BORIS is described as: Polynucleotides encoding a nonfunctional mutant form of the Brother of Regulator of Imprinted Sites (BORIS) molecule, nonfunctional mutated BORIS protein, polypeptide or peptide and modified protein forms of BORIS are described. These molecules are used as a therapeutic vaccine against cancer.
CTCFL is a Unique Onco target for Immunotherapy
The CTCFL was originally discovered by scientists at the National Institutes of Health (NIH), who demonstrated this protein acts as a critical switch for the initiation and propagation of cancer. CTCFL expression has been shown in many solid tumors including breast cancer. Importantly, CTCFL transforms normal cells to cancer cells, and switching off of CTCFL causes cancer cells to die. CTCFL controls expression of the majority, if not all, cancer-specific antigens used today for clinical trials. For example, it was shown that this cancer stem cell specific oncogene orchestrates MAGE-A, BAG-1, NY-ESO-1 , SBSN, TSP50,FerT, NOTCH3 gene and hTERT. Importantly as mentioned above CTCFL is expressed on cancer stem cells, a small, resilient subset of cells that are central to tumor initiation growth, recurrence and metastasis.
To understand better correlation of CTCFL with cancer we used Big Data analysis-Cosmos site http://catalogue.fiware.org/enablers/bigdata-analysis-cosmos and obtained very important results. More specifically, Big Data analysis of exon sequencing of CTCFL in cancerous and normal tissues showed high mutagenesis rate in various cancer tissues. These mutations occurred in DNA binding ZF-region and in N-and C-terminal regions, indicating the essential role of CTCFL for binding to DNA and survival of tumor cells. These mutations are mostly changing a few amino acids (sometimes one) in protein and may change the binding ability with certain DNA sites. Data from NIH scientists have already shown CTCFL mutations in Wilm’s tumor (pediatric kidney cancer) and these mutations change binding properties of CTCFL to WT1 gene.
These novel data along with published results on immunotherapy suggests that targeting CTCFL represents a paradigm shift in the treatment of cancer. Accordingly based on all this data and based on the fact, that CTCFL expression has been shown in ~70% of primary breast cancer we developed our BRS-001 action plan.
Immunotherapy: Using the Immune System to Treat Cancer
The immune system’s natural capacity to detect and destroy abnormal cells may prevent the development of many cancers. However, cancer cells are sometimes able to avoid detection and destruction by the immune system. Cancer cells may:
- reduce the expression of tumor antigens on their surface, making it harder for the immune system to detect them
- express proteins on their surface that induce immune cell inactivation
- induce cells in the surrounding environment (microenvironment) to release substances that suppress immune responses and promote tumor cell proliferation and survival
In the past few years, the rapidly advancing field of cancer immunology has produced several new methods of treating cancer, called immunotherapies, which increase the strength of immune responses against tumors. Immunotherapies either stimulate the activities of specific components of the immune system or counteract signals produced by cancer cells that suppress immune responses.
These advances in cancer immunotherapy are the result of long-term investments in basic research on the immune system—research that continues today. Additional research is currently under way to:
- understand why immunotherapy is effective in some patients but not in others who have the same cancer
- expand the use of immunotherapy to more types of cancer
- increase the effectiveness of immunotherapy by combining it with other types of cancer treatment, such as targeted therapy, chemotherapy, and radiation therapy
Immune Checkpoint Modulators
One immunotherapy approach is to block the ability of certain proteins, called immune checkpoint proteins, to limit the strength and duration of immune responses. These proteins normally keep immune responses in check by preventing overly intense responses that might damage normal cells as well as abnormal cells. But, researchers have learned that tumors can commandeer these proteins and use them to suppress immune responses.
Blocking the activity of immune checkpoint proteins releases the “brakes” on the immune system, increasing its ability to destroy cancer cells. Several immune checkpoint inhibitors have been approved by the Food and Drug Administration (FDA).
