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Foundation Staff .

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Posted: Thu Sep 22nd, 2005 04:23 |
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Inflammation causes cancer
"Everybody knows inflammation causes cancer" and they can readily observe what low levels of cancers are found in the MP cohort. Getting rid of Th1 inflammation apparently is the silver bullet for prevention. Is there a silver bullet for cure? Probably not. At least, nobody has come up with a 100% cure just yet, and I suspect immunopathology will prevent them from doing so. (If any Professionals want a more detailed explanation of the putative pathogenic description please contact me directly)....Trevor...
"Recent research is showing that some of the cytokines (caused by Th1 inflammation) are necessary for Cancers to take hold in the body. So it is most certainly incorrect to view Cancer as a totally separate disease from Th1 immune disease."
Dr. Trevor Marshall, PhD
The Cancer Microbe
Dr Alan Cantwell, who, back in 1982, published photographs showing bacteria at the seat of Sarcoid-inflamed-tissue, is the author of a book called "The Cancer Microbe."
When he published it he was made the laughing stock of many in the medical profession, who ridiculed the concept that Th1 bacteria are at the root of cancer. But he has now drawn a close group of colleagues around him, and we exchange info and ideas as each of the new studies comes out. And to me, as every week passes, it looks more and more likely that Alan was correct all along.
Knowing the pathogenesis is a long way from deriving a cure, but, IMO, we are close to defining the pathogenesis, and papers are being published from many groups who are working along similar lines. Patients (not MP patients) are reaching recovery after antibiotic therapy (not MP) in just a few cases, but cases that IMO, are significant.
I think Alan Cantwell is absolutely correct in saying that the CWD infection creates the environment and cytokines needed for cancer to start and proliferate. CAM apparently provides the adhesion necessary for the cancer cells to adhere to tissue, and to each other.
Since excess Vit D will shut down the cytokines, then it will be (and is being) shown as a cancer "cure" when it fact it is just delaying the inevitable. Another problem with study design - the studies just do not last for long enough to pick up the effects of chronic infection.
The next 20 years will see a lot of change in medicine, IMO.
..Trevor..
Study raises hopes antibiotics may be an alternative
http://www.rense.com/general72/chemo.htm
ps: some of Alan's papers are at JOIMR.org
You might also review Dr Broxmeyer's paper: http://tinyurl.com/afuqp
and this one: http://tinyurl.com/bosvc
pps: Alan has just published a new book "Four Women Against Cancer" ($16.95 approx). His books are available from 'Aries Rising Press,' phone/FAX (323)462-6458
There are some secondhand copies of each at Amazon.com
http://tinyurl.com/ey3cc
http://tinyurl.com/b8ucd
Book review
An incredible book (by Alan Cantwell, MD).I just read it this weekend,and it is excellent.It's very hard to believe that this incredible research has been overlooked for so long.A quote from Florence Nightingale really sums up TH1 disease:"There are no specific diseases, only specific disease CONDITIONS."
Especially fascinating was the section on the struggles between Antoine Bechamp and Louis Pasteur. Pasteur hypothesized that all illness came from external germs, and this is what modern medicine is based on. Bechamp, on the other hand, hypothesized that some illness came from inside of us, and not from external bacteria.This sounds an awful lot like Trevor's theory that TH1 illness is caused by a succession of illnesses, perhaps changing something inside of us, that makes us vulnerable to pleomorphic bacteria.
Fascinating reading, and I highly recomend it.If Dr Alan Cantwell reads this site, I gotta congratulate you. I'm looking forward to reading more of your books! ~Sam
"Cantwell AR: The Russell Body - The Forgotten Clue to the Bacterial Cause of Cancer. JOIMR 2003;1(6):1"
http://www.joimr.org/phorum/read.php?f=2&i=50&t=50
Another good book
Physician/Researcher Lawrence Broxmeyer MD Historically Addresses A Controversial Question: Is Cancer Just An Incurable Disease?
Summary: Recently, Elsevier, foremost publisher of world medical literature peer-reviewed and published Lawrence Broxmeyer MD’s “Is cancer just an incurable infectious disease?” Medical Hypothesis 63 (986-996) 2004.
Here he discusses that publication:
Whitestone, New York -- (ArriveNet - May 16, 2005) -- The word ‘cancer’ is of Latin derivation and means crab. By the turn of the 20th Century organized medicine had come to the conclusion that it was not a matter of whether infectious disease caused cancer, but which one. And in 1912, The Journal of the American Medical Association, (JAMA) in its editorial “Is Cancer of Infectious Nature?”, concluded that one investigator had “a very strong case in favor of his view of the infectious cause of cancer in general.” Just how was this mind set altered, and then totally submerged? It was an interesting subject, and so I decided to ask researcher Lawrence Broxmeyer MD more.
“For over two hundred years a cancer germ had been discovered and rediscovered, named and renamed, each scientist adding to the knowledge, but to no avail,” replied Lawrence Broxmeyer MD. “Then, in 1910, certain American medical powers did a 180-degree rotation, deciding that cancer was not caused by a microbe, and that anyone who thought otherwise was a heretic, a charlatan, or a quack. But Dr. Virginia Livingston MD and her superb network were none of the above, their meticulous peer-reviewed research and publications, done at the height of US post World War II technology. In her group were such world-renowned scientists as Dr. Florence Seibert and Dr. Eleanor Alexander-Jackson of Cornell. And Dean Burk, Head of Cell Chemistry at the National Cancer Institute (NCI) at that time, when asked, went so far as to say that Livingston’s cancer germ was as real and certain as anything known about cancer.”
Videos
Dec 07 Dr Alan Cantwell's two presentations at our LAX 2006 conference are now available on YouTube at these URLs:
"The Cancer Microbe and the Russell Body"
http://youtube.com/watch?v=sSst-APMmzA
"The Cancer Microbe in AIDS and Kaposi's Sarcoma"
http://youtube.com/watch?v=TQm8Xi76AIw
Those of you who haven't yet had a chance to hear Alan talk about "The Cancer Microbe" will now be able to do so. The quality isn't as good as it is on our DVDs, but these are URLs that you can send to any of your friends who might be interested in trying to understand the links between the pleomorphic bacteria, Cancer and AIDS.
Alan also talks briefly about Lupus and Scleroderma.
Cancer and the Marshall Protocol
The VDR transcribes the Metastasis Suppressor #1 (MTSS1) gene, which ends up as the "Missing In Metastasis" (MIM) protein. When the bugs are present this protein is missing. When Olmesartan gets the VDR working again, you can expect that protein to come back.
We have seen no metastasis in our cohort. Some old inactive tumors, yes, but no metastasizing agressive tumors as would normally be expected in a cohort as sick as ours.
..Trevor..
from the topic: Elusive Bacterium -- Russell Bodies ?????
Cancer, Th1 inflammation basic cause????
Dr Trevor Marshall wrote:
I just finished off preparing for my presentation next week at Karolinska Institutet. I edited up a sequence of video I received from Andy Wright that I haven't shown in public yet, a sequence photographed of L-forms in blood of a Cancer/ ME /CFS patient.
What is amazing is the total destruction of the environment by the L-forms, the same shaped L-froms which are seen in lesser abundance on his other videos.
We do have a chicken-and-egg situation, however. Does the cancer weaken the immune system so that it cannot kill the intracellular forms, or do the intracellular forms so weaken the immune system that it cannot stop the cancer cell formation?
Of course, the L-forms are there in any case, so it does make sense to try and get rid of them. But what will be the outcome of doing this?
I will have a copy of the poster, with the video on it, showing at our own conference too. There will be some interesting discussions to be had there, I think 
..Trevor..
ps: the video plays continuously on a tiny hand-held Pocket PC attached to the poster printout
See also:
Bacteria and cancer: cause, coincidence or cure? A review.
J Transl Med. 2006 Mar 28;4:14.
PMID: 16566840
Wikipedia Cancer bacteria page
Can the MP treat cancer?
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Foundation Staff .

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Posted: Thu Sep 22nd, 2005 04:37 |
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Breast cancer
BRCA mutation genes
Question: I recently came across an article while doing a medline search entitled, "Association between low levels of 1,25 dihydroxyvitamin D and breast cancer risk." The conclusions of the study were:"These data are consistent with a protective effect of 1,25-D for breast cancer in white women." This concerns me because I carry the brca-1 mutation and so am already at a very high risk of getting breast cancer and according to the study lowering my 1,25-D will only further increase my risk.
Answer: The brca1 gene has only been shown to be a MARKER of breast cancer, not a cause. Second, Th1 inflammation is almost certainly a necessary precursor to breast cancer (i.e. a cause) Mutations in brca1 and brca2 are associated with increased incidence of cancers, not necessarily causal.
I have just come from a "Diseases of (DNA) Transcription" conference at the Salk Institute where there was not one scientist who knew exactly how genes mutate, or why, or what it means.
Sure, there are statistics linking shifts in haplotypes with certain diseases, but they are just as likely due to the mix of persistent pathogens your family has been passing down, as they are due to any Mendelian variation of the gene pool.
A person has to assess the relative liklihood of dying from Th1 disease and dying from cancer. 1,25-D is a measure of the Th1 reaction and is therefore intimately associated with breast cancer, in ways that this study investigators never dreamed of. If one doesn't understand the subtleties behind this kind of research, then one is going to have trouble assessing relative risks in medicine.
