Have They Found A Cure For Cancer

Yes, you read that correctly. I try to stay on top of things such as new meds, techniques, therapies and such in my cancer fight. As it turns out, it looks like we may have a reason to hope. They have found a way to dissolve the protein that keeps our immune system from attacking the cancer. Here’s a quote from the Stanford School of Medicine.

Stanford researchers have previously shown that CD47, a molecule found on the surface of many cancers, acts as a “don’t eat me” signal that protects the cancer from roving immune cells called macrophages. The scientists found that when they used drugs to block this “don’t eat me” signal, macrophages engulfed and destroyed the cancer cells.   Read More

I read further and they implanted cancer in mice and the cancers just “melted away” when the mouse was given anti-cd47 antibodies. It seems that CD47 is a protein found on all cancer cells.  Here’s a video you should find interesting.

Have they found a Cure for Cancer

So, are we going to see a cure for all cancers? Well, I have to be honest, I have high hopes for this treatment. I read that we may see it commercially available within 5 years but, I think that is optimistic. I HOPE that we will not see the FDA block a potential cure. They have stood in the way of many useful technologies and medicines that have been proven to be useful in the fight against cancer. Just take a look at the long road Gallium 68 has had to travel just to be used in clinical trials. Gallium 68 is a standard in almost every other country but not here in America. It’s a shame because it offers a much more accurate scan for carcinoid cancer patients.

The use of anti-CD47 Antibodies in treating cancer is so promising that they are talking about a future cancer vaccine. Here’s another quote for you.

The fact that T cells become involved in fighting cancer as a result of CD47-blocking antibody therapy could have important clinical implications. The antibody might be used as a personalized cancer vaccine allowing T cells to recognize the unique molecular markers on an individual patient’s cancer. “Because T cells are sensitized to attack a patient’s particular cancer, the administration of CD47-blocking antibodies in a sense could act as a personalized vaccination against that cancer,” Tseng added. Read More


As promising as this treatment seems there are limitations. It seems that if there is a lot of cancer then this does treatment is not as effective. The good news is that doctors are already thinking of ways to shrink the amount of tumors in the body so that they can use this treatment to fight cancer.

The anti-CD47 antibody presents a novel way of combatting cancer however it is not without limitations. The success of obliterating cancer is dependent on the volume of the tumour. Combination treatments are beginning to be explored but the replacement of  radiotherapy and chemotherapy is much preferred to reduce adverse effects on normal cells. The increased concentration of in situ macrophages would perhaps offer a better solution to eliminate bigger and more aggresive tumours. Read More

What Now?

So, this is the new focus of my personal research. Do carcinoid tumors have this CD47 protein? I expect so. I will be looking into this further. Also, what are the actual antibody names and compounds that dissolve these compounds? I’ll keep hoping for a cure from my oncologist, eating organic and taking supplements that make me healthier. I’m staying positive and looking for my own answers as well. If you know anything about anti-cd47 therapies please let me know.

Stay Strong and Keep Fighting,

Ed – To find out how to use my images on your blog for free – Click Here



  1. The fact that they were allowed to use the not-yet-approved drug for the 2 who are suffering from Ebola makes me think that restrictions are being modified. We can hope!

    • Yeah, I think not. 🙂 There are too many medicines that the lawyers tie up for years in FDA litigation. If I want to get a treatment that is standardized in Europe I will either have to leave the country or get into a clinical trial. I’m speaking of PRRT and Gallium 68. Sad but true.

        • You know, I understand the need to make money BUT not at the expense of patients. A lot of people say things like “big pharma” is out to get us. They say things like oncologists are only in it for the $$$. In my opinion it really comes down to the people who “own” the hospitals. The people on the board of directors and other people in power. They do not look at this from a humanitarian perspective but from a financial one. They remove emotions from the equation and treat the entire endeavor like a financial enterprise. So, if people die but profits rise they don’t care. They see patients as numbers and they never see those people face to face like doctors, oncologists, nurses etc. This makes it easier for them to do such things. Patients have to fight for their own health or they will be simply part of a money making system. My opinion.

          • I hate to agree with you, but I do! There have been incidents where people died in front of hospitals because they didn’t have insurance or cash! I get it! Not a non-profit agency, but what about the Hippocratic Code? I guess there’s plenty of blame to go around though.

  2. Wow! That sounds VERY promising! Fingers crossed for it to proceed through the necessary channels to get out there and help people!

  3. Hi Ed, FYI.,,,



        • The company also announced that following a scientific and commercial evaluation of its tigecycline program, as well as the lack of a strategic fit with the company’s current focus and expertise, the license agreement underpinning the program has been terminated and all rights have been returned to University Health Network.
          “We believe that all our efforts and resources should be focused on our immuno-oncology programs, in particular on a greatly expanded SIRPaFc program,” commented Dr. Stiernholm.

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    • That’s pretty interesting. I wonder? Have you read about antiangiogenesis? That’s pretty interesting too. Although, they got carried away with the food list and didn’t really explain if the studies were conducted “in vitro” or “in vivo”.

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  7. Back in 2000 Dr. Oldenborg and colleagues hypothesised that CD47 served as a marker of ‘self.’ Specifically, they proposed that the surface expression of CD47 on red blood cells served as a mechanism to prevent macrophage phagocytosis (ingestion). In immunity this functions as a “don’t eat me” signal when it interacts with SIRP-a on macrophages. Cells that have lower levels of CD47 and higher calreticulin (an ”eat me” signal) are removed by the immune system, whereas cells expressing elevated levels of CD47 are resistant to destruction due to a balance of pro- and anti-phagocytic signals. So in order to avoid phagocytosis by macrophages, cancer cells upregulate CD47. This is observed in nearly all solid and hematological malignancies and is likely a broadly conserved tumour escape mechanism http://www.pnas.org/content/109/17/6662

    • Thanks… I read somewhere that CD47 did not work out so well. The effect was short lived and it seems that the doctor who pioneered the study has gone on to other things. Have you seen any recent news on CD47?

      • The Forty Seven version has shown quite encouraging data in certain types of NHL. In combo with rituximab in DLBCL the response rate (shrinkage) was 40% and in fNHL it was 71% http://abstracts.asco.org/214/AbstView_214_216289.html

        Trillium Therapeutics had a lower response rate in their DLBCL group in part due to the fact they couldn’t give higher doses. Some other data came from the ongoing intratumoral trial. Injections resulted in rapid reduction in CAILS scores (measures of local lesion(s) responses) in 90% (9/10) of mycosis fungoides patients. Additionally, in 3 of 3 patients a reduction in circulating leukemic Sézary cells was observed. Importantly, the injection was well tolerated with no dose-limiting toxicities.

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