Cancer In Plain English – Cancer Information Cancer Information Sat, 04 Apr 2015 14:55:20 +0000 en-US hourly 1 Brain Tumors – new exciting developments Sat, 27 Sep 2014 13:17:55 +0000 Warsaw, Poland
We here at keep an eye out for new and exciting research and report it here when we find it. This is what has just happened with these recent findings with regard to Malignant Gliomas which is a type of brain tumor.
A team of researchers at the Polish Academy of Sciences in Warsaw has come up with potentially ground-breaking new findings with regards to a kind of brain tumor known as a Malignant Glioma.
We have always known that tumors develop and grow because they develop the ability to evade detection by the body’s immune system. Indeed, researchers spent the better half of the 1990s trying to find ways for molecules such as Alpha Interferon and Interleukin-2 to kill tumors. Researchers incubated the body’s immune cells with high doses of Interleukin-2 (IL-2) in an effort to generate what is known as “Lymphocyte Activated Killer Cells” – or LAK cells – and then try to see if these cells were able to kill tumors such as Renal Cell Carcinoma and Malignant Melanoma.
In these new developments, a team in Poland lead by Dr. Bozena Kaminska has discovered that brain tumors known as Malignant Gliomas, seem to evade detection by the body’s immune system by secreting a protein which they have called CSF2. They based their research on this protein on the fact that some of their earlier studies dating back to 2007 had shown that by secreting this protein, Malignant Gliomas are able to “reprogram”, if you will, the surrounding immune system near the Malignant Gliom tumors, to not destroy it.
They followed a hunch. In Breast Cancer, researchers had found that Breast Cancers changed the behavior of the immune system that surrounds them by changing the cells known as Tumor-Infiltrating-Macrophages (or Tumor Infiltrating Lymphocytes – TILs). Breast Cancers did this by secreting a protein which called CSF-1. Well, the team in Poland thought “what if Malignant Gliomas do the same thing?”  – well the answer is no. Malignant Gliomas do NOT secrete CSF-1 as a means to stop the body’s immunce TIL cells from invading them – but the researchers DID find that the Malignant Glioma cells DID secrete a protein which they have called CSF-2! This was their “EUREKA!” moment.
They then blocked the PRODUCTION of CSF-2 by Malignant Glioma cells by blocking the gene which MAKES it – and lo and behold – the Malignant Glioma cells WITHOUT the ability to make and secrete CSF-2 were NOT able to stop the body’s immune TIL cells from invading them and destroying them. Furthermore, it seems that tumor cells that did NOT secreting CSF-2 were found to be “converted” to less aggressive forms (i.e. less “tumor-like”) by the lack of CSF-2 secretion.
This, therefore, immediately presented itself as a possible target for the treatment of Malignant Gliomas.
Dr. Kaminska’s group then took things a logical step further. They asked themselves “What if we could create an “anti-protein” which could actively COMPETE for the binding site of CSF-2?” Well, they did just that. They developed short peptides (which are proteins) which interfere with the binding of CSF-2 to their respective binding site and – as hoped – this seems to have the same effect as removing the gene which makes CSF-2 did in earlier experiments. It stops the Malignant Gliomas and makes them more susceptible to the body’s immune system.
This thus opens up a whole new “can of beans” for possible treatments for Malignant Gliomas. Potentially, we could give patients with Malignant Gliomas these small peptides which compete for the binding site of CSF-2 and their Gliomas would stop growing, become more sensitive to the immune system and – apparently – even become less malignant! As we can expect, the pharmaceutical potential and the financially lucrative possibilities did not escape the notice of those who learned of this. Thus, the “Developed Molecules” and their “relevant genetic tools” for making these molecules are now covered by an International Patent! Surprise, surprise. Oh well. At least we can hope that despite the monetary considerations, if these researchers and others are indeed able to develop a protein which will stop Malignant Gliomas and do so with natural, less aggressive means than radiation and/or chemotherapy, it would be a wonderful step forward in a new direction for the treatment of brain tumors.
We at will continue to keep an eye out for these developments and will report them here as they become available.
‘Till next we speak again,
Mark Sperry for