I have seen a number of Th1 patients erroneously diagnosed with cancer. The diagnosis of cancer is not precise. Flow cytometry senses the presence of both CD10 and bcl2, and these are elevated in Th1 disease. False positives are a fact of life, but patients rarely find out about them. False positives increase the apparent 'success rate' of oncology, and there is therefore little incentive to minimize them.
Please listen to my discussion of these genetics, including the bcl2 issue, on the DVDs of my talk on Familial Aggregation at the conference.
BRCA genes are turning out essentially useless to tell Breast Cancer predisposition, as now they are falling back on the old epidemiological factors before even screening 
The relationship between cancer and inflammation is controversial. (IMO) A good review of the issues is available from JOIMR at URL
http://www.joimr.org/phorum/read.php?f=2&i=50&t=50
Additionally, two of the markers used in Flow Cytometry (used as the 'gold standard' for breast cancer) bcl2 and CD10, are both elevated in the inflammatory diseases, leading to misdiagnosis in a lot of cases, probably in a majority of cases. These misdiagnoses also bias the epidemiological studies.
The BRCA1 and BRCA2 genes are probably not good differential markers of cancer vs inflammation. The pathology report from MD Anderson again states there is no sign of proliferation of the cancer into the surrounding tissues, so the sentinel node biopsy is probably the best way to determine whether the lump is an old cancer or is still active.
Less than 10% of Breast cancers are due to BRCA1, most are due to Estrogen up-regulation. Since the Estrogen receptor transcribes the protein which folds to form the Vitamin D Receptor, excessive estrogen is probably associated with a disabled VDR, IMO.
..Trevor..
BRCA1 and BRCA2 genes are no longer regarded as definitive
BRCA genes get help in causing breast cancer-study
By Andrew Stern
CHICAGO, Jan 8 (Reuters) - The risk of breast cancer among women carrying the well-known BRCA mutations is also affected by other genes, researchers said on Tuesday.
The study of close relatives of breast cancer patients who had one of the BRCA mutations showed the risk of the disease varied greatly between families, indicating that other genes must be involved.
So a woman who knows she has a BRCA1 or BRCA2 mutation still cannot know precisely what her risk of breast cancer is, the researchers reported in the Journal of the American Medical Association. "The implications of that are that there must be other genetic factors involved here," Dr. Colin Begg of Memorial Sloan-Kettering Cancer Center in New York, who led the study, said in a telephone interview.
"Because if some carrier families have higher risks than other carrier families presumably there are other genes being passed through these families that elevate or lower the risks," Begg said.
Begg's team studied 2,000 women diagnosed with breast cancer, and the families of the 181 patients who had BRCA mutations. They found that 5 percent of those with cancer in one breast had a BRCA1 or BRCA2 mutation and 15 percent of those with cancer in both breasts did.
All had been diagnosed early, before the age of 55. But only 25 percent of all the patients had a close relative with breast cancer. And 58 percent of those with BRCA1 or BRCA2 mutations had a mother, sister or other close relative with the disease, the researchers said.
They said this means a close relative of a BRCA carrier with breast cancer has a 40 percent risk of developing the disease herself by age 70. But this is an average risk and they found a considerable amount of variation in risk from one family to another.
Search for more genes
Among carriers, their risk of developing breast cancer by age 70 has been estimated at anywhere between 50 percent and 85 percent, Begg said.
They looked to see if perhaps the type of BRCA mutation might affect risk, but it did not appear to. Many different types of mutations were found but they usually did not significantly affect whether a woman or her relatives had breast cancer, Begg's team said.
"There's a lot of research going on at the moment in general to find additional breast cancer genes. What we're saying here is that research is likely to be successful," Begg said.
The BRCA1 and BRCA2 mutations are most common among Jews of Ashken*** decent -- at least 2 percent of these descendants of Eastern European Jews are carriers. The incidence is lower in the general population, but not enough testing has been done to put a firm estimate on it. About 465,000 women died of breast cancer last year, making it the leading cause of cancer death among women worldwide, according to the World Health Organization.
The vitamin D link to cancer
Many new papers linking Vitamin D / VDR to breast cancer. Here is one that Doc might be interested in looking at:-
http://tinyurl.com/36d693
and another:
http://tinyurl.com/23c5uk
and another:
http://tinyurl.com/23qpc4
See also:
Vitamin D and Cancer
Genomic data
Here is some specific information to help you understand the complexities of making absolute causal inferences from genomic data, such as many oncologists have done with respect to the association between brca mutations and familial incidence of cancers. You will find a summary of the the Staph aureus genome at this URL:
http://tinyurl.com/3rasb
Search for the following annotation:
"Pfam match to entry PF00533 BRCT, BRCA1 C Terminus (BRCT) domain, score 54.4, E-value 2.7e-13"
This means that there are similarities between the way the BRCT gene at the C Terminus of homo sapiens BRCA1, and the way this gene in the Staph aureus bacterium behave.
Please note that I am not concluding that this apparent homology is proof of anything, except that we still have so much to learn about the human body, and the way it works, and the pathogens with which it co-habits this planet.
The more I learn the less I realize I really know. I just wish physicians were trained to recognize the same phenomenon 
..Trevor..
Far more mutations than thought involved in cancer
"A painstaking scan of the DNA of tumor cells shows hundreds of previously unsuspected genes are involved in cancer, researchers said on Wednesday .. They found more than 1,000 different mutations in just one family of genes taken from 200 samples of breast, stomach, colorectal and other common tumors." http://tinyurl.com/226nh6
Prognosis
Using 1,25-D to determine breast cancer prognosis
Dr. Marshall cites this study in his paper, Sarcoidosis Succumbs to Antibiotics – Implications for Autoimmune Disease:
"However, Mawer, et al, reported that 1,25-D is such a sensitive indicator of the Th1 immune response that it can even be used to determine prognosis in breast cancer [23}. As the level of 1,25-D falls, the level of the body’s ability to mount a Th1 response is also falling, and the prognosis becomes less favorable."
The reference listed is:
[23] Mawer EB, Walls J, Howell A, Davies M, Ratcliffe WA, Bundred NJ. Serum 1,25-dihydroxyvitamin D may be related inversely to disease activity in breast cancer patients with bone metastases. J Clin Endocrinol Metab. 1997;82(1):118-22. PMID: 8989244 [Abstract]
This seems to indicate that it might be possible to use the level of 1,25-D as one means of suggesting whether or not breast cancer treatment is effective if doctors know how to interpet the results. But you'll note that the patients in the above study had bone metastasis.
Nobody knows the cause of cancer. But those who are close to a pathogenesis are publishing that the Th1 inflammatory cytokines, especially the chemokine CAM, are key to the cancer getting a hold in the body.
How does this relate to reduced or increased risk from Vit D deprivation? Nobody knows for sure, although it is obviously a pretty good idea to get rid of any Th1 inflammation.
You might also ask Doc how he/she assesses the relative risk factors. There has been a reluctance for clinical medicine to recognize that Vitamin D is not really a vitamin, but is an immune modulator (at least in its active steroidal 1,25-D form). As far as I know, very few cancer researchers have been looking into the biochemistry of Vit D and cancer, although some have. You will find some references to those studies in our paper at URL
http://yarcrip.com/sarcoidosissuccumbs-preprint.htm
Our Russian paper cited some of this work as well. There is beginning to be more research done in this area, but it is still early-days.
Diagnosis
See Diagnosing Cancer Accurately
The key statement is that the growth is "progressive." IMO this is the gold standard. How fast is the lump growing, and does it need immediate intervention. IMO such an evaluation cannot be made with anything other than a series of MRI or CT images, at intervals, with clear signs of progressive growth.
If the growth is not fast, and if Doc is not sure that the mass is B-cells, then there is also no pressing need for intervention (IMO).
Sarcoid granuloma, Th1 cysts and Thymal masses take months to enlarge, and not weeks.
I respectfully disagree with your doctor, it is VERY important to stain the histology of a patient with inflammatory disease in order to differentiate T cells from B cells, and Thymal masses from malignant tumors.
..Trevor..
Breast Biopsy
See Diagnosing cancer accurately
Q: "I have microcalcifications, instead of a lump, which is why a stereostatic biopsy with ultrasound is being done."
Re "microcalcifications" see A Review - Vitamin D and Calcium in Sarcoidosis (7-5-03)
http://www.sarcinfo.com/calcium.htm
It says in part:
At levels above about 42 pg/ml, the 1,25-D (generated by the sarcoid inflammation) begins to stimulate bone osteoclasts[12], causing bone to be resorbed (dissolved) back into the bloodstream. Not only does this lead to osteoporosis, but also to calcium being deposited into soft tissue of the body, including the lungs, breasts, and the kidneys (where it forms kidney stones).
Necrosis and proper testing for granulomatous mastitis versus breast cancer
A case of granulomatous mastitis mimicking breast cancer
Idiopathic granulomatous mastitis: time to avoid unnecessary mastectomies
Idiopathic granulomatous mastitis: case report and review of the literature
Idiopathic granulomatous mastitis (with necrosis). Report of a case diagnosed with fine needle aspiration cytology.
