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    Step forward in leukemia treatment
    by South Australian Health and Medical Research Institute

    An international clinical trial involving Adelaide researchers has demonstrated the safety and efficacy of a next-generation treatment for people with chronic myeloid leukemia (CML).

    The study's lead author, Professor Tim Hughes, says successful development and testing of the new kinase inhibitor called asciminib is the biggest breakthrough in CML treatment this century.

    The development of the original tyrosine kinase inhibitor (TKI) called imatinib in the 1990s changed CML from a death sentence to a disease that in many patients could be managed until they lived to a ripe old age," Professor Hughes said.

    "But while imatinib and subsequent TKIs have been very effective at improving survival, they frequently cause serious side-effects."

    TKIs that are currently approved for use are not well targeted, attacking leukemia cells but also damaging healthy cells. Professor Hughes, a Cancer Council SA Beat Cancer Professor, says asciminib selectively blocks the mutant kinase present in the leukemic cells.

    "This trial of 150 patients showed asciminib is highly effective, even in patients who'd failed to respond to several other TKIs," Professor Hughes said.

    "Equally as important, it's well tolerated by patients and appears to have significantly less long-term ill-effects compared to current treatments."

    The results of this clinical trial were published today in the esteemed New England Journal of Medicine.

    CML is a blood cancer that causes bone marrow to produce too many white blood cells. This excess of mutant white blood cells interferes with normal blood cell production. TKIs slow or stop this excess production of white blood cells.

    Over 4,000 Australians are living with CML currently however the increasingly high survival rate brought about by TKI treatment means the disease is estimated to be the most common form of leukemia by 2040.

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    What Causes Scarring of the Lungs?

    Scarring of lung tissue causes a variety of problems, from difficulty breathing to lack of adequate oxygen intake for optimal function of body organs. Understanding the causes of lung tissue damage helps you make wiser choices about your lifestyle habits. Damage to the bronchi, the two major airways to the lungs; the bronchoiles, the smaller branches of airways; or the alveoli, the small air sacs, may be affected by lifestyle, disease and environmental factors, which can lead to scarring of the lungs.

    Long term exposure to pollutants in the air may lead to lung damage and scarring. For example, metal dust shavings, asbestos or inhaling silica dust particles are environmental hazards of working in the construction industry. A pool cleaner who continually inhales chlorine or acid fumes may also experience some scarring of lung tissues. Farm workers exposed to chicken droppings or dust, moldy hay dust particles or grains grown in crops also face risks of lung damage, according to the Mayo Clinic.

    Radiation Therapy
    If you have been diagnosed and treated for lung cancer with radiation therapy, you may also suffer some lung damage caused by scarred tissues. The degree of damage is determined by the length and duration of radiation treatments and whether or not the person was also treated with chemotherapy drugs congruent with the radiation therapy. Some chemotherapy drugs also cause damage and scarring to the membranes lining and protecting the lungs, according to the Mayo Clinic.

    Pulmonary Fibrosis
    Idiopathic pulmonary fibrosis is caused by a gradual thickening of lung tissues, according to the Pulmonary Fibrosis Foundation. Fibrosis is a medical term for scarring, and idiopathic means there is no known cause for the condition. This thickening leads to large areas of scarring and prevents the affected lung tissues from properly receiving, exchanging or transferring vital oxygen to all parts of the body. Idiopathic pulmonary fibrosis is one of many types of interstitial lung disease processes, which may potentially lead to damage or scarring to the lungs.

    A great majority of lung scarring cases may be caused by pneumonia, according to the University of Maryland Medical Center. Pneumonia inflames lung tissues, causes damage and produces scarring in the interstitium, or fluids in the lungs that lubricate and protect the alveoli, or air sacs in the lungs, according to Medline Plus and the National Institutes of Health.


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    Cancer therapy poised for rapid advances, noted researcher says

    he remarkable cancer treatment that uses a patient’s own immune cells to treat their cancer has saved a growing number of people who were close to death. But sometimes this treatment, known as CAR T cell therapy, fails, and that has perplexed researchers.

    That puzzle is being pieced together, and more effective variations on this therapy are on the way, a pioneer in this therapy said Thursday at a symposium at the UC San Diego Moores Cancer Center.

