"Beauty Secrets" Revealed...Just Read the Label!

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From: www.pronature.com

DANGEROUS BEAUTY: Scientists Warn of Harmful Ingredients In Our Shampoos and Cosmetics
~ by David Lowell Kern

Sodium Laurel Sulfate and Eye Damage in Young Children
The greatest concern of many scientists is sodium lauryl sulfate (SLS), a detergent found in about 90 percent of commercial shampoos. Also known as sodium dodecyl, sodium laureth sulfate (SLFS) this chemical has been shown to damage protein formation in eye tissue in young animals, raising serious concerns about the possibility of ocular tissue malformation, blindness in infants and young children. In animal studies, Sodium Laurel Sulfate penetration and uptake is much greater in neonatal and young animal eye tissue, compared to adult animals, showing "penetration into the eye, as well as systemic tissues (brain, heart, liver, etc.)" SLS also showed long-term retention in tissues, up to 5 days after a single drop.1

Researcher Keith Green, Ph.D., D. Sc., of the Medical College of Georgia, also reports that Sodium Laurel Sulfate extends the healing of corneal tissue by a factor of 5, from 2 days (normal) to more than 10 days. He also has concerns about cataract formation from Sodium Laurel Sulfate. Writing for Research to Prevent Blindness, Inc., Dr. Green states in part: There is an immediate concern relating to the penetration of these chemicals into the eye and other tissues. This is especially important in infants...exposure to SLS results in accumulation in eye tissues, a process that could retard healing and possibly have long-term effects. Dr. Green concludes that exposure to Sodium Laurel Sulfate sulfate causes improper eye development in children and that since Sodium Laurel Sulfate is absorbed systemically through the skin, it doesn't have to enter the eye directly.

Our own research found that SLS is present as a main ingredient in most commercial shampoos for adults or children.

Sodium Laurel Sulfate Toxicity and Cancer - Another serious health concern with SLS is its tendency to react with other ingredients to form NDELA, a nitrosamine and potent carcinogen. According to a 1978 FDA report, shampooing the hair with a product contaminated with this nitrosamine can lead to its absorption into the body at levels much higher than eating nitrate- contaminated foods. (Researchers estimate the nitrate absorption from one shampoo is equal to eating a pound of bacon.) The FDA has recently warned shampoo manufacturers of unacceptable levels of dioxin formation in products containing SLFS (dioxins are also dangerous carcinogenic compounds). Only laboratory testing can determine if a shampoo is contaminated with these powerful carcinogenic compounds.

Damage To Your Skin - Researchers have known for years that Sodium Laurel Sulfate is a skin irritant.

Sodium Laurel Sulfate is implicated in premature hair loss in men and women, and may be one reason for wide-spread incidence of thinning hair.

Sodium Laurel Sulfate is also implicated in scalp irritation, eczema, dandruff, and other scalp conditions. Many shampoos designed to alleviate dandruff, itching, and other scalp disorders may actually be causing the toxicity of Sodium Laurel Sulfate-containing formulas to the skin and scalp. Avoiding contact with this cytotoxic (cell- killing) chemical is all that many people require to completely alleviate scalp disorders.

Natural Brands Offer No Protection - Ingredient reviews of shampoos sold in health food stores under natural brands and labels have turned up many formulas containing Sodium Laurel Sulfate. The cost, reputation, or market position of a shampoo apparently has little to do with its contents. Some of the most reputable and exclusive brands contain Sodium Laurel Sulfate. Don't be fooled by high prices or marketing hype. You must check the ingredients on each product if you want to avoid the harmful effects of Sodium Laurel Sulfate.

References:

1. Clayton et. al., Ed. Chem. Tox., 1985
2. Br J Dermatol 1992 Sep
3. Contact Dermatitis 1992 Jul
4. Acta Derm Venereol (Stockh) 1991
5. Acta Derm Venereol Suppl (Stockh) 1992
6. The Lancet, Feb 3, 1990
7. Contact Dermatitis 1993 Sep
8. Contact Dermatitis 1993 Mar and 1993 Feb
9. Contact Dermatitis 1992 Sep
10. Journal of Toxicology, Cutaneous and Ocular Toxicology, 1992
11. Toxicology Letters, Vol 26, 1985
12. Toxicol Pathol 1992
13. Govt Reports Announcements & Index, 1993
14. Acta Derma Venereol (Stockh) 1992
15. Department of Dermatology, Rigshospitalet, Copenhagen

Here is list of ingredients to steer away from in our cosmetics and beauty products,and why. Unfortunately, due to the lax regulation in the U.S. the majority of these ingredients can be found in most of the products we use daily.