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A new way to detect lung cancer early Thu, 19 Sep 2013 14:58:50 +0000 IDH1 – is this finally the blood test we have all been waiting for in order to find Lung Cancers early?
In a recent paper in the journal Clincal Cancer Research Jie He, MD, PhD of the Peking Union Medical College in Beijing, China reported that a protein in the blood called, IDH1, may indeed be a great new blood test we can use to find lung cancers early. A “biomarker” is a substance – such as a protein – in the blood which may give us a clue that a disease is present in the body of the person who has this protein in their blood.

Dr. He and colleagues at the Laboratory of Thoracic Surgery at the Chinese Academy of Medical Sciences collected blood samples from 943 patients WITH lung cancer and 479 people WITHOUT lung cancer and compared the blood levels of IDH1 in both the patients with lung cancer and the persons without lung cancer.
Dr. He’s team’s findings were that the patients with a type of lung cancer known as Adenocarcinomas had almost 3x higher blood levels of IDH1 than people without lung cancer. They also discovered that patients with a type of lung cancer known as a Squamous Cell lung cancers had almost 2 1/2 times higher blood levels of IDH1 than people without lung cancer.

What this means is that we can conceive the thought that we could take people who have smoked cigarettes for a long time and, if we suspect that they may have lung cancer, draw their blood and study their blood to see if we find IDH1 in their blood. If we do, as we will see below, we can then re-draw their blood and run tests for other blood markers known as CEA, Cyfra21-1 and CA125 and if the person who has smoked cigarettes for many years and who we suspect may have lung cancer has high blood levels of ALL 4 of these biomarkers, we should then have a very high suspicion that this person may indeed have a lung cancer – even if we still can’t see one in his or her chest x ray.

The combination of measuring IDH1 along with other biomarkers in the blood may increase the ability of IDH1 to find lung cancers early: Dr. He and his team further noted that if they combined the detection of IDH1 with the detection of other biomarkers such as CEA, Cyfra21-1 and CA125, the ability to detect cancer versus a false positive increased. This means that the combination of all of these biomarker tests together was better than just measuring IDH1 by itself. On top of that, by combining the detection of IDH1 with these other, more familiar and known biomarkers, the team was able to get a sense of the TYPE of non-small cell lung cancer which was being detected such as Adenocarcinoma versus Squamous Cell carcinoma. This could truly be a wonderful new development if further testing proves that it is indeed as good as it seems.

We do not know if IDH1 – or its combination with other biomarkers such as CEA, Cyfra21-1 and CA125 is the final answer in allowing us to find lung cancers early; but the key is that we – the scientific community – are getting closer to finding a blood test with which we can find lung cancer early. As the world’s – and the US – population grows older, we can unfortunately expect more and more lung cancers to be found. We all know that lung cancer is the most prominent and principle cause of cancer deaths IN MEN AND WOMEN worldwide (and in the USA). We as well know that if we can find lung cancers early, we are able to remove them with surgery and are thus able to very possibly cure the person with the lung cancer. Finding lung cancer early, therefore, can only mean one thing – decreased deaths due to lung cancer.

Till next we speak again,
Mark Sperry for

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Can a cancer drug help treat Diabetes? Mon, 16 Sep 2013 17:49:54 +0000 It turns out that there are signs that a current treatment for Colon Cancer may actually help people who have diabetes.

Cancer therapy – and many therapies really – can produce surprising combinations this way sometimes. We may discover, for example, that one medication which is good for one thing is actually good for something else. For example, the medication Thalidomide was discovered to cause horrible birth defects when given in England years ago for “morning sickness” but we now have discovered that this same medication is now helpful for Multiple Myeloma.