    A deeper understanding of how immune cells fight cancer, and better genetic engineering methods for these cells are fueling the advances, said Dr. Carl June, MD, of the University of Pennsylvania. Besides the T cell therapy, which is the best known, other immune cells called natural killer cells and macrophages are also being brought into service.

    Not only will the treatments get more effective, but it now appears possible that the current cost of several hundred thousand dollars could in the long term drop dramatically, June said. He presented information from research yet to be published pointing to those advances.

    Just one engineered cell can proliferate and defeat a cancer, June said, citing results from one patient. That patient was infused with many genetically engineered immune cells. One of those cells proliferated more than all others, and its descendants eradicated 5 pounds of tumor cells.

    Engineering one cell is far less expensive than growing a batch of cells, June said, and it is conceivable that could bring down the cost of therapy to that of a regular blood transfusion. That cost varies between several hundred to a few thousand dollars.

    Automation will also help, June said in an interview after his speech.

    “It’s very cheap to do this with machines, rather than it being done it by hand, which it is right now with scientists and technicians,” June said.

    However, it’s unclear how difficult it will be to replicate that finding in other patients, June said in the interview. Safety is also an issue — uncontrolled proliferation is a hallmark of cancer. So more research is needed to understand how this process takes place and to minimize risks.

    In his speech, June gave an example of a known danger. Another cancer patient received a batch of engineered immune cells that contained one “rogue” cell. That cell proliferated and killed the patient.

    “It also is the first real proof of the tumor stem cell hypothesis,” June said.

    That hypothesis says that the most dangerous cancer cells have undergone genetic changes that make them in some ways resemble stem cells. They aggressively proliferate and are the hardest to kill.

    This was shown by examining the patient’s cancer cells.

    “We could show at the time he died, every single cell had the (genetic modification), and they're all descendants of one cell,” June said.

    Another discovery is that in patients that fail CAR T cell therapy, their immune cells often have become exhausted fighting the cancer. This T cell exhaustion also occurs in untreated HIV patients.

    What that means is that the cells are unsuitable for therapy, June said. Moreover, certain types of cancers are more likely to produce this exhaustion than others.

    It may be possible to rescue these exhausted cells with appropriate genetic modifications, June said. That’s being tested in a new clinical trial for prostate cancer that has overcome hormone therapy, so-called “castrate resistant” prostate cancer, where the cancer keeps growing even when the amount of testosterone in the body is reduced to very low levels.

    In a second clinical study, the groundbreaking gene editing technique called CRISPR is being used to create better, more precisely engineered CAR T cells. This is now being tested in four cancers, including multiple myeloma and melanoma.

    Both studies are recruiting patients, who can find more information at www.clinicaltrials.gov. The prostate cancer study can be found under number NCT03089203. The multiple myeloma and melanoma study can be found under the number NCT03399448.F

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    Julia Louis-Dreyfus Posts Stunning Photo To Celebrate Kicking Cancer's XXX

    We deserve some good news right about now, so this photo posted by Julia Louis-Dreyfus is just what the doctor ordered. At least, we can only hope the actress' doctors instructed her to host a radiant photoshoot following her surgery. The Veep star announced her "great results" before revealing that she had undergone surgery as part of her breast cancer treatment, and this photo proves she's more than recovered.

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    Would You Be Able To Spot These 7 Symptoms Of Leukemia? Certain forms of the disease can spread quickly—and be fatal.

    If you've ever seen A Walk to Remember or read My Sister's Keeper (and who hasn't?) then you're already somewhat familiar with the term “leukemia.”

    A blood-based cancer, leukemia occurs when bone marrow cells start dividing and multiplying at a rapid pace, severely limiting the body's ability to produce red and white blood cells. In 2014, an estimated 387,000 people in the U.S. were living with a form of leukemia, according to the National Cancer Institute. And as we've seen in the movies, leukemia can be fast-acting, debilitating, and extremely lethal.

    Exactly how lethal leukemia is depends on its type—chronic or acute, says Anne Renteria, M.D., assistant professor of medicine, hematology, and medical oncology at Mt. Sinai Hospital in New York City.

