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    Prostate cancer: Big data unlocks 80 new drug targets

    In the biggest study to analyze the genetics of prostate cancer, scientists find no fewer than 80 new potential drug targets. The project opens broad avenues for the design of new treatments.
    DNA computer code
    Big data provides new ways to approach prostate cancer.
    Extracting genetic data was, once upon a time, a cumbersome and incredibly time-consuming task.

    However, as technology continues to improve, the job has become significantly quicker and cheaper.

    In parallel, the tools available for handling large datasets have vastly improved.

    Taken together, this means that the oceans of information harvested from genetic code can be analyzed, mapped, and combined with relative ease to provide a new level of clarity.

    Recently, an international team used this double-pronged approach of DNA analysis and big data to delve into the genetics of prostate cancer. On the hunt for molecular chinks in the disease's armor, the research was orchestrated by the Institute of Cancer Research in London, United Kingdom.

    Prostate cancer challenges
    Prostate cancer is the second most common cancer among men in the United States. This year, in the U.S., there will be an estimated 164,690 new cases of prostate cancer and almost 30,000 deaths to the disease.

    Although researchers have made headway in understanding and treating prostate cancer, there are still a number of difficulties.

    As study leader Prof. Rosalind Eeles explains, "One of the challenges we face in cancer research is the complexity of the disease and the sheer number of ways we could potentially treat it."

    Dr. Justine Alford, of Cancer Research U.K., outlines another issue in studying and intervening in prostate cancer.

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    "A major hurdle to making further progress against prostate cancer," she explains, "is the lack of ways to accurately predict how a person's disease will progress, making it challenging to know which treatment is best for each patient."

    Harvesting genetic data
    To approach the problem from a new direction, the researchers took genetic information from 112 men with prostate cancer and combined it with data from a range of other studies. In all, samples from 930 patients were used.

    Using the latest big data techniques, the team garnered new insights into genetic changes that spark the development and fuel the progress of prostate cancer. Once they understood which genes were involved, they could create a map of the proteins that are coded by these genes.

    Next, they turned to a database called canSAR, which combines data from studies, applies machine learning, and helps to provide insight into drug discovery.

    On their website, canSAR explain the questions that their database aims to answer: "What is known about a protein, in which cancers is it expressed or mutated, and what chemical tools and cell line models can be used to experimentally probe its activity? What is known about a drug, its cellular sensitivity profile, and what proteins is it known to bind that may explain unusual bioactivity?"

    The scientists found that 80 of the proteins that they had uncovered were potential drug targets. And, 11 of these were targeted by existing drugs, and seven others could be targeted by drugs already in clinical trials.

    Their findings are published this week in the journal Nature Genetics.

    "Our study applied cutting-edge techniques in big data analysis to unlock a wealth of new information about prostate cancer and possible ways to combat the disease."

    Prof. Rosalind Eeles

    Looking to the future
    The discoveries will require further study before they can be used clinically, of course, but they provide a range of new possibilities.

    As co-author Prof. Paul Workman explains, "This study has uncovered a remarkably large number of new genes that drive the development of prostate cancer, and given us vital information about how to exploit the biology of the disease to find potential new treatments."

    He hopes that their work will "stimulate a wave of new research into the genetic changes and potential drug targets [they] have identified, with the aim that patients should benefit as soon as possible."

    Another stumbling block for the design of prostate cancer treatments is the way that the disease progresses differently in each individual. This makes it much more difficult to decide which treatment options are best suited to each patient.

    Dr. Alford hopes that "[b]y greatly enhancing our understanding of the genetics behind the disease, [...] in the future, this knowledge could help doctors better tailor treatments to an individual's cancer, and hopefully see more people survive their disease."

    These are early days, but the findings that will come from the next generation of studies could be transformative to the field.

    From Medical News Today

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    Vaccines are medicine’s most important invention—but they could be even more effective

    After I received a vaccine as a child, my mom would take me to get ice cream. While I inhaled my vanilla twist, my body was mounting a response to the inactive virus or bacteria injected into my left arm.