Immune Cell Therapy
Progress is also being made with an experimental form of immunotherapy called adoptive cell transfer (ACT). In several small clinical trials testing ACT, some patients with very advanced cancer—primarily blood cancers—have had their disease completely eradicated. In some cases, these treatment responses have lasted for years.
In one form of ACT, T cells that have infiltrated a patient’s tumor, called tumor-infiltrating lymphocytes (TILs), are collected from samples of the tumor. TILs that show the greatest recognition of the patient’s tumor cells in laboratory tests are selected, and large populations of these cells are grown in the laboratory. The cells are then activated by treatment with immune system signaling proteins called cytokines and infused into the patient’s bloodstream.
The idea behind this approach is that the TILs have already shown the ability to target tumor cells, but there may not be enough of them within the tumor microenvironment to eradicate the tumor or overcome the immune suppressive signals that are being released there. Introducing massive amounts of activated TILs can help to overcome these barriers and shrink or destroy tumors.
Therapeutic antibodies are antibodies made in the laboratory that are designed to cause the destruction of cancer cells.
One class of therapeutic antibodies, called antibody–drug conjugates (ADCs), has proven to be particularly effective, with several ADCs having been approved by the FDA for the treatment of different cancers.
ADCs are created by chemically linking antibodies, or fragments of antibodies, to a toxic substance. The antibody portion of the ADC allows it to bind to a target molecule that is expressed on the surface of cancer cells. The toxic substance can be a poison, such as a bacterial toxin; a small-molecule drug; or a radioactive compound. Once an ADC binds to a cancer cell, it is taken up by the cell and the toxic substance kills the cell.
Immune System Modulators
Yet another type of immunotherapy uses proteins that normally help regulate, or modulate, immune system activity to enhance the body’s immune response against cancer. These proteins include cytokines and certain growth factors. Two types of cytokines are used to treat patients with cancer: interleukins and interferons.
Immune-modulating agents may work through different mechanisms. One type of interferon, for example, enhances a patient’s immune response to cancer cells by activating certain white blood cells, such as natural killer cells and dendritic cells. Recent advances in understanding how cytokines stimulate immune cells could enable the development of more effective immunotherapies and combinations of these agents.
CAR T-Cell Therapy: Engineering Patients’ Immune Cells to Treat Their Cancers
For years, the cornerstones of cancer treatment have been surgery, chemotherapy, and radiation therapy. Over the last decade, targeted therapies like imatinib (Gleevec®) and trastuzumab (Herceptin®)—drugs that target cancer cells by homing in on specific molecular changes seen primarily in those cells—have also emerged as standard treatments for a number of cancers.
And now, despite years of starts and stutter steps, excitement is growing for immunotherapy—therapies that harness the power of a patient’s immune system to combat their disease, or what some in the research community are calling the “fifth pillar” of cancer treatment.
One approach to immunotherapy involves engineering patients’ own immune cells to recognize and attack their tumors. And although this approach, called adoptive cell transfer (ACT), has been restricted to small clinical trials so far, treatments using these engineered immune cells have generated some remarkable responses in patients with advanced cancer.
For example, in several early-stage trials testing ACT in patients with advanced acute lymphoblastic leukemia (ALL) who had few if any remaining treatment options, many patients’ cancers have disappeared entirely. Several of these patients have remained cancer free for extended periods.
Equally promising results have been reported in several small trials involving patients with lymphoma. These are small clinical trials, their lead investigators cautioned, and much more research is needed.
A Living Drug
Adoptive cell transfer is like giving patients a living drug. That’s because ACT’s building blocks are T cells, a type of immune cell collected from the patient’s own blood. After collection, the T cells are genetically engineered to produce special receptors on their surface called chimeric antigen receptors (CARs). CARs are proteins that allow the T cells to recognize a specific protein (antigen) on tumor cells. These engineered CAR T cells are then grown in the laboratory until they number in the billions.
The expanded population of CAR T cells is then infused into the patient. After the infusion, if all goes as planned, the T cells multiply in the patient’s body and, with guidance from their engineered receptor, recognize and kill cancer cells that harbor the antigen on their surfaces.