The same with a medication called Aflibercept (also known as Eylea or Zaltrap). This medication is a VEGF inhibitor which is useful in the treatment of Colon Cancer. VEGF stands for Vascular Endothelial Growth Factor. VEFG is a protein which colon cancer produces in order to make itself more blood vessels in order to feed itself better as it grows. By doing this, the tumor, as it grows, does not outgrow its blood supply. Well, Aflibercept blocks VEGF and thus makes the tumor outgrow its blood supply and starve/suffocate to death because of lack of  blood supply and oxygen.

Researchers at Stanford have recently discovered that VEGF inhibitors block (as they are supposed to do) the development of new blood vessels. This then leads to decreased oxygen delivery to the cells. Decreased oxygen delivery is known as hypoxia. Hypoxia, then makes the cells to produce a substance known as HIF-2Alpha which in turn produces another protein called IRS2 which thus makes it easier for cells to absorb and work with the glucose that surrounds them. What this means is that, if this research continues to bear fruit, we may discover that it may be possible to give Aflibercept to patients with diabetes as a way to help the cells of diabetic patients to more easily absorb the glucose that surrounds them and thus, have less of the glucose swimming around their bodies (which is the problem with diabetics).

As more of this information comes forward, I will keep you informed. Mark Sperry for Cancer In Plain English

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Breast Cancer: Where are we today? Wed, 03 Mar 2010 12:56:42 +0000 Breast Cancer remains a very serious and important medical problem in the world. Every year, over 170,000 women and over 2,000 men will be found with breast cancer.
In the 1980s, we started to use mammograms in order to screen women for the possibility of having breast cancer. This has been a revolutionary step and a life saver for thousands of women. As we would expect, with the use of mammograms, we now find many cancers very early in their course, which in the past would have never been found until it was too late and the cancer might have already spread.
The question one would ask is: Since women now use mammograms as a way to find breast cancer early before it spreads, does this mean that we no longer find breast cancer that is advanced by the time we find it? Unfortunately, the answer is no. This is truly unfortunate.
It seems that there is a group of women who have a tendency (which is probably genetic in origin) to developing very aggressive breast cancers and that when they are found with breast cancer, their cancers are already spread. Thankfully, this is a small percentage of the women who develop breast cancer. This group of women, the ones who develop a very aggressive breast cancer from the “get go” is made up of only about 5% – 10% of all women who develop breast cancer. Research is currently ongoing to see if we can find other ways to know who are these women who develop aggressive breast cancers from the start and how to find them earlier than what is possible with a mammogram. To this end, the use of things such as the BRCA cancer genes and blood tests are being explored as a possible means of finding these women who have the tendency to develop aggressive breast cancers and to try to catch them as early as possible.
The good news is that we are making progress. The findings of new and promising ways to try to find out who are the women at risk for this aggressive form of breast cancer continue to come frequently. As we learn of them, we here at Cancer In Plain English will post them here for you in easy to understand language. Our desire is to make complicated cancer information very easy to understand so that everyone can know as much as possible. All of these concepts are as well available on the breast cancer audio CD which is available on the internet web site.

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Ghrelin stimulates appetite in cancer patients Tue, 23 Feb 2010 09:11:14 +0000 A new treatment has been discovered which increases the appetite and the nutritional intake of patients with cancer.
A major problem, when it comes to cancer, is the loss of appetite. People with cancer just are not hungry. This loss of hunger in cancer patients (and in anyone who is not hungry) is called “Anorexia”. Unfortunately, this lack of appetite could not come at a worse time. Just when a person needs to eat and take in nutrition in order to build up strength with which to fight the cancer, they lose all desire to eat.
Until the development of this new medication known as Ghrelin, the major means for stimulating appetite in cancer patients was with a medication known as Megesterol (or Megace). This is a hormone which stimulates appetite in many cancer patients and, until now, was the best we could do in order to try to stimulate appetites in patients with cancer.
Well, enter Ghrelin. This is a relatively new hormone which was discovered by Dr. Kojima and colleagues in 1999. Its function is to circulate in the body and to stimulate the development of hunger.
In a study published in February of 2010 in the medical journal Cancer, researchers in Sweden administered Ghrelin as a daily subcutaneous injection for 8 weeks to patients with cancer who had poor appetites. More or less half the patients were given Ghrelin at a low dose and the other half were given Ghrelin at a higher dose.
The results of this study showed that the patients with cancer and a poor appetite who received the higher doses of Ghrelin tended to have significantly improved appetites, improved retention of their body weights and improved levels of energy. What’s more, the patients who received Ghrelin did not have any noteworthy side effects from this medication.
As such, it seems that we have now discovered a new medication for the stimulation of appetite in patients with cancer. For cancer doctors, the finding of this new means to stimulate the appetite of patients with cancer could not come a moment too soon. Lack of appetite has been a difficult problem for patients with cancer for a very long time. All of these concepts and many more are covered and discussed in the Colon Cancer audio CD available on

