Recurrance Free with DIM or Alternatives

Anonymous

Recurrance Free with DIM or Alternatives

Anonymous

I am looking to hear from those who have remained breast cancer who went off hormone therapy or never took it.  I have been on Tamoxifen for the past 14 months and was take off due to bad side effects.  Now I am wondering if I should go back on it, try an AI with Lupron or play the numbers.  I had ILC- ER+, PR+ with an Oncotype score of 12 so my chance of recurrences is about 15% without hormone therapy.  I have been reading more about DIM as a Tamoxifen alternative.  I have also read that ILC might be resistant to Tamoxifen.  While I understand that this is a very personal decision, I would just love to hear from those who have remained recurrance free without hormone therapy.  Thank you, your feedback is appreciated.  

Springtime

Hi Nancy,

I'm interested in this thread. But you say, you've heard, " I have also read that Tamoxifen might be resistant to Tamoxifen. "

If you meant DIM was resistant to Tam, I'd be interested in that as I do both!!! Can you point me to where you found that?

Anonymous

I meant ILC might be resistant to Tamoxifen.  I read it on the ILC thread.  Sorry for the confusion.

Springtime

OH, I see, I had IDC. Good grief though! I had not heard that. Did you see there was a DIM thread? Just FYI... I just noticed it...

kfinnigan

I had ILC and am on Tamoxifen!  YIKES

Anonymous

Thank you, I saw there is a DIM thread, but it did not address recurrence free.  Maybe natural girls would be a better choice for me to post this topic. 

anondenet

15 years recurrence free. ER and PR positive.

No Tamox tho I considered it because I thought back then that the doctors knew how to read the studies. Ha!

If you look up the "absolute risk" stats on Tamox they are feeble. And if you recur on Tamox you are screwed. Tamox creates a less treatable cancer.

trigeek

ok butting in anomdenet.. do you think Tamox creates a less treatable cancer.. or maybe..

Tamox cannot prevent  the less treatable cancer .. but prevents lite cancer(ok I am sounding funny here) .. but you get the picture right, it basically is preventing some c ?

I am on femara.. btw

Alyad

There has been a lot of discussion on a thread called natural girls - lots of info on DIM there

anondenet

Trigeek,

Comparing all women who recur, those taking Tamox have poorer outcome when they recur than those who don't take Tamox. Tamox must damage the receptors or something. You roll the dice with Tamox for very teeny benefit, if any, and it can shorten your survival time if you recur on it.

There is a lot of information to consider here and I don't think anybody can size up the enormity of the misinformation out there in a few months. Even in this group, you see the decision-making comes from the accumulation of a lot of information and people trading book sources and videos.

Also, we have to ask instead of blocking this enzyme or that receptor-- in essence-- making our selves sick, instead could we try to prevent recurrence by normalizing our bodies by addressing deficiencies and detoxing junk?

fairy49

The stats on tamox are incorrect because they lumped in the ladies with DCIS into the stats, this scewed the numbers in favor of tamox.........

vivre

I read the same thing that Anom said, but can't remember where, that cancer is harder to treat after tamox. Plus there is th clotting and fibroid issues, which do not come up with other alternatives.

anondenet

Fairy,

I remember when Tamox first came out, the Brits wouldn't use it and they thought the Americans were nuts because there was so little benefit for such high risk. Your reading is fresher than mine. I knew there was some cooking of the books but I couldn't remember what.

There was cooking the books on Arimidex too. A week after they released  the results, they had to come clean on exaggerating benefit. And it still hasn't shown long time survival.

Welcome to the land of guinea pigs.

<

fairy49

Anom, I am from London, but live here in the states, I think there are a lots of things we do here that raise eyebrows in Europe!   I THOUGHT I had saved the article on the messed up stats issue, but can't find it, I am now on a mission to find it! I will post it when I do!

 Anom, I didn't know you have been recurrance free for 15 years, fan flippin tastic!!!

L

ox

vivre

Okay, this may be a long post, but people seem to ignore links so I am hoping others will read it as it does address the lack of long term benefits with tamox:

Myomin and Angiostop: A Novel Combination Therapy
For Breast and Prostate Cancer

By: Tsu-Tsair Chi, NMD, PhD

 

INTRODUCTION

Cancer is a very invasive disease, not just physically but emotionally and financially as well. There are approximately 10.1 million Americans with a history of cancer and about 1.4 million more cancer cases are expected to be diagnosed this year¹. While these figures seem astronomical, cancer mortality rates have been steadily decreasing in the last two decades, mainly due to advances in diagnosis and treatment methods.

