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I am a Cancer Survivor!
Testimonials
Joan was diagnosed in April, 1979, after her salivary gland was excised. She came to the IAT Clinic following extensive radiation. Her prognosis was "terminal" by a well known head & neck surgeon in NYC. He gave her three options: 30% chance of survival with radical surgery of the face, jaw & tongue. Less percent with less radical surgery, or extension of life for a short period of time with radiation, only. She chose radiation, keeping her face in tact & began the IAT treatment in September of 1979...Now, 32 years later, she continues to be cancer free , thanks to the Immuno Augmentative Therapy. - J.W.“In March 2000 I was diagnosis with mesothelioma and given a few months to live. A week later my husband brought me from England, traveling in a wheelchair, to the Cancer Clinic in the Bahamas. Within a few weeks of the treatment I was much stronger, swimming in the sea and going for long walks on the beach. I have remained completely fit and healthy since then. My last 3 annual CT scans showed no growth of the cancer-HOORAY!” - S.E.
If You Or Someone You Love Have Cancer…

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Cancer Cell Culture and Sensitivity Testing with Genetic Phenotyping
A modern working definition of a gene is “a locatable region of genomic sequence, corresponding to a unit of inheritance, which is associated with regulatory regions, transcribed regions, and or other functional sequence regions“. In biology, and specifically genetics, epigenetics is the study of heritable changes in phenotype (appearance) or gene expression caused by mechanisms other than changes in the underlying DNA sequence, hence the name epi- (Greek: επί- over, above) –genetics. These changes may remain through cell divisions for the remainder of the cell’s life and may also last for multiple generations. However, there is no change in the underlying DNA sequence of the organism, instead, non-genetic factors cause the organism’s genes to behave (or “express themselves”) differently.
When most people refer to someone having a gene for specific trait or disease they are generally using the word incorrectly. The truth is that everyone will have the gene for that trait in question and different people will have a variation of that gene called a phenotype. In the simplest case, the phenotypic variation is called an allele. The phenotypic differences that are observed may be caused by a single nucleotide polymorphism substitution of the allele site in the genetic code. Some of these polymorphic variations on the allele are thus phenotypes that have the potential to cause disease.
Cancer, like all illnesses, is not pre-determined by our genes, it is not even determined by our alleles, nor the polymorphisms in our genetic code. Diseases like cancer are only potentiated by the variable changes in our genetic code. A variation on an allele that has the potential to cause a cell to grow out of control so that that cell line will eventually be called a cancer cell is often called an oncogene, but it is still only a phenotype with the potential to impart a cell with uncontrolled growth. It doesn’t matter if we inherit a variation on one of our alleles, or the mutation is acquired during our life, the polymorphism only has a potential to impart cancer. The regulation of the cancer potential in a genetic phenotype is determined by individual environmental influences. The expression of an oncogene phenotype is subject to the laws of economics and natural selection.
It is precisely because cancer growth is not determined by our genetic polymorphisms that it is vital for us to understand the polymorphisms involved in a cancer to predict how it will respond to treatments. If cancer was determined genetically then there would be nothing we could do to ‘change our fate’, but, thankfully this is not the case. The phenotypic changes in an oncogene only impart a potential for major cell function disruptions. It is the expression of that phenotype that is influenced by epigenetic factors such as the cellular nutritional and biochemical environment, along with the emotional and biophysical environment.
When we determine thru specialized testing, what phenotypic changes are present on known oncogenes for cancer cell regulation in an individual cancer cell, we can then apply what we know about which pharmaceuticals, what nutriceuticals and how electroceuticals can be used to suppress the transcription and translation of the phenotype oncogene. Most important clinically, are the epigenetic factors that are economically selecting the full expression of the cancer related phenotype of the oncogene. In other words, the biochemical, hormonal and cytokine environment of the oncogenic phenotype can be greatly down-regulated with nutritional, hormonal and cytokine therapies (or greatly up-regulated if the correct epigenetic factors are ignored and the incorrect therapies are applied). Thus, for advanced standard of care, it is vital to know the phenotype status of each individual cancer, rather than population based estimates that are the current standard of care.
We now have the technology to functionally asses the activity and expression of polymorphic variations in phenotypes of the genetic code of individual cancer cells. This information can then be used to objectively select what targeted monoclonal immunotherapies, which chemotherapies, nutriceuticals and hormonal therapies would best apply a negative economic influence on the expression of the phenotype oncogene identified through our testing.
The knowledge base for the factors that influence the expressions of our oncogenetic phenotype alleles is vast and extensive, but it is still only a micro fraction of the knowledge needed to fully predict how a cancer will behave when subjected to medications, nutritional and electro-physical therapies.
Because there is so much more to know about the epigenetic regulation of oncogenes, we have thus developed a functional assay that tests most of the pharmaceutical and nutriceutical therapies on living cancer cell cultures. The concept is very analogous to the culture and sensitivity testing that is routinely done for malignant bacterial infections. With a bacterial culture and sensitivity test, the basic steps are: First, we biopsy the infected tissue and screen and identify the malignant bacteria. Then we grow these bacteria in an environment with several antibacterial medications to measure which medication the bacteria is most sensitive to be inhibited in growth.
The process for cancer cells we use is basically the same in principle. The main difference is the type of equipment we use to select the malignant cancer cells. The measurement of cancer cell inhibition is sometimes a simple cell count to measure inhibition compared to an untreated control culture, but, cancer cells are very adaptable and in many cases we need to re-measure the expression of key oncogene protein products to determine if the tested medication has down regulated the oncogene expression. With nutriceutical medications the measurement of the markers for cell death or decreased expression of key oncogene protein expression is the only test we have to help us select what nutriceutical therapies are ideal for the suppression of an individual cancer.
In this way the Cancer Genetic Phenotype Testing and the Cancer Cell Culture and Sensitivity Testing (RGCC Testing) offered thru Bahamas Clinical Services Ltd. at the IAT Clinic (Bahamas) Ltd. is very individualized testing. This type of testing is one of the ways we help individualize treatment protocols for the client with cancer and help the oncologist better select what pharmaceutical, nutriceutical, targeted immunotherapy or targeted gene therapy is objectively rational in your individual case. Our doctors work with your family doctor and your oncology team to get the best treatment available for your cancer.