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A root cause and potential cure for cancer is largely ignored by many conventional oncologists despite an accumulating body of research that we may already have the answer.

From the perspective of conventional cancer treatment, a diagnosis of multi-drug resistant cancer is equivalent to a death sentence. By the time such a diagnosis occurs, the patient's body has likely been irreversibly damaged by chemotherapy and radiation, and an even more aggressive cancer may have emerged to take the place of the original one.

Tragically, these treatments may not only simply fail, but in some cases may make the cancers more malignant. This phenomenon may even be concealed by the name multidrug resistant cancer, which makes it seem as if the cancer was so exceptionally resistant and malignant that the normally effective drugs used to treat it just couldn't do the job.

But wouldn't it be more accurate to call this multi-drug failed cancer, putting the responsibility back on the medical establishment, as it should be, in recognition of the impotence-, or worse, cancer-promoting nature of its treatment choices?

In other words, instead of blaming the treatment failure on the patient's body — or a set of virulent gene mutations within their cancer — it is time we look more closely at why conventional chemotherapy and radiation-based treatments may breed multidrug resistance within the cancer of patients, who may ultimately succumb to the effects of the treatment and not the cancer they were originally diagnosed with.

How Conventional Cancer Treatment May Create Greater Malignancy

Multidrug resistant cancer may be the byproduct of cancer doctors (oncologists) throwing the chemical and radiological kitchen sink at the patient and not only failing to improve their condition, but significantly worsening it. How so? In order to understand how conventional treatment may drive cancer into greater malignancy, we must first understand what cancer is.

Tumors are 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 throwback and not necessarily a byproduct of strictly random mutation.

Because tumors may not simply be 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 a 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.[1] CSCs are slow to replicate, making them less likely to be destroyed by chemotherapy and radiation treatments that target cells that 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 often completely misses 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 lifespans do not exceed two years, tumor relapse is very difficult, if not impossible, to study.

The first round of chemotherapy rarely kills the entire tumor, but rather 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 may have reduced the tumor volume, has actually made the cancer more malignant by increasing the ratio of CSCs to benign daughter cells.

Radiotherapy has also been shown to increase cancer stem cells in the prostate, ultimately resulting in cancer recurrence and worsened prognosis.[2] Cancer stem cells may also explain why castration therapy often fails in prostate cancer treatment.[3]

Non-Toxic Natural Substances That Target and Kill CSCs

Certain natural compounds have been shown to exhibit three properties that 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: Natural compounds have the ability to target only those cells that are cancerous and not healthy cells. CSCs targeting: Natural compounds may have 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) may have the ability to target CSCs:

Curcumin (Turmeric) Resveratrol (Red Wine; Japanese Knotweed) Quercetin (Onion) Sulforaphane (Brocolli sprouts) Parthenolide (Butterbur) Andrographalide (Andrographis) Genistein (Cultured Soy; Coffee) Piperine (Black Pepper)

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

References

[1] 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

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

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

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