Understanding Precision Medicine in Cancer Treatment
Precision medicine is an approach to patient care that allows doctors to select treatments that are most likely to help patients based on a genetic understanding of their disease. This may also be called personalized medicine. The idea of precision medicine is not new, but recent advances in science and technology have helped speed up the pace of this area of research.
Today, when you are diagnosed with cancer, you usually receive the same treatment as others who have same type and stage of cancer. Even so, different people may respond differently, and, until recently, doctors didn’t know why. After decades of research, scientists now understand that patients’ tumors have genetic changes that cause cancer to grow and spread. They have also learned that the changes that occur in one person’s cancer may not occur in others who have the same type of cancer. And, the same cancer-causing changes may be found in different types of cancer.
The Promise of Precision Medicine
The hope of precision medicine is that treatments will one day be tailored to the changes in each person’s cancer. Scientists see a future when patients will receive drugs that their tumors are most likely to respond to and will be spared from receiving drugs that are not likely to help. Research studies are going on now to test whether treating patients with drugs that target the cancer-causing genetic changes in their tumors, no matter where cancer develops in the body, will help them. Many of these drugs are known as targeted therapies.
Though experts believe that precision medicine can become an additional option for people with cancer, it is not likely to replace the cancer treatments we already have. Currently, if you need treatment for cancer, you may receive a combination of treatments, including surgery, chemotherapy, radiation therapy, and immunotherapy. Which treatments you receive will depend on the type of cancer, its size, and whether it has spread. With precision medicine, if your cancer has a genetic change that can be targeted with a known drug, you may also receive that drug.
There are drugs that have been proven effective against specific genetic changes in certain cancers and approved by the FDA. Many of these drugs are discussed in Targeted Cancer Therapies. Approved treatments should be available wherever you have cancer treatment.
Precision Medicine as a Treatment Option
Even though researchers are making progress every day, treatment using precision medicine is not yet part of routine care for most patients. Many new drugs used in precision medicine are being tested right now in clinical trials. Some clinical trials are accepting patients with specific types and stages of cancer. Others accept patients with a variety of cancer types and stages. To be eligible for precision medicine trials, your tumor must have a genetic change that can be targeted by a drug being tested.
Not Every Person with Cancer Will Have Their Cancer Tested for Genetic Changes
If there is a targeted drug approved for your type of cancer, you will likely be tested for a genetic change that might be driving it. For instance, people with melanoma, some leukemia’s, and breast, lung, colon, and rectal cancers usually have their cancers tested for certain genetic changes when they are diagnosed. Since additional genetic changes that can drive cancer may occur over time, you might also have your cancer tested if it comes back or gets worse.
If there is not an approved targeted drug for your type of cancer, you still may be tested for genetic changes. For instance, your cancer may be tested to see if you can join a precision medicine clinical trial.
How Genetic Changes in Your Cancer Are Identified
To figure out which genetic changes are in your cancer, you may need to have a biopsy. A biopsy is a procedure in which your doctor removes a sample of the cancer. This sample will be sent to a special lab, where a machine called a DNA sequencer looks for genetic changes that may be causing cancer to grow. The process of looking for genetic changes in cancer may be called DNA sequencing, genomic testing, molecular profiling, or tumor profiling.
Paying for Precision Medicine
If you have a type of cancer with a genetic change that can be treated with an approved drug, testing for genetic changes in your cancer is part of routine care. Therefore, your insurance company may cover the costs. To make sure, check with your insurance company to find out which costs it will cover.
If you join a precision medicine clinical trial, the cost of testing for genetic changes may be covered by the organization sponsoring the trial. To be sure, check with the trial staff and make sure that you understand your consent form.
If there is not an approved targeted drug for your type of cancer and you are not in a clinical trial using precision medicine, your insurance company will probably not cover the costs of having your cancer tested for genetic changes.
Testing for genetic changes requires the use of complex technology and requires the services of people with specialized training. Therefore, this testing can be expensive.
