Research

Good question! I study the relationships between psychological and physical illness. For example, in my work with obese adults, I have found higher than expected rates of depression. It is the case that depression can lead to weight gain, but also that weight gain can lead to depression. The same is true for other illnesses. We see higher levels of several psychological disorders among individuals with type 2 diabetes, cancer, HIV, chronic pain, and many other illnesses. I recently published a book that comprehensively reviews this area and it can be found at this link: http://www.amazon.com/Psychological-Co-morbidities-Physical-Illness-Perspective/dp/1441900306/ref=sr_1_1?ie=UTF8&qid=1332296518&sr=8-1 Please contact me if you have further interest. Good question! I study the relationships between psychological and physical illness. For example, in my work with obese adults, I have found higher than expected rates of depression. It is the case that depression can lead to weight gain, but also that weight gain can lead to depression. The same is true for other illnesses. We see higher levels of several psychological disorders among individuals with type 2 diabetes, cancer, HIV, chronic pain, and many other illnesses. I recently published a book that comprehensively reviews this area and it can be found at this link: http://www.amazon.com/Psychological-Co-morbidities-Physical-Illness-Perspective/dp/1441900306/ref=sr_1_1?ie=UTF8&qid=1332296518&sr=8-1 Please contact me if you have further interest.

First some history so we understand how we got to where we are today (I’ll limit it to this last century). Around the turn of the century, Cannon was a Harvard physiologist who paid attention to some connections that he felt other investigators were ignoring at the time. He observed that all vertebrates had a common response to a threat which included increased heart and respiratory rates, tension in large muscle groups, coldness and sweatiness, decrease in intestinal activity, and dilatation of the pupils. All of these were manifestations of activity of the sympathetic nervous system (a part of the autonomic nervous system) which primes an animal (or human) to flee or fight. Common to all animals.

In the 1920-30’s, a physician by the name of Hans Selye made the next major contribution to mind-body medicine. He noticed that patients in a hospital all “looked sick” regardless of their specific illness. He set out to find the anatomic and physiologic commonalities among these sick looking patients. He subjected lab animals to all sorts of noxious stimuli (pain, loud noises, electric shock, heat and cold) and he found some consistent responses in all animals. The adrenal cortex (which secretes stress hormones) was enlarged and components of the immune system (such as the thymus, spleen, and lymph nodes) had shrunk. He defined “stress” as the non-specific response of the body to any demand, and the physiologic changes that he noted, he called the “general adaptation syndrome” or more commonly called the stress response today.

Now fast forward to the early 70’s when researchers were beginning to correlate fight or flight and stress responses with the development of certain diseases. Cardiologists Friedman and Rosenman described the angry, time-obsessed, hypertension and heart attack-prone “type A” executive. The type A person was in a chronic state of anxious readiness which produced physical damage. The connection was being made that if stress contributed to things like heart disease and cancer, maybe by reducing stress one might help prevent these illnesses. This gave tremendous energy to the new field of stress reduction.

George Solomon was a psychiatrist at Stanford who in the 1960s showed that by destroying a rat’s hypothalamus, the animal suffered a marked decline in immune function.

Ten years later, Ader at the University of Rochester, demonstrated that the cells of the immune system (long thought to be under automated control) could be conditioned in the same way that Pavlov’s dogs responded to a bell by salivating. His colleague Felton demonstrated direct connections between the fibers of the sympathetic nervous system and the organs and cells of the immune system. Candace Pert and Soloman Snyder at Hopkins suggested that there were “peptide messengers” between the cells of the brain and those of the immune system. They called this new field of looking at connections between psychological processes and the nervous and immune systems psychoneuroimmunology.

I guess the answer to this question depends on what you mean by the word “prove”. If your question is about whether or not we can prove a connection between stress, depression, or anxiety and the development of cancer, that gets a bit trickier. The progression of research noted above would certainly suggest that this is an area for investigation.

A psychologist by the name of Bahnson reviewed the literature on stress, emotions, and cancer in 1980. At that time he felt that there was evidence to demonstrate an association between what he called a “particular configuration” and the development of cancer. That “configuration” was characterized by denial and depression, absence or loss of affection in early childhood, severe loss later in life, and strong and persistent feelings of hopelessness and helplessness. Bahnson based this conclusion on several studies, one being a prospective study of medical students at Hopkins which revealed a correlation between lack of closeness to parents and later development of cancer. The second was an observation that women with suspicious cervical biopsies who had recently suffered a loss were more likely to develop cervical cancer. The third study found that patients who had cancer were significantly more likely than controls to have suffered loss of an important relationship and to have an inability to express hostile feelings.

In the 28 years since this review, studies on personality and cancer have confirmed some of these findings but not all. A recent meta-analysis from the UK showed that stress-related psychological factors are associated with a higher incidence of cancer. There is some association between personality/stress and the development of cancer, and certainly other factors such as genetics, environment, and diet play a significant role.

What impact does stress have after the diagnosis of cancer? Do our patients’ thoughts, feelings, beliefs, and attitudes affect their outcomes? If so, how can we affect positive change?