Alkylphenol Ethoxylates

Found to reduce sperm count

Benzene/Benzoic Acid/Benzyl Benzoate

Considered a carcinogen, is an endocrine disruptor, and is suspected to cause birth defects

Coal Tar

Known human carcinogen. Prohibited for us in cosmetics in the European Union. May contian harmful impurities or breakdown products. Found in dandruff shampoos, anti-itch creams and hair dyes.

Methyl, Propyl, Butyl and Ethyl Paraben

Used as inhibitors of microbial growth and to extend shelf life of products. Have caused many allergic reactions and skin rashes. Studies have shown that they are weakly estrogenic and can be absorbed by the body through the skin. Widely used even though they are known to be toxic.

Dibutyl Phthalate

Prohibited for us in cosmetics in the European Union. Possoble human reproductive or developmental toxin. Endocrine disruptor. Found in some nail polish, perfume and hair spray.

Diethanolamine (DEA), Triethanolamine (TEA)

Often used in cosmetics as emulsifiers and/or foaming agents. They can cause allergic reactions, eye irritation and dryness of hair and skin. DEA and TEA are "amines" (ammonia compounds) and can form cancer-causing nitrosamines when they come in contact with nitrates. Toxic if absorbed into the body over a long period of time. This chemical interferes with the body's ability to absorb choline which is needed for proper fetal brain development.

Diazolidinyl Urea, Imidazolidinyl Urea

These are widely used preservatives. The American Academy of Dermatology has found them to be a primary cause of contact dermatitis. Two trade names for these chemicals are Germall II and Germall 115. Neither of the Germall chemicals contains a good antifungal agent, and they must be combined with other preservatives. Both these chemicals release formaldehyde, which can be toxic.

Formaldehyde

This is an extreme irritant to the mucous membranes with often destructive effects. It is also considered to be a neurotoxin and carcinogen.

Fragrances

The label of "Fragrances" can mask a multitude of toxic, synthetic chemicals, many of which suppress the immune system, are endocrine disruptors, and cause cancer. When looking for scented products, make sure it's scented by essential oils -- which are expensive; therefore, companies usually list what essential oils are contained in the product without reverting to the generic term "Fragrances".

Isopropanol/Isopropyl Alcohol

This is a skin irritant that causes flushing, pulse rate fluctuations, dizziness, headaches, and nausea.

Lead Acetate

Known human reproductive and developmental toxin. Prohibited for use in cosmetics in the European Union. Found in some hair dyes and cleanser.

Mercury

Possible human carcinogen. Possible human reproductive or developmental toxin. Found in some eye drops and ointment.

Methylisothiazoline, or MIT

This can cause skin and eye irritation and is known to cause neurological damage.

Parabens (Isobutylparaben, Butylparaben, Methylparaben, Propylparaben)

Increases a person's risk of breast cancer. These class of chemicals are also endocrine disruptors and have been linked to fertility problems.

Petrolatum

Also known as petroleum jelly, this mineral oil derivative is used for its emollient properties in cosmetics. It has no nutrient value for the skin and can interfere with the body's own natural moisturizing mechanism, leading to dryness and chapping. It often creates the very conditions it claims to alleviate. Manufacturers use petrolatum because it is unbelievably cheap.

Petroleum Distillates

Possible human carcinogen. May contain harmful impurities or breakdown products. Prohibited for use in cosmetics in the European Union. Found in some mascara, perfume, foundation, lipstick and lip balm.

Phthalates

This has been linked to damage of the organs -- kidneys, lungs, and liver -- as well as the reproductive system.

Propylene Glycol

Ideally this is a vegetable glycerin mixed with grain alcohol, both of which are natural. Usually it is a synthetic petrochemical mix used as a humectant. It has been known to cause allergic reactions, hives and eczema. When you see PEG (polyethylene glycol) or PPG (polypropylene glycol) on labels, beware—these are related synthetics. Although exposure to high levels of Propylene Glycol is known to cause serious and potentially irreversible health conditions, the chemical industry tell us that "small" quantities or low level exposure of Propylene Glycol is "safe" to use on the skin and in food. According to the safety data sheets of industrial chemical manufacturers, chemicals such as Ethylene Glycol and Propylene Glycol will cause serious health conditions, including liver and heart damage and damage to the central nervous system if sufficient is absorbed by the body.

