Re: Digest Number 1233

[Guest guest]

I have updated my web page with SV40 frequencies. See:

http://jeffsutherland.com/complementary

Everyone should check for this and eliminate it if present. It

significantly increases the risk of cancer and makes it extremely

difficult to eliminate cancer.

Jeff Sutherland

> Message: 1

> Date: Thu, 13 May 2004 11:36:41 -0600

>

> Subject: RE: Looking for " simian 40 virus " frequencies?

>

> Does anyone know frequencies for the simian 40 virus, a pollutant of the the

> polio vaccine?

[Guest guest]

This illistrates why I like the F105 which does 0.01 Hz steps. If you are

running a device that only does 1 Hz steps, and you are 1 Hz off, at 344,436

you are 64 Hz off. With 0.1 Hz steps, you are 6.4 Hz off. With a F105 you

can run 5553.68 or 5553.69. Or, you can sweep from 5553.6-5553.8 in 0.01 Hz

steps.

Or, with an EMEM device which makes its own frequencies with a 555, there

will be some drift which can accomplish the same thing.

Dick http://www.royalrife.com

Re: Digest Number 1233

>

>

> Jeff,

>

> Can you give me the breakdown for these two cancer numbers with

instructions for the F-150 running an Emem machine? Thanks!

>

> Mike truerife.com

>

> Jeff Sutherland wrote:

> I have updated my web page with SV40 frequencies. See:

> http://jeffsutherland.com/complementary

>

> Everyone should check for this and eliminate it if present. It

> significantly increases the risk of cancer and makes it extremely

> difficult to eliminate cancer.

[Guest guest]

On Sat, 15 May 2004 05:33:59 -0400 Jeff Sutherland

writes:

> Everyone should check for this and eliminate it if present. It

> significantly increases the risk of cancer and makes it extremely

> difficult to eliminate cancer.

It seems Jeff's comment above is accurate, because there is significant

indication in the research literature, that SV40 is found associated with

more and more types of cancer. While numerous studies have focused on

its presence in brain tumors, non-Hodgkins lymphoma, bone cancers, and

mesotheliomas, there are also studies on breast and ovarian, prostate and

uterine cell lines - a few abstracts are included below. Even though

many may not have time to read through the abstracts, it might be helpful

to keep them for future reference if needed.

Rife did his research on the BX virus in the late 1920s and early 1930s.

This was before the polio vaccine contamination with SV40. It is likely

we now must deal with more than one *major* cancer virus in the human

population (and there are undoubtedly others). It is just incredible

that vaccines produced on animal cells, which can contain various types

of viruses including hidden retroviruses in the animal's genome, are

still being administered to humans in a way that bypasses the natural

immune barriers. The flu vaccine is a major vaccine, it is produced on

chicken cells.

Here are some additional suggestions for experimental frequencies

relating to the genome of SV40. Numerous strains have been decoded, and

there is some variation among them. Listed first are the viral strains

that were positively identified in old batches of polio vaccine. After

that, are listed numbers for all currently identified strains, along with

a few additional freqs. Octaves are included in each line for

convenience.

Freqs for strains positively ID'd in polio vaccine (according to publicly

available records):

438.40 876.80 1753.59 3507.18

2121.32 1060.66 530.33

436.96 873.92 1747.83 3495.67

2114.36 1057.18 528.59

430.89 861.77 1723.54 3447.08

2084.96 1042.48 521.24

Freqs for all SV40 strains (octaves not included in this section, sorry.

Multiply or divide by 2 or 4 if you want them higher or lower):

Range from 858-882 hz. Or specifically:

858.83 859.81 861.77 862.26 863.08 863.25 870.72

873.75 873.92 875.27 876.80 878.33 879.35

881.92

Range from 2077-2134 hz. Or specificially:

2077.84 2080.21 2084.96 2086.16 2088.14 2088.54

2106.62 2113.94 2114.36 2117.62 2121.32 2125.02 2127.51

2133.72

Additional freqs that may be helpful:

2159.36 2575.17

2119.91 2128.89 2132.90 2137.94

2573.08

Sorry there are so many numbers, don't mean to overwhelm anyone but do

want to cover the possibilities. Some might notice many of these freqs

fall in the range often recommended by others for cancer-related

conditions.

Disclaimer

These frequencies are for experimental use only. In providing these

frequencies, there is no implication whatsoever that they could cure,

improve, or affect in any way a person's state of health. They are

derived using publicly available information from the sciences of

molecular biology, physics, and mathematics. The person providing these

frequencies is in no way setting himself / herself up as a practitioner

of medicine. You are using these numbers at your own risk.