One measure of the emotional state of a patient is to assess quality of life. Patti Ganz and Allen Coates showed that patients with lung or breast cancer who are more optimistic, more involved in their usual activities, and more hopeful about the future have an improved survival over those who are less optimistic or engaged. This is a finding that is independent of other prognostic factors. In the same meta-analysis from the UK that I just mentioned, Chida found that a stress-prone personality or unfavorable coping styles and negative emotional responses were related to higher cancer incidence and poorer survival. Another review article from JCO a couple of yearsago, showed there was a correlation between patient reported outcomes (such as quality of life measures) and survival. In her conclusion Dr. Gotay called for “studies that go beyond documenting this phenomenon and test hypotheses about why patient reported outcomes may be linked to survival…” And she goes on to conclude that interventions that improve patient reported outcomes have the potential to increase survival.
First some history so we understand how we got to where we are today (I’ll limit it to this last century). Around the turn of the century, Cannon was a Harvard physiologist who paid attention to some connections that he felt other investigators were ignoring at the time. He observed that all vertebrates had a common response to a threat which included increased heart and respiratory rates, tension in large muscle groups, coldness and sweatiness, decrease in intestinal activity, and dilatation of the pupils. All of these were manifestations of activity of the sympathetic nervous system (a part of the autonomic nervous system) which primes an animal (or human) to flee or fight. Common to all animals.

In the 1920-30’s, a physician by the name of Hans Selye made the next major contribution to mind-body medicine. He noticed that patients in a hospital all “looked sick” regardless of their specific illness. He set out to find the anatomic and physiologic commonalities among these sick looking patients. He subjected lab animals to all sorts of noxious stimuli (pain, loud noises, electric shock, heat and cold) and he found some consistent responses in all animals. The adrenal cortex (which secretes stress hormones) was enlarged and components of the immune system (such as the thymus, spleen, and lymph nodes) had shrunk. He defined “stress” as the non-specific response of the body to any demand, and the physiologic changes that he noted, he called the “general adaptation syndrome” or more commonly called the stress response today.

Now fast forward to the early 70’s when researchers were beginning to correlate fight or flight and stress responses with the development of certain diseases. Cardiologists Friedman and Rosenman described the angry, time-obsessed, hypertension and heart attack-prone “type A” executive. The type A person was in a chronic state of anxious readiness which produced physical damage. The connection was being made that if stress contributed to things like heart disease and cancer, maybe by reducing stress one might help prevent these illnesses. This gave tremendous energy to the new field of stress reduction.

George Solomon was a psychiatrist at Stanford who in the 1960s showed that by destroying a rat’s hypothalamus, the animal suffered a marked decline in immune function.

Ten years later, Ader at the University of Rochester, demonstrated that the cells of the immune system (long thought to be under automated control) could be conditioned in the same way that Pavlov’s dogs responded to a bell by salivating. His colleague Felton demonstrated direct connections between the fibers of the sympathetic nervous system and the organs and cells of the immune system. Candace Pert and Soloman Snyder at Hopkins suggested that there were “peptide messengers” between the cells of the brain and those of the immune system. They called this new field of looking at connections between psychological processes and the nervous and immune systems psychoneuroimmunology.

I guess the answer to this question depends on what you mean by the word “prove”. If your question is about whether or not we can prove a connection between stress, depression, or anxiety and the development of cancer, that gets a bit trickier. The progression of research noted above would certainly suggest that this is an area for investigation.

A psychologist by the name of Bahnson reviewed the literature on stress, emotions, and cancer in 1980. At that time he felt that there was evidence to demonstrate an association between what he called a “particular configuration” and the development of cancer. That “configuration” was characterized by denial and depression, absence or loss of affection in early childhood, severe loss later in life, and strong and persistent feelings of hopelessness and helplessness. Bahnson based this conclusion on several studies, one being a prospective study of medical students at Hopkins which revealed a correlation between lack of closeness to parents and later development of cancer. The second was an observation that women with suspicious cervical biopsies who had recently suffered a loss were more likely to develop cervical cancer. The third study found that patients who had cancer were significantly more likely than controls to have suffered loss of an important relationship and to have an inability to express hostile feelings.

In the 28 years since this review, studies on personality and cancer have confirmed some of these findings but not all. A recent meta-analysis from the UK showed that stress-related psychological factors are associated with a higher incidence of cancer. There is some association between personality/stress and the development of cancer, and certainly other factors such as genetics, environment, and diet play a significant role.

What impact does stress have after the diagnosis of cancer? Do our patients’ thoughts, feelings, beliefs, and attitudes affect their outcomes? If so, how can we affect positive change?

One measure of the emotional state of a patient is to assess quality of life. Patti Ganz and Allen Coates showed that patients with lung or breast cancer who are more optimistic, more involved in their usual activities, and more hopeful about the future have an improved survival over those who are less optimistic or engaged. This is a finding that is independent of other prognostic factors. In the same meta-analysis from the UK that I just mentioned, Chida found that a stress-prone personality or unfavorable coping styles and negative emotional responses were related to higher cancer incidence and poorer survival. Another review article from JCO a couple of yearsago, showed there was a correlation between patient reported outcomes (such as quality of life measures) and survival. In her conclusion Dr. Gotay called for “studies that go beyond documenting this phenomenon and test hypotheses about why patient reported outcomes may be linked to survival…” And she goes on to conclude that interventions that improve patient reported outcomes have the potential to increase survival.

