Researchers show stress suppresses response to cancer treatments

New research shows that chronic stress suppresses the immune system’s response to cancer, reducing the effectiveness of immunotherapy treatments.

University of Queensland scientists say they are investigating dual therapies for patients to reduce stress signalling and improve their response to treatments.

UQ Diamantina Institute researcher Dr Stephen Mattarollo said lymphoma progressed more rapidly in mouse models when stress pathways were induced to reflect chronic psychological stress.

“When we used immunotherapies on these mice they were not able to respond as effectively as those which had not been stressed,” Dr Mattarollo said.

“This is because the stress led to poor function against the cancer by T-cells, which are very important in the immune system’s control and surveillance of tumours and are a major target in many immunotherapy treatments.”

Dr Mattarollo said increased anxiety was natural with a cancer diagnosis, and it should be managed to ensure the best possible outcome for patients.

“Absolutely there is now pre-clinical evidence to suggest that treatments and lifestyle interventions to manage or reduce stress levels will improve the chances of these patients responding to therapies,” he said.

“This applies particularly to immunotherapies, but many conventional therapies such as chemotherapy also rely on components of the immune system for their effectiveness.

“It is quite possible that by increasing the immune function in patients they will also respond better to some other therapies.”

PhD candidate Michael Nissen said as immunotherapies became more widely available, it was important to build on the knowledge of factors which influence their effectiveness.

“The more we know, the better chance we have of designing them effectively and efficiently to work in cancer patients,” Mr Nissen said.

Dr Mattarollo said the lab was hoping to combine immunotherapy treatments with commonly used blood pressure drugs that block the effects of stress hormones.

“We hope this will reduce the stress-induced neural signalling and improve immune function,” Dr Mattarollo said.

“We are about to test this combination in animal models.”

Dr Mattarollo said psychoneuroimmunology – or the interaction between the mind, the nervous system and the immune system – is a rapidly growing discipline and is becoming an increasing focus of the lab’s cancer research.

The research is published in Cancer Immunology Research.

Dr Mattarollo’s lab is located at the Translational Research Institute.

New strategy for multiple myeloma immunotherapy

In recent decades monoclonal antibody-based treatment of cancer has been established as one of the most successful therapeutic strategies for both solid tumors and blood cancers. Monoclonal antibodies (mAb), as the name implies, are antibodies that are made by clonal cells derived from a single parent cells and therefore share the identical amino acid sequences.

One of the leading technologies to emerge in mAb-based treatment is CAR-T, where CAR stands for “chimeric antigen receptor”, and T represents T cells, a type of white blood cells that have pivotal roles in immune defenses. CARs are produced by combining together the gene for an antibody that recognizes a tumor antigen with the gene for a receptor that resides on the surface of the T cells; insert this new gene into a T cell and it will be precisely targeted at the tumor.

Theoretically, new antigens – molecules capable of inducing an immune response to produce an antibody – that arise from cancer-specific mutations of cell-surface proteins are excellent targets. However, mAb therapy targeting such antigens is impractical because of these proteins’ vast diversity within and between individual tumors, which renders identifying new cancer-specific target antigens difficult.

However, such challenges have driven researchers centered at Japan’s Osaka University to think outside of the box; cancer-specific antigen formed by the modification of proteins during or after synthesis, such as glycosylation (attachment of sugar moieties to protein) or conformational changes, might have been missed in previous analyses. The team believed new antigen epitopes, which is the part of an antigen recognized by the immune cells, could be discovered by thoroughly searching for cancer-specific mAbs and characterizing the antigens they recognize.

“We applied this strategy to identify novel therapeutic targets for multiple myeloma (MM), a cancer that forms in a type of white blood cell called a plasma cell,” explains Naoki Hosen, lead author of the study, which was recently published in Nature Medicine. “Despite advances in MM treatment, relapse remains common. As such, there is an ongoing need for new therapeutic approaches, including mAb-based therapies.”