    In an orchestral sequence of events, the body processes antigens, substances that provoke an immune reaction, in the vaccine and produces antibodies to defend itself. In vaccines, these antigens are commonly live, weakened, parts of, or dead pathogens. When we encounter these invaders in the future, antibodies identify the antigen, call in backup, and the threat is eliminated. This specific reaction is known as the adaptive immune response, one of two pillars that make up our immune system.

    This symphony is wildly successful in many cases—the vaccine is the most important invention in medicine. Hundreds of millions of people saved, millions of disease cases and deaths prevented, billions of dollars saved in healthcare. Take polio, for example: an injection of inactivated poliovirus has nearly wiped it from existence.

    However, in some of the biggest threats in our generation, current attempts to produce a vaccine for HIV, malaria, RSV-F, and Tuberculosis are struggling. To be clear, the reasons behind these failures are complex and could range from how the clinical trial was conducted to the design of the vaccine. But new studies suggest that the innate response has immense potential to help fix these failures. It’s time to design therapies aimed at both pillars of the immune system, not just the adaptive response.

    Before the doctor injected that vaccine into my arm all those years ago, the other pillar, termed the innate immune system, was prepared to respond to invaders. This response is the natural, front-line defense we are born with. If the adaptive immune response is the SWAT backup, then our innate response consists of the physical barriers, alarm systems, and first responders. These two systems work hand in hand against enemies of our cells. All walks of life have innate immune systems, from plants to fungi to our multicellular ancestors.

    Recent evidence suggests that innate immunity can be trained to respond more effectively.

    Until recently, our innate immunity was thought to lack the memory that makes our adaptive response so powerful in response to specific disease-causing pathogens. This idea is now being challenged: Maziar Divangahi at McGill University and his team recently published evidence suggesting that the cells and processes that form our innate immunity can be trained to respond more effectively the second time it encounters that pathogen.

    Divangahi studied this phenomenon using the most administered vaccine in the world, Bacillus Calmette-Guerin (BCG). BCG contains live Mycobacterium bovis, a non-pathogenic strain closely related to Mycobacterium tuberculosis.

    The BCG vaccine does a good job at preventing childhood tuberculous meningitis, but its performance for other Mycobacterium tuberculosis-caused diseases is debated and unconvincing. Considering 1.7 million people die annually from tuberculosis, primarily in the lungs, this is an issue. Motivated by efforts to develop an effective tuberculosis vaccine and by growing tuberculosis (TB) antibiotic resistance, Divangahi and his team tested if administering the BCG vaccine directly into the bloodstream, rather than in the top skin layer, in mice could improve the response to Mycobacterium tuberculosis.

    Intravenous, rather than localized, administration allows the vaccine to reach the bone marrow, home to hematopoietic stem cells, a self-renewing factory that produces an army of immune and blood cells. In this army of cells are those commonly responsible for our innate immune response: macrophages, natural killer cells, neutrophils, and dendritic cells.

    Trained immunity
    Instead of relying on the vaccine to ignite the adaptive immune response, the researchers hypothesized that they could educate the stem cells to produce better-trained innate immune cells—better first responders. And they were right. Exposure to the live, weakened bacteria from the BCG vaccine resulted in greater protection in the mice they studied. This protection was sustainable for several weeks afterward. To make their case stronger, mice without T-cells in their bone marrow were used to compare, which allowed them to confirm it was the innate system at work, not the adaptive. The changes researchers found in which genes were expressed and how they were regulated in the study suggests that how and where we administer vaccines can fundamentally alter the ability of our innate immune system to respond to disease-causing pathogens.

    Despite these convincing results, this research is still in its infancy. For starters, the study was done in mice, and mice are not humans. Any vaccine design stemming from this study or others like it, like all vaccines, will face a gauntlet of excruciating safety and efficacy testing before reaching patients. Nevertheless, Divangahi and his co-authors explicitly consider the failure of T cell-targeted vaccines combined with their results as reason to revisit the design of TB vaccines.

    The vaccine created in 1921 for tuberculosis is still used for attracting and priming our immune cells—to eat cancer cells.