Those are excellent questions, and they are the basis for my evidence-based book, A Cancer Prevention Guide for the Human Race (http://www.amazon.com/Cancer-Prevention-Guide-Human-Race/dp/1608446913), which is the only current research-based cancer prevention book written specifically for lay readers. First, let me start by noting that the overwhelming majority of disease prevention research (http://www.doctorwascher.com/tag/prevention), including cancer prevention research, is based upon rather “low-level” types of research, including survey-based public health studies and retrospective clinical studies. While these methods of research are relatively quick and inexpensive to perform, the data that they produce is highly prone to various forms of bias. That is to say, their conclusions are often not highly accurate. On the other hand, prospective, randomized, placebo-controlled clinical research trials, when performed properly, provide the highest level of research evidence available. However, because this type of research is so demanding, and so expensive to perform, very few cancer prevention studies are performed using this “high-level” research approach. With this in mind, even rather conservative estimates of cancer risk associated with lifestyle and dietary factors suggest that somewhere between 40 and 60 percent of all cancer cases are directly linked to modifiable lifestyle, dietary, and environmental factors. (Some important cancer risk factors cannot be modified at this time, including the genes that we inherit from our parents, increasing age, and gender.) What is especially important to note is that some of the very worst cancer killers are the very same cancers that are most closely linked to modifiable lifestyle and dietary factors, including lung cancer, breast cancer, pancreatic cancer, esophageal cancer, stomach (gastric) cancer, and other common major cancers. At this time, we are able to effectively cure approximately 60 to 65 percent of all cancers. However, for many of the “bad actor” cancers, the likelihood of cure, even with aggressive treatment, remains very low at this time. As I say in A Cancer Prevention Guide for the Human Race, “…an ounce of cancer prevention is worth a ton of cancer cure!” Those are excellent questions, and they are the basis for my evidence-based book, A Cancer Prevention Guide for the Human Race (http://www.amazon.com/Cancer-Prevention-Guide-Human-Race/dp/1608446913), which is the only current research-based cancer prevention book written specifically for lay readers. First, let me start by noting that the overwhelming majority of disease prevention research (http://www.doctorwascher.com/tag/prevention), including cancer prevention research, is based upon rather “low-level” types of research, including survey-based public health studies and retrospective clinical studies. While these methods of research are relatively quick and inexpensive to perform, the data that they produce is highly prone to various forms of bias. That is to say, their conclusions are often not highly accurate. On the other hand, prospective, randomized, placebo-controlled clinical research trials, when performed properly, provide the highest level of research evidence available. However, because this type of research is so demanding, and so expensive to perform, very few cancer prevention studies are performed using this “high-level” research approach. With this in mind, even rather conservative estimates of cancer risk associated with lifestyle and dietary factors suggest that somewhere between 40 and 60 percent of all cancer cases are directly linked to modifiable lifestyle, dietary, and environmental factors. (Some important cancer risk factors cannot be modified at this time, including the genes that we inherit from our parents, increasing age, and gender.) What is especially important to note is that some of the very worst cancer killers are the very same cancers that are most closely linked to modifiable lifestyle and dietary factors, including lung cancer, breast cancer, pancreatic cancer, esophageal cancer, stomach (gastric) cancer, and other common major cancers. At this time, we are able to effectively cure approximately 60 to 65 percent of all cancers. However, for many of the “bad actor” cancers, the likelihood of cure, even with aggressive treatment, remains very low at this time. As I say in A Cancer Prevention Guide for the Human Race, “…an ounce of cancer prevention is worth a ton of cancer cure!”

Please visit our website at www.rational-t.com for additional information and references. In addition, the Ralph Moss’ book, “Customized Chemotherapy” Equinox Press 2011, is an excellent source regarding the history and application of these techniques. Please visit our website at www.rational-t.com for additional information and references. In addition, the Ralph Moss’ book, “Customized Chemotherapy” Equinox Press 2011, is an excellent source regarding the history and application of these techniques.

It looks like a Phase 2 study was just completed on metestatic women http://clinicaltrials.gov/ct2/show/NCT00842998?term=herceptin+only&rank=5

and a phase three is ongoing
and recruiting metestatic women

http://clinicaltrials.gov/ct2/show/NCT00968968?term=herceptin+only&rank=9

to view all clinic trials go to http://clinicaltrials.gov It looks like a Phase 2 study was just completed on metestatic women http://clinicaltrials.gov/ct2/show/NCT00842998?term=herceptin+only&rank=5

and a phase three is ongoing
and recruiting metestatic women

http://clinicaltrials.gov/ct2/show/NCT00968968?term=herceptin+only&rank=9

to view all clinic trials go to http://clinicaltrials.gov

Most of the pioneering and breakthrough studies in the field are mentioned in our book and I also write a blog (www.YourBrainAfterChemo.blogspot.com) that is completely devoted to the topic. There you'll find some of the more important recent studies, summarized for a general audience. PubMed.gov of the U.S. National Library of Medicine is also an excellent source.
Most of the pioneering and breakthrough studies in the field are mentioned in our book and I also write a blog (www.YourBrainAfterChemo.blogspot.com) that is completely devoted to the topic. There you'll find some of the more important recent studies, summarized for a general audience. PubMed.gov of the U.S. National Library of Medicine is also an excellent source.