PVP/VA Copolymer

A petroleum-derived chemical used in hairsprays, styling aids and other cosmetics. It can be considered toxic, since inhaled particles can damage the lungs of sensitive persons.

Sodium Lauryl/Laureth Sulfate

A cheap, harsh detergent used in shampoos for its cleansing and foam-building properties. Often derived from petroleum, it is frequently disguised in pseudo-natural cosmetics with the phrase "comes from coconuts." It causes eye irritation, scalp scurf similar to dandruff, skin rashes and other allergic reactions. (See detailed report, above.)

Stearalkonium Chloride

A quaternary ammonium compound used in hair conditioners and creams. Developed by the fabric industry as a fabric softener, it is a lot cheaper and easier to use in hair conditioning formulas than proteins or herbals, which are beneficial to the hair. Causes allergic reactions. Toxic.

Synthetic Colors

Used to make cosmetics "pretty," synthetic colors, along with synthetic hair dyes, should be avoided at all costs. They will be labeled as FD&C or D&C, followed by a color and a number. Example: FD&C Red No. 6 / D&C Green No. 6. Many synthetic colors can be carcinogenic. If a cosmetic contains them, don't use it.

Synthetic Fragrances

The synthetic fragrances used in cosmetics can have as many as 200 ingredients. There is no way to know what the chemicals are, since on the label it will simply read "fragrance." Some problems caused by these chemicals include headaches, dizziness, rash, hyperpigmentation, violent coughing, vomiting, skin irritation—the list goes on. Advice: Don't buy a cosmetic that has the word "fragrance" on the ingredients label.

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Stress Fuels Breast Cancer Metastasis to Bone

ScienceDaily (July 17, 2012) — Stress can promote breast cancer cell colonization of bone, Vanderbilt Center for Bone Biology investigators have discovered.

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The studies, reported July 17 in PLoS Biology, demonstrate in mice that activation of the sympathetic nervous system -- the "fight-or-flight" response to stress -- primes the bone environment for breast cancer cell metastasis. The researchers were able to prevent breast cancer cell lesions in bone using propranolol, a cardiovascular medicine that inhibits sympathetic nervous system signals.

Metastasis -- the spread of cancer cells to distant organs, including bone -- is more likely to kill patients than a primary breast tumor, said Florent Elefteriou, Ph.D., director of the Vanderbilt Center for Bone Biology.

"Preventing metastasis is really the goal we want to achieve," he said.

Elefteriou and his colleagues knew from their previous studies that the sympathetic nervous system stimulated bone remodeling, and that it used some of the same signaling molecules that have been implicated in breast cancer metastasis to bone.

"We came to the hypothesis that sympathetic activation might remodel the bone environment and make it more favorable for cancer cells to metastasize there," Elefteriou said.

Evidence from the clinic supported this notion. Breast cancer patients who suffered from stress or depression following their primary treatment had shorter survival times. Both stress and depression activate the sympathetic nervous system.

To explore this possible link, the researchers studied cancer cell metastasis in mice. They followed fluorescently "tagged" human breast cancer cells that were injected into the mouse heart to model the stage of metastasis when breast cancer cells leave the primary site and move through the circulation.
They found that treating the mice with a drug that mimics sympathetic nervous system activation caused more cancer lesions in bone. Using physical restraint to stress the mice and activate the sympathetic nervous system also caused more cancer lesions in bone. Treating the restrained mice with propranolol, one of a family of blood pressure medicines called "beta-blockers," reduced the number of bone lesions.

The investigators demonstrated that sympathetic nervous system activation increases bone levels of a signaling molecule called RANKL, which is known to promote the formation of osteoclasts -- bone cells that break down bone tissue. RANKL has also been implicated in cell migration, and Elefteriou and colleagues were able to show that breast cancer cell migration to the bone depends on RANKL.
The findings suggest that beta-blockers or drugs that interfere with RANKL signaling, such as denosumab, may be useful in preventing breast cancer cell metastasis to bone. Propranolol and other beta-blockers are inexpensive, well characterized, and safe in most patients. They may be a good choice for long-term treatment if future studies in patients with breast cancer confirm their ability to block cancer cell metastasis to bone, Elefteriou said.

"If something as simple as a beta blocker could prevent cancer metastasis to bone, this would impact the treatment of millions of patients worldwide," he said.

Efforts to reduce stress and depression in patients with cancer may have unappreciated benefits in terms of metastasis prevention, he added

“For every life saved by breast cancer screening up to 10 women ‘have unnecessary treatment’.”

