Winning The War Against Cancer


Good News Is Always Welcome

Report from Jan 2020

Mortality from cancer in the United States has been falling continuously since 1991, when cancer-related death rates peaked, resulting in a 29% overall decline in mortality from cancer through 2017, notes a new report from the American Cancer Society.

“The big news is that despite slowing progress for other leading causes of death, the cancer death rate is not only continuing to drop but had the largest one-year drop ever from 2016 to 2017,” lead author Rebecca Siegel, MPH, American Cancer Society, Atlanta, Georgia, told Medscape Medical News in an email.

“This is driven by accelerating progress against lung cancer,” she added — a reflection of both steady reductions in smoking cessation in the past several years and major advances in treatment.

The observed reductions in cancer-related mortality seen in the United States are primarily being driven by long-term declines in mortality from the four leading malignancies in the United States today: lung, breast, colorectal, and prostate cancer.

For example, as of 2017, the mortality rate from lung cancer has dropped by more than 50% among men since 1990 and by 26% among women since 2002. (That said, lung cancer still causes more deaths than breast cancer, colorectal cancer [CRC], and prostate cancer combined and remains the leading cause of cancer-related mortality for both men and women today, Siegel observed.)

Death from female breast cancer has dropped by 40% from 1989 levels, and death from prostate cancer has dropped by 52% since 1993.

Reductions in mortality from CRC have been of the same order of magnitude, dropping by 53% among men since 1980 and by 57% among women since 1969.

“Recent mortality declines are even more rapid for melanoma of the skin, most likely reflecting improved survival in the wake of promising new treatments for metastatic disease,” the authors note.

“Lung cancer has always been the biggest driver in the 26-year trend of declining age-adjusted cancer mortality. However, the decline we are seeing between 2016 and 2017 is unprecedented: Lung cancer age-adjusted death rate for men dropped by 5%. For women, it dropped by 4%.”

The progress that has been made in the treatment of lung cancer ― and the impact this has had on the cancer mortality statistics ― is emphasized in an op-ed piece in the Cancer Letter written by Otis Brawley, MD, currently Bloomberg Distinguished Professor of Oncology and Epidemiology at Johns Hopkins University and former chief medical officer at the American Cancer Society.

Otis Brawley, Bloomberg Distinguished Professor of Oncology and Epidemiology at Johns Hopkins University

Brawley attributes the dramatic decline to changes in treatment.

“Immunotherapy is showing such a dramatic impact in the treatment of locally advanced and advanced non–small cell lung cancer that this effect elevates the statistics for all lung cancer and ― this I find astonishing ― you can even see its effect in age-adjusted cancer mortality overall.

He acknowledges the role of prevention: “it is undeniable that tobacco control dating back to the 1960s is a major element in the decline in lung cancer deaths,” he writes, but adds that this decline is small and steady. And so far, screening for lung cancer has had little impact, mainly because it is still not widely used (in fewer than 2% of smokers).

So that leaves treatment, he says. This includes improvements in imaging and staging, in radiotherapy, but also in the many new drugs that have been approved for the treatment of lung cancer, in particular, the immunotherapies.

[Note: Immunotherapies are, of course, the “smart” way to treat cancer; it’s all about harnessing the innate wisdom of the immune system in bringing the cancer under control! KS-M].

The one notable exception is liver cancer, which has continued to increase by 2% to 3% a year from 2007 through 2016, although the pace of the increase has slowed from that of previous years.

For all cancers combined, the 5-year relative survival rate for those diagnosed with cancer between 2009 and 2015 was 67%.

“For all stages combined, survival is highest for prostate cancer (98%), melanoma of the skin (92%), and female breast cancer (90%) and lowest for cancers of the pancreas (9%), liver (18%), lung (19%), and esophagus (20%),” the researchers report.

From Medscape Oncology News, Jan 8th, 2020: “Unprecedented’ Drop in US Cancer Deaths, Driven by Lung Cancer.

Japanese Study Confirms Vitamin D Reduces Cancer Risk

Vitamin D is an essential nutrient that is good for the health, and scientists continue to explore its other health benefits. In fact, a new study published in The British Medical Journal (BMJ) found that vitamin D reduces the risk of cancer.