The study presented by Dr. Grace Smith at the San Antonio Breast Cancer Symposium entitled Partial Breast Brachytherapy is Associated with Inferior Effectiveness and Increased Toxicity Compared with Whole Breast Irradiation in Older Patients has garnered a tremendous amount of print and internet media attention. After reading the abstract (paper not in press yet), seeing the talk live in San Antonio, and discussing the study with many colleagues in the breast surgery and radiation oncology fields, it has become necessary to try to clarify the data on APBI, discuss the 'information' in the abstract and the hyperbole in the lay press that is distressing our patients.

First and unequivocally, Acellerated Partial Breast Irradiation is a safe and effective form of treating the breast after appropriately performed lumpectomy in patients over age 45-50 with early stage invasive (typically <3cm primaries and lymph node negative) and non-invasive breast cancer. Numerous retrospective studies and 2 prospective randomized (the gold standard) studies have shown no difference in survival, local-regional recurrence rates or complications between APBI and Whole Breast Irradiation (WBI). The American Society of Breast Surgeons Mammosite Registry has published more than 16 papes showing the safety and efficacy (comparable to WBI) of Mammosite APBI.

The abstract and presentation is drawn from the Medicare claims-SEER database which is a large database with cancer patient data linked to Medicare claims data. The database is managed by the NCI and sold to institutions to do research. The linked database has information about cancer type and treatments but no specific data on margin status, prognostic factors such as ER/PR and Her2Neu, or even local, regional or distant recurrence. The study stated that 'subsequent mastectomy' is a 'validated surrogate for local failure' although I am unaware of any literature that states this. The 'two-fold increased risk for subsequent mastectomy' is misleading (and inaccurate - it's 4.0% for APBI vs. 2.2% for Whole Breast Irradiation in their study). Both of these rates are quite small and questionable whether there is any clinical significance between the two. Not emphasized but equally (?more) important is the overall survival rates which were equivalent. The study also stated that infections were higher for APBI (not surprising since it involves the insertion of one or more catheters in the breast) but there is no statement regarding severity (were the APBI patients just placed on prophylactic antiobiotics and that is how an infection was defined?). Fat necrosis and breast pain were also significantly higher in the APBI group although there is absolutely no uniform definition of what fat necrosis is nor a statement about the severity or the fat necrosis or breast pain. Lastly, they state there was a 9.6% hospitalization rate for APBI patients vs 5.7% for WBI patients. This is quizzical since no diagnosis was given for hospitalization nor the time period over which they were hospitalized (was it APBI related[doubtful] or related to first chemotherapy cycle [perhaps] or other unrelated health issues [APBI often used in older, sicker patients who may not be candidates for 6-7 weeks of WBI]). In summary, this retrospective study of an inherently inacurate (no data on tumor characteristics and margin status - both known to be significant determiners of local recurrence) database with questionable outcomes (admission rate) and non-validated 'surrogate endpoints' (subsequent mastectomy=local recurrence) should be looked at with appropriate skepticism in the face of 20 years of retrospective studies and 2 prospective randomized trial to the contrary.
Thanks for the question! The San Antonio Breast Cancer Symposium is one of the largest and most prestigious breast cancer conferences, and often exciting and innovative research is presented. However at the recent meeting, a study was presented by a group from MD Anderson, questioning the safety and effectiveness of accelerated partial breast irradiation (APBI) for early-stage breast cancer - specifically they noted that patients undergoing this treatment have a higher rate of complications and eventual mastectomy. Unfortunately before the study was even presented, it received national media attention, leading to significant anxiety and confusion among women. This stresses the importance of reading the study, not just listening to the sound bite - here are some facts:
- The study used retrospective (after the fact) "claims data" to do their evaluation. That means they took Medicare billing information, not actual patient data, and drew some conclusions. It is NOT possible to accurately determine complication rates from claims data as they are not always reported. It is also not possible (and the authors admitted this) to determine why the women treated with APBI subsequently underwent mastectomy - it could have been for an entirely different cancer, even one in the other breast!
- The absolute increased risk of mastectomy was 1.8% which is quite low, and again we have no way to know why the women underwent mastectomy
- APBI has been the subject of multiple prospective (going-forward) and peer-reviewed studies, and has been shown to have an equivalent or in some cases better rate of breast cancer control compared to whole-breast irradiation; the complication rate is also equivalent.

3 respected professional medical societies published responses critical of the MD Anderson study, and I expect more criticism will come. The responses are from the American Society of Breast Surgeons: https://www.breastsurgeons.org/news/article.php?id=122, the American Brachytherapy Society: http://campaign.r20.constantcontact.com/render?llr=kdofiegab&v=001rj64Pj8NTf4ISgwN4cSdZYtZBR53GjAi73j4En_qeygPzWmSUe1qgGI7U-jt8HRV7NouL9sMViv1IOOeGT2QHMAaDWrfEuOApREAHj-8Z60%3D and the American Society for Radiation Oncology: https://astro.org/News-and-Media/News-Releases/2011/ASTRO--APBI-safe,-effective-for-some-breast-cancer-patients.aspx

It is again unfortunate that this poorly designed study with no real valid clinical data was allowed to be presented at such a prestigious meeting, and that it received immense national media attention before the scientific community was allowed to interpret the study and respond. I am hopeful that this will not happen in the future, as many women (and many physicians) were caused unnecessary anxiety regarding their breast cancer treatment options.