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Breast screening risks and benefits

Published on Saturday 14 July 2012 01:22

“For every life saved by breast cancer screening up to 10 women ‘have unnecessary treatment’,” the Daily Mail reported today.

The news is based on a study that looked at the impact of screening in Norway, and how often it led to “overdiagnosis”. Overdiagnosis is the phenomenon where women are correctly diagnosed but given treatment even though it will not improve their survival. This could be because the tumour identified would not have progressed to a clinical stage (would never have caused symptoms) or because the woman would have died from another cause, such as old age, before the cancer reached a clinical stage. Using nearly 20 years of data, researchers estimated that Norway’s screening programme had an overdiagnosis rate of 15–25%. This equated to 6 to 10 women being overdiagnosed for every 2,500 women invited for screening. In comparison, 20 in 2,500 women screened were diagnosed with breast cancer that was not overdiagnosed. Screening 2,500 women was estimated to prevent one death from breast cancer.

The issue of screening is of key interest to many people, and this study provides further data that could be relevant to the UK's current review of breast screening, which was announced in late 2011. This independent review will look at both screening in the UK and the type information that is given to women when deciding whether screening is right for them.

Where did the story come from?

The study was carried out by researchers from Harvard School of Public Health, Bringham and Women’s Hospital, and Harvard Medical School in the US, the Karolinska Institute in Sweden, and Oslo University Hospital Rikshospitalet in Norway. It was funded by the Norwegian Research Council and Frontier Science.

The study was published in the peer-reviewed medical journal Annals of Internal Medicine.
This story was widely reported, and most news sources provided accurate coverage of the research.

What kind of research was this?

There are several key considerations surrounding the use of routine breast cancer screening. These are primarily the need to ensure it can detect cancers and save lives, and that it does not cause unnecessary invasive treatments. In particular, there is currently a great deal of debate over the extent to which screening leads to overdiagnosis. This is where a woman is diagnosed and treated with no survival benefit, either because the tumour identified would not have progressed to a clinical stage or because the woman would have died from other causes before the cancer reached a clinical stage.
In late 2011, it was announced that the UK’s breast screening policy would be independently reviewed after some people questioned the overall benefit of the programme. The review will be performed by independent researchers but led by Professor Richards of the Department of Health and Harpal Kumar, chief executive at Cancer Research UK. The publication date for the review has not yet been announced.

This research compared the incidence of invasive breast cancer in women with and without screening. It estimated the percentage of overdiagnoses that might be attributed to mammography screening. It did this by comparing the number of cases of breast cancer found in screened women to the number of cases in matched unscreened women in Norway, where mammography screening was rolled out over a decade by geographical region. The researchers took into account the improvements in breast cancer care and changes in new breast cancer rates that have occurred over time.
The researchers stated that a randomised controlled trial with a lifelong follow-up of participants assigned to screening or a control group with no screening would be the ideal way to estimate the rate of overdiagnosis in research terms, but that due to practical reasons such a trial is unlikely ever to be performed. In this study, the researchers tried to take into account the many variables that affect the calculation of overdiagnosis, including changes in breast cancer incidence over time and “lead time”, the variation in length of time when a breast cancer can go undetected, between the groups.

What did the research involve?

The researchers retrieved details on the female population from the Statistics Norway national database, and information on all women with a first diagnosis of invasive breast cancer between January 1 1986 and December 31 2005 from the Cancer Registry of Norway.
The women were divided into four groups:

• current screening group – a group of women living in counties with screening between 1996 and 2005
• historical screening group – women living in these counties between 1986 and 1995, before screening
• current non-screening – women diagnosed in counties without screening between 1996 and 2005
• historical non-screening – women living in these counties between 1986 and 1995

By comparing current groups against historical groups, the researchers accounted for changes in breast cancer incidence over time. The researchers then used two different approaches to account for lead time, where an earlier diagnosis is made when women are younger in the screened group. The researchers also analysed the results by stage of cancer.

What were the basic results?

The researchers included 39,888 patients with invasive breast cancer diagnosed over twenty years, between 1986 and 2005. There were 18,708 cases in women aged between 50 and 69 years old, the age range invited for screening, and 7,793 of these women were diagnosed after the screening programme started, making them part of the “current screening group”.

Combining the two statistical approaches, the researchers calculated that the estimated rate of overdiagnosis due to the mammography screening programme was 15–25%. In other words, this proportion of women were diagnosed with breast cancer and potentially received treatment unnecessarily. They also estimated that over the 10 years of biennial mammography screening in Norway, for every 2,500 women invited for screening:

• 6 to 10 women were overdiagnosed
• 20 women were diagnosed with breast cancer that was not overdiagnosed
• 1 death from breast cancer was prevented

How did the researchers interpret the results?

