Anything on Creutzfeldt-Jakob Disease
kerrr at CRYPTIC.RCH.UNIMELB.EDU.AU
Thu Aug 17 01:46:20 EST 1995
>You say just because the dwarfs in the 1950's got bovine growth hormine
>injections (bovine=cow) and the dwarfs got a "cow" disease, how do we
>know they got Creutzfeldt-Jakob Disease from this? Isn't that sort of
>like saying you don't get rose petals from roses?
was the growth hormone extracted from pooled bovine pituitary glands ?
if it was, then some of those cows probably had bovine spongiform
encephalitis , which is a prion disease & has little to do with the
regulation or metabolism of IGF or GH. unfortunately, the prion diseases
weren't known in the 1950s so they couldn't screen for them. The prion is
the causative agent in CJD not "aberrant" hormone levels.
>As to the references I'll be glad to go over them. The insulin growth
>factor is the regulator of cancer! Milk is an enzyme inhibitor and
>hormones survive digestion.
Iv'e shifted all of the scientific refs to the bottom of the post. I agree
that IGF & it's receptor are implicated in some cancers in some situations.
However to extrapolate these findings to the growth of every cancer ,
disregarding the roles of other factors, such as TGF beta, FGF, BDGF , stem
cell factor, LIF etc
is not accurate, nor is it good scientific practice. Actually, it steps
very close to scaremongering..Please don't disregard the finding that IGFs
are a piece of the woodwind section, not the entire orchestra.
the last paragraphs I've pasted below in the appendix
>On November 8, 1994 the New York Times published a story written by Gina
>Kolata which revealed:
again< i reiterate, the function of a news paper is to sell copy, not
provide unbiased comment. To quote from the NY Times as a piece of
supporting evidence for a complex topic such as the regulation of cellular
metabolism is irresponsible. did this article have a reference list that
quoted peer reviewed work?
>1. There is good reason to believe that many very early cancers never
>become clinically significant.
>2. Although 1% of women between the ages of 40 and 50 are diagnosed with
>breast cancer, autopsy studies reveal that 39% of women in that age group
>have tumors in their breasts.
are these tumours malignant or benign ?
further, are they tumours at all ? or hyperplasia, which is distinct from
>3. Forty-six percent of men between the age of 60 and seventy have
>prostate cancer although only 1% are clinically diagnosed.
is this prostate cancer, prostate thickening or what. To cut off the line
of retort that all these things are merely stepping stones to prostate
cancer , the answer is no, they are not.
>4. Virtually all people over 50 have thyroid tumors.
why? do you know?
>5. Cancerous tumors are the ones that have somehow thrown off the
>usually tight genetic controls on unwanted divison and growth. (Remember
>the match I mentioned?!)
>The FDA now has information indicating that data was manipaulated and
>withheld from peer review. In addition, new information has surfaced
>indicating that the product which was approved for use after many years
>of testing is not the same product that is now being used. (Remember the
>freak amino acid - epsilon-N-acetyllysine - in place of lysine in the
do you have a reference for this assertion that the FDA has this info. ?
how did you get it, or did you read of it somewhere?
>Armed with the knowledge that virtually all humans hae tumors waiting to
>proliferate, and milk hormones (IGFs) cause proliferation of cancer, and
>that treatment of cows with recombinant bovine growth hormone causes an
>increase in IGF levels in milk, it is now time for science, industry and
>the FDA to re-investigate and re-evaluate this controversy.
>According to Sciene News in 1988 when human growth hormone was given to
>dwarfs some got leukemia.
>Monsanto doesn't want it labeled because consumers won't buy it. That's
>why in 10 or 11 major cities of the U.S. on Thursday there will be
>protests sponsed by PURE FOODS in Washington. The one in Atlanta is in
>cooperation with Mission Possible and includes aspartame, another
>Monsanto monster. (10:30 A.M., Thursday, August 17 in front of Return to
>Eden, Cheshire Square Shopping Center at Cheshire Bridge and LaVista).
>Robert Cohen who has done this research is trying to stop this insanity
>and save our children who are drinking this milk.
>I hope this further information is helpful. I know that scientists are
>only interested in peer review journals but many times data is compromised.
The notion that data is compromised again raises the X-files conspiracy
flavour of a lot of your posts Betty. misquotation & changes in context ,
exxageration and scaremongering are usually charges levelled at supporters
of different points of view when the accusser is running low on
If IGF from milk was the regulator of cancer then where are the quotes for
increases in GI tract cancer, where the exposure of the cells would be
also, how about studies comparing rates of these cancers in people or
animals that drink cows milk vs no cows milk ( there will be people who
have to do this as they are lactose intolerant or just don't have access to
cows milk )
the other *hypothetical* course would be (if you assume your argument to
be correct, which is a mighty leap of faith) to inoculate experimental
animals with tumour that is somehow attenuated then feed the mice cows milk
& sit back & wait for the tumours to appear. do you have any data such as
till the next fun filled episode
repositioned article quotes.>
>The most recent research would tend to support the dramatic role that IGF
>plays in cellular growth. Kleinman report that IGF-I is found to be
>involved in the growth regulation of endometrial tumor cells and is 30
>fold more potent than insulin, suggesting the effects of these growth
>factors are mediated by the IGF-I receptor. D-Errico notes that results
>obtained using molecular biology techniques suggest a possible role for
>insulin-like growth factor II (IGF-II) in the pathogenesis of
>hepatocellular carcinoma (HCC). Kwok has found that the biological
>effects of IGF-I are initiated by its binding to the IGF-I receptor,
>which is able to transduce mitogenic and metabolic signals, supporting
>the hypothesis that the IGF-I receptor is involved in the development of
>diabetic vascular complications. Wimalasena found IGF-I to increase cell
>growth, and a maximal effect of 3-5 fold increase in cell number was
>There is evidence that IGF functions on a nanomolecular level. MCF-7
>cancer cells proliferate in response to nanomolar concentrations of IGF-I
>and IGF-II. De-Leon reported that the actions of both peptides are
>mediated through the IGF-I receptor concluding that IGF-I and IGF-II are
>potent mitogens in MCF-7 cells and can stimulate cell proliferation
>through all three receptors. Martin reports that IGF-II stimulates cell
>proliferation via the type I IGF receptor. The type I IGF receptor
>mediates IGF-II induced autocrine neuroblastoma cell growth.