VEGF is an acronym for the vascular endothelial derived growth factor. VEGF is a protein produced by the cells that make up the lining of blood vessels (and others) and its role is to promote the development of blood vessels (angiogenesis). VEGF binds to a receptor located on the surface of some cells. This makes VEGF the 'ligand' for that receptor. (Please see my answer re: ligands for more details on that term.) Both VEGF and its receptor (VEGFR) are proteins.

Tumor cells are abnormal but they still need the nutrients provided by blood and need to get rid of waste products. Tumors that don't get a blood supply can only grow to an extremely small size. Tumors that do get a blood supply can get larger and also use the blood vessels to move to other parts of the body (metastasize). Cancer cells can either produce VEGF themselves or 'trick' nearby cells into making it. Either way, they cause blood vessels to come over to the tumor, feeding it. There are many other factors beside VEGF that can cause blood vessels to grow.

There are approved cancer drugs that block the VEGF:VEGFR interaction. An example is Avastin®. One reason why cancer can progress even when Avastin® is used is the presence of other things that can cause angiogenesis. Much current work is going into identifying the different factors that cause blood vessels to grow and to the development of drugs that can block these factors. Probably the best approach will be a 'cocktail' of different drugs that target several angiogenesis factors at once.

VEGF is an acronym for the vascular endothelial derived growth factor. VEGF is a protein produced by the cells that make up the lining of blood vessels (and others) and its role is to promote the development of blood vessels (angiogenesis). VEGF binds to a receptor located on the surface of some cells. This makes VEGF the 'ligand' for that receptor. (Please see my answer re: ligands for more details on that term.) Both VEGF and its receptor (VEGFR) are proteins.

Tumor cells are abnormal but they still need the nutrients provided by blood and need to get rid of waste products. Tumors that don't get a blood supply can only grow to an extremely small size. Tumors that do get a blood supply can get larger and also use the blood vessels to move to other parts of the body (metastasize). Cancer cells can either produce VEGF themselves or 'trick' nearby cells into making it. Either way, they cause blood vessels to come over to the tumor, feeding it. There are many other factors beside VEGF that can cause blood vessels to grow.

There are approved cancer drugs that block the VEGF:VEGFR interaction. An example is Avastin®. One reason why cancer can progress even when Avastin® is used is the presence of other things that can cause angiogenesis. Much current work is going into identifying the different factors that cause blood vessels to grow and to the development of drugs that can block these factors. Probably the best approach will be a 'cocktail' of different drugs that target several angiogenesis factors at once.

Of course we would suggest the Inflammatory Breast Cancer Research Foundation, www.ibcresearch.org, which would include the website, Facebook page, and e-newsletter. Content is regularly updated and reviewed for accuracy and usefulness.

For current medical journal articles it is always best to go to PubMed and type in "inflammatory breast cancer" to locate the most recently published articles. Unfortunately those are often in subscription only journals so you may only be able to read the abstract but can contact the corresponding author for more information.

The National Cancer Institute has a good fact sheet:
http://www.cancer.gov/cancertopics/factsheet/Sites-Types/IBC

Many major medical centers have information about inflammatory breast cancer and those who see more cases may have some research data as well as clinical trials.

It's important to be cautious when exploring the internet for health related information. Not all websites have physician overview and may contain more personal opinion than unbiased medical information. Of course we would suggest the Inflammatory Breast Cancer Research Foundation, www.ibcresearch.org, which would include the website, Facebook page, and e-newsletter. Content is regularly updated and reviewed for accuracy and usefulness.

For current medical journal articles it is always best to go to PubMed and type in "inflammatory breast cancer" to locate the most recently published articles. Unfortunately those are often in subscription only journals so you may only be able to read the abstract but can contact the corresponding author for more information.

The National Cancer Institute has a good fact sheet:
http://www.cancer.gov/cancertopics/factsheet/Sites-Types/IBC

Many major medical centers have information about inflammatory breast cancer and those who see more cases may have some research data as well as clinical trials.

It's important to be cautious when exploring the internet for health related information. Not all websites have physician overview and may contain more personal opinion than unbiased medical information.

Yes, I can except that I cannot give a specific. Angiogenesis is triggered by three main receptor VEGFR 1, VEGFR 2, and VEGFR 3. You can inhibit one of these receptor or two receptors, or three receptors. Further, some people approach inhibit the ligand (stimulant of receptor). Stopping the ligand is the approach of Bevacizumab (Avastin).

So the main question is wether the ligands or the receptors important in creating new blood vessels that can nurture the cancer more. The answer is that we do not have a clear cut answer. Therefore, the thought is why not inhibit all three receptors. Because we speculate that all three receptors promote inflammatory breast cancer to be aggressive, we feel that is worth testing a drug that inhibit all three receptors.
Yes, I can except that I cannot give a specific. Angiogenesis is triggered by three main receptor VEGFR 1, VEGFR 2, and VEGFR 3. You can inhibit one of these receptor or two receptors, or three receptors. Further, some people approach inhibit the ligand (stimulant of receptor). Stopping the ligand is the approach of Bevacizumab (Avastin).