The researchers concluded that “mammography screening entails a substantial amount of overdiagnosis”.

Conclusion

The benefits and risks of breast cancer screening have come under much scrutiny in recent years, not just from the press and the public, but also within the medical community. Many of the key arguments centre on the rates of legitimate treatment and treatment that would have otherwise proved unnecessary following screening. The issue is highly complex as it relies on finding high-quality data that can reliably indicate what would happen with the presence and absence of screening in a particular population.

This study looked at screened and unscreened segments of the Norwegian population to estimate the percentage of overdiagnoses of invasive breast cancer due to mammography screening. Overdiagnosis occurs where a woman is diagnosed and treated with no survival benefit even though the diagnosis is correct. This can be because the tumour identified would not have progressed to a clinical stage (i.e. it would never have caused symptoms) or because the woman would have died from other causes before the cancer reached a clinical stage.

The authors estimated the rate of overdiagnosis due to mammography screening as 15–25%. They calculated that for every 2,500 women invited for screening, 6 to 10 women are overdiagnosed, 20 women are diagnosed with breast cancer that is not overdiagnosed, and 1 death from breast cancer is prevented.

This study has some limitations. It was based on data taken from registries rather than gathered to specifically assess screening. Also, the researchers could not adjust for all factors that could have influenced the results, some of which might have offered alternative explanations for the results. In addition, another type of breast cancer called ductal carcinoma in situ was not studied.
However, despite its limitations, the study’s findings are similar to those in other recent publications, including some that have prompted a UK review of breast cancer screening and the type of information offered to women. This review is currently being conducted, although its expected completion date has not yet been announced.

Analysis by Bazian

Breast Cancer Clinical Trials Should Aim to Prevent Metastases.

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Breast Cancer Clinical Trials Should Aim to Prevent Metastases

By Patricia S. Steeg, PhD¹ |July 12, 2012

¹Chief, Women’s Cancers Section, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland
Interviewed by Anna Azvolinsky, PhD

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CancerNetwork speaks with Patricia S. Steeg, PhD, chief of the women’s cancers section at the Center for Cancer Research at the National Cancer Institute in Bethesda, Maryland. Dr. Steeg has recently written a perspective in the journal Nature calling for a shift in both the types of drugs that are developed for breast cancer and in the way clinical trials are designed and executed.
The breast cancer field has come a long way. The 10-year overall survival rate, according to a United Kingdom study, has increased from around 51% in the early 1980s to 77% in 2007. Tumors of patients diagnosed with breast cancer are now genetically and histologically characterized to better tailor treatment. We are able to identify a subset of high-risk disease patients who likely need more aggressive treatment, and novel and next-generation treatments to treat aggressive tumors are in late stages of development.

But patients whose breast cancer has progressed to metastatic disease are unlikely to be cured or even survive for very long. Dr. Steeg believes that rather than solely focusing on drugs that can shrink existing tumors, we need to develop and test drugs that will prevent not only existing tumor growth, but the spread of cancer, or metastasis.

CancerNetwork: Dr. Steeg, you propose that drug developers should start to focus on preventing metastatic disease rather than stopping the existing tumor from further growth, could you explain the rationale for this?

Dr. Steeg: Certainly. I am a molecular biologist, and I study tumor metastasis, which is the movement of tumor cells from the primary tumor to other sites in the body where they progressively grow. This is the major contributor to cancer patient death. We study metastasis in model systems—usually in mice. We inject mice with a tumor, and like in the human process, it forms a primary tumor, and then it spreads. And what I and many other metastasis researchers have noticed is that we have found a number of drugs that, when given to mice soon after the mice develop a primary tumor, will significantly prevent the development of metastases. Now, if we give that drug later, once the mouse has already developed metastases, it does not shrink them. It doesn’t obliterate them. But it will prevent them from developing. And so we see this opportunity to prevent metastases in people. And now we need a clinical trial system that will enable us to test this.

CancerNetwork: Are there examples of these types of drugs that have been developed for either

Dr. Steeg: Yes. The metastasis literature has a lot of examples of this kind of work. My own research focuses on brain metastasis in breast cancer—10, 20 years ago, breast cancer rarely went to the brain, and when it did, the patient was usually terminally ill and was given some medication for the symptoms. But now, with better systemic therapy, or therapy that goes through your body, a number of women with metastatic breast cancer are getting their first-line of chemotherapy and are now relapsing with brain metastases. This is particularly devastating because we don’t have very good treatments for them and they cause a lot of neurocognitive consequences. In other words they impair mental function, they can cause seizures, etc.