Treatment using precision medicine can also be expensive. It takes many years, sometimes decades, of research to develop drugs that target the changes that cause cancer to develop, grow, and spread. So, by the time these drugs are available on the market, they are often very expensive.
Precision Medicine Research Moving Forward
Researchers have not yet discovered all the genetic changes that can cause cancer to develop, grow, and spread. But, they are making progress and discover new changes every day. Information from this research is being collected in databases where researchers from across the country can access the data and use them in their own studies. This sharing of data helps move the field of precision medicine forward.
Once genetic changes are discovered, another active area of research involves looking for drugs that can target these changes, then testing these drugs with people in clinical trials. Clinical trials are going on across the United States.
Researchers are also working to understand and solve the problem of drug resistance that can limit how well targeted therapies work. Many researchers believe that precision medicine is the key to unlocking these secrets.
Cancer has a major impact on society in the United States and across the world. Cancer statistics describe what happens in large groups of people and provide a picture in time of the burden of cancer on society. Statistics tell us things such as how many people are diagnosed with and die from cancer each year, the number of people who are currently living after a cancer diagnosis, the average age at diagnosis, and the numbers of people who are still alive at a given time after diagnosis. They also tell us about differences among groups defined by age, sex, racial/ethnic group, geographic location, and other categories.
- Cancer accounts for 8 million deaths per year worldwide
- About 1,300,000 new cases of cancer were diagnosed yearly in the US
- Every year about 560,000 Americans are expected to die of cancer; more than 1,500 people a day
- Based on the Surveillance, Epidemiology, and End Results (SEER) program database of the National Cancer Institute, the number of all cancer patients is expected to more than double from 1.36 million in 2000 to almost 3.0 million in 2050, both due to the aging as well as the growth of the U.S. population
- Prostate cancer is the most common malignancy and the second leading cause of cancer-related deaths amongst men in the United States. An estimated 186,000 men were diagnosed with prostate cancer in 2008, and there were 28,660 deaths. In Europe in the same year, there were 190,000 new cases diagnosed and there were 80,000 prostate cancer related deaths. The incidence of prostate cancer in Asia is significantly lower, with the total worldwide burden of prostate cancer thought to be in the 650,000 to 700,000 range
- By 2010, 1.5 million deaths/yr due to lung cancer are projected worldwide.
- More than 108,070 people in the United States were diagnosed with colon cancerin 2008 accord to the American Cancer Society. The estimated cancer deaths this year will be 50,000.
- Approximately 35,000 Americans are diagnosed each year with oral cancer
- Leukemiais a serious white blood cell cancer that more than 44,000 Americans develop every year. Currently there are approximately 218,000 people in the U.S. living with the disease, and each year 21,000 people die from leukemia.
- Pancreas canceraffects 38,500 patients each year and the current 5-year survival rate is about 5%. Pancreas cancer ranks fourth in cancer related deaths. Current therapies for this disease are woefully inadequate. The cost to provide this ineffective health care is estimated at 4.1 billion annually.
- Melanomais the most rapidly increasing cancer in the United States, according to the National Cancer Institute, with more than 62,000 people diagnosed with the disease annually. Of these, it is estimated that more than 8,000 will die within three to four years after a form of the recurrent disease spreads, or metastasizes, to other sites in the body.
- The number of new non-melanoma skin cancer cases in the USA is estimated to be between 900,000 and 1,200,000.
- Multiple myelomais a B cell malignancy characterized by the accumulation of mature clonal plasma cells in the bone marrow, which leads to progressive bone destruction and marrow failure. Myeloma is the 2nd most common hematologic malignancy, with an estimated 19,900 new cases diagnosed each year and almost 11,000 deaths each year in the US.