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Cigarette smoking and Colon Cancer Mon, 22 Feb 2010 00:47:30 +0000 Inheriting a gene that increases one’s risk for the development of cancer is like inheriting a loaded gun. That gun never needs to go off unless someone or something pulls the trigger.
When we think of cigarette smoking and the health risks that come with that activity, we think of lung cancer, emphysema and other breathing ailments; however, we typically do not think of Colon Cancer.
Well, as per an article published in February of 2010 in the journal Clinical Cancer Research that thinking may soon change.
Researchers have known for years that cigarette smoking is not only related lung cancer. It is as well associated with other cancers such as Kidney Cancer and Throat Cancer.
The findings in this recent study indicate, however, that it may as well increase the chances of developing Colon Cancer in people who inherit a gene that makes them more susceptible to the development of colon cancer.
Drs. Pandel and Lynch of the MD Anderson Cancer Center in Houston, Texas studied a total of 752 people who were known to have inherited a gene for a form of colon cancer known as the Lynch Syndrome type of colon cancer. This form of colon cancer is also called the HNPCC syndrome. What they found is that patients who inherited the gene for this form of cancer and who smoked had a much higher chance of developing colon cancer than in patients who inherited that gene and who did not smoke – or who had quit smoking for at least 2 years or more.
The key here is that cigarette smoking seems to increase the risk of colon cancer in these people who have already inherited a gene that places them at an increased risk of cancer. As we mentioned earlier, this is comparable to having inherited a loaded gun, but it did not go off until cigarette smoking comes along and pulls the trigger.
What we can “take away” from the findings of these researchers is that cigarette smoking, although known to be harmful to the lungs can hurt us in ways that we never imagined. If, by chance, a person has inherited the gene for this form of colon cancer, does not know it AND starts to smoke cigarettes, his or her risk of colon cancer is thus increased. As such, it is important to not start smoking and if we already smoke, to do all we can to stop smoking. As we can see from this recent journal article, like a sinister and stealthy assailant, cigarette smoking can cause us harm in many and sometimes unexpected ways. All of these concepts and many more are discussed in easy to understand language in the Colon Cancer Audio CD available on the Internet web site