So my lab, again, using mouse models, has developed models for brain metastasis of brain cancer, and we have now published three or four drugs—not in common use in breast cancer—that in the model will meaningfully prevent brain metastasis. One of these is vorinostat. It is a histone deacetylase inhibitor. It is an FDA-approved drug for a different kind of cancer. One of them is pazopanib, also an FDA-approved drug for a different kind of cancer. But our models propose that these drugs may be effective in preventing brain metastasis.

CancerNetwork: Could you briefly summarize your viewpoint about clinical trial design? How are our current clinical trials designed and what do you propose that the field should be doing that it is currently not doing?

Dr. Steeg: This is actually a very simple concept. When a drug is developed today, and this is my understanding as a PhD, it is first tested in phase I clinical trials, and this is a dosing and toxicity study largely. So the dose is escalated. You give more and more of the drug to patients and are looking for side effects because you are looking for a safe dose that may have efficacy. Once you find that dose in phase I studies, you go to phase II studies where you are now looking for a hint of efficacy that this drug actually works. And the main endpoint in these trials is shrinkage of tumors.
So these are patients who have had multiple lines of therapy and already have metastases. And what they are asking this drug to do is to shrink those metastases, and that is exactly what I said these experiment drugs won’t do in our mouse models. So, for a drug to move on from phase II to phase III trials the drug either has to shrink those metastases by itself or it has to synergize with the current chemotherapy to make the chemotherapy shrink those tumors even better. The drug then goes to phase III trials, which is the large trial against the standard of care—so will this drug, alone, or with the standard of care, improve patient outcomes? And then it goes for approval to the FDA.
After that, there can be what are called adjuvant trials. Now these are metastasis prevention trials. These are when the drug is finally given to women who don’t have metastases already. They usually have either large primary tumors or primary tumor cells that have already moved into the lymph nodes. And we are then asking these drugs to prevent metastasis. However, as you can see, this is a very long process and the only drugs that will get there are the ones that shrunk metastatic tumors back in the phase II and III trials.

So what I am proposing is that we need a detour to test for metastasis prevention. We need to get more drugs into metastasis prevention trials. We need smaller trials that we can conduct more often and start getting some more information. And what I have proposed is really quite simple. And that is, after the phase II setting—so we know that the drug is not too toxic, and we have a dose and we have a hint of efficacy and we know what we can combine this drug with in terms of the normal chemotherapy that the patients are given—what I have proposed are one of two types of randomized, metastasis-prevention phase II trials. And it is a pretty simple concept. For instance, we could take patients who have come in for very early chemotherapy, and the chemotherapy hasn’t worked so they will be very high risk for full-blown metastatic disease. They would get standard chemotherapy, and then be randomized to either placebo or this metastasis preventive, this compound we think will prevent metastasis. And what would be the endpoint? It would not be shrinkage of a lesion—there are no lesions. It would be time to the development of a first metastasis.

A second flavor of this trial would be those patients who have limited metastases already and they have been treated with whatever the standard treatment is. These patients are doing OK, but they are at extraordinary high risk for additional metastasis. Again, they would get standard of care and be randomized to vehicle or the metastasis preventive. And here, the endpoint would not be shrinkage of their metastatic lesion. It would be time to development of new metastases. I think if we try these trials we could get a signal that this drug may have efficacy in preventing metastasis, and that could lead to new consideration of these drugs.

CancerNetwork: Sure. So the types of trials that you propose, these have been done with tamoxifen(Drug information on tamoxifen) and trastuzumab(Drug information on trastuzumab) (Herceptin), at least for breast cancer. Trastuzumab was first developed to shrink tumors in the metastatic setting, so is there something that is unique about tamoxifen and trastuzumab, and can we further develop what you described earlier to prevent metastasis?

Dr. Steeg: Well, we were really lucky with trastuzumab and tamoxifen because those drugs have two abilities. One, they shrink tumors and that is what got them through phase I, II, and III trials. And two, they prevent metastases and that is where they were beneficial in the adjuvant setting. So these drugs do both. But unfortunately, there are not that many drugs that will do both functions—shrink tumors and prevent metastasis. If you think about metastasis, you are talking about the ability of the cell to move, not divide, and so you can imagine that there would be drugs that can prevent a cell from moving and invading through tissue to get to where it is going that necessarily wouldn’t have a toxic effect or growth inhibitory effect on those cells. And so my point is that there are probably a large number of drugs out there with these capabilities, but we are losing them in the current clinical trial scenario.

