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Please note that we are unable to respond back directly to your questions or provide medical advice. As the fastest growing consumer health information site a€” with 65 million monthly visitors a€” Healthlinea€™s mission is to be your most trusted ally in your pursuit of health and well-being. Finding a cure for cancer would save more than 580,000 lives and billions of dollars each year for research.
Here are two of the more prominent studies that report breakthroughs in the quest to find a cure for cancer. An article published in August 2013 in BMC Biology reports the results of 50 of the subjects. Researchers believe that getting to know more about the rats’ ability to combat a disease that they are not normally prone to in the first place may provide key insights into how to fight cancer in humans.
DCA—dichloracetic acid—was touted as another miracle cure when studies conducted at the University of Alberta in Canada suggested that the chemical could slow the growth of certain types of cancer cells. The results of the study were published in Cancer Cell back in January 2007, and, like the Spalax studies, immediately garnered lots of attention from the media.
DCA is typically used to remove warts and other skin growths, but it also has “shown some promise” for cancer treatment in lab studies, according to the American Cancer Society (ACS).
But it’s not yet clear how or even if DCA could potentially be used as a cancer treatment or cure. As cancer researchers work in the labs to find a cure for cancer, many patients and surgeons are taking matters into their own hands.  The issue of preventive surgery to cure cancer for people with a strong genetic risk is a controversial topic. The most common preventive cancer surgeries include hysterectomies for women with a family history or cervical or ovarian cancer, and mastectomies for women with a strong family history of breast cancer. Preventive surgery to remove both breasts—has been shown to reduce the risk of breast cancer by up to 90 percent in women who have a strong family history of breast cancer.
If you think you are at an increased risk for these types of cancers because of genetics or family history, talk to your doctor about your options. Understanding the Science behind Angelman Syndrome will help illustrate how close we are to a cure. Angelman Syndrome is unique because it is caused by loss of function of a single gene rather than many genes and the gene is known – UBE3A. The next step is to understand how the paternal copy is being silenced so that we can unsilence it.
A good way to look at this scenario is that our DNA is extremely active – there is a constant flow of delivery trucks (transcription enzymes) attaching to their docking station and copying genes. Knowing this, a possible solution is to custom build a protein which will bind to those genes just upstream of UBE3A, preventing all those trucks from going to work there.
There are still many steps that need to be taken – further trials in higher order species, analysis of findings, evaluation of possible side effects (short and long term), and hopefully the development of more feasible delivery systems are just the first of these steps. We cannot thank everybody enough for the love and support they have given our family during this time. For decades, governments, charities and pharmaceutical companies have all poured tens of billions of dollars into breast cancer research.
Helping extend those strides is research in liquid diagnostics, a method aimed at finding early signs of cancer  in blood or urine before symptoms arise. Just weeks ago, for example, the journal Nature published the development of a blood test for pancreatic cancer, one of the deadliest kinds.
Meanwhile, researchers at the University of Freiburg, Germany, have developed a breast cancer test that needs only a few millilitres of urine. This is giving rise to both the development of target-specific drugs (up to about 50 today from just 15 in 2008) and to theragnostic tests themselves. Understanding the genomics of tumours may aid in the understanding of the third and perhaps most crucial area of breast cancer research: the metastasis of the primary tumour itself. She cautions that cancer is highly complicated and that parsing out the “enormous” number of possible mutations in a bulk tumour is the key to personalised, highly targeted medicine.
Image: “Umbrellas”, the sculpture by Giorgos Zogolopoulos is illuminated in pink light to mark Breast Cancer Awareness Month in Thessaloniki in northern Greece. Simplicity of delivery will be critical if a ‘cure’ is going to be deliverable in the parts of the world where HIV is endemic. Bridget Haire receives funding from the National Health and Medical Research Council (NHMRC).
Finding a cure for HIV is a powerful concept, often spoken of as the Holy Grail of HIV research. An affordable, scalable HIV cure that worked as well in rural Malawi as in urban Sydney would put the global eradication of new HIV infections within reach, while also transforming the lives of those now living with the virus. Given the effectiveness of antiretroviral drugs in both treating and preventing HIV infection, however, cure research raises a range of important questions about priority setting in global health. Curing HIV – or at least achieving long-term remission – is possible, under the right circumstances.
In 2007, Timothy Rae Brown, formerly known as “the Berlin patient”, required a bone marrow transplant to treat his leukaemia. A matching donor with the CCR5 mutations was found, the harrowing transplant was performed, and it was successful.
While it is unknown whether HIV has been completely eradicated from his body, in 2016 Brown still has no detectable HIV in his blood, and does not require antiretroviral drugs.