Best wishes,

Char

==============================================

[breast]

[This study is interesting because it also indicates *pleomorphic*

tendencies in SV40-transformed mammary cells].

In Vitro Cell Dev Biol. 1991 Feb;27A(2):103-12.

Morphogenetic behavior of simian virus 40-transformed human mammary

epithelial stem cell lines on collagen gels.

Rudland PS, Ollerhead GE, Platt-Higgins AM.

Department of Biochemistry, University of Liverpool, United Kingdom.

Transformation of primary cultures of human breast cells with simian

virus 40 and clonal selection has yielded single-cell-cloned, epithelial

cell lines, as well as myoepithelial-related cell lines. When grown on

floating collagen gels, the epithelial cell lines give rise to branching

rays of cells, thick fingerlike protrusions, saclike structures, and

degenerating areas. The myoepithelial-related cell lines give rise only

to the branching rays. Epidermal growth factor stimulates the production

of the thick protrusions, whereas cholera toxin stimulates the production

of the degenerating areas. Immunocytochemical staining of these cultures

using reagents directed against the cell surface-extracellular matrix or

the cellular cytoskeleton confirms the epithelial and myoepithelial

nature of the cells, and demonstrates that the degenerating areas are

undergoing squamous metaplasia. The fingerlike protrusions consist of

cords of cells composed of inner, epithelial and outer,

myoepithelial-related cells sometimes surrounding a central lumen

reminiscent of ducts. The saclike structures resemble alveoli.

Ultrastructural analysis confirms the identification of the basic cell

types and also identifies indeterminate cells possessing features of both

epithelial and myoepithelial cells. It is suggested that the epithelial

cell lines represent human mammary stem cells that can undergo processes

of morphogenesis and differentiation in vitro to form many of the

three-dimensional structures found within the breast.

PMID: 1708370 [PubMed - indexed for MEDLINE]

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-

[breast]

Br J Cancer. 1993 Nov;68(5):868-73.

Malignant progression of SV40-immortalised human milk epithelial cells.

Yilmaz A, Gaide AC, Sordat B, Borbenyi Z, Lahm H, Imam A, Schreyer M,

Odartchenko N.

Swiss Institute for Experimental Cancer Research, Epalinges.

A human breast epithelial cell line (Hu-MI), established by

microinjecting SV40 DNA into human milk epithelial cells, exhibits the

phenotype of luminal epithelial cells and is neither clonogenic nor

tumorigenic. From this cell line we have selected two sublines, HuMI-T

and HuMI-TTul, reflecting different stages of spontaneous transformation.

HuMI-T cells grow anchorage-independently, but do not induce tumours in

nude mice. HuMI-TTul cells are clonogenic as well as tumorigenic. Cells

from both lines exhibit polymorphic structural and numerical chromosome

aberrations. Immortalisation of normal luminal epithelial cells from

human mammary gland with SV40 DNA alone may thus cause random genetic

changes eventually resulting in tumorigenic cell lines. Since Hu-MI,

HuMI-T and HuMI-TTul represent some of the consecutive stages taking

place during cellular transformation, they are particularly suited as a

novel in vitro model system to study progression of human breast cancer.

PMID: 8217602 [PubMed - indexed for MEDLINE]

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[Ovarian]

Gynecol Oncol. 2001 Apr;81(1):10-7.

Characterization and tumorigenicity of human ovarian surface epithelial

cells immortalized by SV40 large T antigen.

Nitta M, Katabuchi H, Ohtake H, Tashiro H, Yamaizumi M, Okamura H.

Department of Obstetrics and Gynecology, Kumamoto University School of

Medicine, Kumamoto 860-8556, Japan.

OBJECTIVES: Epithelial ovarian cancers are considered to arise from

neoplastic transformation of the ovarian surface epithelium (OSE).

However, the earliest events in ovarian carcinogenesis have not been

clearly defined because patients are often diagnosed in the advanced

stages and useful in vivo and in vitro experimental systems using human

OSE cells are lacking. We aimed to improve the availability of

experimental models for the study of human ovarian carcinogenesis.