Granulomatous mastitis (with necrosis): a clinicopathological review of 26 cases.
"Microcalcifications" are a hallmark of Th1, and I am puzzled why they are now regarded as a sign of 'cancer'. Still, given the lack of knowledge generally being exhibited by Oncologists these days (my 'exhibit 1' is this paper from Reuters earlier today, "Vitamin D may help slow breast cancer -study" http://tinyurl.com/yk7w5v )
The key thing to remember is that cancer kills because it is progressive. The cells grow too fast for your immune system to deal with. Since you are now in Phase 3, your immune system should be capable of doing a pretty good job of cleaning up any cancer cells which happen to form. So I would not be too eager to intervene until I knew that I really had a proliferative disease.
Finally, here is a quote for Doc - "Everybody knows Inflammation induces Cancer"- Francesco Marincola MD, Senior Investigator, NIH (spoken during his presentation at the "Host Defences" conference at UCSD last week).
I would be happy to chat with your oncologist about the problems with the flow cytometry markers, if that would help. to make sure they are not relying on flow cytometry markers.
At the very least, you need to have the biopsy tissue stained to differentiate B-cells and T-cells. You also need to get a better assessment of what the rate of proliferation might be." <<
Be sure to get an "open" biopsy or an "excised" biopsy (not a needle biopsy).
-If necessary have someone to support you as a patient advocate to understand and assist you in achieving your best interest.
-Prepare in advance by asking on the Board about your situation.
-Discuss your needs with your Dr before the surgery.
-Ask the Dr to confer with Dr Marshall.
There is little doubt amongst some of my professional colleagues that many cancers are rooted in Th1 inflammation. See, for example, Dr Alan Cantwell's papers at http://www.joimr.org
It is dangerous to assume that the MP in any way harms the prognosis of a cancer. There is no data indicating that this would be so, and there is one case history indicating that it doesn't.
~Trevor
CA 27.29
This article published in 2003 in the journal of the American Family Physician explains that "CA 27.29 also can be found in patients with benign disorders of the breast, liver, and kidney, and in patients with ovarian cysts."
Sarcoidosis would be considered a benign (non-malignant) disorder that can affect the breast, liver, kidney or ovary.
The CA 27.29 test is not reliable in all cases. Information from the FDA says, "Because the (CA 27.29) test did not detect the cancer antigen in all cases and detected it falsely in others, FDA based its approval on use of the test in conjunction with other procedures to monitor the recurrence of Stage II or Stage III breast cancer.
I don't understand what my pathology report means
This puts me in a difficult position. I am not an oncologist, I am a scientist. I am interested in the pathogenesis of cancer. I am far less interested in the tests which are currently thought to be indicative of cancers,as these tests change from year-to-year.
If this was a report on, for example, my wife, I would want her to discuss the following with Doc.
1. A needle biopsy is usually not capable of preserving the granulomatous structure characteristic of Sarcoidosis. The diameter of the needle is small, and granuloma are often large by comparison. This makes microscopic histological examination somewhat uncertain without specific staining.
2. I see no attempt to stain for T cells or B cells.
3. The issue is not that a 'mass' was found - I would ask if it is a Thymal mass (indicating T-cell immune disease) or a proliferative mass (B-cell cancer)
4. The marker "c-erbB-2" which is supposed to indicate a bad prognosis for Breast Cancer is reported as negative.
5. Only one out of the three markers was positive, and that marker seems to be a pretty general marker to me (an Estrogen Receptor Protein)
I would want to at least ask Doc to wait for the remaining test results to come back before I had to see a surgeon. I know what the surgeon's specialty is, and I know what he is going to want to discuss.
Again, I am not trying to give you advice, but only guidance as to what a scientist sees in the data you posted. Only your Doc and Surgeon can help you decide what course to follow. Only they are licensed to look after your health. I would be happy to discuss the T-cell vs B-cell issue with Doc, if that would help.
..Trevor..
Mammography
Mammography is a diagnostic procedure using x-rays to create images of breast tissue. It is used to detect and evaluate abnormalities such as tumors and cysts. There are two basic forms of mammography: screening and diagnostic.
" Even the best radiologists are will inaccurately read a mammogram in 2 to 3 percent of cases, while some series show that other doctors incorrectly read the images in 20 percent or more. " Chapter 8. The Eye of the Beholder, How Doctors Think by Jerome Groopman, MD.
Screening mammography
A screening mammogram is used to evaluate for cancer in women with no symptoms and no history of breast surgery. Mammograms are used for comparative study: to compare the left breast to the right, and to compare current films to older films. The goal of regular screening is to detect small cancers (when they are still small) because they are easier to treat and usually have a better prognosis for the patient. It is suggested women have a mammogram around age 35 to provide a baseline study for comparison with mammograms taken when they are 40 and older.
How often women younger than age 50 should have a screening mammogram is controversial. Most agree that women between 50-69 may significantly reduce their risk of dying from breast cancer by having a mammogram every 1-2 years, but there is insufficient evidence supporting the same benefit for women between age 40-49.
The National Cancer Institute and the American Cancer Society recommend that women 40 and older have a mammogram every 1-2 years, and that women with significant risk factors should discuss earlier screening, and how often, with their own physicians.
In standard mammogram studies, one breast is positioned between two panels and slowly compressed. Two images of each breast are obtained: a side view (from the center of body to the side) and a view from above. X-rays penetrate the breast tissue to produce images recorded on film. Different tissues in the breast absorb x-rays differently, resulting in shades of black, gray, and white on the film:
Fatty tissue absorbs little of the x-rays to appear black or dark gray.
Normal fibrous and glandular tissues (such as milk glands, lymph nodes) contain fluid, which causes them to absorb a moderate amount of x-rays and appear light gray.
Fibrous and glandular tissues may contain calcium and appear nearly white or completely white.
Cancerous tissues contain fluid and sometimes calcium, which makes small cancers difficult to distinguish from normal breast tissue. As a cancer grows, it begins to appear whiter than breast tissue on film.
Comparison with prior mammograms helps identify changes in patterns on the film that may identify small breast cancers.
Findings from screening mammograms
Because small cancers are difficult to distinguish from normal breast tissue on a mammogram and may not be palpable during a breast exam, some will be undetected. Cases that escape diagnosis are referred to as false negatives. These cancers are usually found after they have grown to a size that can be seen or felt.
Other conditions in the breasts may look similar to cancer, such as calcifications, fibrosis or cysts. The radiologist will order additional studies focusing on the area of the breast with any suspicious lesion. If additional studies are inconclusive, a biopsy may be recommended. If the biopsy eventually proves to be non-cancerous, the finding is called a false positive.
Calcifications often develop in women's breasts because breasts produce milk, which contains calcium. Because many breast cancers contain calcifications, the doctor will want to determine whether any calcification is in cancerous tissue. Most calcifications can be evaluated using additional mammogram views. Some that are difficult will require additional studies.
A mass, or a lump, found on a mammogram may be a lymph node, cyst, or fibroadenoma (fibrous milk gland). These types of masses usually are easy to identify and do not require additional studies. A new mass or a mass that has changed or grown since the last mammogram will usually be evaluated using ultrasound. A mass may be due to an inflammatory disease such as sarcoidosis. Sarcoidosis should be considered in the differential diagnosis of a mass in any patient with a previously suspected or confirmed diagnosis of sarcoidosis.
Several masses can be seen in women who have fibrocystic disease. If there is a change in the size or shape of the edges of a mass, or if a suspicious calcification is seen within a mass, the radiologist may order additional studies.
An area in one breast that has a distinctly different appearance than the same area in the other breast is referred to as asymmetric density. This finding usually requires additional studies using mammography and/or ultrasound.
Dense breast tissue can make mammogram evaluation difficult because the tissue can obscure small cancers. Pre-menopausal women usually have denser breast tissue than women who are past menopause.
Diagnostic Mammography
Diagnostic imaging is required under these conditions:
Breast implants
Severe fibrocystic disease
After surgery for early breast cancer that did not remove the entire breast
Abnormal findings on a screening mammogram (change in a mass)
New findings during a clinical breast exam (lump, nipple discharge)
Types of imaging used for diagnosis include special mammography views, views from different angles and ultrasound. If the findings obtained from additional studies indicate that there is a solid lesion, a biopsy will be recommended.
Special mammogram views
Magnification produces larger imaging of a portion of the breast that contains calcifications or masses.
Spot compression applies more pressure to a small region in the breast. This thins out an area of dense tissue so the x-rays produce a clearer image, making it easier for the radiologist to see if the tissue is normal or abnormal. This is useful in women with denser breast tissue, where it is difficult to get adequate compression for best imaging.
Sometimes views of the breast from different angles are required to see a questionable area. Typical additional views include:
Cleavage view - Both breasts are compressed between a set of panels at the same time and a top-to-bottom view of a suspicious finding in tissue between the breasts.
Rolled view - The breast is rolled to the right or left, compressed, and a top-to-bottom view is taken of a questionable area located in dense tissue.
Mediolateral view - The view is taken from the center of the chest to the outer side of the breast.
Lateromedial view - The view is taken from the outer side of the breast to the center of the chest.