>Ambrose observed that the interaction of insulin-like growth factors with
>the IGF-I receptor is an important step in the control of cell
>proliferation and development. In particular, IGF-I and IGF-II are key
>regulators of central nervous sytem development and may modulate the
>growth of glital tumors. Nielsen noted that the transcription of IGF-II
>genes lead to the production of significant amounts of IGF-II which
>stimulate the proliferation of MSRCT (cancerous growths) by interaction
>with IGF-I receptors on the cells.
>FDA, based upon Monsanto's research, continues to proclaim that IGF in
>milk has no effect on human metabolism. IGF-I is a mitogenic growth
>factor. Prager found rat cells responding so in vitro IGF-I treatment by
>increased proliferation and DNA synthesis. Tumor cell assays confirmed
>continued expression of IGF-I receptors. Raile observed similar
>effects. Insulin-like growth factor I and II were implicated in the
>growth promotion of in vivo tumors and tumor cells in vitro. Tumor cells
>responded to an addition of exogenous insulin growth factor with an
>increase of DNA synthesis.
>Langford found that IGF-I has multiple metabolic actions and effects on
>the differentiation and proliferation of a wide variety of cell types.
>IGF-I and II have been identified as autocrine and endocrine growth
>regulators which accelerate various types of carcinomas. IGF-I is
>considered to play an important role in the proliferation of pancreatic
>cancer cells, according to Gillespie.
>Glick noted that IGFs play an important role in the regulation and
>glucose metabolism in CNS tumors.
>It was reported by Atig that insulin-like growth factor II is associated
>with human primary colorectal tumors and colincarcinoma cell lines.
>Yashiro found IGF-bp activity was significantly higher in cancer
>extracts, suggesting that higher IGF-bp activity in cancer tissue is
>involved in regulating growth of thyroid papillary carcinoma cells.
>Robbins (Genentech, Inc.) found IGF-I increased lymphocyte numbers in all
>of the peripheral lymphoid organs examined. This increase had functional
>significance, and Robbins concluded that IGF-I produced locally by thymic
>and bone marrow cells may be a natural component of B and T cell
>Yun demonstrated that IGF transcripts were 32-64 fold more abundant in
>Wilms tumors than in the adjacent uninvolved kidneys. IGF-II is
>suggested as playing a role in transforming growth factor in Wilms
>Minniti concluded that insulin-like growth factor II (IGF-II) acts as an
>autocrine growth and motility factor in human rhabdomyosarcoma cell
>lines. Analyses of tumor biopsy specimens demonstrate high levels of
>IGF-II mRNA expression. All tumor specimens examined expressed the gene
>for IGF-II, and this expression was localized to the tumor cells and not
>to surrounding stroma. These data suggest that the IGF-II autocrine loop
>may be operating not only in vitro but also in vivo.
>Developing osteogenic sarcoma were researched by Kappel who wrote that
>this type of cancer is the most common bone tumor of childhood and
>typically occurs during adolescent growth spurts when growth hormone and
>insulin-like growth factor-I (IGF-I) may be at their highest lifetime
>levels. He noted that human osteogenic sarcoma cell lines are dependent
>on signaling through IGF-I receptors for invitro survival and
>proliferation. Furthermore, they suggest modulation of the growth
>hormone IGF-I axis may affect the growth of these tumors in vivo.
>Lippman, as early as 1991, had implicated IGF-I as being critically
>involved in the aberrant growth of human breast cancer cells.
>Lee observed the processing of insulin-like growth factor by human breast
>tissue and commented:
>"This indicates, for the first time, that oestrogen regulation of IGF-I
>peptide in breast cancer cells would support the hypothesis that IGF-II
>has an autocrine regulatory function in breast cancer.
>Chen notes that IGFs are potent mitogens for malignant cell proliferation
>in the human breast carcinoma cell line.
>Figueroa confirmed that insulin-like growth factors (IGFs) are potent
>mitogens for breast cancer cells and their activity is modulated by high
>affinity binding proteins.
>Li treated breast cancer cells (MCF-7) with IGF-I and observed a 10-fold
>increase in mRNA levels of cancer cells and concluded that IGF-I
>modulation of gene expression appears to be an important step in cellular
>proliferation. Krasnick furnishes another clue to this puzzle by
>revealing that IGF-I may have a role in the regulation of human ovarian
>cancer. His data support a role for IGF-I in proliferation of ovarian
>cancer and suggests that IGF-I and estradiol interact in a synergistic
>manner and regulate this malignancy.
>Musgrove states that growth factors play a major role in the control of
>human breast cancer cell proliferation.
>Here's your missing link:
>Regards Betty OPERATION MISSION POSSIBLE
>Domain: betty at pd.org
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