- Primary kidney cancers comprise approximately 3.8% of malignancies with an estimated 54,390 new cases and 13,010 deaths in 2008. Additionally, the rate of kidney cancer has increased over the past 65 years by 2% per year. When compared to other malignancies, kidney cancer is the seventh most common cancer diagnosis in men and the ninth most common in women, with the peak incidence occurring in the sixth decade. Renal cell carcinoma(RCC) represents 90% of kidney cancers and 30% of persons affected present with metastatic disease. It has been reported that of these, 85% are clear cell carcinomas with the remaining 15% being papillary, chromophobe, and collecting duct carcinomas. In Europe, more than 63 000 new cases of renal cell carcinoma and 26 000 deaths were reported in 2006. Historically, the prognosis for patients with metastatic RCC has been poor, with a 5-year survival rate of 10%.
Cancer Treatment Vaccines
The use of cancer treatment (or therapeutic) vaccines is another approach to immunotherapy. These vaccines are usually made from a patient’s own tumor cells or from substances produced by tumor cells. They are designed to treat cancers that have already developed by strengthening the body’s natural defenses against the cancer.
In 2010, the FDA approved the first cancer treatment vaccine, sipuleucel-T (Provenge®), for use in some men with metastatic prostate cancer. Other therapeutic vaccines are being tested in clinical trials to treat a range of cancers, including brain, breast, and lung cancer.
Our Approach is BORIS: Universal Cancer vaccine based on Brother of Regulator of Imprinted Sites Molecule
Polynucleotides encoding a nonfunctional mutant form of the Brother of Regulator of Imprinted Sites (BORIS) molecule, nonfunctional mutated BORIS protein, polypeptide or peptide and modified protein forms of BORIS are described. These molecules are used as a therapeutic vaccine against cancer.
What is BORIS?
BORIS = Brother of the Regulator of Imprinted Site
- Discovered by Victor Lobanenkov at NIH
- “Regulator of Imprinted Sites” is CTCF
- CTCF is a tumor suppressor gene
- CTCF is involved in keeping silent parts of DNA that are supposed to be silent
- BORIS is “bad brother” in that it displaces CTCF from DNA, thus allowing for genes that should not be transcribed to be transcribed
“BORIS is a gene that is essential for cancer to be cancer – if a tumor mutates BORIS, then it no longer is a tumor”
– Thomas Ichim, PhD
BORIS Causes Cancer to be Cancer:
BORIS is Expressed only in Cancer Tissues:
Left Panel: Brown staining indicates the presence of BORIS. As you can see, it only shows up in the bottom rows, which are cancer tissues whereas the top rows are normal tissues from the same patient and organ.
Right Panel: Another way of quantifying BORIS levels. Red bars are from cancer tissues and black bars are from the same tissue, but the non-cancerous part of it.
In Patients Higher Levels of BORIS Equals Lower Survival:
Killing Cancer Stem Cells is Key to Curing Cancer: If you don’t specifically kill the stem cells, the tumor regrows.
BORIS is Found Only in Cancer Stem Cells:
Silencing BORIS Blocks Cancer Stem Cells:
Here, cancer stem cells were prevented from producing BORIS using two different inhibitors (left and middle bars) and they stopped growing. The right bar is a control and those cells kept growing.
How to Kill BORIS? – BRS-001 Cancer Vaccine
BRS-001: Cancer Stem Cell Targeted Immunotherapy
BRS-001 is a patent-pending cellular immunotherapy developed by scientists at Therapeutic Solutions International, Inc., a San Diego Biotechnology Company, which is available at the Pan Am Cancer Treatment Center in Tijuana Mexico to treat stages 1-4 in breast cancer.
BRS-001 activates the immune system to seek and destroy cancer stem cells, based on their expression of a protein named Brother of the Regulator of Imprinted Sites (BORIS). BRS-001 is generated using white blood cells of the patient, which are grown outside of the body to create dendritic cells. The patient’s own dendritic cells are treated in vitro with peptides derived from BORIS, and subsequently are injected back into the patient in order to program the immune response to kill cells that express the protein BORIS, which are cancer stem cells.
Without Killing of Cancer Stem Cells it is Impossible to Cure Cancer
All tumor cells are the offspring of a single, aberrant cell, but they are not all alike. Only a few retain the capacity of the original cell to create an entire tumor. Such cancer stem cells can migrate to other tissues and become fatal metastases. To fully cure a patient’s cancer, it is crucial to find and eliminate all of these cells because any that escape can regenerate the tumor and trigger its spread through the body.