CancerNetwork: I see. I think one of the troubles with testing efficacy of a drug that could potentially prevent metastasis is that it may be difficult to predict which patients and which tumors would spread if they were not exposed to therapy. So initially these trials will have to be pursued specifically in patients that are high risk, is that right?

Dr. Steeg: I completely agree. For breast cancer, we know enough about the molecular biology of progression of breast cancer so we can predict groups of patients who are at very high risk for metastatic progression within what I would call a few years—2 to 3 years. One of those groups would be those patients who come in with very large primary tumors, that just grew too fast and they get up-front chemotherapy, they don’t go straight to surgery—this is called neoadjuvant chemotherapy. So they get up-front chemotherapy to shrink that tumor down. There are cases where that up-front chemotherapy shrinks that tumor away to nothing and these patients are associated with very good outcomes. But unfortunately, there are a lot of cases where that up-front chemotherapy does not significantly shrink that tumor and the patient goes to surgery. And those patients are at very high risk in a couple of years for metastatic disease. Now the FDA just issued guidance on doing clinical trials in that neoadjuvant setting but I think a perfect opportunity would be for those patients where that up-front chemotherapy didn’t have a profound effect and these women remain at very high risk. This would be this kind of population that would be perfect for these metastasis prevention trials. There are other types of patients that could qualify. And, you know, in other types of cancers this concept could also apply and I think you could identify these patients at high risk.

CancerNetwork: And so the last question. We know that microscopic metastases likely exist before we are able to detect them but we do not yet have the developed tools to detect these yet. Do you think that this needs to happen before this shift to test prevention of metastases drugs comes about?

Dr. Steeg: This is a fascinating question, but no I don’t. In the neoadjuvant population, we can now identify these patients that are at very high risk. So for instance, in breast cancer: the neoadjuvant population where the tumor didn’t shrink; women who go to surgery and have a large number of lymph nodes with tumor in them, so that tumor has already spread past the primary site and has gotten at least that far; women with limited metastatic disease. And I think we are making progress in finding smaller and smaller deposits of tumors which is going to open its own Pandora’s box into "When do we treat?" but I think we can do these trials now with the tools that we have.

CancerNetwork: Thank you so much for joining us, Dr. Steeg.

Dr. Steeg: It was a pleasure.

Top Ten [Excuses] for a Sabbatical from Blogging About Cancer

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10.  Life gets in the way...that quirky [mis]fortune of having so many other time-consuming, energy-sucking, mundane LIFE-activities that at times it is a challenge to walk down daily to the mailbox, let alone log into Blogger Dashboard.

9.  Anger to the point of Void...being so overwhelmed by the daily onslaught of "cancer" whether it is the incessant commercials and billboards, the parade of promises, the seemingly daily diagnosis - or death - of someone as a result of cancer (I have to stop reading obits). An emotional void surrounds and drowns me till I feel like I am a middle-schooler caught in perpetual swirly-nightmare.

8.  Endearing Caustic Rachel...her passing chilled and sobered me to the inanity of all that is cancer; driving home the reality that no matter how loudly we YELL into the rabbit hole women are being diagnosed with breast cancer at a rate of over 200,000 per year, and dying at a rate of nearly 40,000 per year -- still.

7.  Lovely Hannah...seeing a vibrant, intelligent and amazing teenager fall into the abyss that is cancer has wrested words from my fingers and the air from my soul. Hannah got an all-clear in her lymphatic system only to be stricken down with meningitis as an after-gift of chemo. The roller coaster of cancer-world. Just when your stomach inches back from your pelvis where it was unceremoniously lodged during a drop with 5.4 g-force, as the ride slows down on the straight-away, the momentum unexpectedly picks up again and thrusts you sideways on an unexpected bank and your breath gets knocked out of you, along with your equilibrium.

 6.  Boredom...I am tired of being a person with MBC; tired of writing about it; tired of thinking about it; and I am sure people must be tired of reading my tone-deaf cancer-operetta. After all, how many ways can you spell C-A-N-C-E-R?

5.  Children ...totally privileged to be included (and not just with the checkbook) in the busy lives of my two eldest daughters as they launch themselves into full-blown adulthood, well almost; and the daily (and nightly - aka sleepless in Phoenix) schedule and needs of my emerging tween.