So the main question is wether the ligands or the receptors important in creating new blood vessels that can nurture the cancer more. The answer is that we do not have a clear cut answer. Therefore, the thought is why not inhibit all three receptors. Because we speculate that all three receptors promote inflammatory breast cancer to be aggressive, we feel that is worth testing a drug that inhibit all three receptors.

Widespread use is something that will not happen easily in any research related to cancer. Sorry.

Most of the advancement in cancer research is an increment. Step by step. Further, IBC is under funded so it makes the situation more difficult.

MD Anderson Cancer Center focuses now on targeting EGFR, HDAC, VEGFR, c-Met, HER2, IGFR and etc. There are many targeted therapy trials conducted specially targeting IBC or including IBC. Widespread use is something that will not happen easily in any research related to cancer. Sorry.

Most of the advancement in cancer research is an increment. Step by step. Further, IBC is under funded so it makes the situation more difficult.

MD Anderson Cancer Center focuses now on targeting EGFR, HDAC, VEGFR, c-Met, HER2, IGFR and etc. There are many targeted therapy trials conducted specially targeting IBC or including IBC.

If you are looking for serious medical articles, you can go to a medical library and ask for the followng articles to be pulled. I hope that this will guide you.

The other is for you to learn how to use PubMed (http://www.ncbi.nlm.nih.gov)
And do a search by inflammatory breast cancer.

The other website for the latest update related to inflammatory breast cancer is
http://www.facebook.com/InflammatoryBreastCancer


Inflammatory breast cancer: the disease, the biology, the treatment.
Robertson FM, Bondy M, Yang W, Yamauchi H, Wiggins S, Kamrudin S, Krishnamurthy S, Le-Petross H, Bidaut L, Player AN, Barsky SH, Woodward WA, Buchholz T, Lucci A, Ueno NT, Cristofanilli M.
CA Cancer J Clin. 2010 Nov-Dec;60(6):351-75. Epub 2010 Oct 19. Review. Erratum in: CA Cancer J Clin. 2011 Mar-Apr;61(2):134. Ueno, Naoto [corrected to Ueno, Naoto T].
PMID: 20959401 [PubMed - indexed for MEDLINE] Free Article
Related citations

2.
International expert panel on inflammatory breast cancer: consensus statement for standardized diagnosis and treatment.
Dawood S, Merajver SD, Viens P, Vermeulen PB, Swain SM, Buchholz TA, Dirix LY, Levine PH, Lucci A, Krishnamurthy S, Robertson FM, Woodward WA, Yang WT, Ueno NT, Cristofanilli M.
Ann Oncol. 2011 Mar;22(3):515-23. Epub 2010 Jul 5.
PMID: 20603440 [PubMed - indexed for MEDLINE]
Related citations

3.
Molecular targets for treatment of inflammatory breast cancer.
Yamauchi H, Cristofanilli M, Nakamura S, Hortobagyi GN, Ueno NT.
Nat Rev Clin Oncol. 2009 Jul;6(7):387-94. Epub 2009 May 26. Review.
PMID: 19468291 [PubMed - indexed for MEDLINE]
Related citations

4.
The medical treatment of inflammatory breast cancer.
Dawood S, Ueno NT, Cristofanilli M.
Semin Oncol. 2008 Feb;35(1):64-71. Review. If you are looking for serious medical articles, you can go to a medical library and ask for the followng articles to be pulled. I hope that this will guide you.

The other is for you to learn how to use PubMed (http://www.ncbi.nlm.nih.gov)
And do a search by inflammatory breast cancer.

The other website for the latest update related to inflammatory breast cancer is
http://www.facebook.com/InflammatoryBreastCancer


Inflammatory breast cancer: the disease, the biology, the treatment.
Robertson FM, Bondy M, Yang W, Yamauchi H, Wiggins S, Kamrudin S, Krishnamurthy S, Le-Petross H, Bidaut L, Player AN, Barsky SH, Woodward WA, Buchholz T, Lucci A, Ueno NT, Cristofanilli M.
CA Cancer J Clin. 2010 Nov-Dec;60(6):351-75. Epub 2010 Oct 19. Review. Erratum in: CA Cancer J Clin. 2011 Mar-Apr;61(2):134. Ueno, Naoto [corrected to Ueno, Naoto T].
PMID: 20959401 [PubMed - indexed for MEDLINE] Free Article
Related citations

2.
International expert panel on inflammatory breast cancer: consensus statement for standardized diagnosis and treatment.
Dawood S, Merajver SD, Viens P, Vermeulen PB, Swain SM, Buchholz TA, Dirix LY, Levine PH, Lucci A, Krishnamurthy S, Robertson FM, Woodward WA, Yang WT, Ueno NT, Cristofanilli M.
Ann Oncol. 2011 Mar;22(3):515-23. Epub 2010 Jul 5.
PMID: 20603440 [PubMed - indexed for MEDLINE]
Related citations

3.
Molecular targets for treatment of inflammatory breast cancer.
Yamauchi H, Cristofanilli M, Nakamura S, Hortobagyi GN, Ueno NT.
Nat Rev Clin Oncol. 2009 Jul;6(7):387-94. Epub 2009 May 26. Review.
PMID: 19468291 [PubMed - indexed for MEDLINE]
Related citations

4.
The medical treatment of inflammatory breast cancer.
Dawood S, Ueno NT, Cristofanilli M.
Semin Oncol. 2008 Feb;35(1):64-71. Review.