BORIS is Essential for Cancer “To be Cancer”
The BORIS protein functions to disable a tumor suppressor termed “CTCF”. The role of CTCF is to ensure that parts of DNA that should not be activated, indeed are not activated. For example, one of the roles of CTCF is to block expression of genes that cause cancer. In cancer stem cells, BORIS blocks the function of CTCF, thus allowing for propagation of cancer. It has been shown that if BORIS is blocked in cancer stem cells, the cancer stem cells no longer form tumors.
BRS-001 is Selective Immunotherapy
Dendritic cells are the most potent immune stimulatory cell of the body. Currently, dendritic cell therapy is approved in the USA in the form of the drug Provenge. BRS-001 consists of dendritic cells that are treated with parts of the BORIS protein in order to stimulate killer T cell responses against any cell that expresses BORIS. Using dendritic cells to stimulate immunity offers the advantage of inducing immunological memory against the tumor. Published studies by us in collaboration with the NIH showed immunity to BORIS results in tumor killing,.
The BRS-001 construct is capable of stimulating immune responses that cross over to wild-type tumors without having the potential of causing cancer. This ability to induce tumor immunity was validated across a broad variety of tissue types making the BRS-001 approach broadly applicable for numerous cancers. This was described in peer-reviewed papers by Company scientists demonstrating that immunization with BRS-001 not only inhibits growth of aggressive breast cancer 4T1 cells in BALB/c mice, but also that mice immunized with BRS-001 contain high numbers of CD8+ T cells that have spontaneous cytolytic activity against breast, leukemia, and glioma cells in vitro.
The BRS-001 construct is capable of stimulating immune responses that crossover to wild-type tumors without having the potential of causing cancer. This ability to induce tumor immunity was validated across a broad variety of tissue types making the BORIS approach broadly applicable for numerous cancers. This was described in peer-reviewed papers by Company scientists demonstrating that immunization with BRS-001 not only inhibits growth of aggressive breast cancer 4T1 cells in BALB/c mice, but also that mice immunized with BRS-001 contain high numbers of CD8+ T cells that have spontaneous cytolytic activity against breast, leukemia, and glioma cells
Company scientists have determined that vaccination with BRS-001 in the context of various immune stimulatory technologies induces a CD8 cytotoxic T cell response that recognizes tumors independent of tissue origin.
NanoStilbene: Patented Augmenter of Cancer ImmunotherapyNanoStilbene, a nanoparticle formulation of pterostilbene, is covered for use in cancer immunotherapy under the Company’s issued U.S. Patent No.: 9,682,047 and is included as part of the Breast Cancer Protocol with StemVacs.
NanoStilbene is an easily absorbed nanoemulsion of nanoparticle pterostilbene in the range of 75-100nm at a concentration of 200 milligrams per milliliter. The pterostilbene placed in a nanoemulsion droplet is free from air, light, and hard environment; therefore, as a delivery system, nanoemulsion can not only improve the bioavailability of pterostilbene but also protect it from oxidation and hydrolysis, while it possesses an ability of sustained release at the same time. Therapeutic uses of nanotechnology typically involve the delivery of small-molecule drugs, peptides, proteins, and nucleic acids. Nanoparticles have advanced pharmacological effects compared with the therapeutic entities they contain. Active intracellular delivery and improved pharmacokinetics and pharmacodynamics of drug nanoparticles depend on various factors, including their size and surface properties. Nanoparticle therapeutics is an emerging treatment modality in cancer and other inflammatory disorders. The National Cancer Institute has recognized nanotechnology as an emerging field with the potential to revolutionize modern medicine for detection, treatment, and prevention of cancer.