The researchers conducted the study using data of 33,736 participants, aged between 40 and 69 years, from the Japan Public Health Center-based Prospective (JPHC) Study. A baseline survey provided detailed information on their medical history, diet, and lifestyle. Blood samples were also taken to measure baseline vitamin D levels.

The researchers divided the participants into four groups, depending on their levels of vitamin D. After that, they followed the participants for an average of 16 years, in which time they recorded more than 3,300 new cases of cancer. The study also included 4,044 randomly selected sub-cohort participants.

After cancer risk factors, such as age, weight, physical activity levels, smoking, alcohol consumption, and diet, were compensated for, the researchers found that participants with a higher level of vitamin D had a 20 to 25 percent lower risk for all cancers. For liver cancer, they showed an even bigger 30 to 55 percent lower risk of cancer, and the association was more evident in men than in women.

In addition, they found that vitamin D levels lower the risk for pre-menopausal breast cancer, but not for prostate and lung cancer.

Furthermore, they observed a ceiling effect for total cancer risk, meaning no further benefit would be obtained by further increases in vitamin D blood concentration. However, they failed to determine the optimal vitamin D concentration that reduced the risk of cancer. I’m suggesting therefore that 5,000 IU daily would seem about right.

“We observed that a higher circulating concentration of vitamin D was associated with a lower risk of subsequent cancer in a large Japanese population. Our findings support the hypothesis that vitamin D may confer protection against the risk of cancer,” said Sanjeev Budhathoki, first author of the study.

Rebel Oncologists Sings To Her Patients

This is a marvelous interview with medical rebel Laura Esserman MD, who passionately believes in individualizing patient care. In most cases that means NOT rushing to treat…

I stole the whole interview from MedScape but I’m sure Higher Power will forgive me, for the pursuit of love and knowledge for all!

Editor’s Note: In this One-on-One, Eric Topol talks with UCSF breast cancer specialist Laura Esserman about her approach to individualizing patient care at every stage of cancer screening and treatment, which has both made her an iconoclast and occasionally put her at odds with conventional wisdom in the field.

A Vision of Care for Women With Breast Cancer

Eric J. Topol, MD: Hello. I am Eric Topol, editor-in-chief of Medscape. With me today is Dr Laura Esserman, who heads up the Carol Franc Buck Breast Care Center at the University of California, San Francisco (UCSF), and who has really been pioneering a whole different path for breast cancer. Your background is interesting: You were at Harvard for undergrad, you were at Stanford for medicine and for your MBA, and you have been running this breast cancer program for 20 years. Over this period of time, there have been a lot of changes and there is still a lot of controversy over how to manage breast cancer. What is your take on all of this?

Laura J. Esserman, MD, MBA: When I started the program, I had an idea; there were a couple of things that I wanted to create. I wanted to create a place that really served the women who had breast cancer—to create a place that was “one-stop shopping” for breast cancer. That was organized around patients. It would have a very high-touch, patient-centered program where all the different specialties would revolve around the patients and where we would really think about reducing morbidity and complications, improve the specificity of what we were treating, and create a team that was interested in innovation. Some of those things we have been able to do very well. To really drive innovation, however, you need a bigger platform. You need to have a larger, more population-based focus. The lesson of biology is that one size does not fit all. Cancer is not one disease, and, actually, some of what we call cancer is not even cancer. If you really want to make progress, you have to get your denominator right.

Cancer is not one disease, and, actually, some of what we call cancer is not even cancer.

The other thing that I have been pushing for, and it’s sad that it has taken me so long to get there, is to make sure that people had feedback on performance. I have always had this idea—now people call it precision medicine—that we should treat people based on biology, patient preference and situation, and clinical performance. If you figure out how to get the resources and the structures in place to allow that to happen, then you are going to do the best with what you have; you will be able to work together to create a better future and be able to create that future by constantly being able to look at and improve your situation.

A Screening-Created ‘Cancer’?

Dr Topol: There is no question that you have been emphasizing this individualized approach at multiple levels, but you have also been termed a rebel who is fighting the status quo. Let’s go into a very important area—ductal carcinoma in situ (DCIS), which I think you would prefer to have renamed and re-identified.