Two of the most common causes of cancer deaths are breast and prostate cancer. In 2006, about 214,640 new breast cancer cases (both men and women) are expected while 234,460 new prostate cancer cases are estimated¹. The prognosis of those who suffer from these diseases depends largely on their treatment method. Traditionally, chemotherapy is the first treatment of choice by doctors. But recently, two types of therapy have shown major progress in increasing survival in cancer patients: aromatase inhibitors and angiogenesis or receptor tyrosine kinase (RTK) inhibitors. This combination is particularly relevant for breast and prostate cancer, both of which are estrogen-related.

Aromatase expression promotes estrogen production, especially at the site of estrogen-responsive tumors such as in breast, ovarian^2,3 and prostate cancer^4,5. Aromatase inhibitors seek to block the aromatase enzyme from converting androgens into estrogen. This will diminish estrogen production, eventually leading to tumor suppression and apoptosis.

Angiogenesis and RTK inhibitors work by blocking certain proteins overexpressed by cancer cells and which promote tumor growth. They selectively attack cancer cells and leave healthy cells unharmed. These types of drugs have shown favorable results in many types of cancer, most notably in solid tumors such as breast cancer.

Two natural supplements show a very promising future as natural alternatives to aromatase and angiogenesis/RTK inhibitor drugs in the market today. Myomin^©, a combination of herbs, has been shown to inhibit aromatase in vitro and in vivo. Furthermore, it has been used effectively for cysts and fibroids in humans⁶. A sea cucumber extract, Angiostop^©, has exhibited in vitro and in vivo anti-angiogenic properties^7-11.

 

Angiostop^© and Myomin^© combination for breast and prostate cancer

 

Myomin^© inhibits aromatase

The aromatase enzyme contributes to the production of estrogen through two pathways: androstenedione to estrone and testosterone to estradiol (Figure 1). By inhibiting these two pathways, estrone and estradiol (both carcinogenic forms of estrogen) levels are reduced and the production of estriol, the good estrogen, is continued. This is especially important in men because, as they get older, an increasing amount of testosterone is being converted into estradiol, leading to problems such as prostate cancer and decreased libido. Those who are using progesterone supplements should also be aware that the hormone can eventually be synthesized into estradiol and estrone (Figure 1) and create problems. For this reason, an aromatase inhibitor should be taken with the progesterone to prevent an increase in estrogen from progesterone use.

Figure 1. Biochemical pathways of reproductive hormones

Myomin^© is a combination of different herbs shown to inhibit the aromatase enzyme and consequently reduce estrogen levels. In rat endometrial and ovarian tissues, Myomin^© was shown to reduce aromatase expression tremendously after 28 days of administration⁶.

In one study, the estrogen-reducing action of Myomin^© was evident, this time on postmenopausal women with fibroids and cysts. Sixty women were involved with an average estradiol (the most potent form of estrogen) level of 74.52 pg/ml. After 10 days on Myomin^©, their average estradiol level reduced to 38.84 pg/ml. The size of the fibroids/cysts, as well as the pain associated with them, was also diminished⁶.

Another study illustrates that Myomin^© is effective in cysts, another estrogen-mediated condition. This study involved 85 pre- and postmenopausal women with ovarian cysts. After 1 to 3 courses of Myomin, the cysts and symptoms of 15 patients completely cleared with no recurrence 3 months after the study while 34 women experienced a 50% reduction in the size of the cyst⁶.

Inhibiting aromatase and reducing estrogen levels do have a significant effect on estrogen-mediated growths, as illustrated in the following study. Fifty cases of fibrocystic breasts (45 women and 5 men) were treated with Myomin^© for one month. Sixty five percent of the women were under 35 years old. In 14 cases, the growth cleared completely while the fibrocystic breast reduced by 50% in 16 cases. Of the five men in the study, the cyst cleared completely in 3 cases⁶.

