induced EAE.

Neurology 1992;42(Suppl 3):301

60. Lamont AG, Gordon M, Ferguson A. Oral tolerance in

protein deprived mice. II. Evidence of normal ‘gut

processing’ of ovalbumin, but suppressor cell deficiency, in

deprived mice. Immunology 1987;61:339-343

61. Hanson DG, Vaz NM, Maia LC, Hornbrook MM, Lynch JM, Roy

CA. Inhibition of specific immune responses by feeding

protein antigens. Int Arch Allergy Appl Immunol

1977;55:526-532

62. Matthews JB, Fivaz BH, Sewell HF. Serum and salivary

antibody responses and the development of oral tolerance

after oral and intragastric antigen administration. Int Arch

Allergy Appl Immunol 1981;65:107-113

63. Higgins P, Weiner HL. Suppression of experimental

autoimmune encephalomyelitis by oral administration of

myelin basic protein and its fragments. J Immunol

1988;140:440-445

64. Miller A, Lider O, Al-Sabbagh A, Weiner HL. Suppression

of experimental autoimmune encephalomyelitis by oral

administration of myelin basic protein. J Neuroimmunol

1992;39:243-250

65. Jausion H. Sur l’auto-ouro-therapie. Journal D’Urologie

1935;39:58-59

66. Cimino T. Premiers essais de vaccine-proteine-therapie

des infections non gonococciques ni tuberculeuses des voies

urinaires a l’aide des injections sous-cutanees de l’urine

purulente du sujet, sterilisee par l’ebullition

(ouro-therapie). Rivista Sanitaria 1927;186

67. Rabinowitch IM. Auto-urine-therapy in gonarthritis.

Vratchebnaia gazeta 1931;35:677-8

68. Jausion H, Giard R, Martinaud G. L’auto-ouro-therapie.

La Presse Medicale 1933;76:1467-1470

69. Day HB. Treatment of glomerulonephritis by antigen.

Lancet 1936;1456-9

70. Sandweiss DJ, Saltzstein HC, Farbman AA. The prevention

or healing of experimental ulcer in Mann-Williamson dogs

with the Anterior-Pituitary-Like hormone (Antuitrin-S). Am J

Dig Dis 1938;5:24-30

71. Sandweiss DJ, Saltzstein HC, Farbman AA. The relation of

sex hormones to peptic ulcer. Am J Dig Dis 1939;6:6-12

72. Seiffert L. Die “Darn-Siphonblase”. Arch fur Klin Chir

1935;183:569

73. Bricker EM. Bladder substitution after pelvic

evisceration. Surg Clin North Am 1950;30:1511

74. Hammer E. Cancer du colon sigmoide dix ans apres

implantation des ureteres d’une vessie exstrophiee. J Urol

Nephrol 1929;28:260

75. Miller-Schoop JW, Good RA. Functional studies of Peyer`s

patches: Evidence for their participation in intestinal

immune responses. J Immunol 1975;144:1757

76. Barclay THC, Schapira DV. Malignant tumors of the small

bowel. Cancer 1983;51:878-881

77. Loeffler M, Stein R, Wichmann HE, Potten CS, Kaur P,

Chwalinski S. Intestinal cell proliferation. I. A

comprehensive model of steady-state proliferation in the

crypt. Cell Tissue Kinet 1986;19:627-645

78. Tapper D, Folkman J. Lymphoid depletion in ileal loops:

Mechanism and clinical implications. J Pediatr Surg

1976;11:871-880

79. Wilson WEC, Kirkpatrick CH, Talmage DW. Suppression of

immunologic responsiveness in uremia. Ann Intern Med

1965;62:1

80. Starkey RH, Cohen S, Orth DN. Epidural growth factor:

Identification of a new hormone in human urine. Science

1975;189:800-802

81. Urdaneta LF, Duffell D, Creevy CD, Aust JB. Late

development of primary carcinoma of the colon following

ureterosigmoidostomy: report of three cases and literature

review. Ann Surg 1966;164:503-13

82. Harguindey SS, Colbeck RC, Bransome ED JR.

Ureterosigmoidostomy and cancer: new observations (letter).

Ann Intern Med 1975;83:833

83. Rivard JY, Bedard A, Dionne L. Colonic neoplasms

following ureterosigmoidostomy. J Urol 1975;113:781-6

84. Carswell JJ III, Skeel DA, Witherington R, Otken LB Jr.

Neoplasia at the site of ureterosigmoidostomy. J Urol

1976;115:750-2

85. Lasser A, Acosta AE. Colonic neoplasms complicating

ureterosigmoidostomy. Cancer 1975;35:1218-22

86. Sooriyaarachchi GS, Johnson RO, Carbone PP. Neoplasms of

the large bowel following ureterosigmoidostomy. Arch Surg

1977;112:1174-7

87. Eraklis AJ, Folkman MJ. Adenocarcinoma at the site of

ureterosigmoidostomies for exstrophy of the bladder. J

Pediatr Surg 1978;13:730-4

88. Everson T. Spontaneous regression of cancer. Ann NY Acad

Sci 1964;114:721-35

89. Stephenson H, Delmez J, Renden D, Kimpton R, Todd P,

Charron T, Lindberg D. Host immunity and spontaneous

regression of cancer evaluated by computerized data

reduction study. Surg Gynecol Obstet 1971;133:649-55

90. Cole W. Spontaneous regression of cancer: The metabolic

triumph of the host? Ann NY Acad Sci 1974;230:111-41

91. Burnet F. Immunological aspects of malignant disease.

Lancet 1967;II:1171-4

92. Droller M. Immunotherapy and genitourinary neoplasia.

Urol Clin N Am 1980;7:831-46

93. Enomoto K, Kawakita M, Kishimoto S, Katayama N, Miyake

T. Thrombopoiesis and megakaryocyte colony stimulating

factor in the urine of patients with aplastic anemia. Br J

Haematol 1980;45:551-556

94. Kawakita M, Enomoto K, Katayama N, Kishimoto S, Miyake

T. Thrombopoiesis and megakaryocyte colony stimulating

factors in the urine of patients with idiopathic

thrombocytopenic purpura. Br J Haematol 1981;48:609-615

95. Stanley ER, McNeill TA, Chan SH. Antibody production to

the factor in human urine stimulating colony formation in

vitro by bone marrow cells. Br J Haematol 1970;18:585-590

96. Galdston I. The ideological basis of discovery. Bull

Hist Med 1939;7:729-735

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