4. It's always something...same ol' daily grind. For every step I take toward slowing down and gaining the upper hand on the onslaught of stress, I am pulled back two steps with another "need" or "crisis." The adage is that the universe only lays upon us that which we can handle. Ah, the universe's generosity can be quite insufferable at times. Check out:

Right-Wing Judges Seek to Close the Courthouse Doors to Public Interest Claims

http://www.huffingtonpost.com/bennet-kelley/rightwing-judges-seek-to-_b_1625309.html
to see how our lives can get turned upside down without the help of a cancer diagnosis.

3.  Fifty Shades of Indulgence...oh yeah, I did. All three of this insipid rehash of the trite Beauty and the Beast story. Although, this time the beast does not swing from the Empire State Building swatting at planes, but rather he perches himself above the skyline of Seattle and swats at psychologically vacuous brunettes with braided leather floggers. (By the end of the second installment I wanted to b*tch slap Ana's inner goddess...oh!)

2.  I am just too tired...whether it is [finally] the onset of peri-menopause; mid-life crisis [again? I had a baby the last time in went into mid-life crisis mode!]; or a combo of ##s 3-10; I find that I am just cranium-tired (as opposed to bone-tired) all the time. Thank the goddess for coffee and a nice pinot noir (grenache is not bad either!)

.......and the #1 reason to take a blogging sabbatical....wait for it!

1.   Making a concerted effort not to have the reality of living within the shadow of cancer define me
                                                 ...the rest is all commentary!

Insurance (??), Anniversaries & Cosmos (Not Necessarily in that Order)

******

Mutual of Omaha Insurance Company sent me a solicitation in yesterday's (July 7, 2012) post: Supplemental Cancer Protection. The advert proudly announces that it PAYS for, in what looks to be a thoughtful descending order of consideration,







...screening and/or procedures
...hospital room and ICU
...drug and medication
...radiation, chemo and immunotherapy
...surgery
...doctor visits
...follow up doctor visits
...anesthesia (okay, this should have been up there with the surgery)
...blood and blood plasma benefits
...hospice care (they are hoping for this benefit before having to pay for the following)
...ambulance services
...x-rays and labs
...home health care
...skilled nursing facility or rehab ...all for the low monthly rate of $9.07.

The hook in this solicitation is: DON'T WAIT over 1.5 million new cancer cases are expected to be diagnosed in 2010 alone* (*American Cancer Society). Um...guess Mutual of OH-maha is using up past years' surplus.  According to the American Cancer Society Facts & Figures for 2012, 1,638,910 new cancer diagnosis are anticipated in the U.S. (and yes...that is over 1.5M) And, it is expected that the U.S. will see 577,190 cancer-related deaths by year's end. 39,510 of these are expected to be due to breast cancer.

The catch?  You can request coverage, even if you have had cancer...as long as it been more than five years.

I guess I am on the cancer junk mail solicitation list. Luck me.

I won't be sending in my request, however. Not just because I have a modicum of good sense and do not fall prey to undesired solicitations. But, because I wouldn't qualify. I don't meet the 5-year prerequisite.

Three years ago, TODAY, I received the diagnosis of stage III-B invasive lobular carcinoma. One year (actually 362 days ago) TODAY, I received the re diagnosis of stage IV metastatic breast cancer. Despite these ominous edicts, I am still here. Why?  or rather...WHY NOT?

Could be because I did not venture down the oft-traveled rabbit hole of conventional treatment?

Could be because I did explore alternative therapies and supplements that quite possibly worked?

Could be because I am undeniably one tenacious b*tch?

Could be because I have an overblown sense of my own importance, so much so that I feel my family and work (and avocations) cannot get on without me?

Could be that the course and manifestation of cancer cells is still such a conundrum to the medical arts, that without the predictability of imposed variables (e.g. radiation, chemotherapy, Tamoxifen, etc) the course of cancer cannot be predicted?

Could be I have an overdeveloped grasp on denial?

Whatever the reason or rationale, I am here. Enjoying (through gritted teeth) the onset of grey hairs; discovering new "character lines" in my caricature of a 50-something punim; wondering at the capriciousness of my weight and waistline; and taking each day as a new challenge. And, giddy as a toddler that I am here to b*tch about such shallow and pedestrian concerns, as well as everything else.

Bring on the shallow and mix up the Cosmos ... and HAPPY ANNIVERSARY to batsh*t b*tchy me!