Ultrasound
Ultrasound is used to help determine if a mass is a cyst or a possible cancer. Ultrasound is performed with a small, handheld device called a transducer. First, a gel is spread on the skin. Then the technician passes the transducer over the breast, which directs sound waves through the skin into the body. The sound waves create an image of the breast on a computer monitor
MRI
-Recent research (June 2007 published in August) indicates that an MRI which doesn't give off radiation detects 97% of breast tumors, but is known to give false positives. Researchers also indicated that needle biopsies can be guaged better by MRI's, but it is essential one gets the procedure done by one of only a handful of experienced rad doc in the US. Mammograms detect around 51% of tumors depending on whose research one reads. Specifically they are better for detecting microcalcifications to test for DCIS stage 0 than tumors.
MRIs do not hurt, nor do the Ultrasounds which is one of the reasons I refused (and will continue, LOL) to have mammograms and they don't give off radiation. Had the rad doc told me she was looking for microcalcifications, I would not have had the mammogram at all. I guess it was my mistake for not pushing the issue. The place I now go for treatment is at a major cancer center of a top medical school. We'll see how the next MRI goes in January. If something questionable shows up, then I will PM you for further info on Thermal Imaging. ~DNStog
Thermal imaging
-I did some research into thermal imaging (breast thermography) as an alternative and ended up calling Dr. George E. Chapman, who has written a number of texts on using thermal imaging and interpreting the results of thermal imaging, especially for early detection of breast cancer to learn more about it. (He did say that a baseline mammogram is important for interpreting any future results showing changes large enough to register on a mammogram.)
If I can remember this right, he said that the heat generated by the extra blood flow to a tumor will show up on a thermal image photo (they use special heat sensing cameras) up to ten years before the tumor would be large enough to be detected by a mammogram. Of course, heat caused by other reasons (such as infection) would show up as well, so having a qualified person, such as Dr. Chapman, interpret the results is as important as the training of the technician who takes the images.
My images showed some areas of black (cold temperatures) that were interpreted as stastically being most frequently associated with cystic and fibrocystic breasts (suggestive of hormone imbalance).
Here is part of the report: "performed 20 minutes post onset of examination and following a 60 second hand soak in 50 degree water. This provides an autonomic challenge and a response of sympathetic vaso-constriction. The skins microcirculation is further shut down and we are able to contrast any non-responsive blood vessels that may be associated with malignant neoplasms. This includes the neo-angiogenic blood vessels and those that are dilated because of nitric oxide."
At the time I was also having abdominal pain and paid for an additional set of images of the abdomen. The report stated: "Increased heat is observed above the umbilicus and prmarily at the right upper abdominal quadrant. Question pancreatitis and/or gall bladder dysfunction based on thermal patterns. May be associated with 'Head Zones'. Additional clinical information is needed for confirmation."
Kind of interesting, but I would not pay for it out of pocket unless I felt it would provide more clarity on an important health issue. Perhaps such a procedure is available in your area. I was told that Kaiser in Northern California is using it as a standard diagnostic tool now. I am sure it was much kinder and gentler than what you describe above.
I also remember him making a comment about the equipment for mammograms being 1970's (?need to check this date?) technology, approved for use at around the same time as the thermal imaging technology. But while the mammogram equipment is basically the same to this day, the equipment for thermography has moved forward significantly with computer analysis, etc. ~Joyful
Breast cancer treatment
See Chemotherapy and Radiation
Where did you get the idea that chemotherapy was in any way compatible with healing from your Th1 disease? Chemotherapy is immunosuppressive, aggressively so, and chemo will allow your bacterial load to return, by shutting down your immune system.
My assessment of your situation is that the MP has restored your immune system, allowed it to fight the cancer, which was an aggressive ductal carcinoma, but has (reportedly) been inactived by your immune system. You have dodged the bullet that killed your forebears. I know how tough it is to tread the line between old-school and new-school medical knowledge, but that is what your oncologists are forcing you to do.
Take another hard look at Alan Cantwell's presentations at the LAX conference. You are being given a choice, and those who are putting pressure on you to begin chemotherapy do not seem to have any concept of where you have been, or where you are capable of going.
..Trevor..
Members' experiences
-I was first diagnosed with Sarcoid in 1977, and like most of you have years of in and out of what seems like remission. To cut a long stroy short, I finally had a double mastectomy in 2006, and both my breasts came back from the lab, yes, with sarcoid throughout. It shows like a ca in my body. ~Debra
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Posted: Thu Sep 22nd, 2005 05:17 |
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(filelink)
Skin Cancer
"Cantwell AR: Cell-Wall-Deficient Bacteria as a Possible Cause of Basal Cell Carcinoma JOIMR 2003;1(4):1"
http://www.joimr.org/phorum/read.php?f=2&i=42&t=42
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Posted: Thu Sep 22nd, 2005 05:17 |
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(filelink)
Prostate Cancer
"Cantwell AR Jr.: Acid-Fast Bacteria In-Vivo in Prostate Cancer and the Connection between Prostate Cancer, Other Cancers, and the Kaposi’s Sarcoma Virus. JOIMR 2004;2(3):1"
http://www.joimr.org/phorum/read.php?f=2&i=57&t=57
Full paper on acid-fast bacteria in prostate cancer/Ronnie Cohen et al from Journal of Urology/ June 2005
-Excellent pioneering paper out of Perth, Australia, which for the first time suggests that BACTERIA may play a role in prostate cancer.
BBC News-- US researchers say there may be a better marker to indicate when a man has a more aggressive form of prostate cancer.
Test spots severe prostate cancer
"Investigating the reasons for this rapid growth, we discovered that the omega-6 was turning on a dozen inflammatory genes that are known to be important in cancer," lead author Dr. Millie Hughes-Fulford, from the San Francisco VA Medical Center, said in a statement.
http://tinyurl.com/apbtc
If either of these cancer tests (colonoscopy and PSA) gave a precise answer, a definite prognosis, and a clear treatment path for every possible outcome, then they would be very worthwhile indeed. You can find studies both supporting and denigrating every pathway. Medicine just doesn't have the answers yet, unfortunately. ..Trevor..
PSA 'largely produced by benign prostate disease'
13 March 2007 BJU Int 2007; 99: 554558
A study published this month provides further evidence against the use of prostate-specific antigen (PSA) as a screening tool for prostate cancer in healthy men.
The research, by a team from Charing Cross Hospital in London, UK, shows that PSA levelcorrelates poorly with prostate volume and supports the hypothesis that PSA is largely produced by benign prostatic hyperplasia (BPH).
Mathias Winkler and colleagues evaluated data on 97 prostates removed at radical cystoprostatectomy. These specimens represented a "fairly random" sample of prostates from asymptomatic men whose prostates had been examined digitally, removed whole, and were amenable to histopathological examination and clinical follow-up.
Prostate cancer was detected in 60% of the specimens, Winkler and colleagues report in BJU International.
Of these tumors, 53% were deemed clinically significant on the basis of Gleason score, tumor stage, surgical margins, perineural invasion, and presence of high-grade prostatic intraepithelial neoplasia.
However, PSA level correlated poorly with tumor volume and did not differ significantly between men with and without prostate cancer (3.1 vs 1.1 ng/ml, p=0.06).
Moreover, after a median follow-up of 3 years, there was just one distant metastasis and seven biochemical recurrences among 35 survivors with prostate cancer. Furthermore, none of the men with clinically insignificant cancers had a biochemical recurrence.
"Most incidental prostate cancers in cystoprostatectomy specimens are significant, contrary to previous analyses, but have little practical importance in terms of oncological outcome," Winkler and co-authors write.
They say that the lack of correlation between PSA values and presence of prostate cancer represents further supportive evidence that most of the PSA in prostates with cancer is produced by BPH.
"PSA is therefore confirmed as a poor screening tool, which appears to cause a serendipitous detection of prostate cancer," they conclude. "Meanwhile the search for a better prostate cancer biomarker continues.
Members' experiences
-My PSA was through the roof during the first 18 months on the MP (3 - 4 times the safe leve). I had a biopsy and a colonoscopy, all were good. As the inflamation in my glands settled so did the PSA. It has fallen well within the safe zone and remained there for nearly 2 years. Hope this gives you some comfort, although my Dr was insistent that I get it checked to be sure. ~ Sydney Chris
-My prostate and urine flow issues started 20 years ago. I am pretty pleased with all my improvements on MP in that department. Although I never had an elevated PSA my gland was large enough that my urologist wanted to microwave it. Now it is normal size and typical upon rectal exam. ~P.B.
Last edited on Thu Jul 17th, 2008 04:45 by Foundation Staff
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Posted: Sat Sep 24th, 2005 17:06 |
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(filelink)
Diagnosing Cancer Accurately
One has to be awfully careful of cancer diagnoses when one has a Th1 disease.
The gold-standard Flow Cytometry test gives false positives, as it uses two markers BCL2 (bcl2) and CD10, which are both abnormal in Th1 disease.
It is critical that no cancer diagnosis be given unless the pathologist has stained for both Thymal masses (by using a T-cell stain) in addition to a B-cell stain. This is becoming more and more rare these days.
After all, once the oncologist gets to see you, he is unlikely to see Th1, if he/she thinks it looks a bit like cancer. Worse, many oncologists think that Chemo will 'fix' Th1 diseases like sarcoidosis. Of course, they couldn't be more wrong.