I am guessing that you are asking how you develop a novel biomarkers or a new targeted therapy for breast cancer or inflammatory breast cancer.


There are several ways to approach this issues.

1. You collect large amoung of tissue and blood samples from breast cancer. Then you do a comprehensive analysis of genetic and protein changes (DNA, RNA, and protein). You link this data to a clinica data and find the one or them that can impact surveil or disease recurrence.

2. The other approach is discovery from basic research needs to be mined. And take their knowledge to apply by conducting a hypothesis oriented research. This means that you build up the puzzle one by one to prove the target is truly relevant in breast cancer.

Both approaches are important. Therefore, we do both and spend tremendous amount of time an money to come out with a strong scientific rationale before we can test this in human being. The problem we face is that there is not enough money and those who qualified to do this type of research.

Please asks me a more specific question. This may help me to answer this more accurately. I am guessing that you are asking how you develop a novel biomarkers or a new targeted therapy for breast cancer or inflammatory breast cancer.


There are several ways to approach this issues.

1. You collect large amoung of tissue and blood samples from breast cancer. Then you do a comprehensive analysis of genetic and protein changes (DNA, RNA, and protein). You link this data to a clinica data and find the one or them that can impact surveil or disease recurrence.

2. The other approach is discovery from basic research needs to be mined. And take their knowledge to apply by conducting a hypothesis oriented research. This means that you build up the puzzle one by one to prove the target is truly relevant in breast cancer.

Both approaches are important. Therefore, we do both and spend tremendous amount of time an money to come out with a strong scientific rationale before we can test this in human being. The problem we face is that there is not enough money and those who qualified to do this type of research.

Please asks me a more specific question. This may help me to answer this more accurately.

By research I believe they are not looking for a cure but researching more toxic and more expensive chemotherapy drugs. What about alternative care? Why isn't that funded by my insurance-is the medical profession so scared that they won't get their billions? It is about time that the insurances include naturopathic, acupuncture, and holistic practitioners to their list of providers. I think private enterprise is sufficiently motivated by the huge profits they make off cancer.

The obvious answer is to prevent metastasis by improving early detection. If you ignore that, there are several new technologies that are very promising. One of the main problems with the systemic treatments (like chemotherapy) that are used to treat cancer is that they affect many normal cells, leading to unwanted side-effects. The best new treatments will have to limit their side-effects. These include:
1. Nanotechnology - this field uses microscopic particles to deliver drugs to cancer cells. They 'home' in to the cancer cells and don't hurt normal cells.
2. Anti-angiogenesis treatments- Angiogenesis is the development of blood vessels. Tumors 'trick' the body into providing them with blood vessels, giving them access to nutrients, oxygen and a way to spread. Because angiogenesis is limited to only a few normal conditions (i.e. pregnancy) in adults, these treatments have the ability to starve tumors. Anti-angiogenesis drugs (including Avastin) DO have side effects and do not always work.

They key is to find something that is UNIQUE to the particular cancer cells being treated, whether it is the things they need (like lots of sugar) or don't need. Newer targeted therapies are a step in this direction but they still affect normal cells to an extent. The obvious answer is to prevent metastasis by improving early detection. If you ignore that, there are several new technologies that are very promising. One of the main problems with the systemic treatments (like chemotherapy) that are used to treat cancer is that they affect many normal cells, leading to unwanted side-effects. The best new treatments will have to limit their side-effects. These include:
1. Nanotechnology - this field uses microscopic particles to deliver drugs to cancer cells. They 'home' in to the cancer cells and don't hurt normal cells.
2. Anti-angiogenesis treatments- Angiogenesis is the development of blood vessels. Tumors 'trick' the body into providing them with blood vessels, giving them access to nutrients, oxygen and a way to spread. Because angiogenesis is limited to only a few normal conditions (i.e. pregnancy) in adults, these treatments have the ability to starve tumors. Anti-angiogenesis drugs (including Avastin) DO have side effects and do not always work.

They key is to find something that is UNIQUE to the particular cancer cells being treated, whether it is the things they need (like lots of sugar) or don't need. Newer targeted therapies are a step in this direction but they still affect normal cells to an extent.

Yes, I'd be happy to.

To recap, I study and analyze cases of Non-Allopathic Remission, which are cancer remissions that occur either without Western (allopathic) medicine, or after allopathic medicine has failed to remit the disease. They are rare, and not always permanent, but they are nevertheless (in my opinion) still worth studying, because they have the potential to reveal how and why cancer goes away.