 

Angiostop^© inhibits angiogenesis and RTK

Angiostop^© contains the active ingredient Philinopside A, which has been shown through various studies to inhibit four different RTKs: vascular endothelial growth factor receptor (VEGFR), epidermal growth factor receptor (EGFR), platelet-derived growth factor receptor (PDGFR) and fibroblast growth factor receptor (FGFR)⁷. The number of RTKs it targets is significant because angiogenesis, or new blood vessel formation, is a complex process that likely involves multiple RTK signaling pathways. Inhibiting more than one RTK may prove to be more effective in blocking angiogenesis and other processes involved with cancer (Figure 2).

 

Figure 2. Angiostop^© mechanism

The VEGFR is of particular importance because VEGF is specifically associated with vascularity and is highly expressed in solid tumors such as breast and prostate cancer. Results of clinical trials indicate that addition of a VEGFR inhibitor to standard cancer therapy produces better survival rates than standard cancer therapy alone. Even when given by itself, a VEGFR inhibitor produces better results on patients with no prior treatment¹².

In studies, Angiostop^© was shown to inhibit VEGFR with an IC₅₀ of 2.6mM, comparable to that of SU5416 (semaxanib), a selective VEGFR inhibitor drug with an IC₅₀ of 2.9mM⁸. This means that angiogenesis can be effectively stopped, cutting off nutrient and blood supply to the tumor and eventually causing it to die.

Angiostop^©'s effect was evident in the case of a 42-year-old woman from Florida who tested positive on a mammogram and ultrasound (Figure 3a). Through thermal imaging performed by Medi-Therm Imaging, angiogenesis evidently increased around the tumors from April to June, 2005 (Figure 3b), during which time she did not undergo any type of treatment. Beginning June 28, 2005, she took Angiostop^© and the result has been remarkable. It appears that angiogenesis has significantly receded after two months of taking Angiostop^© (Figure 3c).

Figure 3a. April 11, 2005
Dark areas signify angiogenesis.

 

 

Figure 3b. June 28, 2005
Without treatment, angiogenesis apparently increased around the area.

 

Figure 3c. August 24, 2005
Angiogenesis has receded after 2 months on Angiostop.

 

 

Further studies support Angiostop^©'s anti-angiogenesis activity in vivo. Two mouse models were employed: one with tumors induced by implanting sarcoma 180 cells, the other with tumors induced by hepatoma 22 cells. Administration of Angiostop^© for 7 days at concentrations of 2, 3 and 4 mg/kg inhibited sarcoma 180 tumor growth by 28.2, 55.6, and 60.7%, respectively. In the other group, administration of 1, 2, and 3 mg/kg Angiostop^© for 7 days suppressed hepatoma 22 tumor growth by 20.6, 46.1 and 59.4%, respectively⁸.

Inhibiting angiogenesis alone can be effective in some cases of cancer. But for breast and prostate cancer, addition of an aromatase inhibitor may prove to be a more effective regimen because many aspects of the cancer are being targeted at the same time. First, the formation of blood vessels that feed the tumor is prevented. Second, by precluding the action of aromatase, estrogen production is greatly diminished, helping prevent the proliferation of tumor cells.

 

Discussion

Treatment with either an angiogenesis or an aromatase inhibitor by itself certainly has merit. But combining both therapies, particularly for estrogen-responsive diseases like breast and prostate cancer, has such tremendous potential success that it should be considered a standard combination of treatment.

Reiterating what was mentioned in an earlier section, this combination of therapies deals with many facets of breast and prostate cancer. Obviously, the growth of the tumor should be suppressed to prevent it from getting worse and spreading to other tissues. An angiogenesis inhibitor like Angiostop^© will manage that issue. By inhibiting the VEGFR, it blocks the RTK directly associated with new blood vessel formation and accordingly cuts off the nutrient and blood supply to the tumor. But because Angiostop^© also inhibits three other RTKs, it may produce a more complete and long-term anti-angiogenic effect than other therapies that target only one RTK.

In the last decade, several RTK inhibitor drugs have been approved for treatment of different types of cancer. Among these are Avastin^© (bevacizumab), a VEGFR inhibitor for colorectal cancer; Gleevec^© (imatinib), which inhibits PDGFR and Bcr-Abl for leukemia and gastrointestinal stromal tumor (GIST); Tarceva^© (erlotinib), an EGFR inhibitor for non small cell lung carcinoma and pancreatic cancer; Herceptin^© (trastuzumab), an EGFR and HER2 inhibitor for breast cancer; and Sutent^© (sunitinib), a multi-RTK inhibitor for GIST and advanced kidney cancer.