Additional StemVacs Platform Immunotherapeutics
Cancer Metabolic DeTox: This is an orally administered agent that is derived from various herbs termed apigenin. The unique property of apigenin is that it inhibits a cancer associated metabolic pathway that degrades the amino acid tryptophan. Specifically, apigenin inhibits the enzyme indolamine 2,3 deoxygenase (IDO), which is responsible for breaking down tryptophan in the vicinity of the tumor and generating by-products such as kynurenine. It is known that immune activation is dependent on tryptophan being present in the tumor environment. The depletion of tryptophan and generation of kynurenine by tumor cells and tumor associated cells is a major cause of immune suppression in cancer. By administering Cancer Metabolic DeTox, the innate arm of the immune system has a chance to regenerate. This positions the patient for better outcome after administration of specific immune stimulating vaccines.
Patent Title: Targeting the Tumor Microenvironment through Nutraceutical Based Immunoadjuvants
Disclosed are compositions useful for the treatment of cancer which modulate tumor associated immunosuppression, thus acting as immunoadjuvants. In one embodiment a composition containing apigenin, is provided, said composition useful for inhibition of tumor associated immune suppression mediated through the molecule indolamine 2,3 deoxygenase (IDO). In another embodiment, liposomal apigenin is administered as a means of decreasing IDO expression.
innaMune: This is a biological product derived from tissue culture of blood cells derived from healthy donors. It is a combination of cytokines that maintain activity of innate immune system cells, as well as having ability to shift M2 macrophages to M1.
Patent Title: Activated Leukocyte Extract for Repair of Innate Immunity in Cancer Patients
Disclosed are compositions, methods of use, and pharmaceutical preparations useful for modulation of immune responses. In one embodiment a composition is extracted polyvalently activated peripheral blood mononuclear cells through dialysis. Said immune modulator is useful for treatment of cancer and alleviation of cancer associated immune depression. In one embodiment, said immunomodulator acts as a costimulatory of T cell activation by modulation of cytokine production. In one embodiment said immune modulator is concentrated for miRNA species capable of activating innate immune cells.
LymphoBoost: LymphoBoost is a proprietary formulation of Mifepristone, a drug approved for another indication, which we have shown to be capable of stimulating lymphocytes, particularly NK cells and T cells, both critical in maintaining anti-tumor immunity.
Augmentation of Anti-Tumor Immunity by Mifepristone and Analogues Thereof
The present invention relates to compositions of matter and methods useful for improving a treatment outcome and/or an alteration of immunity in a condition that benefits from immune stimulation. In particular, one embodiment of the invention teaches administration of sufficient doses of mifepristone or a derivative, alone, or in combination with an immunotherapeutic such as, but not limited to, an antibody, a vaccine, a cytokine, or a medicament whose therapeutic activity is associated with immune modulation.
MemoryMune: This is a product derived from a two-step culture process of donor blood cells. The product MemoryMune reawakens dormant immune memory cells. It is known that many cancer patients possess memory T cells that enter the tumor, however, once inside the tumor these cells are inactivated. MemoryMune contains a unique combination of growth factors specific for immune system cells called “cytokines”.
Patent Title: Methods of Re-Activating Dormant Memory Cells with Anticancer Activity
Disclosed are methods, protocols and compositions of matter useful for stimulation of anticancer immune responses. In one embodiment of the invention culture of buffy coat cells is performed in an environment resembling non-physiological conditions. Buffy coat derived products are subsequently harvested, concentrated, and added to a culture of monocytes and lymphocytes. Conditioned media from said second culture is subsequently utilized as an injectable solution for stimulation of anticancer immunity.
Conclusion: This type of immune response is usually associated with remission of the tumor. Based on this mechanism of action, Therapeutic Solutions International, Inc. has decided to develop a dendritic cell BORIS-peptide pulsed candidate as the most promising method of stimulating immune responses to BORIS in cancer patients. The Pan American Cancer Treatment Center is located a few miles south of sunny San Diego, in Tijuana, Mexico. The Pan Am facilities are state of art and offer access to cutting-edge cancer immunotherapies outside of clinical trials. After we receive you in San Diego, you will travel by air-conditioned transportation to our new and modern treatment center, where you will have access to cellular, small molecule, and protein therapies through accelerated means.
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