METHODS: Subcultured human OSE cells were transfected with SV40 large T

antigen. Resulting OSE cell lines were characterized using

immunocytochemistry and tested tumorigenicity. RESULTS: Six immortalized

OSE cell lines were obtained. All cell lines essentially retained the

original morphological features of normal OSE cells and showed higher

proliferation rates and saturation density. Although they were all

nontumorigenic in athymic mice, OSE2b-2 sv cells, which were selected in

soft agar from colonies of an SV40 large T antigen-expressing

transfectant, OSE2b sv, produced tumors on the peritoneal surface,

mesothelium, and diaphragm and induced ascites after being injected

intraperitoneally. Solid tumors also grew when mice were inoculated

subcutaneously. The tumor cells were formed in a solid sheet arrangement

and no evidence of glandular or squamous differentiation was present.

They were weakly immunostained with an antibody against cytokeratin, and

intercellular junctions resembling attachment devices were

ultrastructurally present between cells. The tumors were histologically

diagnosed as undifferentiated carcinomas. CONCLUSIONS: The established

cell lines may provide a model system to investigate the mechanisms of

cytogenic and molecular changes from normal OSE cells through the various

steps of transformation. Copyright 2001 Academic Press.

PMID: 11277643 [PubMed - indexed for MEDLINE]

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[uterine]

Am J Pathol. 1999 Apr;154(4):1245-57.

Physiological and cytogenetic characterization of immortalized human

endometriotic cells containing episomal simian virus 40 DNA.

Akoum A, Lavoie J, Drouin R, Jolicoeur C, Lemay A, Maheux R, Khandjian

EW.

Laboratoire d'Endocrinologie de la Reproduction, Centre de Recherche,

Pavillon Saint-Francois d'Assise, Centre Hospitalier Universitaire de

Quebec, Universite Laval, Quebec, Canada. ali.akoum@...

The study of misplaced endometrial cells, which abnormally implant and

grow outside the uterine cavity, is of considerable interest for the

understanding of the pathophysiology of endometriosis. However,

endometriotic cells, particularly epithelial cells, required for primary

cell culture are not easily available. We report here the

characterization of an endometriotic cell line immortalized after

infection of primary endometriotic cell cultures with simian virus 40.

Transformed cells express T-antigen, and blot hybridization analysis

showed that the viral genome is present as an episome. Cytogenetic

analysis revealed a polyploid karyotype with numerical and structural

rearrangements involving mainly the same chromosomes (6, 10, 11, 15, and

17). The cell line has been maintained in culture for over 80 passages

and was still proliferating without any noticeable change in the

biological properties investigated. Transformed endometriotic cells

expressed both progesterone and estradiol receptors and were stimulated

by these ovarian hormones to secrete monocyte chemotactic protein-1, a

factor that may play an important role in the recruitment and activation

of peritoneal macrophages. In addition, this response was enhanced in

interleukin-1-treated cells. Taken together, these findings support the

view that this cell line may be an interesting tool for the study of the

pathophysiology of endometriosis.

PMID: 10233862 [PubMed - indexed for MEDLINE]

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[Prostate]

Proc Natl Acad Sci U S A. 1998 Dec 22;95(26):15382-7.

A transgenic mouse model of metastatic prostate cancer originating from

neuroendocrine cells.

Garabedian EM, Humphrey PA, Gordon JI.

Department of Molecular Biology and Pharmacology, Washington University

School of Medicine, St. Louis, MO 63110, USA.

A transgenic mouse model of metastatic prostate cancer has been developed

that is 100% penetrant in multiple pedigrees. Nucleotides -6500 to +34 of

the mouse cryptdin-2 gene were used to direct expression of simian virus

40 T antigen to a subset of neuroendocrine cells in all lobes of the

FVB/N mouse prostate. Transgene expression is initiated between 7 and 8

weeks of age and leads to development of prostatic intraepithelial

neoplasia within a week. Prostatic intraepithelial neoplasia progresses

rapidly to local invasion. Metastases to lymph nodes, liver, lung, and

bone are common by 6 months. Tumorigenesis is not dependent on androgens.

This model indicates that the neuroendocrine cell lineage of the prostate

is exquisitely sensitive to transformation and provides insights about

the significance of neuroendocrine differentiation in human prostate

cancer.

PMID: 9860977 [PubMed - indexed for MEDLINE]

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-----------------

[Prostate]

J Urol. 1991 Sep;146(3):881-6.

Immortalization of human adult normal prostatic epithelial cells by

liposomes containing large T-SV40 gene.

Cussenot O, Berthon P, Berger R, Mowszowicz I, Faille A, Hojman F,

Teillac P, Le Duc A, Calvo F.