While Brown’s case demonstrates HIV can be forced into remission, it has not resulted in a reproducible form of cure.

The particular CCR5 mutations required is and generally only found in Northern Europe, where an estimated 1% has one copy of this genetic variation. Current approaches to cure research are focused on achieving a “functional cure” or remission of HIV rather than a sterilising cure, which would aim at removing all traces of HIV from the body.
If a safe, limited dose combination of drugs could be developed, this approach could prove potentially deliverable in disparate settings globally. Another approach is bolstering the human immune system to control HIV replication without antiretroviral drugs using therapeutic vaccines and antibody-based therapeutics. If a therapeutic vaccine was developed that controlled HIV replication without antiretroviral drugs and required limited dosing (ideally one-off dosing), this would be an improvement on the current need to take medication daily to control HIV.
Particular properties of the developing infant immune system make such an approach more likely to work in newborns than in adults.
Finally there are cell-based therapies: genetic modification or “gene editing” in people with HIV, including stem-cell transplantation.
While these have the advantage of being one-off intervention, they carry the serious disadvantage of being extremely intensive in the use of medical technology and potentially risky to patients. As antiretroviral treatment for HIV is now highly effective and relatively simple (often just a pill a day), approaches to a potential HIV cure need to be evaluated according to whether they might offer a real advantage over lifelong therapy at both individual and population levels. Evaluating the social value of particular cure strategies is a critical aspect of ensuring that the right kinds of research are prioritised – those that have the potential to transform the epidemic in resource poor contexts.
Treatment has transformed the outlook for people living with HIV from almost certain death to a manageable chronic condition. Just three decades ago at the start of the AIDS epidemic, testing positive for HIV, the human immunodeficiency virus that causes AIDS, was essentially a death sentence. HIV attacks a person's immune system by destroying cells in the body, called T-cells, which fight off disease and infection. CRISPR could help rid of diseases like cystic fibrosis, muscular dystrophy and even HIV and cancer. Both of which will support, guide, and inspire you toward the best possible health outcomes for you and your family. Other people say that these remedies are just treatments—not cures—because the cancer could come back. Some people even go so far as to say that a cure would eliminate cancer from our diagnosis dictionary altogether, just like the polio vaccine. On the one hand, we’ve made leaps and bounds of progress since we first figured out what exactly cancer is and how it works, but at the same time we’ve got miles to go before we can say we’re anywhere near having a full understanding of this devastating disease and being able to come up with a cure. For 50 years, researchers have been studying the cancer-resisting abilities of Spalax, or blind mole rats. But even when they are artificially exposed to cancer, the blind mole rats’ bodies are still able to kill the cancerous cells. While having a genetic marker does not guarantee that you will get cancer, preventive surgery may still be the best option in some cases. In children with Angelman Syndrome the maternal copy has either been mutated or is missing (via deletion or UPD).
However, only the bottom mouse suffers dwarfism because, due to imprinting, in this case the mutated gene must be on the paternal copy to have an effect.
On one hand, it is due to this uniqueness in UBE3A that a child would even have Angelman Syndrome, however, on the other hand, it lends itself to a possible cure.
Garrett could learn to talk and develop as a typical person – living a fully functional life! Tracking proteins allow for real time imaging of the spread of the medicine throughout the cells of the body.
Measurement of Ubiquitin-protein ligase E3A enzyme allows scientists to confirm successful expression of the silenced gene. Behavioral scientists who specialize in mice, rat, pig and other animal behaviors can evaluate changes and determine the theoretical implications in humans. Angelman Syndrome could be the first neurogenetic syndrome cured and that would cause a renaissance in modern medicine!
Donations through The Angelman Syndrome Foundation (ASF) and The Foundation for Angelman Syndrome Therapeutics (FAST) will help drive scientific research.
The area is so promising that it could become part of a $20bn market for cancer blood tests within five years, according to a JP Morgan analyst.
As exciting as this is for those working to eradicate pancreatic cancer, the test could also prove useful for breast cancer screening: Biomarkers in blood from breast cancer patients also “lit up” during the study. It detects concentrations of microRNAs that have crossed into the sample from the patient’s blood.
Scanning a person’s blood for tiny fragments of DNA released by tumours—a field known as theragnostics—can help doctors prescribe tailored drugs that work directly against a specific kind of tumour, for example. Analysis of the genetic sequence of more than 2,000 breast cancer samples by the Cambridge Cancer Centre, for example, revealed that there are at least ten genetically distinct, different kinds of breast cancer tumour types. Understanding the makeup of those mutations and using nanotech platforms to deliver targeted therapies could be key to long-term survival, she says.