..Trevor...
Diagnosing a biopsy correctly (staining for B-cells and T-cells)
Flow Cytometry tests for cancerous tissue, which are the latest technology, use some markers (such as Bcl2) which are also present in sarcoidosis and other Th1 inflammatory conditions.
If you are going to let your oncologist operate, make sure that they use the older technique of MANUALLY STAINING for B or T cell proliferation in the tissue they biopsy. This will distinguish better whether the lymph nodes (or tissue from any suspicious area) are inflamed by Th1 inflammation or by a B-cell, possible cancerous, proliferation.
..Trevor..
Cancer diagnosis in sarcoidosis patients
We caution sarcoidosis patients that Sarcoidosis can be misdiagnosed as cancer. Patients need to be their own advocate on this issue. This topic is covered in these threads:
Cancer Diagnosis in Sarcoid Patients
Explanation of Biopsy (How to read a biopsy report)
There have recently been published reports of sarc misread as cancer in PET with F-18 fluorodeoxyglucose (FDG).
False-Positive Uptake of FDG in Hepatic Sarcoidosis.
Clin Nucl Med. 2006 Mar;31(3):175.
PMID: 16495745 [PubMed - as supplied by publisher]
http://tinyurl.com/kuaoc
Cancer and inflammation are tightly intwined and the physicians don't understand that yet. An oncologist always looks for/at cancer. All the PET is doing is looking at the radioactive decay when the glucose is metabolized in the tissue. Look at this animation for more detail of how the glucose gets broken down as its energy is released
http://www.johnkyrk.com/glycolysis.html
..Trevor..
A member's experience with a request to stain tissues
I had a somewhat similar problem in trying to arrange the staining to determine the relative proportion of T and B cells for my dad’s lung biopsy sample. The doctors did not know what I was talking about and they asked the pathology department who simply said, "we will do all the appropriate tests, don’t worry about it."
So, what I did was ask the doctor if it was O.K. if I spoke to the pathologist and he said fine. The doctor had already agreed he would go along with what came of my discussion with the pathologist, when I told the doctor how important it was to me. I told the doctor, that based on research on sarcoidosis, that this test was important to help distinguish whether a mass was really cancer or actually sarcoidosis, according to a sarcoidosis expert that I had a great deal of faith in (Dr. Marshall).
So, I spoke to the pathologist and although it took a little discussion, and he may not have been wholly convinced of its necessity, he said that it was easy to do and if the doctor would order it, he could do it. So, then he talked to the doctor and they arranged for the proper order for the test. It is a fairly basic test, as I understand it, that has been around a long time. Hopefully, they will have enough of a sample from your biopsy still frozen so they can do it.
Joyce Waterhouse
Errors in cancer diagnosis common
Mon Oct 10, 2005
NEW YORK (Reuters Health) - In a review of patient specimens, errors in cancer diagnosis were seen in up to 11.8 percent of cases, according to a report in the medical journal Cancer. Moreover, in a substantial proportion of cases, the error caused some degree of harm for the patient.
The frequency and clinical impact of pathology errors in cancer diagnosis have not been well characterized, lead author Dr. Stephen S. Raab, from the University of Pittsburgh in Pennsylvania, and colleagues note.
In the present study, the authors evaluated diagnostic errors in patients who were seen at one of four hospitals in 2002 for a cancer work-up.
The frequency of errors varied between hospitals and ranged from 1.79 percent to 9.42 percent for gynecologics cases and from 4.87 percent to 11.8 percent for other cases, the researchers note. A significant link between the institution and the error cause was observed.
As for the cause of errors, up to 50 percent were due to misinterpretation with the remainder being due to poor tissue sampling.
The clinical impact of the error was significantly associated with the institution. On further analysis, it appeared that up to 45 percent of errors resulted in harm to the patient, ranging from further unnecessary diagnostic tests to loss of life or limb.
"It is exceedingly difficult to measure the true frequency of errors in cancer diagnosis because of the variety of detection methods used, bias, and the inability of institutions to secondarily review large case volumes," the authors state.
"As part of a multi-institutional, national effort to improve practice, we are in the process of standardizing methods, decreasing bias by sharing cases and data among institutions, and establishing more accurate error frequencies by detecting errors using multiple methods," they add.
SOURCE: Cancer, November 15, 2005.
Other diagnostic tests
"You are correct to insist on every test which could provide support for the diagnosis. Cancer is a disease which is not well understood, and for which there is no certain cure (quality of life is poor in many patients who are declared 'cured' after Chemo). Every effort should be taken to ensure that the diagnosis is correct since chemotherapy will destroy the immune system and allow CWD bacteria to mulitply...then, when the chemo is discontinued, chronic inflammation exacerbates.
Cancer kills when it is "invasive." It spreads from the primary site to other sites, and proliferates there. The only sure way to know the disease is cancer is to allow it to progress to a point where there is no question you have a proliferative disease. This is not usually an approach taken by 'modern medicine' but I mention it because it does contrast the risks of misdiagnosis and early intervention with those of late diagnosis and inability to intervene.
The two considerations have to be balanced, and I personally don't believe today's oncologists fully understand that balance. I also believe that they have been overtaken by the epidemic in Th1 immune disease, and therefore do not understand how it factors into the liklihood of misdiagnosis.
Ultimately, the immune system and Cancers are very closely related. There is a paper talking about the complexity of this relationship which I was reviewing last night
http://www.tbiomed.com/content/3/1/6
We will be discussing the links between Cancers, AIDS and th1 Immune disease at our LAX conference." (See the 2006 LAX DVDs)
..Trevor..
Members' experiences
- I wanted the DC4 and the T&B cells stained. They had to be sent out to do this. I spoke to Dr. Marshall and expressed my concern of the insurance not covering it. He told me not to worry about them if that was the case. His concern was to watch the rate of proliferation (growth rate) if their usual tests were positive. Therefore, I called and did not have them done. ~Lori
Last edited on Sun Dec 16th, 2007 04:24 by Foundation Staff
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Posted: Mon Sep 26th, 2005 03:57 |
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(filelink)
Are cellular changes caused by cancer permanent?
I am sure the damage is reversible, otherwise the bacterial load would not gradually reduce.
Many cancers grow on Th1 inflammation. One of the Th1 Chemokines is called CAM (cellular Adhesion molecule) and it is a key component both of how the plaque macrophages adhere to the arterial wall in atherosclerosis and also of how the initial cancerous cells stick to the tissue in cancer, and protect themselves from the immune system. More papers are coming out on both these things every month, but mainstream medicine has still to tie CAM to occult Th1 inflammation. It will take a decade for that to happen, IMO.
..Trevor..
from Dr Marshall's Perspective: Host Defences - UCSD 2006
Quotable quote:
"Everybody knows Inflammation induces Cancer"
- Francesco Marincola MD, Senior Investigator, NIH
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Aussie Barb Member in Phase 3

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Posted: Wed Oct 5th, 2005 20:33 |
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Book review of Four Women Against Cancer
Scooker48 wrote:
Over the last weekend I read Alan Cantwell's new book, "Four Women Against Cancer." It has a good scientific overview of pioneers who identified CWD forms of bacteria, the medical politics involved, and the author's own experience with four dedicated research scientists.
There is even an entry in the index for "Marshall, Trevor G." and the JOIMR.
It made me realize this fight has been going on for a long, long time.
see another comprehensive review of the book..
____________________ Barb: Dx Inflammatory Disease Endocrine Imbalance 2003| Depression| 24+ years not Dx| MP Aug04| ABC of MP| MP Search|
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Posted: Sat Oct 15th, 2005 23:11 |
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(filelink)
Studies of cancer and Th1 inflammation
Cancer, inflammation and the AT1 and AT2 receptors
1Research Department, Perses Biosystems Limited, University of Warwick Science Park, Coventry, CV4 7EZ, UK
2Chemistry Department, The Open University, Walton Hall, Milton Keynes MK7 6AA, UK
Journal of Inflammation 2004
Here are some studies which make it appear that taking an angiotensin receptor blocker would not seem totally foreign or harmful to an oncologist:
Antiproliferative efficacy of angiotensin II recep...[Curr Cancer Drug Targets (this one cites one of Dr. Marshall's papers)
Angiotensin II, cell proliferation and angiogenesi...[Curr Vasc Pharmacol. 200
Functional expression of the angiotensin II type 1...[Clin Cancer Res. 2005] -
Pilot study of angiotensin II receptor blocker in ...[Int J Clin Oncol. 2005]
And this one is a 2006 review on it:
Angiotensin II receptor blocker: possibility of an...[Mini Rev Med Chem. 2006]
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Posted: Fri Nov 4th, 2005 04:09 |
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Studies of Cancer and Infection
(filelink)
INTERNATIONAL | November 1, 2005
Study Links Bacteria, Lymphoma Around Eye
By THE ASSOCIATED PRESS
PARIS (AP) -- New research suggests that infection with bacteria from the Chlamydia family may play a role in the development of a type of lymphoma that affects the tissue around the eye, raising hopes that antibiotics may one day prove to be an alternative to chemotherapy or radiation.
