Oncologists doing more harm than good

Dr. Weeks’ Comment:   As much as I enjoy being right and at least under my breath saying “I told you so”, it is not so fun when people have to die because of ignorance and refusal on the part of the responsible professionals to listen to reason.  For the past 6 years, I have been lecturing around the world teaching doctors three revolutionary concepts:

  1. the standard of care for cancer (chemotherapy and radiation) makes your cancer worse
  2. the cancer cell we should be targeting is not the cancer TUMOR cell but the cancer STEM cell
  3. cancer spreads by inflammation and the optimal treatment for cancer is safe and effective anti-inflammatory foods (especially seeds) as well as immune enhancement (onco-immunology)

Still today, overly trusting and overly naive cancer patients, like innocent sheep, are being led to the slaughter despite the scientific evidence that the standard of care for cancer treatment is more dangerous than cancer itself.

For a summary of Dr. Weeks’ three-fold approach to helping people get past cancer – Corrective Cancer Care – see these two lectures:

The Truth about Cancer – Strike the Root 

The Revolution in Cancer Care 

This article below, published two days ago should sound the death knell for standard of care cancer treatments and encourage people to take anti-inflammatory agents and immune enhancing agents. While they promote a synthetic, patented drug Rebastinib – an inhibitor of multiple tyrosine kinases which is also an inhibitor of TMEM) please, dear reader, know that safe and effective anti-inflammatory foods are the way to start:  eat the anti-inflammatory diet and caloric restricted ketogenic diet.  

Neoadjuvant chemotherapy induces breast cancer metastasis through a TMEM-mediated mechanism

Science Translational Medicine  05 Jul 2017:  Vol. 9, Issue 397, eaan0026
DOI: 10.1126/scitranslmed.aan0026

Closing the door to cancer cells

Breast cancer is one of the most common tumor types, and metastasis greatly increases the risk of death from this disease. By studying the process of intravasation or entry of cells into the vasculature, Karagiannis et al. discovered that, in addition to killing tumor cells, chemotherapy treatment can also increase intravasation. Groups of cells collectively known as tumor microenvironment of metastasis (TMEM) can serve as gateways for tumor cells entering the vasculature, and the authors discovered that several types of chemotherapy can increase the amounts of TMEM complexes and circulating tumor cells in the bloodstream. The researchers also determined that a drug called rebastinib can interfere with TMEM activity and help overcome the increased risk of cancer cell dissemination.


Breast cancer cells disseminate through TIE2/MENACalc/MENAINV-dependent cancer cell intravasation sites, called tumor microenvironment of metastasis (TMEM), which are clinically validated as prognostic markers of metastasis in breast cancer patients. Using fixed tissue and intravital imaging of a PyMT murine model and patient-derived xenografts, we show that chemotherapy increases the density and activity of TMEM sites and Mena expression and promotes distant metastasis. Moreover, in the residual breast cancers of patients treated with neoadjuvant paclitaxel after doxorubicin plus cyclophosphamide, TMEM score and its mechanistically connected MENAINV isoform expression pattern were both increased, suggesting that chemotherapy, despite decreasing tumor size, increases the risk of metastatic dissemination. Chemotherapy-induced TMEM activity and cancer cell dissemination were reversed by either administration of the TIE2 inhibitor rebastinib or knockdown of the MENA gene. Our results indicate that TMEM score increases and MENA isoform expression pattern changes with chemotherapy and can be used in predicting prometastatic changes in response to chemotherapy. Furthermore, inhibitors of TMEM function may improve clinical benefits of chemotherapy in the neoadjuvant setting or in metastatic disease.

This is an article distributed under the terms of the Science Journals Default License.


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