Dr Esserman: Correct. DCIS is in many ways a disease that we created because of screening. It’s important for us to put screening into perspective. It is not a question of whether screening is good or bad. Let’s understand what made us think that screening was a good idea. What have we learned with 3 or 4 decades of screening, not just in breast cancer but in breast, prostate, cervical, lung, and colon cancer? What are the lessons we have learned? How do we then apply them? Let’s try to take some of the emotion out of it. I think I understand why people react the way they do; I am not for or against anybody. I am trying to create something better for patients and for women.

Back in the 1970s and 1980s, we were looking at this from a population basis. The people who had cancer in stage III and IV did much worse than the people who had stage I cancer. It stands to reason that if we could only find that disease earlier, we would do a much better job—we would prevent death. That assumed, however, that cancer was one disease. That was a long time ago and that is what we thought then. In fact, we have learned so much more. Cancer is very complicated. It is heterogeneous, and if we accept that scientific reality, that has to impact our clinical practice.

What have we learned? We have learned that in fact there is a range of behavior, from indolent to very aggressive.

Dr Topol: And most [of the DCIS] are indolent? That is why you want to call it IDLE?

Dr Esserman: Yes—indolent lesions of epithelial origin. If you screen, you are necessarily going to find this reservoir of indolent disease. The problem is that we see it and go after it. People understand this in prostate cancer, and, actually, screening may have a greater impact on prostate cancer than it does in breast cancer. When you screen you find more indolent disease in prostate cancer, so people understand that. In breast cancer, young women who have more aggressive disease are the faces of breast cancer, and people are very frightened of it. It is not that it is not a serious disease, but you do not help the people with more aggressive or serious disease by overtreating the people who are never going to get there.

DCIS: Just Another Risk Factor

Dr Topol: A lot of women are referred to you who have already been told that they should have a bilateral mastectomy. You say, “Time out.”

Dr Esserman: My email is full of this. I get calls and the women themselves seek me out; it’s not just referrals. We assumed that DCIS was the obligate precursor. That is how we thought. Think about cervical cancer for a minute. We used to call it “cervical carcinoma in situ,” but they changed the name to “cervical intraepithelial neoplasia” (CIN) because it made people pause and not be so aggressive. Where are we now? If you watch CIN1 for a year, 50% of those lesions go away. This is the lesson. It’s not, “If you do not do this, your breast is going to come off and you are going to die.” We have to stop telling people that because we have no basis in fact for that. All we know is, this might or might not progress. In itself, it’s just a risk factor. The reason why the pathologist probably cannot tell the difference between atypia and low-grade DCIS is because biologically they are the same thing. They are a risk factor.

We should ask, “Do you have any other risk factors? Are there things that we can do to reduce your risk?” What about endocrine risk-reducing therapy? We spend hundreds of millions of dollars on prevention research, so why not apply it here? Why not start figuring out who is at risk and who is responding to these features and start thinking about alternative therapies? I also wonder why it is that we are accepting of interventions without data, but we’re anxious to withdraw interventions when we have no data to suggest that they are working.

For example, there is no evidence that we make a mortality difference with radiation for DCIS. With the exception of some very high-risk situations, why are we radiating people with DCIS? This is [an intervention for which], even though that risk is very low, the mortality, in fact, is probably not zero. Why are we doing that?

Screening the Right People

Dr Topol: I am glad that you are questioning that. I actually think the questions here go even broader. What you are saying, though, is that the model of breast cancer applies, as you have already asserted, across many other cancers. Prostate is another perfect example. There are many others where we overtreat, we do too much, we overreact, and we do not appreciate the individualized story here. Why do we do mammography routinely? This seems really crazy. The data suggest a net harm that is really profound.

Dr Esserman: You do not necessarily want to throw the baby out with the bathwater. One thing to do is figure out who is at risk for what kind of cancer. Which groups and which populations of people should be screened? Just as today, no medical oncologist and no surgeon would treat everyone with breast cancer the same. Why are we screening everybody the same? That cannot make sense either.

Dr Topol: You are working on a really big cohort of the WISDOM study, with hundreds of thousands of women, to understand this better. Recently, a JAMA Oncology study[1] of 37,000 women with 92 single-nucleotide polymorphisms (SNPs) was published. They could sort out risk for mortality and breast cancer from 3% to 25%. We know that there are better ways than just clinical data to do this.

