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    CancerNews asked a questionCancer

    A short and simple poll. Are you optimistic about your treatment path or pessimistic?

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    CancerNews posted an update

    Pill for breast cancer diagnosis may outperform mammograms

    As many as one in three women treated for breast cancer undergo unnecessary procedures, but a new method for diagnosing it could do a better job distinguishing between benign and aggressive tumors.

    More from Science Daily .com https://www.sciencedaily.com/releases/2018/04/180430131433.htm

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    CancerNews posted an update

    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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    CancerNews posted an update

    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.

    1 Comment
  • CancerNews' Avatar

    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.

      2 months 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.

      2 months ago
    • Ellie59's Avatar

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

      2 months ago