The team screened more than 10,000 anti-MM mAb clones and identified MMG49 as an MM-specific mAb specifically recognizing a subset of integrin β7, a cell-surface receptors that facilitate cell-extracellular matrix adhesion. MMG49 reacted to MM cells, but not other bone marrow cell types in MM patient samples. This prompted the researchers to design a CAR that incorporates a fragment derived from MMG49. The resulting MMG49 CAR T was found to have anti-MM effects without damaging normal blood cells.

“Our results also demonstrate that the active conformer of integrin β7 can serve as an immunotherapeutic target against MM, even though the expression of the protein itself is not specific to MM,” study coauthor Yukiko Matsunaga says. “Therefore it’s highly plausible that there are other cancer immunotherapeutic targets that have yet to be identified in many cell-surface proteins that undergo conformational changes, even if the expression of the proteins themselves is not cancer-specific.”

Gilead to buy Kite Pharma in $11.9 billion deal

Reuters — Gilead Sciences agreed to buy Kite Pharma in a $11.9 billion deal on Monday, as it looks to fuel growth with an emerging class of cancer immunotherapies that are expected to generate billions.

Gilead will pay $180 per share in an all-cash deal, representing a 29.4 percent premium over Kite’s Friday close. Kite’s shares were trading up at $178.15 before the bell.

Santa Monica, California-based Kite is developing a CAR-T, or chimeric antigen receptor T-cell therapy, which harnesses the body’s own immune cells to recognize and attack malignant cells.

Gilead’s growth has been fueled by its pricey but revolutionary hepatitis C drugs but with fewer eligible patients and rising competition, sales have begun to fall.

Second-quarter sales of its hepatitis C drugs — Sovaldi, Harvoni and Epclusa — totaled $2.9 billion, down from $4 billion a year earlier.

Wall Street and Gilead shareholders have long been expecting Gilead to use its cash pile for a big-ticket acquisition.

The deal for Kite, which has been approved by the boards of both companies, is expected to close in the fourth quarter.

Kite is one of the leading players in the emerging field of CAR-T, and is competing with rivals Novartis, Juno Therapeutics, and Bluebird bio in a race to get the first approved therapy.

If approved, these drugs are expected to cost up to $500,000 and generate billions of dollars. Success would also help advance a cancer-fighting technique that scientists have been trying to perfect for decades.

The U.S. Food and Drug Administration (FDA) is expected to decide by Nov. 29 whether to approve Kite’s CAR-T, axi-cel, for treatment of adults with advanced lymphoma.

Gilead has a market value of $96.36 billion, according to Thomson Reuters data. The company was once the world’s largest maker of HIV drugs, and in 2011 agreed to acquire hep C drug developer Pharmasset for $11 billion.

Last year, Gilead generated total sales of $30.39 billion, of which $14.8 billion came from hep C treatments.

Bank of America/Merrill Lynch and Lazard are acting as financial advisers to Gilead, while Centerview Partners is Kite’s exclusive financial adviser.

Skadden, Arps, Slate, Meagher & Flom is the legal counsel to Gilead and Sullivan & Cromwell and Cooley for Kite.

The Wall Street Journal reported first reported the deal.

Gilead’s shares were little changed in premarket trading, while Juno’s shares rose nearly 14 percent and Bluebird’s 2.6 percent.

UH Seidman Cancer Center Expert Presents Novel Triple-Negative Breast Cancer Immunotherapy Trial at 2016 San Antonio Breast Cancer Symposium

Meeting focuses on state-of-the-art breast cancer research, including immunotherapeutic approaches

A researcher from University Hospitals Seidman Cancer Center discussed his upcoming immunotherapy clinical trial for triple-negative breast cancer at the 2016 San Antonio Breast Cancer Symposium. The annual symposium is the premier meeting for more than 7,500 physicians and scientists dedicated to breast cancer treatment, featuring state-of-the-art breast cancer research such as experimental biology, etiology, prevention, diagnosis, and therapy of both breast cancer and premalignant breast disease.