    When a patient has chronic leukemia, cancer cells are found in the patient's blood and bone marrow, but they don't rapidly and aggressively divide. Chronic leukemias are most often found during routine blood work and are managed either with observation or a chemotherapy pill. “Very often the cancer is in your bone marrow, but it's not making you sick. People with CML and CLL work and pretty much live a normal life,” she says.

    But acute leukemias are a different beast altogether, and you're likely seeing an acute form of the cancer when you see leukemia portrayed on the big screen. Acute leukemias are aggressive, and typically exhibit extreme symptoms before they're diagnosed, she explains.

    Read Full Article on Womens Health: https://www.womenshealthmag.com/health/leukemia-symptoms/slide/1

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    Killer cells target leukemia broadcasting ‘come and get me’

    Researchers used CRISPR gene-editing to equip certain immune cells with a homing beacon to target leukemia.

    Leukemia is a deadly cancer in which rogue white blood cells roam the bloodstream, slowly killing the body that gave them life. But it has an Achilles’ heel. Many leukemia cells are betrayed by a molecule on their exterior surfaces known as CD19.

    “We’re trying to design smarter cells.”

    When activated, CD19 will kill the cancer cell to which it is attached. To cancer biochemists, CD19 is like a tiny radio signal broadcasting to the world, “I’m leukemia. Come and get me.” But when a body is without the immune cells equipped to hear CD19’s siren song, the leukemia is free to carry on its lethal business undeterred.

    So, researchers created leukemia-specific human immune cells that track down and kill any leukemia cell exhibiting the CD19 signal.

    Developing better hunter-killer cells to target cancers is part of what goes on in the lab of Stanley Qi, assistant professor of bioengineering and of chemical systems biology.

    Though this is still basic research, Qi’s approach could one day lead to new ways to treat the roughly 170,000 Americans who were diagnosed with leukemia and other blood-related cancers last year.

    Beyond leukemia
    But leukemia is just the beginning. Cancers of the blood system account for a mere fraction of all cancers, most of which are solid tumors—clumps of cells that grow inappropriately in breasts, ovaries, lungs, and prostate, for example.

    Solid tumors take refuge within a complex microenvironment of molecules, hormones, and growth factors that help these unwanted cells spread and suppress the immune system agents that seek to kill the tumor.

    Qi hopes to prove that his technique could work on all cancers because it targets a beacon found not just on leukemia, but on almost every type of cell in the body, including solid cancers.

    By using CRISPR to hack ever more precisely into the genome, Qi believes it may one day be possible to bioengineer therapeutic agents to dial in on not just cancers, but other diseases that use the same radio-like signaling that has already used to attack leukemia.

    Read Full Article From http://www.futurity.org/immune-cells-targeting-cd19-leukemia-1671742/

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    A helpful list of questions to ask your oncologist about your diagnosis.

    Questions to ask about diagnosis

    The following are questions that you can ask the healthcare team about stem cell transplant. Choose the questions that fit your situation and add questions of your own. You may find it helpful to take the list to the next appointment and to write down the answers.
    What test(s) are needed to find cancer? How are they done?
    Will a biopsy be done?
    When will the test(s) be scheduled? Is there a waiting list?
    Who makes the arrangements or appointments for the test(s)?
    Can a support person (such as a partner, parent or friend) be present during the test(s)?
    Where will the test(s) be done?
    Will the procedure be done as an inpatient or outpatient procedure?
    Is an anesthetic or sedation used? If so, what kind?
    Is any preparation needed for the test(s)?
    How long will the test(s) take?
    Are there any side effects to the test(s)? Is the procedure painful?
    Are there any risks involved with the test(s)? What are they?
    Are there special instructions to follow after the test(s)?
    Do I need to arrange a ride home after the test(s)?
    How long does it take to get the results of the test(s)?
    Who will explain the test results?
    May I have a copy of the test results?
    What happens if the results are not normal?
    What other tests will need to be done? Why?

    Read more: http://www.cancer.ca/en/cancer-info...

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    What is hairy cell leukemia and how is it treated?

    Hairy cell leukemia is a type of hematologic cancer. This type of cancer starts in the tissues that form blood, such as the bone marrow, or in the cells of the immune system.
    Hairy cell leukemia accounts for approximately 2 percent of all leukemias, is more common in men than in women, and is also more frequent in older people. Around 1,000 new cases are reported every year in the United States.