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Although effective anti-HIV drugs have transformed HIV into a chronic manageable condition – a condition you live with, rather than die from – taking life-long therapy is a very different proposition to being definitively cured.
This must the goal of cure research: to prioritise interventions that have potential application worldwide, not limited to settings with highly developed health systems.

Global investment in cure research has more than doubled in the last four years, in contrast with investment in other HIV programs. Brown also had HIV, and his doctor suggested that if they could find a bone marrow match from a donor who had rare genetic mutation on the CCR5 receptors – receptors that HIV uses to get inside cells – this could potentially cure Brown of HIV.
So transplanting bone marrow using a donor who lacks HIV receptors means that the new bone marrow would produce immune cells that were resistant to HIV infection. Brown was able to cease antiretroviral therapy, and has not had a viral rebound since (though his leukaemia did relapse and he required a second transplant). Even fewer have the two copies that are required for high-level resistance to HIV infection. It uses latency-reversing agents (chemotherapy-like drugs) to activate cells that have been latently infected with HIV and then kill the HIV. This strategy relies on intensive use of antiretroviral drug in infants who acquired HIV from their mothers.
There is a documented case of a child who controlled HIV successfully for 27 months following cessation of treatment (known as the Mississippi baby).
Simplicity of delivery will be critical if an intervention is going to be deliverable in the parts of the world where HIV is endemic. It's a sexually transmitted virus that spreads through semen and vaginal fluid, and it can also be spread by blood, sharing needles, or during pregnancy and breast-feeding.While advancements in treatment have made it possible to control the virus -- and also greatly reduce the risk of transmitting HIV to others -- the drugs fall short of permanently curing a person of HIV. Scientists have developed a type of "genetic scissors" that would allow them to potentially cut and alter the genome of infected cells.
A lot of the fear comes from the fact that while there are many effective ways to treat cancer, there isn’t a cure for cancer. Since every child carries a silent healthy paternal copy of UBE3A, unsilencing that gene would allow the brain to produce Ubiquitin-protein ligase E3A. Their behavior and physiological conditions are quite similar to conditions in human Angelman Syndrome individuals. This is such an amazing thing to hope for and that is why it is so important that we push for a cure as soon as possible! We need the UBE3A gene to produce its protein – Ubiquitin-protein ligase E3A – but there are just too many trucks going in and out of the genes nearby!
Just this type of solution is now being shown to work at UCDavis and other research institutions – it is absolutely cutting edge science. Angelman Syndrome model mice were injected with a protein with the goal of blocking the nearby genes and unsilencing the paternal UBE3A gene.
To support these genomics efforts, the Addenbrooke’s Charitable Trust just launched the “Bracode” Campaign (a play on the word “barcode”) to study 450 volunteer patients at the Cambridge Breast Unit for the next five years.
This is vexing for researchers because metastasis tends to be what kills patients, says Dr Merajver.
It would be highly unethical to transplant bone marrow in a person who did not require this for another serious illness such as leukaemia. So finding ways of flushing HIV out of the places where it lies dormant is an important aspect of cure research. World AIDS Day is observed on December 1 every year to raise the awareness in the fight against HIV. If patients are diagnosed early and take antiretroviral medication as directed, doctors say they can live a normal lifespan.
Researchers are currently trying to figure out how to utilize this new technology to find a cure for HIV.When asked how far off the reality of a cure might be, experts say it's hard to gauge, but they are very hopeful. That means we each have a pair of UBE3A genes – a paternal copy from our father and a maternal copy from our mother.
Scientists have shown that reintroduction of Ubiquitin-protein ligase E3A into an Angelman Syndrome mouse model causes reversal of symptoms – the mice are able to learn and develop as a typical mouse would. This is why you actually do see some very low levels of Ubiquitin-protein ligase E3A being expressed in Angelman Syndrome individuals. The test, which involved 48 women, looked for concentrations of these microRNAS and was 91% accurate, according to the researchers. But there is still no cure."To see the pace from the days that we could do very little other than watch our patients die to finding the first treatments and then working hard to make those treatments better to where we are now has been remarkable," Dr. Carlos del Rio, professor of medicine and public health at Emory University and co-director of the Emory Center for AIDS research, told CBS News.
Ubiquitin-protein ligase E3A was confirmed to be produced by the cells at near normal levels and behavior improved in some areas! Paul Volberding, a professor in the department of medicine and director of the Center for AIDS Research at the University of California, San Francisco, told CBS News. But I think it's realistic to think that at the end of five years we will be a lot further along than we are now."For del Rio, he said he hopes to see a cure before he ends his scientific career. A major challenge in finding a cure is that even after treatment reduces HIV in the blood to an undetectable level, the virus lays dormant in areas of the body known as HIV reservoirs.

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