Department of Urology, INSERM Unit 301, Hospital Saint-Louis, Paris,

France.

Simian virus SV40 has been widely used to immortalize epithelial cells of

mammalian origin. We report here, for the first time to our knowledge,

the immortalization of normal adult prostatic epithelial cells in culture

by transfection of a plasmid containing SV40 genome with a defective

replication origin (SV40 ori-) encapsulated into liposomes. These cells

(PNT1) have now been cultured for more than 12 months, and shown to

contain the SV40 genome. They express large T protein, present the

phenotype of differentiated luminal prostatic cells (positive with

antibodies to cytokeratin 18, 19, weakly positive for prostatic acid

phosphatase and prostatic specific antigen, negative with anticytokeratin

14 and KL2 antibody). PNT1 cells contain high affinity receptors for

dihydrotestosterone. These cells provide a useful tool to study the

biology and the pathology of adult prostatic epithelial cells, specially

to understand the steps leading to prostatic transformation.

PMID: 1714974 [PubMed - indexed for MEDLINE]

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[Prostate and breast]

Proc Natl Acad Sci U S A. 1994 Nov 8;91(23):11236-40.

Prostate and mammary adenocarcinoma in transgenic mice carrying a rat

C3(1) simian virus 40 large tumor antigen fusion gene.

Maroulakou IG, Anver M, Garrett L, Green JE.

Laboratory of Molecular Oncology, National Cancer Institute, Frederick,

MD 21702-1201.

A transgenic mouse model for prostate and mammary cancer has been

developed in mice containing a recombinant gene expressing the simian

virus 40 early-region transforming sequences under the regulatory control

of the rat prostatic steroid binding protein [C3(1)] gene. Male

transgenic mice develop prostatic hyperplasia in early life that

progresses to adenoma or adenocarcinoma in most animals surviving to

longer than 7 months of age. Prostate cancer metastases to lung have been

observed. Female animals from the same founder lines generally develop

mammary hyperplasia by 3 months of age with subsequent development of

mammary adenocarcinoma by 6 months of age in 100% of the animals. The

development of tumors correlates with the expression of the transgene as

determined by Northern blot and immunohistochemical analyses. The results

of these experiments demonstrate that the C3(1) regulatory region used in

these experiments is useful for targeting expression to the prostate and

mammary gland. To our knowledge, this experimental system is the first

reported transgenic mouse model for prostate cancer. These transgenic

animals offer the opportunity to study hormone response elements in vivo

and the multistage progression from normal tissue to carcinoma in the

prostate and mammary glands.

PMID: 7972041 [PubMed - indexed for MEDLINE]

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[Prostate]

Proc Natl Acad Sci U S A. 1995 Apr 11;92(8):3439-43.

Prostate cancer in a transgenic mouse.

Greenberg NM, DeMayo F, Finegold MJ, Medina D, Tilley WD, Aspinall JO,

Cunha GR, Donjacour AA, Matusik RJ, Rosen JM.

Department of Cell Biology, Baylor College of Medicine, Houston, TX

77030, USA.

Progress toward understanding the biology of prostate cancer has been

slow due to the few animal research models available to study the

spectrum of this uniquely human disease. To develop an animal model for

prostate cancer, several lines of transgenic mice were generated by using

the prostate-specific rat probasin promoter to derive expression of the

simian virus 40 large tumor antigen-coding region. Mice expressing high

levels of the transgene display progressive forms of prostatic disease

that histologically resemble human prostate cancer, ranging from mild

intraepithelial hyperplasia to large multinodular malignant neoplasia.

Prostate tumors have been detected specifically in the prostate as early

as 10 weeks of age. Immunohistochemical analysis of tumor tissue has

demonstrated that dorsolateral prostate-specific secretory proteins were

confined to well-differentiated ductal epithelial cells adjacent to, or

within, the poorly differentiated tumor mass. Prostate tumors in the mice

also display elevated levels of nuclear p53 and a decreased heterogeneous

pattern of androgen-receptor expression, as observed in advanced human

prostate cancer. The establishment of breeding lines of transgenic mice

that reproducibly develop prostate cancer provides an animal model system

to study the molecular basis of transformation of normal prostatic cells

and the factors influencing the progression to metastatic prostate

cancer.

PMID: 7724580 [PubMed - indexed for MEDLINE]

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Additional PubMed articles on prostate-SV40 immortal cell lines:

8900919, 11272117, and numerous others (click on " related articles " )

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