Dec 29, 2009 - 9:12 am
I simply cannot stress strongly enough the relationship between cancer and inflammation. The first step in getting a handle on cancer should really be to get a handle on inflammation that is going on in your body.
Please have your CR-P LEVELS tested. It is your body's inflammation marker, is a simple inexpensive blood test. Be sure to inform your doctors that do you not want the cardiac panel as that is limited in its scope. Inform them that you have cancer. Mention the NIH, NCI and a whole slew of other abbreviated things, recognize inflammation as a factor in the development and spread of cancer, and you would like to know where you stand in the inflammation aspect of your disease. What you would like to see once you get your results is ideally as close to zero as one can get. I have been reading that less than 10 is predictive of a better outcome than over ten, but there are simple things one can do to bring the number down. But first you have to know what it is. If you're interested there are a few very good books out there to read. I'm getting back on track on the first. Right now I'm developing a plan of attack and in the information gathering mode.
And yes, I absolutely got up on the bossy side of the bed. But honestly, if you all thought you had things that might save my life or help me to save my life, wouldn't you have, absolutely positively have to tell me, or someone you loved who wasn't quite so bossy, since today you might not be so concerned with my life as you might just wish I would quit telling you what to do. Jeez, what a nag! Hey, I wouldn't nag you, if I didn't care about you.
Love, kisses and hugs to you all,
And, once you know stuff, your brain starts to put pieces together to figure out other things and light bulbs start going off all over the place, and then you too can become as annoying as I am. " ~ )
What follows all comes before the introduction.
Executive Summary of Inflammation and Cancer Think Tank
Inflammation is a response to acute tissue damage, whether resulting from physical injury, ischemic injury, infection, exposure to toxins, or other types of trauma. It can play a role in tumor suppression by stimulating an antitumor immune response, but more often it appears to stimulate tumor development. Epidemiologic and clinical research indicates an increased risk of certain cancers in the setting of chronic inflammation. For example, two inflammatory bowel diseases, ulcerative colitis and Crohn’s disease, predispose to cancers of the intestinal tract. Basic research, in turn, has shown that many of the processes involved in inflammation (e.g., leukocyte migration, dilatation of local vasculature with increased permeability and blood flow, angiogenesis), when found in association with tumors, are more likely to contribute to tumor growth, progression, and metastasis than to elicit an effective host anti-tumor response.
Interestingly, inflammation functions at all three stages of tumor development: initiation, progression and metastasis. Inflammation contributes to initiation by inducing the release of a variety of cytokines and chemokines that alert the vasculature to release inflammatory cells and factors into the tissue milieu, thereby causing oxidative damage, DNA mutations, and other changes in the microenvironment, making it more conducive to cell transformation, increased survival and proliferation.
Chronic inflammation appears to contribute to tumor progression by establishing a milieu conducive to development of different cancers. However the precise mechanism by which it does so remains to be determined. Infection is a common cause of inflammation, and evidence indicates that the presence of microbes can be a cofactor in the tumor promoting effects of inflammation.
Tumor cells produce various substances that attract inflammatory cells, which then secrete an array of soluble mediators. These further stimulate proliferation of the initiated cell, tissue disruption in the stroma, and tumor growth. Leukocyte infiltration, and particularly macrophages, can lead to enhanced angiogenesis, which is associated with a poor prognosis in some tissues.
The role of inflammation in metastasis is less well defined than its roles in cancer initiation and progression. The soluble mediators secreted by tumor-associated leukocytes promote cell motility, and induce angiogenesis, vascular dilation and extravasation of tumor cells. Particularly interesting is the recent finding that metastatic cells leave the tumor as microcolonies, containing lymphocytes and platelets as well as the tumor cell. Inflammation continues to play a role at metastatic sites by creating a cytokine milieu conducive to tumor growth.
Although there is a strong association between chronic inflammation and cancer, investigators have not yet uncovered all the molecules, pathways, and mechanisms involved, and numerous questions remain to be resolved about the mechanisms and targets of pro-inflammatory mediators of tumor development. These are articulated in the body of the report and the recommendations that follow. Furthermore, to understand the role of inflammation in tumor formation and progression, we also need to understand its role in maintaining homeostasis and responding to damage in normal tissue. An appreciation of the importance of inflammation has already led to clinical trials of anti-inflammatory drugs (e.g., COX-2 inhibitors) for cancer prophylaxis and treatment. The results obtained will provide clues to the dominant mechanisms at work, and will help in the design of a new generation of interventions.
These represent very small potions of the articles.