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Ramucirumab – no food supply for you! Sat, 20 Feb 2010 12:26:31 +0000 There is a promising new medicine for the treatment of various forms of cancer. This new medicine is known as RAMUCIRUMAB.
Cancer is a formidable foe. It not only starts out quietly and often grows quietly, it also makes sure that it creates its own blood supply to feed its growing appetite as it grows.
Lately, researchers have focused on this ability of cancer to create its own blood supply – its supply lines as it were – as an Achilles’ heel with which to attack and kill growing cancers. If we stop a cancer’s ability to feed itself, we thereby stop its ability to grow and ultimately to survive.
The way that cancers make new blood supplies is by making a protein in the blood called a VEGF. Think of VEGF as a baseball that comes to the baseball glove. The baseball glove is the VEGF RECEPTOR.
Well, when the baseball (the VEGF) arrives at the baseball glove (the VEGF RECEPTOR) this triggers the production of new blood vessels which in turn bring more blood and nutrition to the growing cancer.
Well, a relatively new medication which has been recently approved for the treatment of both Colon Cancer and Lung Cancer is called Bevacizumab (or Avastin). Avastin binds to the baseball (the VEGF) BEFORE it has a chance to be caught by the baseball glove (the VEGF RECEPTOR). Thus, if VEGF can never get to the VEGF RECEPTOR, then the reaction that happens when those two get together can never happen and, thus, no new blood vessels are made.
Well, what if we were to now make a new medicine to target not the baseball but the baseball GLOVE?
Well that is what the experimental medicine, Ramucirumab is. This is the first medicine that targets the baseball GLOVE (the VEGF RECEPTOR). What’s more, it SPECIFICALLY targets a very SPECIFIC TYPE of baseball glove. In other words, it specifically targets a type of VEGF Receptor known as the TYPE 2 VEGF Receptor. Thus, if the VEGF Receptor is taken out of commission, then, again, as with the medicine Bevacizumab (Avastin), the cancer cannot make new blood vessels to feed itself.
In a recent article in the February 10th, 2010 issue of the Journal of Clinical Oncology, researches prove that this new medicine can be safely given to patients and it is reasonably well tolerated. It also promises to be a new addition to our armaments and weapons for treating cancer. Even though this medicine, Ramucirumab, is still investigational, it promises to be a wonderful new addition to our treatments for possibly Colon Cancer, Lung Cancer and possibly Kidney Cancer.
All of these concepts and more are covered in easy to understand language in the the Lung Cancer and Colon Cancer audio CDs available on

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Degarelix for the treatment of Prostate Cancer Sat, 13 Feb 2010 07:33:51 +0000 There is an exciting new medication which was just recently approved by the FDA (Food and Drug Administration of the USA) on December 24th, 2008 for the treatment of advanced Prostate Cancer. This new medicine is known as Degarelix and it is made by a company known as Ferring Pharmaceuticals.
Once prostate cancer has grown and has spread outside of the prostate gland, it is typically no longer able to be cured but is able to be controlled for years with what is known as hormonal therapy. The types of hormone therapies that have been available for us to use until now have been of two basic types.
One is the “LHRH agonists” of which Leupron or Zoladex are common examples and the other is the “Antiandrogens” of which Casodex or Eulexin are common examples.
Well, we now have a third type of hormone therapy that has been approved by the FDA and this one is called Degarelix. What Degarelix does is to actually BLOCK the GnRH RECEPTOR. GnRH stands for “Gonadotropin Releasing Hormone” and this is a hormone that originates in the part of the brain called the hypothalamus which stimulates the production of another hormone called LH (Leutenizing Lormone). This LH hormone, then, in turn causes the testicles to produce testosterone.
There are “receptors” in the brain that, when triggered, cause the brain (i.e. the hypothalamus part of the brain as we mentioned earlier) to produce GnRH which in turn, as we have seen, causes the production of LH which in turn stimulates the testicles to produce Testosterone. Thus, by blocking the RECEPTOR for GnRH in the brain, the brain is not stimulated to produce GnRH. Thus, since no GnRH is made, then no LH is made and thus finally, no testosterone is made thus by the testicles. Prostate cancer depends on the presence of testosterone in the body as its stimulus for growth and spread. Therefore, without testosterone, the cancer stops growing and shrinks – often for years.
The best part about this new medication known as Degarelix, is that it avoids what is known as the “flare” reaction that is sometimes a problem with the use of the more classic “LHRH agonists”. All of these concepts and many more are covered in very easy-to-understand language in the Prostate Cancer audio CD available on