Dr Esserman: We are doing that. In the WISDOM study we are using 157 SNPs.[2] We are taking the Breast Cancer Surveillance Consortium model, which has been validated in a million people. We have validated it with the SNPs; these are the SNPs that we are talking about—these small variations. There are also probably nine genes—not just BRCA1 and 2—that are associated with significant risk for breast cancer. It’s not the majority of the population but that 1%-2% of the population who have the most risk. Let’s make sure we get those. Let’s add breast density, exposures, and the SNPs and put that into a model and do two things. Let’s identify the groups of people who are most at risk. We will make sure that we screen them, make sure that we think about prevention. We should integrate screening and prevention. There are many tools. These SNPs tell us whether you are at risk for ER-negative disease or ER-positive disease.

You can imagine, as we are starting to figure out what is actually working to treat some of these hormone receptor–negative cancers—and many probably have something to do with the immune environment—that if we can understand who is at risk for them, maybe we can start to think about other things. Maybe that is where we start to think about the microbiome and prevention.

We are starting with a framework that is within the US Preventive Services Task Force guidelines because we do not have room to do it differently. We are going to adapt over time. We are going to learn. I am not going to start with a model that, 20 years from now, everyone is going to argue about. The whole idea is to have living learning systems and adaptation.

More Is Just More

Dr Topol: Absolutely. You have been a standout. You are somewhat of a maverick, because the rest of the breast cancer community is much more aggressive. They are not exactly adopting this “less is more” position, wouldn’t you say?

Dr Esserman: The funny thing is, I am not a therapeutic nihilist. With my other hat on, I run the I-SPY trial where I am trying to figure out how to do better for the people at most risk. Last time I checked, 40,000 women a year are still dying of breast cancer, and people don’t like the treatments that we have to offer. As far as I am concerned, until we get those numbers down and the morbidity of our treatments goes down, we have a long way to go to improve what we are doing. If you keep doing the same thing, how are you going to make it better?

Dr Topol: That is the key point; there has not been a substantive change in the landscape here.

Dr Esserman: I have started to see a sea change. I will tell you another thing that I am working on. More is not better. But people feel that; it is an emotional reaction. “I did everything I could. I am going to fight it. I am going to do everything I can.” More is just more. Sometimes more is worse.

Let’s talk about the MINDACT study[3] for a minute. They spent 70 million Euros on this trial. They are trying to say, “Look at the people who have the 70-gene test who are low-risk.” It does not mean low-risk ever. It just means low early risk. They are trying to say, “Does chemotherapy really help these people?” They set as their primary endpoint that there would be less than a 2% variation in that outcome of 94%; the survival of this group was 94.7%, so with confidence, it was above the 92.5% survival. The maximum benefit you could have from chemotherapy in that group, as they showed, for low-risk patients with up to three positive nodes was 2%. If you want to do chemotherapy for that benefit, have at it. I would bet you that a lot of people would say they did not absolutely prove there was no benefit. My point? Take it to the patients.

If we just stop doing the things that we do every day that actually do not have that much value, there is plenty of room to pay for new things.

Dr Topol: Yes, give them the choice.

Dr Esserman: Here is the thing. We already know that the higher the proliferation, the more the chance that chemotherapy is going to benefit those people. With lower proliferation, it is not that you never have risk, but what is going to help you are endocrine manipulation and other targeted therapies that are coming along. People talk about how expensive all of these new therapies are. I say, honestly, if we just stop doing the things that we do every day that actually do not have that much value, there is plenty of room to pay for new things.

Dr Topol: It sure seems that way.

Dr Esserman: For example, radiation therapy for women over age 55 with luminal A disease or people over 70. I gave a talk to an internal medicine review course yesterday morning, all about screening across all five major cancers. I gave some great examples around DCIS. This woman came up to me afterward and said, “I had this patient who had about a centimeter and a half of DCIS, and she had a little bit of microinvasion, was strongly hormone positive, and they want to radiate her.” I said that if she had an invasive cancer that was 2 cm and is strongly hormone positive, there is no indication that radiation will have any improvement in mortality. Why would you do that? I gave the discussion at the American Society of Clinical Oncology (ASCO) meeting in 2005 over these data that were in the New England Journal of Medicine.