It is apparent that some types of cancer express different RTKs. For example, colorectal cancer expresses both VEGFR and EGFR. Breast cancer also expresses EGFR, HER2 and possibly VEGFR. Therefore, inhibiting one RTK may not be enough to completely suppress the tumor. A wide-range RTK inhibitor like Angiostop^© is more likely to produce better results in blocking angiogenesis and preventing invasion and metastasis.

Aromatase inhibition is another aspect targeted by the combinational therapy. A major portion of breast cancer cases are estrogen-responsive and will therefore benefit from treatments that reduce estrogen production: treatments such as aromatase inhibitors. In fact, aromatase inhibitors are considered "critically important" for improving breast cancer outcomes¹³. Although aromatase activity has been detected in malignant prostate cancer tissues, the use of aromatase inhibitors as standard prostate cancer treatment is not yet considered the norm. But they are currently being explored as potential therapy because of emerging research linking aromatase expression, estrogen dominance and prostate cancer.

In recent years, aromatase inhibitors have been more widely used than other hormone-related therapy for breast cancer. Antagonizing the effect of estrogen used to be the main objective of these therapies rather than lowering estrogen levels. Most notable among drugs with this mechanism is Tamoxifen^©. Latest studies, however, have shown that long-term use of Tamoxifen^© provides no apparent benefits. Aromatase inhibitors, on the other hand, produce better long-term effects and improve quality of life¹³. Arimidex^© (anastrozole), Aromasin^© (exemestane) and Femara^© (letrozole) are just some of the aromatase inhibitor drugs in the market today. The drawback to these drugs, however, is that they are indicated for postmenopausal women only. Myomin^©, on the other hand, can be used by men as well as pre- and postmenopausal women. In the study on fibrocystic breasts, a majority of the women in the study were premenopausal, demonstrating that Myomin^© is not limited to postmenopausal women. It was also effective in three of the five men in the study. Furthermore, it was shown to be effective on cysts in both pre- and postmenopausal women.

Recently, researchers have found that estrogen increased VEGF levels in normal breast tissue, promoting angiogenesis¹⁴. Further investigation is certainly warranted to establish the direct link between estradiol and VEGF. But if this is indeed true, then the use of an angiogenesis and aromatase inhibitor is even more imperative to achieve more comprehensive and effective results.

fairy49

great info vivre, I checked out the Myomin, based on the info it says 2-3 capsules 2-3 times daily, would you/one also take DIM?

Anonymous

Great Information.  What exactly is "menopausal"?  I have heard of pre and post menopausal, but am confused about just menopausal.  Thank you.

ibeejojo

I considered doing Myomin and took the ingredient list to my acupuncturist/chinese med guy and there was one or two ingredients that he could not document.  People please understand that cancer is a big business even in the alternative world.  I'm not taking anything that's not regulated or that's questionable.  You can do more by cutting the crap out of your diet than taking one of these pills.  Read the "Anti Estrogenic Diet". 

Nancy...have your doc do a blood test to determine your status.  Pre is before...meopausal is during and post is after.  Your homones blood tests will let you know where your at....you should be menopausal for at least a year...no menses (naturally) before they consider you for post status.  Chemo and hormonal therapy screws all that up of course.

I do natural estrogen reducing things like passion flower, chamomile, heal all (prunella vulgaris), indole3, IP6/Inositol and D3.  Exercise and diet are key.......4 yr survivor... ILC....no chemo...no nodes.....some hormonals.....lots of alternatives.....JO

vivre

Fairy-I decided to just try the myomin alone for now. That way, when I test again, I will be sure which one I am testing results for.

Nancy, you are right about the menopause confusion. We really should be only using the terms perimenopause(still having periods) and menopause(no periods for at least a year). But I think we tend to add the post and pre because most people have no idea which is which.LOL

JO-You are right that there is no magic pill. We have to be very conscious of our diets, exercise and other supplements. I took I3C and got mixed results so that is why my compounding pharmacist recommended I try the myomin instead. I buy it from him so I am more confindent that it is purer than something over the internet. He is very knowlegeable on lots of alternatives. And congrats on the 4 years. You give us confidence that we are on the right path.