Study Links Bacteria, Lymphoma Around Eye - New York Times
http://tinyurl.com/985or
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Posted: Fri Dec 16th, 2005 01:57 |
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Cancer gene therapy
(filelink)
...the researchers fiddling with gene therapy really don't have it all together just yet. Until they figure out that the CWD pathogens are the things actually causing the mutations in the genes they are measuring, and that all the major diseases are all tied together by a common etiology, then they will be unable to understand what their data is actually telling them.
Dr. Trevor Marshall, PhD
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Posted: Fri Dec 16th, 2005 04:31 |
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Cancer Research in Flames
(filelink)
Research | Vision
Cancer Research in Flames
Tracking inflammation's role in promoting malignancy could lead to better treatments
Michael Karin
Volume 19 | Issue 23 | Page 24 | Dec. 5, 2005
http://www.the-scientist.com/article/display/15898/
One problem with the current war on cancer is that much of it focuses on destroying the malignant cell itself while paying little attention to some of cancer's allies that are more prone to attack.
Cancer undoubtedly starts and ends with the malignant cell, and through tremendous efforts, we have identified many of the molecular and cellular attributes that define such cells. Genetic changes that lead to activation of oncogenes and/or inactivation of tumor suppressors result in aberrant control of cell proliferation and death, endowing the malignant cell with migratory and invasive properties. These changes, however, represent only the initial spark that ignites cancer's fire. Without fuel a fire cannot spread, and in cancer's case, inflammation feeds the blaze. Current cancer therapies that induce necrosis and inflammation may further fan the flames.
INSTIGATING NF-êB
Two pathways lead to NF-êB activation. In the classical pathway, pro-inflammatory stimuli and genotoxic stress leads to IKKâ- and IKK-dependent phosphorylation of IêB, which results in proteasomal degradation and subsequent release of the NF-êB dimers. Activation of this pathway leads to increased transcription of genes in three functional classes, all of which contribute to tumor promotion and progression. The alternative pathway works independently of IKKâ and IKK.
Click for larger version Click for larger version
A link between inflammation and cancer may have been suspected for millennia (see sidebar). Nevertheless, the connection has failed to catch on with most oncologists and has hardly been a mainstay of cancer research. Fortunately, however, this situation is quickly changing.
HINTS OF A LINK
One of the problems in the inflammation-cancer field was the absence of well-defined molecular mechanisms linking chronic inflammation to tumor initiation and promotion. As is often the case, the solution came from another field. NF-êB, the transcription factor identified by David Baltimore and colleagues in 1986, has caught the attention of investigators interested in cell signaling and immunity. NF-êB is rapidly activated in response to numerous proinflammatory stimuli, as well as bacterial or viral infections. Once activated, it contributes to expression of many genes, whose products regulate immune and inflammatory responses.
Early connections between NF-êB and cancer were realized when its p65 subunit was identified as RelA, a relative of v-Rel, the oncogene of the reticuloendoblastosis virus. Thus, much of the early research sought out oncogenic mutations that would result in NF-êB's constitutive activation in malignant cells. A few such mutations were found, but were relatively rare and failed to explain the rather ubiquitous NF-êB activation in most types of cancer.1
My own interest in studying the NF-êB-cancer connection started with our observation, made simultaneously with the labs of Baltimore, Inder Verma, and Albert Baldwin, that NF-êB activation inhibits programmed cell death.2 Diminished apoptosis is an important contributor to malignancy, and infections and inflammation result in activation of NF-êB. So, the proposal that NF-êB provides a molecular link between inflammation and cancer was not too far-fetched.1
The challenge was to critically test this hypothesis in a convenient animal model. While it's impossible to completely inactivate NF-êB in the laboratory mouse, two general approaches allow its conditional inhibition in a given cell type. The first is based on conditional expression of a mutant form of a specific NF-êB inhibitor, IêBá, that is resistant to phosphorylation-induced degradation the so-called IêB super-repressor. IêB-SR expression retains NF-êB in the cytoplasm and selectively inhibits NF-êB-driven gene expression. The second approach is based on conditional inactivation of the IêB kinase (IKK) complex, responsible for signal-induced phosphorylation that leads to IêB degradation and NF-êB activation. Through inducible expression of IêB-SR in hepatocytes, Eli Pikarsky, Yinon Ben-Neriah, and colleagues tested the effect of NF-êB inhibition on the development of a type of liver cancer caused by chronic inflammation.
DOUBLE DUTY
Inhibiting NF-êB in older animals already exhibiting chronic liver inflammation greatly retarded cancer development not because inflammation was prevented, but rather through the accelerated death of preneoplastic hepatocytes.3 We obtained similar results using cell type-specific deletion of the IKKâ gene in intestinal epithelial cells and a model of inflammation-associated colorectal cancer.4 Preventing NF-êB activation in intestinal epithelial cells dramatically inhibited tumor development, again by accelerating the death of preneoplastic cells.
We also examined the effect of selective interference with NF-êB activation in macrophages and neutrophils, two cell types that do not undergo malignant conversion in inflammation-associated cancers but are likely to contribute to their development. In this case we also observed inhibition of tumor development in epithelial cells but due to a different cause. Here, inhibiting NF-êB prevented production of cytokines and chemokines stimulate the growth of preneoplastic epithelial cells.
These studies not only established NF-êB's role in linking chronic inflammation to tumor development but also indicate two distinct mechanisms through which NF-êB promotes carcinogenesis. In the epithelial cell that had undergone malignant conversion, NF-êB inhibits apoptosis. At the same time, NF-êB in inflammatory cells provides early malignant epithelial cells with a variety of growth factors to accelerate tumor growth and progression.
The two types of experimental cancer described above belong to a group representing 15% to 20% of all cancers, in which underlying causes of chronic inflammation are easily detected. But what about the remaining cancers in which an underlying chronic inflammation or infection is not known to exist? Does inflammation play a causative role there as well?
To answer this question we used a model of chemically induced liver cancer in which no chronic inflammation is deliberately induced. Here, conditional deletion of IKKâ in either hepatocytes or inflammatory cells produced surprising results. Instead of reducing cancer load, selective NF-êB inactivation in hepatocytes greatly enhanced tumor development, but additional deletion of IKKâ in inflammatory cells resulted in a dramatic reduction in tumor number and size.5
We propose that in tissues such as the liver, excess cell death caused by inhibition of NF-êB and exposure to a cytotoxic carcinogen triggers compensatory cell proliferation. Nonetheless, the driving force is NF-êB in inflammatory cells, which provides surviving epithelial cells including cells that harbor potentially oncogenic mutations with growth factors. We propose that the release of cellular constituents during necrotic cell death drives this NF-êB activation.5
EXTINGUISHING THE BLAZE
These studies, I believe, establish inflammation's role in providing and maintaining the fuel for many types of cancer, even those not associated with preexisting inflammation. And I think they bear relevance for cancer therapy as well. Most current anticancer drugs, as well as therapeutic radiation, kill tumors by inducing necrosis rather than pure apoptosis. And unlike apoptosis, necrosis results in activation and chemotactic attraction of additional inflammatory cells. This results in production of vast amounts of proinflammatory cytokines and chemokines that enhance the proliferation of surviving malignant cells. A single round of chemotherapy or radiotherapy is never 100% efficient, after all.
High levels of necrosis are commonly associated with rapidly growing tumors and are considered a sign of poor prognosis. Thus this cycle of necrosis, inflammation, and regeneration can be a major driving force in tumor development and progression. In the future, we need to find practical and selective ways to block this inflammatory response and combine anti-inflammatory drugs with preexisting chemotherapeutic and radiotherapeutic procedures. Thus, by attacking not only the malignant cell, but also inflammation, we should achieve much better survival rates than currently possible.
Michael Karin is a professor of pharmacology at the University of California, San Diego School of Medicine and an American Cancer Society Research Professor. He is a cofounder of Signal Pharmaceuticals (now Celgene), and was elected this year to the National Academy of Sciences.
Mounting Evidence
A cancer inflammation connection has long been suspected. Some have pegged its origins on Galen of ancient Greece. Modern connections were made in the 19th century by Rudolph Virchow.1 Yet this work was nearly forgotten until Harold Dvorak compared tumors to wounds that never heal.2 Later, Alberto Mantovani and colleagues implicated inflammatory chemokines in cancer growth and its spread through macrophage recruitment,3 whose role in cancer progression was demonstrated by Pollard.4
Fran Balkwill showed that the major pro-inflammatory cytokine tumor necrosis factor (TNF) may actually operate as a tumor promoter,5 and Ray Dubois and Mark Taketo demonstrated the importance of the pro-inflammatory enzyme cyclo-oxygenase-2 (COX2) and some of its products (the prostaglandins) in tumor progression and angiogenesis.6 Further, epidemiological studies demonstrate that chronic infections and inflammatory conditions such as hepatitis, gastritis, and chronic silicosis or asbestosis are major risk factors for cancer.7
Why, then, is so much effort focused on the malignant cell rather than the inflammatory cell?
References
1. F Balkwill, A Mantovani "Inflammation and cancer: back to Virchow?" Lancet 2001, 357: 539-45.
2. HF Dvorak "Tumors: wounds that do not heal. Similarities between tumor stroma generation and wound healing," N Engl J Med 1986, 315: 1650-9.