Joseph Baar, MD, PhD, Director of Breast Cancer Research at UH Seidman Cancer Center and Associate Professor at Case Western Reserve University School of Medicine, shared details about a phase II clinical trial testing the effectiveness of combining the chemotherapy drugs carboplatin and nab-paclitaxel with an immunotherapeutic agent called pembrolizumab (Keytruda) for use in patients with metastatic triple-negative breast cancer. Dr. Baar’s poster presentation was part of the Ongoing Trials-Targeted Therapy session on Dec. 8, 2016.

“Up until now, women with triple-negative breast cancer have only had one treatment option, which is chemotherapy. However, more recently, we’ve seen that the immune modulator pembrolizumab improves outcomes in patients with metastatic triple-negative breast cancer,” said Dr. Baar. “As a result, it is now critical to explore how the addition of pembrolizumab to chemotherapy might improve survival in patients with this type of breast cancer.”

Triple-negative breast cancer is a highly aggressive form which comprises 10-15 percent of newly diagnosed early-stage breast cancer. Most triple-negative tumors are high grade and have a high incidence of recurrence and metastases (spreading to other organs). Unlike other types of breast cancer, there is no standard follow-up treatment for triple-negative breast cancer to prevent recurrence.

As triple-negative breast cancer progresses, tumor cells express a protein ligand called PD-L1, which interacts with the PD-1 receptor on T-cells. T-cells are the immune system’s primary mechanism for fighting back against harmful foreign invaders. The PD-L1 to PD-1 interaction prevents the T-cell from responding to the tumor as a threat. Pembrolizumab binds to the T-cell’s PD-1 receptors and therefore blocks the PD-1 to PD-L1 interaction, allowing the T-cells to be activated against the tumor cells. The research team hypothesizes that the addition of such an immunotherapeutic agent to chemotherapy will allow the body’s natural immune response to reduce disease recurrence to a greater extent than either modality alone.

This is the first phase II trial to study the effectiveness of combining these two chemotherapeutic agents with the immunotherapeutic agent pembrolizumab for this type of cancer.

The trial will enroll approximately 30 patients beginning in early 2017. Eligible patients must have radiologically measurable and documented metastatic triple negative breast cancer, be mostly functional day to day as measured by an ECOG performance status of between zero and one, must not have received more than two prior therapies for this disease, and must be willing to undergo a preliminary biopsy for research purposes. The trial is sponsored by Merck, which produces pembrolizumab as Keytruda.

“Trials our faculty members present at SABCS and other research meetings around the world illustrate the remarkable advances in oncology taking place today,” says Neal J. Meropol, MD, Chief, Division of Hematology and Oncology, University Hospitals Seidman Cancer Center and Associate Director for Clinical Research, Case Comprehensive Cancer Center at Case Western Reserve.

The symposium, which began Dec. 6 and continues until Dec. 10, 2016, is hosted by The Cancer Therapy & Research Center at the University of Texas Health Science Center at San Antonio, the American Association for Cancer Research, and Baylor College of Medicine.

Molecular Switch Controlling Immune Suppression May Help Turn Up Immunotherapies

Researchers at University of California San Diego School of Medicine and Moores Cancer Center have identified a strategy to maximize the effectiveness of anti-cancer immune therapy. The researchers identified a molecular switch that controls immune suppression, opening the possibility to further improving and refining emerging immunotherapies that boost the body’s own abilities to fight diseases ranging from cancer to Alzheimer’s and Crohn’s disease.

The findings are published in the September 19 online issue of Nature.

“Immunotherapies, such as T cell checkpoint inhibitors, are showing great promise in early treatments and trials, but they are not universally effective,” said Judith A. Varner, PhD, professor in the Departments of Pathology and Medicine at UC San Diego School of Medicine. “We have identified a new method to boost the effectiveness of current immune therapy. Our findings also improve our understanding of key mechanisms that control cancer immune suppression and could lead to the development of more effective immunotherapies.”

When confronted by pathogens, injury or disease, the initial response of the body’s immune system comes in the form of macrophages, a type of white blood cell that express pro-inflammatory proteins called cytokines that, in turn, activate T cells, another immune cell, to attack the health threat. The macrophages then switch gears to express other cytokines that dampen T cell activation, stimulating tissue repair.