    Trained immunity may be a viable option, alone or as a supplement, to bolster our defenses. Interestingly, we may have already been doing this without fully realizing it. Numerous studies have shown that live vaccines, like BCG, provide protection beyond their intention. In fact, BCG has been used to treat bladder cancer, leukemia, melanoma, and lymphoma. This vaccine, created in 1921 for tuberculosis, is still the primary immunotherapy for bladder cancer for its ability to attract and prime our immune cells—to eat cancer cells, in this case.

    This idea of trained immunity is catching on. Cancer chemotherapies are being tested in combination with tiny fragments of protein derived from the wall of Mycobacterium. A new pertussis vaccine seeks to utilize both the innate and adaptive responses. Even the widely covered cancer vaccine, from Ronald Levy at Stanford, that cured nearly 97% of mice of solid tumors all over their bodies, employs a similar strategy. Direct administration of immunotherapy and an innate activating chemical caused an incredibly effective response.

    Two themes emerge: where and how the immune system is engaged can dramatically impact the outcome. In the case of tuberculosis vaccination, exposing the birthplace of our immune cells to bacteria trains them to be more fundamentally more effective defenders against tuberculosis and, as it turns out, many other invaders.

    It’s also worth mentioning the blurring of lines between what is considered innate and adaptive. And this response may not always be desired. Researchers have shown issues arising in innate immunity during vulnerable states like sepsis or chronic inflammatory conditions.

    These insights about how and where we administer vaccines hold promise about new strategies to tackle diseases. Compounded with new curative, mRNA vaccines—a topic for another time—and economics in favor of widespread commercial support, I feel optimistic that the next decade will be the vaccine’s time to shine.

    This piece was originally published on Massive, a site that publishes science stories by scientists on the cutting edge of research. Subscribe to their newsletter or visit them on Facebook or Twitter for more.

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    CancerNews asked a questionCancer

    How long did your neuropathy last after treatment stops?

    9 answers
    • IKickedIt's Avatar

      I finished chemo 6+ years ago and at that time, the neuropathy was crippling. It improved significantly for the first year or two, but very, very little since then. I've been to several doctors (including a top neurologist at one of the top university hospitals/cancer center in the country) and have been told any more improvement is unlikely. I can function within a normal range, although on the low end. Never really sure if new shoes truly fit and I have poor fine motor skills (I do miss playing the piano). It's more of a reminder than a hindrance, though.

      13 days ago
    • Skyemberr's Avatar

      I have had Xeloda and FOLFOX so far. The numbness is a bit better since I had them in 2016 and 2017, but I often still notice it in my hands and arms, sometimes my foot. It seems to hit me when I am holding an object for too long.

      12 days ago
    • Ellie59's Avatar

      7 years two months 2 months and 22 hours so far.

      10 days ago
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    CancerNews posted an update

    Non-Hodgkin's lymphoma-Symptoms & causes-Diagnosis & treatment-Doctors & departments-Care at Mayo Clinic

    A needle suctioning out liquid bone marrow from hipbone
    Bone marrow biopsy
    Your doctor will likely ask you about your personal and family medical history. He or she may then have you undergo tests and procedures used to diagnose non-Hodgkin's lymphoma, including:

    Physical exam. Your doctor checks for swollen lymph nodes, including in your neck, underarm and groin, as well as for a swollen spleen or liver.
    Blood and urine tests. Blood and urine tests may help rule out an infection or other disease.
    Imaging tests. Your doctor may recommend imaging tests to look for tumors in your body. Tests may include X-ray, CT, MRI and positron emission tomography (PET).
    Lymph node test. Your doctor may recommend a lymph node biopsy procedure to remove all or part of a lymph node for laboratory testing. Analyzing lymph node tissue in a lab may reveal whether you have non-Hodgkin's lymphoma and, if so, which type.
    Bone marrow test. A bone marrow biopsy and aspiration procedure involves inserting a needle into your hipbone to remove a sample of bone marrow. The sample is analyzed to look for non-Hodgkin's lymphoma cells.
    Other tests and procedures may be used depending on your situation.
    Full Article at Mayo Clinic

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    Metastases – the real cancer risk

    Metastases are often more dangerous than the primary tumor that gives rise to them. They are responsible for 90% of all cancer deaths. Here are the most important facts on these deadly ‘sleeper’ tumors.