    It is a rare form of leukemia, in which the bone marrow produces an excessive amount of a type of white blood cell called B cells. These abnormal B cells do not develop into healthy cells but instead become harmful cells known as leukemia cells.

    Leukemia cells can build up in the blood or the bone marrow, taking up space from healthy cells. This may weaken the body's immune system and make it more prone to infections, anemia, and bleeding.

    The name "hairy" comes from the way the leukemia cells look under a microscope — they resemble hair.

    Read the full article from Medical News Today

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    Revealed: adult leukemia can be caused by gene implicated in breast cancer and obesity

    When people think of leukemia, they usually think of blood cancers that affect children. These mostly come under the category of acute lymphoblastic leukemia – or ALL – and are different to the group of blood cancers which predominantly affect adults over the age of 60, known as acute myeloid leukemia (AML).

    AML accounts for about 90% of all leukemias in adults, though it affects some children too. With some 3,000 new cases each year in the UK alone, it is tougher to treat than ALL.

    Where advances in ALL treatment have raised survival rates to around 90% over the past several decades, the rates for surviving the less well-researched AML are more like 65%. Older adults respond least well to treatment, with only 5% of over-65s surviving more than five years.

    I am therefore pleased to report a promising discovery. Work in which I have been involved has shown that a particular gene can play a critical role in the development of the disease. This could be the precursor to a breakthrough that could be life-saving for patients.

    Cells and treatments
    Your bone marrow contains stem cells which divide and differentiate into red blood cells and the main groups of white blood cells – myeloid cells, neutrophils, and lymphocytes. Normally this happens in a very controlled manner, ensuring you have all the red blood cells needed to carry oxygen around your body, and all the white blood cells needed to fight off infections.

    In AML too many immature myeloid cells are produced too quickly by the bone marrow. They are mutant cells which don’t mature, meaning they fail to defend against infection.

    For this reason, early signs of AML include flu-like symptoms, aches, and pains in the joints and rapid weight loss. As the abnormal cells build up inside the bone marrow or the blood they grow and divide aggressively. Left untreated, AML patients can have only weeks to live.

    Patients are normally treated by two stages of chemotherapy over a few months: an induction phase which reduces the number of cancer cells to undetectable levels, then a consolidation phase to kill any cancerous cells hiding in the body. Patients often also receive a bone marrow transplant, effectively giving them a new immune system.

    Treating AML is complicated by patients generally being older, since they tolerate the intensive chemotherapy less well. In many cases, they receive some treatment and end up only living a few months. Better understanding the mutations to develop more targeted and less harsh treatments looks like the key to improving survival.

    Step forward, PTPN1
    A number of mutations are associated with AML and often occur in combinations. It’s these mixtures of mutations that are thought to cause the complex subtypes of cancers within the AML group. One common mutation is called Del20q. It involves the deletion of part of chromosome 20, one of the 23 pairs of chromosomes most humans have in all their cells.

    It has long been suspected that genes on this part of the chromosome may function, either individually or together, to suppress cancer. Until recently, however, researchers have found it hard to say which genes are responsible.

    One candidate is known as PTPN1, or protein tyrosine phosphatase, non-receptor type 1. First discovered in the late 1980s and linked to metabolic function, it is more famously known for its roles in breast cancer and type 2 diabetes. Its location on chromosome 20 has long made specialists suspect it could also be involved in AML.

    It was shown recently that when you switch off the equivalent gene in mice, it leads to what are known as myeloproliferative neoplasm, which is the wider family of blood cancers of which AML is a member. In our new study, we have taken this a step forward: we have shown that if you delete this gene in older mice, it specifically gives rise to AML – and in a similar way to how the disease develops in older humans.

    The previous study showed that PTPN1 is deleted from chromosome 20 in the cells of patients in around 17% of AML cases, which raises questions about the remaining majority of cases. We were able to show that deleting the mouse equivalent of PTPN1 activates a molecule called STAT3, which is important to regulating cell growth and division.