In chronic inflammatory diseases such as Alzheimer’s and Crohn’s, however, macrophages associated with the malignancy continue to produce pro-inflammatory cytokines and other substances that kill or transform normal cells. In cancer, highly abundant microphages express anti-inflammatory cytokines that induce immune suppression, effectively stopping the healing process.

In the Nature paper, Varner and colleagues pinpoint a key, suspected player: an enzyme in macrophages called PI-3 kinase gamma (PI3Ky). In mouse studies, they found that macrophage PI3Ky signaling promotes immune suppression by inhibiting activation of anti-tumor T cells. Blocking PI3Ky activated the immune response and significantly suppressed growth of implanted tumors in animal models. It also boosted sensitivity of some tumors to existing anti-cancer drugs and synergized with existing immune therapy to eradicate tumors. Varner and her colleagues at the Moores Cancer Center also identified a molecular signature of immune suppression and response in mice and cancer patients that may be used to track the effectiveness of immunotherapy.

“Recently developed cancer immunotherapeutics, including T cell checkpoint inhibitors and vaccines, have shown encouraging results in stimulating the body’s own adaptive immune response,” said co-author Ezra Cohen, MD, who heads the cancer immunotherapy program at Moores Cancer Center. “But they are effective only on a subset of patients, probably because they do not alter the profoundly immunosuppressive microenvironment created by tumor-associated macrophages. Our work offers a strategy to maximize patient responses to immune therapy and to eradicate tumors. ”

The Nature paper builds upon other work by Varner and colleagues. In a paper first published online in May in Cancer Discovery, Varner’s team reported that blocking PI3Ky in tumor-associated macrophages stimulated the immune response and inhibited tumor cell invasion, metastasis and fibrotic scarring caused by pancreatic ductal adenocarcinoma (PDAC) in animal models.

In humans, PDAC is the most common malignancy of the pancreas It’s aggressive and difficult to treat. Though only the 12th most common type of cancer in the United States, pancreatic cancer is the fourth most common cause of cancer-related death.

“PDAC has one of the worst 5-year survival rates of all solid tumors, so new treatment strategies are urgently needed,” said Megan M. Kaneda, PhD, an assistant project scientist in Varner’s lab and collaborator on all of the papers.

In a December 2015 paper published online in Cancer Discovery, Varner and colleagues described animal studies that revealed how disrupting cross-talk between B cells (another type of immune cell) and tumor-associated macrophages inhibited PDAC growth and improved responsiveness to standard-of-care chemotherapy.

Specifically, that research team, which included scientists in San Francisco, Oregon and Switzerland, reported that inhibiting Bruton tyrosine kinase, an enzyme that plays a crucial role in B cell and macrophage functions, restored T cell-dependent anti-tumor immune response. In other words, it reactivated the natural, adaptive immune response in tested mice.

Q&A with TapImmune CEO Dr. Glynn Wilson, on a Vaccine to Prevent Cancer Recurrence, in Multiple Phase II Trials

A vaccine that can prevent the recurrence and metastasis of cancer would save countless lives. In the past century, vaccines have virtually eradicated life threatening diseases including polio and tuberculosis. Medical science may soon be at the point of delivering a cancer vaccine.
Scientists at TapImmune are working closely with leading institutions and a big pharma collaborator including the Mayo Clinic, Memorial Sloan Kettering Cancer Center, the U.S. Department of Defense, and AstraZeneca, to bring such a cancer vaccine to market.
TapImmune’s lead cancer vaccine candidate, TPIV 200 is slated for four Phase II trials this year. Outstanding Phase I results from previous studies conducted at the Mayo Clinic are the impetus for Phase II trials in ovarian and breast cancer.
The Bio Connection recently spoke with TapImmune CEO Dr. Glynn Wilson about TPIV 200.

Q: Tell us about TPIV 200 and what makes it a vaccine, rather than a drug or a treatment?