My exploratory research - which means it should not be generalized to a larger population - showed that, among the 20 exceptional survivors that I found and interviewed, six actions were common among almost all of them. They were:
1) Dietary changes (more veggies and whole foods; less meat, sugars, dairy)
2) Herbal and vitamin supplementation
3) Releasing repressed emotions
4) Increasing love and joy
5) Using intuition to help inform medical decisions
6) Deepening spirituality

It will take many years and a lot of funding before we can determine definitively whether or not these actions have any significant effect on cancer survival. However, in the meantime, these actions have not been shown to cause harm (although herbs and vitamins must be medically supervised), and the initial research shows that they may improve immune function.

Three underlying beliefs about cancer always emerged from my 20 interviews. They were:
1) To remove cancer, you must change the underlying conditions in the body that allow it to thrive.
2) Illness indicates a blockage or "slowness" on either the physical, mental, or spiritual level. Health, on the other hand, represents a state of movement or freedom.
3) There is a body-mind-spirit interaction that can be capitalized on for healing purposes.

That's a brief summary of my research so far. I will be describing it in more detail in my upcoming book.

Hope that's helpful,
Kelly Turner, PhD
www.ShuniyaHealing.com
Twitter @ShuniyaHealing
Yes, I'd be happy to.

To recap, I study and analyze cases of Non-Allopathic Remission, which are cancer remissions that occur either without Western (allopathic) medicine, or after allopathic medicine has failed to remit the disease. They are rare, and not always permanent, but they are nevertheless (in my opinion) still worth studying, because they have the potential to reveal how and why cancer goes away.

My exploratory research - which means it should not be generalized to a larger population - showed that, among the 20 exceptional survivors that I found and interviewed, six actions were common among almost all of them. They were:
1) Dietary changes (more veggies and whole foods; less meat, sugars, dairy)
2) Herbal and vitamin supplementation
3) Releasing repressed emotions
4) Increasing love and joy
5) Using intuition to help inform medical decisions
6) Deepening spirituality

It will take many years and a lot of funding before we can determine definitively whether or not these actions have any significant effect on cancer survival. However, in the meantime, these actions have not been shown to cause harm (although herbs and vitamins must be medically supervised), and the initial research shows that they may improve immune function.

Three underlying beliefs about cancer always emerged from my 20 interviews. They were:
1) To remove cancer, you must change the underlying conditions in the body that allow it to thrive.
2) Illness indicates a blockage or "slowness" on either the physical, mental, or spiritual level. Health, on the other hand, represents a state of movement or freedom.
3) There is a body-mind-spirit interaction that can be capitalized on for healing purposes.

That's a brief summary of my research so far. I will be describing it in more detail in my upcoming book.

Hope that's helpful,
Kelly Turner, PhD
www.ShuniyaHealing.com
Twitter @ShuniyaHealing

Research studies indicate that there is, indeed, a human virus (HMTV) and it is 95-98% similar to the mouse virus (MMTV) - suggesting they are really the same virus.

Cats become infected with the virus from infected mice.

There are some scientists who think humans can become infected from mice or cats.

Also, MMTV is passed in seminal fluid to infect female mice. We ought to see if there is any evidence of HMTV in human seminal fluid.

Obviously, there are many questions to answer - all of them interesting and important! Research studies indicate that there is, indeed, a human virus (HMTV) and it is 95-98% similar to the mouse virus (MMTV) - suggesting they are really the same virus.

Cats become infected with the virus from infected mice.

There are some scientists who think humans can become infected from mice or cats.

Also, MMTV is passed in seminal fluid to infect female mice. We ought to see if there is any evidence of HMTV in human seminal fluid.

Obviously, there are many questions to answer - all of them interesting and important!

Therapeutic vaccines targeting specific proteins are being tested, some with promising results. The first preventive breast cancer vaccine was developed by Professor Vincent Tuohy of the Cleveland Clinic and published last year in Nature Medicine (May 2010). The vaccine is 100% effective in preventing breast cancer in mice and also capable of slowing the growth of tumors that have already formed. It was also effective against a cell line of triple-negative breast cancer. Tuohy's vaccine is ready to Phase I studies in women, provided he receives the funding necessary to get the clinical trials funded: approximately 5 million to start and, likely, 20 million to fund through Phase III studies. Therapeutic vaccines targeting specific proteins are being tested, some with promising results. The first preventive breast cancer vaccine was developed by Professor Vincent Tuohy of the Cleveland Clinic and published last year in Nature Medicine (May 2010). The vaccine is 100% effective in preventing breast cancer in mice and also capable of slowing the growth of tumors that have already formed. It was also effective against a cell line of triple-negative breast cancer. Tuohy's vaccine is ready to Phase I studies in women, provided he receives the funding necessary to get the clinical trials funded: approximately 5 million to start and, likely, 20 million to fund through Phase III studies.

Here is a link to the Library I created at The PInk Squadron (thepinksquadron.org), an online registry of women interested in issues related to the breast cancer virus.

It is a good starter list of peer-reviewed articles on MMTV and HMTV.

http://www.thepinksquadron.org/research-library/37-bibliography Here is a link to the Library I created at The PInk Squadron (thepinksquadron.org), an online registry of women interested in issues related to the breast cancer virus.

It is a good starter list of peer-reviewed articles on MMTV and HMTV.

http://www.thepinksquadron.org/research-library/37-bibliography