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Following on the heels of recent revelations that x-ray mammography may be contributing to an epidemic of future radiation-induced breast cancers, in a new article titled, "Radiation Treatment Generates Therapy Resistant Cancer Stem Cells From Aggressive Breast Cancer Cells," published in the journal Cancer July 1st, 2012, researchers from the Department of Radiation Oncology at the UCLA Jonsson Comprehensive Cancer Center report that radiation treatment actually drives breast cancer cells into greater malignancy.

The researchers found that even when radiation kills half of the tumor cells treated, the surviving cells which are resistant to treatment, known as induced breast cancer stem cells (iBCSCs), were up to 30 times more likely to form tumors than the nonirradiated breast cancer cells. In other words, the radiation treatment regresses the total population of cancer cells, generating the false appearance that the treatment is working, but actually increases the ratio of highly malignant to benign cells within that tumor, eventually leading to the iatrogenic (treatment-induced) death of the patient.

Last month, a related study published in the journal Stem Cells titled, "Radiation-induced reprogramming of breast cells," found that ionizing radiation reprogrammed less malignant (more differentiated) breast cancer cells into iBCSCs, helping to explain why conventional treatment actually enriches the tumor population with higher levels of treatment-resistant cells. [i]

A growing body of research now indicts conventional cancer treatment with chemotherapy and radiation as a major contributing cause of cancer patient mortality. The primary reason for this is the fact that cancer stem cells, which are almost exclusively resistant to conventional treatment, are not being targeted, but to the contrary, are encouraged to thrive when exposed to chemotherapy and radiotherapy.

In order to understand how conventional treatment drives the cancer into greater malignancy, we must first understand what cancer is....

What Are Cancer Stem Cells, And Why Are They Resistant To Treatment?

Tumors are actually highly organized assemblages of cells, which are surprisingly well-coordinated for cells that are supposed to be the result of strictly random mutation. They are capable of building their own blood supply (angiogenesis), are able to defend themselves by silencing cancer-suppression genes, secreting corrosive enzymes to move freely throughout the body, alter their metabolism to live in low oxygen and acidic environments, and know how to remove their own surface-receptor proteins to escape detection by white blood cells. In a previous article titled "Is Cancer An Ancient Survival Program Unmasked?" we delved deeper into this emerging view of cancer as an evolutionary throw-back and not a byproduct of strictly random mutation.

Because tumors are not simply the result of one or more mutated cells "going rogue" and producing exact clones of itself (multi-mutational and clonal hypotheses), but are a diverse group of cells having radically different phenotypal characteristics, chemotherapy and radiation will affect each cell type differently.

Tumors are composed of a wide range of cells, many of which are entirely benign.

The most deadly cell type within a tumor or blood cancer, known as cancer stem cells (CSCs), has the ability to give rise to all the cell types found within that cancer.

They are capable of dividing by mitosis to form either two stem cells (increasing the size of the stem population), or one daughter cell that goes on to differentiate into a variety of cell types, and one daughter cell that retains stem-cell properties.

This means CSCs are tumorigenic (tumor-forming) and should be the primary target of cancer treatment because they are capable of both initiating and sustaining cancer. They are also increasingly recognized to be the cause of relapse and metastasis following conventional treatment.

CSCs are exceptionally resistant to conventional treatment for the following reasons

CSCs account for less than 1 in 10,000 cells within a particular cancer, making them difficult to destroy without destroying the vast majority of other cells comprising the tumor.[ii]

CSCs are slow to replicate, making them less likely to be destroyed by chemotherapy and radiation treatments that target cells which are more rapidly dividing.

Conventional chemotherapies target differentiated and differentiating cells, which form the bulk of the tumor, but these are unable to generate new cells like the CSCs which are undifferentiated.

The existence of CSCs explains why conventional cancer treatment has completely missed the boat when it comes to targeting the root cause of tumors. One reason for this is because existing cancer treatments have mostly been developed in animal models where the goal is to shrink a tumor. Because mice are most often used and their life spans do not exceed two years, tumor relapse is very difficult, if not impossible to study.

The first round of chemotherapy never kills the entire tumor, but only a percentage. This phenomenon is called the fractional kill. The goal is to use repeated treatment cycles (usually six) to regress the tumor population down to zero, without killing the patient.

What normally occurs is that the treatment selectively kills the less harmful populations of cells (daughter cells), increasing the ratio of CSCs to benign and/or less malignant cells. This is not unlike what happens when antibiotics are used to treat certain infections. The drug may wipe out 99.9% of the target bacteria, but .1% have or develop resistance to the agent, enabling the .1% to come back even stronger with time.

The antibiotic, also, kills the other beneficial bacteria that help the body fight infection naturally, in the same way that chemotherapy kills the patient's immune system (white blood cells and bone marrow), ultimately supporting the underlying conditions making disease recurrence more likely.

The reality is that the chemotherapy, even though it has reduced the tumor volume, by increasing the ratio of CSCs to benign daughter cells, has actually made the cancer more malignant.

Radiotherapy has also been shown to increase cancer stem cells in the prostate, ultimately resulting in cancer recurrence and worsened prognosis.[iii] Cancer stem cells may also explain why castration therapy often fails in prostate cancer treatment.[iv]

Non-Toxic Natural Substances Which Target and Kill CSCs

Natural compounds have been shown to exhibit three properties which make them suitable alternatives to conventional chemotherapy and radiotherapy:

High margin of safety: Relative to chemotherapy agents such as 5-fluorouracil natural compounds are two orders of magnitude safer Selective Cytotoxicity: The ability to target only those cells that are cancerous and not healthy cells CSCs Targeting: The ability to target the cancer stem cells within a tumor population.

The primary reason why these substances are not used in conventional treatment is because they are not patentable, nor profitable. Sadly, the criteria for drug selection are not safety, effectiveness, accessibility and affordability. If this were so, natural compounds would form an integral part of the standard of care in modern cancer treatment.

Research indicates that the following compounds (along with common dietary sources) have the ability to target CSCs:

Resveratrol (Red Wine; Japanese Knotweed)

Parthenolide (Butterbur)

Additional research found on the GreenMedInfo.com Multidrug Resistance page indicate over 50 compounds inhibit multidrug resistance cancers in experimental models.

[i] Radiation-induced reprogramming of breast cancer cells. Stem Cells. 2012 May ;30(5):833-44. PMID: 22489015

[ii] Human acute myeloid leukemia is organized as a hierarchy that originates from a primitive hematopoietic cell. Nat Med. 1997 Jul ;3(7):730-7. PMID: 9212098

[iii] Long-term recovery of irradiated prostate cancer increases cancer stem cells. Prostate. 2012 Apr 18. Epub 2012 Apr 18. PMID: 22513891

[iv] Stem-Like Cells with Luminal Progenitor Phenotype Survive Castration in Human Prostate Cancer. Stem Cells. 2012 Mar 21. Epub 2012 Mar 21. PMID: 22438320