TPIV 200 works much like vaccines that target other disease such as polio and tuberculosis because it stimulates the body’s cellular immune system to recognize and fight the disease. In this case, TPIV 200 targets cancer cells and in particular, it targets metastatic cancer, which is the biggest threat to survival. TPIV 200 broadly stimulates T-cells to recognize, remember, and attack specific targets (antigens) on tumor cells throughout the body.
TPIV 200 is also an off-the-shelf product, like most other vaccines today. It has been formulated and manufactured as a lyophilized (frozen) product with a long shelf life that can be administered via injection, without having to customize it for a specific person’s cancer cells.
Our clinical trials are designed to test TPIV 200’s efficacy in preventing cancer from recurring in people who have already been diagnosed with, and treated for, cancer, thus serving as a vaccine against cancer recurrence.

Q: Would TPIV 200 only be used in people who have already had cancer? What about people using it in a preventative way?

Since a majority of cancer deaths are caused by cancer recurrence and metastasis, not the original tumor, we see this as the area of greatest need. Indeed, in our target indications, ovarian and triple negative breast cancer, patients are at a high risk of cancer recurrence following standard treatments. That’s why we are evaluating the efficacy of TPIV 200 in preventing or delaying recurrence and metastasis.
We certainly see the possibility of developing a prophylactic, or preventative vaccine, for people who have not had cancer, but to do this you will normally need to demonstrate efficacy in a therapeutic setting. There is growing evidence, in preclinical studies, that a preventive vaccine may be viable. We are currently exploring additional studies in this area. A prophylactic cancer vaccine may potentially be developed based on either the TPIV 200 or TPIV 110 platforms. Or, our own in-house developed PolyStart platform also shows great promise for this.

Q: For a company your size, conducting four simultaneous Phase II trials is really impressive. How are you managing this strategy and why four at the same time?

Two of our upcoming Phase II trials are being conducted and financed in collaboration with world-class organizations. These reduce our clinical development costs significantly and they bring on board some of the top minds in immuno-oncology to work on TPIV 200.
With a $13.3 million grant, the U.S. Department of Defense is fully funding a double-blinded, placebo controlled Phase II study of TPIV 200 in 280 patients with triple negative breast cancer to be conducted at the Mayor Clinic in Jacksonville, Florida.
TapImmune is also collaborating with AstraZeneca on a Phase II trial in 40 patients with platinum resistant ovarian cancer, for a combination therapy of TPIV 200 with AstraZeneca’s anti-PD-L1 checkpoint inhibitor, durvalumab (MEDI4736). This study has begun enrollment and is being conducted at the Memorial Sloan Kettering Cancer Center in New York.
Two other Phase II studies are being funded and conducted by us. We recently dosed the first patient in our Phase II trial of TPIV 200 in triple negative breast cancer. This study, which will enroll 80 patients, is being conducted and funded by TapImmune. Later this year, we plan to commence another company conducted and funded Phase II trial in platinum sensitive ovarian cancer patients. Because we are conducting and funding these trials ourselves, we have greater control over the timing and pace of the trial. This is very helpful in terms of seeing data in the relative near term, and advancing our development timeline.
Our strategy is to move TPIV 200 along on multiple fronts via both our own company sponsored trials and by collaborating with others, to reduce our development costs.

Q: Why do you think AstraZeneca, which can partner with just about anyone chose TapImmune’s TPIV 200? Do you see this collaboration with AstraZeneca expanding into something more?

The collaboration started with the Principal Investigator at Memorial Sloan Kettering, Dr. Jason Konner, who saw the potential of combining a leading checkpoint inhibitor with a T-cell vaccine in ovarian cancer patients. Clinicians at AstraZeneca then reviewed the technical and clinical data on TPIV 200, resulting in the current collaboration. They are a big believer in testing combination therapies and are conducting over a dozen clinical trials of their checkpoint inhibitor durvalumab in combination with other compounds.
It’s premature to say anything about a deepening relationship AstraZeneca at this point, but we are very pleased they saw enough promise in TPIV 200 to conduct a collaborative trial with us. If favorable data emerges from the Phase II trial, that may be the impetus for us to discuss an expanded relationship with AstraZeneca.

Q: Can you tell us more about your other cancer vaccine, TPIV 110?