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Prolia: A promising new drug for Prostate Cancer Thu, 11 Feb 2010 09:01:46 +0000 Prolia (or, as it is also known, Denosumab) is an exciting new medication which promises to help men with prostate cancer with the damage to their bones that can result from the treatments that are given to control their prostate cancers.
Just as cars use gasoline for fuel and jet planes use airplane fuel, prostate cancer uses the hormone known as Testosterone as its fuel. Testosterone stimulates the growth and spread of prostate cancer. An excellent and easy way to stop prostate cancer, then, is to shut down the production and/or the effects of Testosterone in the body. This is readily and reliably achieved by “anti-Testosterone” medications known as LHRH agonists, antiandrogens or both given together. Over time, however, these wonderful “anti-Testosterone” medications, which do so much good for men with prostate cancer, can cause the bones of the body to become weaker, brittle and possibly even break or fracture.
Prolia, which is also known by the more scientific name of Denosumab, is a new and exciting medication produced by a company known as Amgen in California, which is showing excellent promise for helping to improve the bone loss that results from the use of the Testosterone-stopping medications mentioned earlier.
There are other medications on the market that help to stop bone loss – particularly one known as Zometa made by a company known as Novartis, which until now has been pretty much the “go to” medication when it comes to treating the bone loss resultant from the use of Testosterone-stopping medications. The key with this new medicine known as Prolia (also known as Denosumab), however, is that it works in a very new way to combat the bone loss.
How does Prolia (Denosumab) work? Well, in order to understand how Prolia works, we first need to talk a little bit about how our bones work in general. The way the bones of our bodies work is that they are constantly breaking themselves down and building themselves back up again over and over again constanly in order to keep our bones fresh and strong. Really? Yes, really. The key, however, is that this happens constantly but very slowly and so we do not notice it. All we notice is that our bones remain hard and strong and they continue to support our bodies.
Well, Prolia (Denosumab) STOPS the “break down” part of the “break down and build up” cycle we just mentioned earlier. By stopping the “break down” half of the cycle, the bones of the body will only continue to “build up” and get stronger and not get weaker.
The nice thing about Prolia (Denosumab) is that it seems to promise to be good not only for the bone loss that happens to men who are receiving Testosterone-stopping medicines as part of their treatment for prostate cancer, but it also promises to be good for women with breast cancer who are being treated with hormone therapies for their breast cancers. What is even better is that Prolia does not seem to have any worse side effects than Zometa (which has been pretty much the “standard” medicine to help avoid bone loss until now) – except, perhaps, a few more episodes of low calcium blood levels. This is an easy situation to monitor with a blood test from time to time and then to treat.
All of the above concepts and much more information is covered in very easy-to-understand language in the Prostate Cancer audio CD which is available on the web site.

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Inflammatory Breast Cancer Sat, 30 Jan 2010 14:12:16 +0000 Inflammatory breast cancer is a very aggressive form of breast cancer that is very different from the other forms of breast cancer and one which is very important to know.
This form of breast cancer is an infrequent form of breast cancer. It accounts for only 1% – 5% of newly diagnosed and newly found breast cancers. As such, thankfully since it is such an aggressive cancer, it is very infrequent.
A key fact to remember with inflammatory breast cancer is that there is usually NO LUMP! A woman with inflammatory breast cancer will not feel a mass or a lump. In inflammatory breast cancer, the whole breast is usually red and warm and the skin of the breast looks thick and dimpled. In fact, the skin of the breast looks so much the way the skin of an orange looks that textbooks describe the way the skin of the breast appears in inflammatory breast cancer as a “Peau d’orange” look – which literally means the “skin of an orange” look.
What this means is that breast cancer has been able to slowly infiltrate the skin of the breast and is spread all through the breast under the skin. This is such, that many times one can make a diagnosis of inflammatory breast cancer by just taking a punch biopsy of the skin of the breast.
It is very important to know that inflammatory breast cancer is a particularly aggressive and fast moving form of breast cancer. If left alone, this form of breast cancer can be rapidly fatal for the woman – sometimes in as little as three months!
As such, if a woman feels that her entire breast is red, tender, warm to the touch and the skin is thickened, she needs to see a physician right away. It is important to know that a mild infection of the skin of the breast, which is sometimes called a “mastitis” can look just like inflammatory breast cancer. Thus, if your doctor tells you that the skin of your breast is red, tender, warm to the touch and thickened because you have an infection in your breast, please make sure to ask him or her if it is possible that what is happening in your breast is not an infection of the breast but possibly an inflammatory breast cancer. All of these concepts are explained in very easy to understand language in the Breast Cancer audio CD available on the web site

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