3. A Mantovani et al, "The origin and function of tumor-associated macrophages," Immunol Today 1992, 13: 265-70.
4. JW Pollard "Tumour-educated macrophages promote tumour progression and metastasis," Nat Rev Cancer 2004, 4: 71-8.
5. F Balkwill "Tumor necrosis factor or tumor promoting factor?" Cytokine Growth Factor Rev 2002, 13: 135-41.
6. RA Gupta, RN Dubois "Colorectal cancer prevention and treatment by inhibition of cyclooxygenase-2," Nat Rev Cancer 2001, 1: 11-21.
7. H Kuper et al, "Infections as a major preventable cause of human cancer," J Intern Med 2000, 248: 171-83.
References
1. M Karin et al, "NF-êB in cancer: from innocent bystander to major culprit," Nat Rev Cancer 2002, 2: 301-10. [PubMed Abstract][Publisher Full Text]
2. Z-G Liu "Dissection of TNF receptor 1 effector functions: JNK activation is not linked to apoptosis, while NF-êB activation prevents cell death," Cell 1996, 87: 565-76. [PubMed Abstract] [Publisher Full Text]
3. E Pikarsky et al, "NF-êB functions as a tumour promoter in inflammation-associated cancer," Nature 2004, 431: 461-6. [PubMed Abstract][Publisher Full Text]
4. FR Greten et al, "IKKâ links inflammation and tumorigenesis in a mouse model of colitis-associated cancer." Cell 2004, 118: 285-96. [PubMed Abstract][Publisher Full Text]
5. S Maeda et al, "IKKâ couples hepatocyte death to cytokine-driven compensatory proliferation that promotes chemical hepatocarcinogenesis," Cell 2005, 121: 977-90. [PubMed Abstract][Publisher Full Text]
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Posted: Fri Dec 30th, 2005 15:35 |
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Vitamin D and cancer
(filelink)
Question: Why are studies showing that increased Vitamin D reduces the risk of cancer?
Answer: These studies are faulty, because the researchers did not understand the close relationship between inflammation and cancer. They draw inferences which are not supported by the data. That is why they use the word "may" so often. Most epidemiological studies on cancer and 1,25-D are flawed, for they fail to take into account the underlying biochemistry.
Th1 inflammation feeds the initial proliferative stage of Cancer. Without Th1 inflammation the cancer cells can't get adhesion to the 'healthy' cells and tissues, and can't become proliferative. Then, as the cancer starts to metastasize the inflamed stem cells are critical in enabling the spread of the inflammation, and the metastasis of the Cancer.
There are a number of groups in conventional-medicine who are coming to this understanding, although I am still only a small part of the only group to have comprehended that the Th1 inflammation is due to occult bacterial infection, and can be treated - (Alan Cantwell's group).
Vitamin D ingestion shuts down the ability of the immune system to to attack the Th1 microbes. The Vitamin D hype is so overwhelming, and the depth of ignorance about the VDR and how it controls the immune system is also overwhelming.
The epidemiological relationships between Cancers and Vitamin-D are short-term. Vitamin-D acts in a similar fashion to steroids, and reduces the incidence of cancers short-term, while enhancing the proliferation of the bacteria which will cause uncontrollable inflammation ten years, or so, down the line. Theoretical Biology allows one to understand this action, but the folks who are doing the Epidemiological studies have no interest in understanding the underlying processes. So they mis-interpret their data, and are funded by the manufacturing industry to continue doing so.
The early studies on Vitamin D and cancer were poorly done. More recent studies have shown that, if anything, the overall risk of cancer is raised in the presence of high levels of 25-D (risk raised above 80 nmol/ml or 32 ng/ml)
http://www.msnbc.msn.com/id/21548773/
..Trevor..
..............................................
Professor Colin Cooper, of the Institute of Cancer Research, said further research was needed to provide definitive proof of the benefits of vitamin D.
................................................
Immunology
Volume 90 Issue 2 Page 286 - February 1997
doi:10.1046/j.1365-2567.1997.00148.x
Effects of 1,25-dihydroxyvitamin D3 and cytokines on the expression of MHC antigens, complement receptors and other antigens on human blood monocytes and U937 cells: role in cell differentiation, activation and phagocytosis
A. SPITTLER, M. WILLHEIM, F. LEUTMEZER, R. ÖHLER, W. KRUGLUGER, C. REISSNER, T. LUCAS, T. BRODOWICZ, E. ROTH & G. BOLTZ-NITULESCU
" Our results demonstrate that calcitriol, alone or in combination with cytokines, modulates expression of MHC, CD11b, CD11c, CD14 and CD71 Ag on both monocytes and U937 cells, and impairs the phagocytic property of monocytes.
==========================
Th1 inflammation feeds the initial proliferative stage of Cancer. Without Th1 inflammation the cancer cells can't get adhesion to the 'healthy' cells and tissues, and can't become proliferative. Then, as the cancer starts to metastasize the inflamed stem cells are critical in enabling the spread of the inflammation, and the metastasis of the Cancer.
There are a number of groups in conventional-medicine who are coming to this understanding, although I am still only a small part of the only group to have comprehended that the Th1 inflammation is due to occult bacterial infection, and can be treated - (Alan Cantwell's group).
Vitamin D ingestion shuts down the ability of the immune system to to attack the Th1 microbes. I have a paper in the works which shows exactly how this happens, but I doubt that any journal would allow it to be published right now. The Vitamin D hype is so overwhelming, and the depth of ignorance about the VDR and how it controls the immune system is also overwhelming.
The epidemiological relationships between Cancers and Vitamin-D are short-term. Vitamin-D acts in a similar fashion to steroids, and reduces the incidence of cancers short-term, while enhancing the proliferation of the bacteria which will cause uncontrollable inflammation ten years, or so, down the line. Theoretical Biology allows one to understand this action, but the folks who are doing the Epidemiological studies have no interest in understanding the underlying processes. So they mis-interpret their data, and are funded by the manufacturing industry to continue doing so."
Dr. Trevor Marshall, PhD
I gave a presentation at Harvard last May, for DMM2007, which explained why animal models of immune disease and cancers do not work, because of the lack of homology between the animal VDR and the VDR of Homo sapiens:
http://autoimmunityresearch.org/transcripts/dmm2007-harvard.pdf
Further, the behavior of Homo sapiens' VDR is different in healthy and Th1 diseased individuals, as the Th1 bacteria act to directly block the VDR's action. I gave a presentation on this at the Metagenomics Conference at UCSD last July:
http://autoimmunityresearch.org/transcripts/metagenomics2007.pdf
So animal studies, such as the one you cite, can never come up with meaningful data in immune disease, data which translates directly to clinical practice, and indeed, they never have done.
Look, for example, at the TeGenero, study, which was even checked in primates (apes), prior to its disastrous introduction into the human environment:
http://en.wikipedia.org/wiki/TGN1412
Further discussion of the topics of both the above papers can be found in "Dr Marshall's Perspective" http://www.marshallprotocol.com/forum39/
See also Extra Vitamin D does not reduce the risk of cancer.
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Posted: Tue Mar 7th, 2006 01:03 |
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Omega-6 turns on inflammatory genes important in cancer
"Investigating the reasons for this rapid growth, we discovered that the omega-6 was turning on a dozen inflammatory genes that are known to be important in cancer," lead author Dr. Millie Hughes-Fulford, from the San Francisco VA Medical Center, said in a statement.
http://tinyurl.com/apbtc
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Posted: Thu Mar 9th, 2006 04:57 |
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Hodgkin's disease
"Pleomorphic Bacteria as a Cause of Hodgkin's Disease (Hodgkin's lymphoma): A Review of the Literature."
by Dr. Alan Cantwell, M.D.
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Posted: Tue Apr 11th, 2006 15:56 |
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[filelink]
Ovarian Cancer
CA 125
Sarcoid inflammation can cause elevated CA 125. See the following abstracts indexed in PubMed.
PMID: 15857040, 1923245
Merck says that any peritoneal inflammatory process can increase CA 125 levels.
Sometimes patients do not realize how unreliable tests can be, depending on the circumstances, and how Th1 inflammation can give false impressions in interpreting results.
Read here why CA 125 is not a reliable screening test for ovarian cancer.
Read here how the menstrual cycle affects CA 125 test results.
Sarcoidosis can cause false positives in cancer tests
Be aware that some of the tests used to identify cancer can be elevated in sarcoidosis, resulting in a "false positive."
Sarcoidosis Associated With an Elevated Serum CA 125 Level
American Journal of the Medical Sciences. 334(6):441-443, December 2007.
Kalluri, Meena MD; Judson, Marc A. MD
CA 125 is a glycoprotein expressed by a variety of tissues of mesothelial origin. It has classically been associated with ovarian carcinoma. It has also been reported to be elevated in certain granulomatous conditions. We describe a patient with sarcoidosis and an elevated serum CA 125 level and review the medical literature on this topic.
Conclusions: Peritoneal sarcoidosis may "mimic" ovarian carcinoma in that it may present with peritoneal or abdominal findings and an elevated serum CA 125 level.