We plan to initiate a Phase II clinical trial of TPIV 110 at the start of 2017. TPIV 110 is a proprietary HER2neu vaccine technology. The HER2neu antigen is a well-established therapeutic target and plays a role in breast, ovarian and colorectal cancer. Each of these is a potential indication for this vaccine. Like TPIV 200, TPIV 110 was originally developed at the Mayo Clinic and TapImmune has a worldwide exclusive license on these technologies. The Mayo Clinic successfully concluded a Phase I trial in HER2neu breast cancer patients that evaluated TPIV 100, a precursor to TPIV 110 which has 4 Class II antigens. TPIV 100 was found to be safe, well-tolerated, and provided a robust immune response across a broad patient population. 19 out of 20 patients showed a robust T-cell response to two antigens and 15 out of 20 patients showed a response to all four antigens. TPIV 110 has been formulated with an additional 5th antigen, which is a Class I antigen, expected to make it more potent than TPIV 100. We believe TPIV 110 shows great promise and it helps round out our cancer vaccine portfolio.
For more information on TapImmune visit http://www.tapimmune.com (Ticker: TPIV)

Q&A with Denis Corin, Q Bio Med Inc – Getting Past the “Pharma Bro” – Smaller Biotech Continue to Strive for Well-Being of Patients

There has been a vast amount of mixed feelings surrounding the biotech/drug company development of drugs and the final price consumers/patients are paying. Especially when one biotech CEO, Martin Shkreli (aka ‘Pharma Bro”) decided to massively increase of a very cheap drug vital to patients with HIV from $13.50 to $750. The actions of one CEO has cast an unjust dark shadow on peers in the industry.

According to Denis Corin, CEO of Q BioMed Inc, a biomedical acceleration and development company, Shkreli’s actions drowned the positive work of hundreds of thousands good corporate citizens in the industry – all judgment cast by one greedy arrogant pharma exec.

“The reason innovators, scientists, well-meaning drug company executives and entrepreneurs, do what we do, has to be rooted in the well- being of the patients we ultimately want to treat. We want to make their lives better. Period. Whether its adding a few healthy years with less pain, or perhaps it’s a life changing cure that will add months or years of comfortable life for patients and their families,” believes Corin.

Life-saving drugs are expensive to develop and for every one that makes it through an overly regulated FDA, over 500 fail. The money has to come from somewhere. Corin believes that there is a balance and what we have seen in the headlines this past while or so is way off the mark and can attest it’s not the way the biotech sector thinks or behaves.

Corin’s own company, Q BioMed Inc, has been working hard to find innovative products and drugs that can accelerate through the development process with the best human capital and least money possible. He recently spoke with The Bio Connection:

Q: What impact did Martin Shkreli (aka “Pharma Bro”) have to the industry?
Corin: I am not sure what the lasting impact is. For the moment its put a spotlight on the cost of drugs and the profit margins associated with those drugs. I think the increased focus on these issues and the overall cost of healthcare, especially in US and the continuing debate around ‘the affordable healthcare act’ and its cost are all contributing to a healthy dialogue. Ultimately it’s making the pharma and biotech’s be more conscious of the issues and what’s going to need to happen to address them.

Q: Why do existing profits makes the pharma system work efficiently? How does providing incentives to keep innovating, making enough profit to make it work, and encourage reinvestment in new ideas and products help?

Corin: Companies need to be profitable to continue to deliver product. But, more so in the pharma industry, we are working new drugs and treatments that have a low probability of making it from concept to revenue. So significant amounts of money need to be invested in innovation and Research & Development that doesn’t always deliver a return on that investment. So, if pharma companies are not making a significant amount of money they simply can’t invest capital into those areas and we’ll have less new drug discovery and testing. That’s not the idea. We need to be continually reinvesting in pipelines of drugs and new potential therapeutics and making old ones better and more affordable.

Q: How we can strike the right balance between price and innovation?

Corin: I am not sure if there’s a silver bullet or a simple answer to that. I believe that as technology improves and diagnoses are made earlier, and regulatory hurdles are lowered, more competition will help make that balance more meaningful.

