The Basics: What is important to know when discussing cancer treatment options with you doctor.
A primary tumor controls the growth of cancer seeds in your body – they are kept dormant. Remove the tumor and there is no further control over the growth cycles of cancer seeds already in your body.
How many cancer seeds do you have? It cannot be determined – many are microscopic. The big question, are they genetically the same as the primary tumor you had removed? Again, it cannot be determined.
Cancer treatment after surgery is a fight at the cellular level. The more you know about the tumor you had removed and what each cancer treatment drug does, the better armed you are to make intelligent decisions.
Find and develop a good rapport with your oncologist and discuss the details to your satisfaction. It is your decision – there are many options.
The Details: Not all cancer cells react the same to treatment options. This brief blog will attempt to give you some insight into the myriad of cancer treatment options.
Cancer seeds are in your body. Some are circulating in your blood stream. Others have found a home buried in an organ, node or other body part. The cancer seeds are kept in a state of dormancy by the primary cancer tumor. It doesn’t want competition for the resources to continue growing. Remove the primary tumor with surgery and the biochemical controls are removed for all the cancer seeds.
Not all cancer seeds do not develop into a cancer tumor. Some die – wither away because they can’t get the nourishment needed for growth. Circulating tumor cells (CTC) are removed from your body if they can’t find a home; and, it is difficult to find one in many cases.
The two key concerns you should have are how many cancer seeds or CTC are flowing throughout your body; and, secondly, how genetically different are they? There is a strong likelihood that you have cancer seeds in your blood stream, and that those cancer seeds are genetically different than your primary tumor.
Let’s explore the defenses that your tumor has to fight conventional chemotherapy. Two-thirds of all breast cancer cells are HER2 (Human Epidermal growth factor Receptor 2) negative and estrogen receptor (ER) positive. A standard chemotherapy treatment for breast cancer is a combination of three chemo drugs – Adriamycin, Cytoxan and Taxol. Taxol has been shown to be minimally effective, if at all, if HER2 is negative and the patient’s ER is positive. So, what about the other two chemo drugs used in that combination treatment? Adriamycin is also ineffective in treating breast cancer patients with a negative HER2 (which is approximately 80%). Four out of five women would receive no benefit from Adriamycin. Taxol and Adriamycin have some serious side effects. Why give it as part of your treatment if it is not effective?
Wouldn’t it be nice to know ahead of time what the genetic disposition of your cancer is before starting your cancer treatment? To confuse thing further, your primary tumor can be the reverse of your circulating cancer cells – you treat the primary tumor and the circulating cancer seeds are not impacted at all by the chemotherapy regimen. My wife is going through chemotherapy now and is receiving Adriamycin and Cytoxan. She is barely HER2 negative and ER positive. We asked lots of questions regarding the efficacy of this treatment before starting it.
The battle against cancer must be fought at the cellular level. You need to know as much as possible about the primary tumor and the circulating tumor cells as possible before treatment. The chemo drug fluorouracil (5-FU) requires activation by the cancer cell by the enzyme uridine phosphorylase. There are cancer cells that are resistant to 5-FU. Why use 5-FU if you know ahead of time if the cancer cell is resistant to that particular chemo drug? Gemzar is another chemo drug which requires activation by the cancer cell by another enzyme – deoxycytidine kinase (DCK). Cancer cells vary the amount of DCK they produce – hence, if you know that your primary and/or circulating cancer seeds are deficient or have little DCK, why use Gemzar as the prescribed treatment? Adriamycin (doxorubicin) targets an essential enzyme, topoisomerase 2 to be effective. The level of topoisomerase 2 varies in the tumor. Those with high levels of this enzyme respond well to Adriamycin.
Note: I’ve used 5-FU in several treatments over the years as a topical treatment for skin cancer. I’ve found it to be very effective with no side effects (none that I noticed). If you are light-skinned and have been in the sun a lot in your youth, you might want to talk to your dermatologist about the benefits of 5-FU or other drugs in the proactive treatment of skin cancer.
There are some tumors that can actually take the chemo drug and modify it or make it nearly ineffective. 5-FU is degraded by dihydropyrimidine dehydrogenase (DPD). Some cancer cells have very high levels of DPD and render 5-FU useless. Cytoxan (cyclophosphamide) requires the cancer cell to produce the enzyme gamma-glutamylcysteine synthetase (GCS). Tumors produce varying amounts of GCS – those tumors with higher levels of GCS negate a large effect of Cytoxan in attempting to kill the cancer cell. There are a series of platinum chemo drugs (cisplatin, carboplatin, oxaliplatin, etc.). Platinum chemo drugs work effectively when they can attack the cancer cell’s DNA. Some cancer cells produce a ‘repair mechanism’ to combat platinum chemo drugs. It is called excision repair cross-complementation 1 (ERCC1) protein. Cancer cells with high levels of the ERCC1 protein can repair the damage done by the platinum chemo drugs to the cancer cell’s DNA making the tumor nearly immune to platinum chemo drugs.
Methotrexate works by blocking an enzyme (dihydrofolate reductase – DHFR) inside the cancer cell. Some tumors can recognize the presence of an enzyme blocker and produce more DHFR to reverse the effect of Methotrexate. An interesting cancer capability is seen when MDR1 (multidrug resistance 1) gene is used to convey certain chemo drugs completely through the tumor without allowing any activation while the chemo drug was present inside the cancer cell. Tumors that have high amounts of MDR1 are very resilient to the chemo drugs, vincristine, Taxol, mitimycin C, and Adriamycin. Wouldn’t it be nice to know how much MDR1 is present in the cancer cell before beginning treatment?
There are some natural supplements that can be used effectively to help combat some of the cancer cell’s defenses. Nuclear factor-kappaB (Nf-kB) is used by some cancers to grow. Curcumin inhibits Nf-kB. A patient with cancer cells containing high amounts of NF-kB would probably benefit from using the natural supplement, curcumin. Several cancer cells produce glutathione S-transferase pi (GST-pi). GST-pi is used to withstand the effects of numerous chemo drugs. Pomegranate contains ellagic acid which prevents the effectiveness of GST-pi.
Why do so many people develop the same or different cancer five or ten years after cancer surgery? It is difficult to determine the reason why. There are many causes of cancer. If you do not change something in your lifestyle to prevent the disruption of your DNA that will cause cancer cells to find life, then you most likely will develop more of the same kind of cancer. If you are treating cancer seeds based on the analysis of the primary tumor and the cancer seeds are genetically different, then the chemotherapy treatment is not as effective as it can be.
The traditional ‘one size fits all’ approach to treat cancer has new hope in CTC (circulating tumor cell) analysis. CTC analysis can tell the details your doctor needs to know before recommending a treatment. CTC analysis examines the nuances of the circulating cancer seeds and provides a better, more viable option in the total treatment of your primary and any floating metastatic cancer cells. Don’t accept the ‘standard’ treatment. Demand to know what kind of cancer cell you have and whether a particular chemo drug is effective against the cancer cell’s defenses. Google CTC analysis if you want more details.
Red O’Laughlin – aka The Prosperity Professor