    Created by cells released by the primary tumor that have been transported to other organs or body parts, metastases – secondary cancer growths that spread through the body – are often viewed as its ‘deadly offspring'. At these secondary sites, the cells proliferate and grow into dangerous metastatic tumors.

    "Usually cells have their dedicated place in the body – they don't migrate,” explains Susanne Weg-Remers from the German Cancer Research Center in Heidelberg. "But malignant cells from solid tumors can in some instances cross anatomical boundaries. Those malignant cells then invade other environs and destroy the surrounding tissue.”

    When the malignant cells enter the bloodstream or lymphatic system, they are transported throughout the body, and can dock onto and enter tissue in other areas. Once there, they establish themselves and begin to divide, eventually turning into metastases. Those metastatic tumors are no longer localized, meaning they can spread elsewhere in the body and can no longer be controlled.

    Under what conditions do metastases form?

    Cancer begins when the DNA in previously healthy cells changes during the course of life. That gives rise to cells with new characteristics. For example, growth behavior can change. Cells can begin to divide in an uncontrolled way, and no longer heed the body's signals to stop.

    To host a metastasis, a particular location in the body has to fulfil a range of conditions. The malignant cells need access to the circulatory system. "The cells have to stimulate the growth of blood vessels in the area. These have to penetrate the newly-forming tumor to ensure it's hooked up to the bloodstream,” says Weg-Remers. The vessels supply the forming metastasis with blood that carries oxygen and nutrients, allowing the cells in it to multiply.

    Types of cancer that frequently metastasize

    Lung cancer is one type of carcinoma that has frequently already metastasized by the time an initial diagnosis is confirmed. Pancreatic cancer, liver cancer and bile duct cancer are also very aggressive forms of the disease. One big problem with these conditions is that sufferers rarely have any physical complaints until the cancer has progressed significantly. "They're often only recognized when the metastases have already formed. At that point, the cancer is no longer curable,” explains Weg-Remers.

    Cancer treatments are most successful when the tumor is confined to a single location and surgeons can remove it without causing potentially life-threatening damage. That is what makes brain tumors a challenge to treat. While they are usually confined to the brain, complete surgical removal is often difficult.

    Read more: New blood test could detect eight types of cancer before symptoms show

    Brain cancer – a special case

    Primary brain tumors grow directly out of the organ's tissue or the surrounding connective tissue, and only rarely metastasize. When they do, the metastases appear in the areas filled with cerebrospinal fluid, a liquid that surrounds and cushions the brain.

    Even though they so seldom metastasize, brain tumors still often prove deadly when vital functions in the brain are affected. Many brain cancers are also secondary tumors, meaning cancers that have spread from other parts of the body. "The brain apparently offers good docking opportunities for metastases,” says Weg-Remers. "The molecular mechanisms that play a role in the process are the subject of ongoing studies.”

    Metastases and their preferred organs

    Although brain tumors rarely metastasize, other types of cancer – such as lung cancer – can spread to the brain. Breast cancer on the other hand often spreads to nearby lymph nodes. When breast cancer metastasizes, it often affects the bones, lungs or liver.

    Prostate cancer also often metastasizes to the bones and lymph nodes, and at times to the liver or lungs. Metastases from bowel cancer often spread to the peritoneum or lymphatic system.

    Is slowing metastasized cancer the only option? Or can it be stopped?

    Once metastases have appeared, the progression of the disease can generally only be slowed.

    Researchers are working hard to clarify the mechanisms behind metastasis. Many scientists believe that in order to develop new treatments, we first have to fully understand the docking mechanism used by cancer cells to gain a foothold elsewhere in the body, as well as how the tumor ensures a steady supply of blood.

    Many of the interactions that take place between cancer cells and cells in the surrounding healthy tissue remain unexplained. "For example, the body produces a range of hormones that eventually cause reprogramming in the surrounding blood vessels,” explains Weg-Remers. "When researchers are able to trace and understand these mechanisms, that will likely open the door to new therapeutic approaches.”