Q: What can CEO do to raise good will and trust among investors?

Corin: I think just by working hard at delivering good product at reasonable prices and providing a decent return. It sounds simple and the kind of principle any business should run on.

Q: Why are capital markets key to fueling innovation and keeping prices manageable?

Corin: So much innovation and new product development is coming out of the junior biotech sector and academia. This is where the capital markets are funding this development and the future pipelines of big pharma. Most new drugs these days are not organically developed at the big name pharma companies, they are coming from smaller biotech start-ups and that requires the capital markets to be actively funding them.

Q: What sectors are going to experience new innovations, new medicines and drive patient care costs down.

Corin: I think there are number of companies looking to repurpose older drugs and generic drugs. Due to the fact that these may have lower development costs, they should provide better access and better price points. I think the new frontier in oncology is immuno-oncology, checkpoint inhibitors and the newer CAR-T type approaches. There have been some very exciting developments in those areas that give hope that there are some major breakthroughs on the horizon. While the results are encouraging, the fact that they are new and costly to produce and administer, I don’t see the price coming down in the near term, but expect that the economic climate and burdened healthcare system, will encourage reasonable price policies.

For more information about http://www.Qbiomed.com (OTCQB: QBIO)

Cancer Immunotherapies take Center Stage

The newly created task force on cancer, in what Vice President Joe Biden has called a “moon shot” to cure the disease, is to put the US on a path to achieve in just five years research and treatment that otherwise might take a decades or more.  Although the memorandum does not commit the government to major new spending, the task force’s role will be to focus on making the most of federal investments, targeted incentives, private sector efforts from industry and philanthropy, patient engagement initiatives and other mechanisms to support cancer research and enable progress in treatment and care.

One area of promise in oncology, has been cancer immunotherapy, which harness the power of the immune system to eradicate cancer and prime the immune system to fight off relapses. For decades, most cancers have been treated with the standard of care treatments which typically include surgery, radiation and/or chemotherapy.

Immunotherapy is a wide area of cancer treatment and research that has built momentum in recent years. Many different types of immunotherapies have been effective in treating and even potentially curing melanomas, B-cell Chronic lymphocytic leukemia, and non-Hodgkin lymphoma, and are currently being developed to treat nearly every time of cancer, including breast cancer. Recent research showed that 70 percent of multiple myeloma patients recovered with immunotherapy.

New Thinking in Head & Neck Cancer

CEL-SCI Corporation, a Vienna-based biotech firm is currently investigating their flagship investigational cancer immunotherapy, Multikine (Leukocyte Interleukin, Injection), in a global Phase 3 clinical study  in head and neck cancers, in what they believe is the logical next step in immunotherapy development. Based on the results of earlier human studies, researchers at CEL-SCI believe that cancer  immunotherapy should be administered as an initial therapy before a patient’s immune system has been debilitated by surgery, radiation and chemotherapy. Data from earlier Multikine Phase 2 human studies, demonstrated that when Multikine was administered for only 3 weeks immediately after diagnosis, the treatment reduced and in some cases eliminated all signs of a tumor before surgery, radiation and/or chemotherapy, for head and neck cancer patients, were administered.

Other investigational cancer treatments and immunotherapies are usually tested as a last resort on patients who have already undergone and failed standard of care treatments. Therapies which are used as a last resort and show some efficacy, will have reached their clinical study primary endpoint in a fairly short period of time. That is because patients with end-stage disease generally have a shorter life expectancy.

The company is the first to advance its investigational cancer immunotherapy into Phase 3 studies where it is actually administered as a first-line treatment immediately after diagnosis within a three-week window before any standard-of-care treatments. Most other cancer immunotherapy treatment regimens must be administered over longer periods of time and cannot be given in the brief three-week period before the current standard of care (surgery and/or radiation and chemotherapy) must be administered. If this treatment regimen is proven successful, the drug will, (1) reduce the number of cancer recurrences and, (2) increased the overall survival of the patients who were treated with the drug.

The hope is that someday Multikine will be administered as the first treatment right after initial cancer diagnosis for many different types of cancers.