Belinda
____________________ Barb: Dx Inflammatory Disease Endocrine Imbalance 2003| Depression| 24+ years not Dx| MP Aug04| ABC of MP| MP Search|
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Posted: Fri Apr 28th, 2006 22:52 |
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Lung cancer
from A visit with Dr Alan Cantwell
Dr Trevor Marshall wrote:
If you print out a copy of this Reuters news service article
"Positive CT scan for lung cancer may resolve"
http://tinyurl.com/h2h86
and give it to Doc, you might find that he is prepared to continue your husband on antibiotics.
(you might also print out the actual abstract at:
http://www.chestjournal.org/cgi/content/abstract/129/4/1039 )
The article is fascinating in that it again points out that the only certain way to know if cancer is present is to allow the passage of time, so that the cellular proliferation can become obvious. Unfortunately, because cancer therapies are ineffective unless started early, few oncologists have been allowing patients to "make sure" that their CT shadows were really cancer before pushing them into chemotherapy. This study shows that a large proportion of Lung cancers might be misdiagnosed.
The researchers note that possible cancer diagnosis in 12 of 41 patients had fully or partially resolved when therapy was delayed 2 months. In another group, 29 of 39 had full or partial resolution.
While this alone ought to be a bombshell, what is intriguing is their concluding statement:
we recommend a course of antibiotics followed by another CT within 2 months to people with patchy consolidation or nonsolid opacities detected on the baseline screening and all those with new nodules on repeat screening. It must be emphasized that the use of antibiotics and short-term CT follow-up is only one of the options in the regimen of CT screening for lung cancer," the researchers add, "and further research in this area promises to continue to improve the efficiency of CT screening for lung cancer.
These researchers are prepared to prescribe antibiotics, just in case, and it is possible your Doc may do so, too. But I would ask Doc for Minocyline, rather than Doxycycline, as Mino is more effective against one of the nasty plasmid-bearing species, Staph. In any case, Doc might well be more familiar with Mino, since he/she is probably prescribing Mino to his/her Acne patients
...........................................................................
Smoking
"Having spent 50 years of my life desperately trying to escape from secondhand smoke, I feel strange having to say that I am not nearly so sure that the diseases attributed to smoking are indeed caused by smoking. There are too many "wide-brush" statements about "XXX lives lost to smoking" yet the people making them have no idea of the underlying disease process by which smoking is supposed to cause death.
It isn't cancer, as it is now pretty clear that cancer rises from Th1 inflammation and an incompetent immune system (for example, review the paper at http://www.tbiomed.com/content/pdf/1742-4682-3-6.pdf - especially the observation about Kaposi's sarcoma).
Nobody has come up with a molecular rationale for how smoking causes cancer. Maybe they are all making the same mistake of over-reaching which we see in the Vitamin D research
In no way am I saying that smoking is not bad for the immune system, and for the body as a whole, am just not convinced it is quite as bad as most folks would have us believe. We need to make sure we focus our energies on the cause of disease, for it is the cause which we have to defeat.
..Trevor..
Last edited on Fri Jul 27th, 2007 19:43 by
____________________ Barb: Dx Inflammatory Disease Endocrine Imbalance 2003| Depression| 24+ years not Dx| MP Aug04| ABC of MP| MP Search|
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Posted: Sun May 21st, 2006 01:19 |
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Colon cancer
Colonoscopy
A colonoscopy may be warranted if you are at high risk and is not contraindicated on the MP. It's okay to continue MP meds but you may want to adjust them to reduce immunopathology so you are feeling your best during this time.
"If either of these cancer tests (PSA) gave a precise answer, a definite prognosis, and a clear treatment path for every possible outcome, then they would be very worthwhile indeed. You can find studies both supporting and denigrating every pathway. Medicine just doesn't have the answers yet, unfortunately." ..Trevor..
____________________ Barb: Dx Inflammatory Disease Endocrine Imbalance 2003| Depression| 24+ years not Dx| MP Aug04| ABC of MP| MP Search|
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Posted: Sun Sep 10th, 2006 15:04 |
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(filelink)
The MP and cancer treatment
"Everybody knows Inflammation induces Cancer", stated Francesco Marincola MD, Senior Investigator, NIH at the Host Defenses: From Bench to Bedside conference, Oct 6, 2006, UCSD. And not a single researcher in that room at UCSD disagreed with him.
The MP will keep your immune system strong so it can fight the cancer proliferation. Sure, I can't prove this, absolutely, definitely, right at this moment, but I have staked my future on the vision that in 10 years time there will be an entirely different treatment for your cancer diagnosis than you are now being given.
Never, ever, ever, underestimate the importance of dealing with the microbes causing the Th1 inflammation. It drives everything - including cancer proliferation.
I will state that, based on everything I have seen in the last several years, one definitely cannot 'cure' cancer without removing the causative Th1 pathogens.
Unless the pathology report indicates proliferation, the tumor is probably less dangerous than the underlying Th1 inflammation.
Dr. Trevor Marshall, Ph.
Can the MP treat cancer?
Although Th1 inflammation causes the cancer it is not possible to resolve that inflammation quickly. With the MP, it takes several years to get down the bacterial load to a point where the body's immune system is working properly again. It would need to be a quite benign cancer to not proliferate significantly in that time.
So reducing inflammation is a way to prevent, but we have zero data on whether inflammation reduction can be part of a cure. It may be, it may not be. As far as I know, there is no cancer therapy which is compatible with removing the bacterial load which is at the source of the problem.
It might be possible to partly reactivate the VDR during chemotherapy, with the agonist Benicar, and maybe one day we will try a study doing that. Since the VDR is responsible for transcribing a number of the genes which help deal the body with cancers, reactivating the VDR may be beneficial, I have no data...
The innate immune system is responsible for cleaning up cancer cells, but the bacteria disable the innate immune response, and it cannot be fully corrected in weeks, it takes years...
When you start reactiving the VDR with Benicar it will start to translate genes which have been shut off by the bacteria. One of these genes produces the protein "Metastasis Suppressing Protein." It will certainly help your body to be producing that again. But will it be enough to affect the whole picture? It is impossible to predict.
I can tell you that in our cohort, which is made up of patients at very high risk of developing cancer, it is reported only very rarely, and then only in non-aggressive presentations.
..Trevor..
Oct08 While it is pretty certain that Benicar's reactivation of the VDR (and MTSS1) will likely reduce metastasis, that has little application once the cancerous cells have already started to spread. While the MP can probably stop metastasis from developing, once a tumor is in place, and growing, it is almost certainly too late to contemplate non-invasive therapies like the MP.
..Trevor..
Can the lab tell from the tissue whether my body was actively "cleaning up" the diseased tissue (cancer) while on the MP?
The lab doesn't look for "cleaning up" because it is assumed that cancer never gets better unless it is hit with a "nuclear bomb therapy" like chemo or radiation.
The key is always metastasis, and its presence or absence.
As I noted earlier, unless the Oncologist wants to aggressively search for metastasis, it is a pretty good bet that he is not too concerned about what he is describing as a 'tumor.'
..Trevor..
June 08 The VDR transcribes the Metastasis Suppressor #1 (MTSS1) gene, which ends up as the "Missing In Metastasis" (MIM) protein. When the bugs are present this protein is missing. When Olmesartan gets the VDR working again, you can expect that protein to come back.
We have seen no metastasis in our cohort. Some old inactive tumors, yes, but no metastasizing agressive tumors as would normally be expected in a cohort as sick as ours.
..Trevor..
Last edited on Sat Oct 4th, 2008 19:01 by Foundation Staff
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Posted: Thu Sep 14th, 2006 05:56 |
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(filelink)
Liver cancer
Anti-Inflammatory Drug Prevents Liver Cancer in at-Risk Liver Patients
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Posted: Sat Sep 16th, 2006 00:18 |
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Granulomas versus cancer
(filelink)
No one can measure many granulomas you had a few months ago to compare with how many you might have now. It's only upon autopsy that pathologists can get a small idea of the granuloma load.
As we've explained, lymph nodes enlarge due to infection, inflammation or cancer. You already have biopsy-verified sarcoidosis, which is the gold standard for diagnosing sarcoidosis. Try to understand that most physicians do not believe sarcoidosis can cause the damage it makes in reality. Most patients look pretty good and the internal damage is not visible. And most doctors have not dealt with sarcoidosis patients who are very ill.
Because of that, good, well-meaning doctors look for other explanations for sarcoidosis symptoms such as your inflammed lymph nodes. Add to that the fact that you have been losing weight (which is consistent with our experiences with the MP) and how litigious our society is in medical malpractice cases concerning missed cancer diagnoses, and you can see why your doctor is motivated to rule out cancer.
You alone can determine how much you are willing to expend time and energy to be poked, prodded and scanned to rule out cancers or any other differential diagnosis your physicians may suspect. But that testing can be expensive, time consuming and lead to nowhere. And you are the only one who knows how much of this you need before you are reassured.
Part of being an active member of your medical team sometimes means reassuring the doctor. Sarcoidosis is a scary disease for physicians, which is part of why they tend to get several specialists involved and do lots of testing. And they tend to want to do that whether the patient is stable or getting worse.
Sometimes a simple nap or brief rest can ease the discomfort of Herx. Our Tool List to check when Herxing is a great review to determine steps to take to keep Herxing manageable. If any of these work, it lends credibility to the concept that you are experiencing a Herx.
Belinda
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