    If a patient has too much STAT3, it leads to the generation of too many immature myeloid cells – that hallmark of AML I mentioned earlier. This is potentially a very useful finding for further studies into the genetics behind the disease: in the two other most common mutations linked to AML, which relate to a protein called JAK2 and a receptor called FLT-3, STAT3 is also over-activated. In all, STAT3 is relevant to maybe three-quarters of all AML cases. Uncovering exactly how they relate looks critical to developing an eventual cure.

    The future
    In short, we’re closing in on understanding the links between PTPN1, STAT3, and AML. A few years from now, as the cost of genome sequencing falls, it will become a question of identifying which combination of mutations has affected a patient and prescribing a treatment accordingly.

    This treatment will probably be more bespoke chemotherapy for patients that can tolerate it, and perhaps gene editing using tools such as CRISPR for those that cannot. Doctors would edit the correct versions of genes like PTPN1 back into the patient’s bone marrow, potentially restoring normal function and negating the often difficult search for a compatible bone marrow donor.

    There is much research still to be done. We need to understand what PTPN1 is doing in healthy myeloid cells to grasp which processes are disturbed when it becomes deleted. The other big question is whether instead of getting deleted, PTPN1 sometimes more subtly mutates and how this relates to AML. Besides this, there are many other genes on the Del20q deletion that we need to better understand, too.

    In the meantime, showing that removing PTPN1 leads to AML is an important piece of the puzzle. It brings the day closer when survival rates for AML make the same climb that we have seen in other kinds of leukemia, and hopefully even beyond.

    From The Conversation.com

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    Time for Congress to Look at the Real Drivers of Health Costs

    No one should have to put a price tag on their life.

    In 2014, I was diagnosed with a rare but aggressive form of leukemia called acute myeloid leukemia. According to the New England Journal of Medicine, in people over 60, the survival rate is only 5 to 15 percent, and I am over 60. Besides that, because I had a rare and complicated case, my treatment cost a lot more than average.

    How much is a lot more than average? My treatment cost over four million dollars, that’s how much. Four million dollars!

    Read the full article from The Morning Consult follow this link>> https://morningconsult.com/opinions/time-for-congress-to-look-at-the-real-drivers-of-health-costs/

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    If you have Chronic Lymphocytic Leukemia, you may have your spleen taken out.

    Removing your spleen

    Surgery is not a common treatment for chronic leukemia. But some people with chronic lymphocytic leukemia (CLL) need an operation to remove the spleen (splenectomy).

    The spleen
    The spleen is an organ on the upper left side of your tummy (abdomen).

    It is part of the lymphatic system and filters the blood, removing worn-out red blood cells. It also stores red blood cells and contains lymph node tissue and many lymphocytes. Lymphocytes are types of white blood cells. Your white blood cells help fight infection.

    Why you might have your spleen removed
    The spleen is quite a large organ. In chronic leukemia, it sometimes becomes bigger and can cause problems.

    The spleen's normal job is to filter the blood and to destroy and break down worn-out red blood cells. When you have CLL your spleen can become so clogged up with abnormal cells that it doesn't work properly. The spleen swells because there are too many blood vessels.

    An operation to remove the spleen is called a splenectomy. You might have this because your spleen:

    is so large it is making you uncomfortable or causing you pain
    is destroying too many red blood cells or platelets
    has not shrunk after chemotherapy
    Your enlarged spleen might destroy too many red blood cells and platelets. This can make you tired and breathless. Or you might find you are bleeding more than usual.

    Removing the spleen can relieve these symptoms. In chronic lymphocytic leukemia, this operation might relieve the low red blood cells and low platelets for up to 3 years.

    Your specialist might suggest a short course of radiotherapy to the spleen if you can't have surgery for any reason.

    Read full article from Cancer Research UK>> http://www.cancerresearchuk.org/about-cancer/chronic-lymphocytic-leukaemia-cll/treatment/surgery/removing-spleen

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    A revolutionary leukemia treatment could soon be approved – here’s what it means for patients


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    One of our partners is looking for patients with acute myeloid leukemia willing to participate in a 60-minute telephone interview. I thought you or someone you know might be interested in participating.

    Participants who qualify, and complete the interview, will receive a $125 Amazon gift card.


    Just click the link above to see if you will qualify for the survey. If anyone has any questions feel free to message me.