Dr Topol: I applaud you for asking these questions.

Dr Esserman: I think people are afraid, and as the physician community, we make them afraid. We are afraid that we will be blamed if they have a recurrence or that something bad will happen. If anything, you cannot prevent bad things from happening. Bad things happen all the time. That is not in our purview.

Dr Topol: What you are getting at is that by having as much information about the individual as possible, you would minimize your chances of doing that. The outcomes would be better by giving choices.

Their Personal Lullaby

Dr Topol: I want to get into something that you do that is unique and goes beyond medicine: singing to your patients. Is that a frequent thing?

Dr Esserman: Every person I operate on.

Dr Topol: Really?

Dr Esserman: If they have a song that they like, they can request it. I tell them that if it is an aria, they have to give me a week; otherwise I can learn it the night before or usually 20 minutes beforehand. I know a lot of songs.

Dr Topol: Have you been singing for a long time?

Dr Esserman: I have been singing for a long time. It is my hobby, it is my avocation. I love to sing. The other day, someone asked me to sing the song “Good Morning Starshine” from the musical Hair. It is such a happy song; it was so great. You could see the mood; it was something that was meaningful to her. I sang it. Actually, a couple of people in the operating room sang it with me. It changes the culture. It changes the dynamic from a scary operation to something where everyone is focused on that patient, and you change it from being a horrible, scary time.

Dr Topol: So the person comes in to the OR, and before they are actually put under, you sing?

Dr Esserman: I am the pre-anesthetic induction. Everybody falls asleep on me.

Dr Topol: Does anybody say, “I do not want you to sing”?

Dr Esserman: No, nobody.

Dr Topol: You have been doing this for all these years.

Dr Esserman: I have. It started when I was an early attending. Someone had a complication, and we were waiting for the anesthesiologist to come in the room. Everyone was just really anxious. I was anxious, the patient was getting more and more anxious, and she was on the blood pressure monitor. I could not think of anything else to do. I had just seen Phantom of the Opera the night before, so I just started singing “All I Ask of You.” It’s a beautiful song; it starts with “No more talk of darkness…” Her systolic blood pressure dropped about 40 points. I am sure mine did too. She told me afterwards that that was the most incredible thing that had ever happened to her. I thought, now I can blend another skill that I bring to the table and something that I love to do.

Dr Topol: That is fantastic.

Dr Esserman: It creates a connection, that you are doing something for them to take their mind off of what is about to happen. You think about something that is meaningful in this moment. The wonderful thing about medicine is the relationships you create. One of the songs that I particularly love to sing is the song “For Good.” It is about how you have been changed for the better because of the people that you know and the experiences that you have had. I think that is true as a physician.

The wonderful thing about medicine is the relationships you create.

Every person you meet changes you and informs you. It is part of your own heuristic about how you can tailor treatments to an individual person. If someone says, “I really do not want to have this,” I don’t say that someone refused therapy; I say that this person was told what the choices were. If they do not like what we have to offer, that is their choice. If you give someone a choice, you have to allow them to make a choice that you would not make. It is not you; it is not for you. It is for them.

I think that is the essence of what I do. I do not browbeat people into doing what I think they should do. I can advise them and try to explain the outcomes, but they have to make their own choices.

A ‘Top 100 Most Influential’ Person

Dr Topol: It is really refreshing. You question a lot of the sacred cows in medicine and surgery. Recently you were recognized by Time as one of the 100 most influential people in the world—not just in medicine but in the world. Congratulations on that.

Dr Esserman: Thank you.

Dr Topol: How was that event? Did you meet a lot of interesting people?

Dr Esserman: Yes. I also met Trevor Noah, which was very exciting. He was someone I have admired quite a lot. These are people who say some of the things that should be said and make us think and make us question. Melissa McCarthy said that she thought people were picked because they were iconoclasts.

Dr Topol: They are out there a little bit.

Dr Esserman: Out there, but making people think—making people change. I do not say that I am right; I say, let these ideas have their day in court and let us test them. In the WISDOM study, I am saying that I think personalized screening is the way to go. I do not know that. If the radiologists say, “We think annual screening is right” and primary care says something else, and the people who are paying for it say, “I do not like it,” then everyone is fighting and putting people in the middle. Someone is sending a letter saying, “Come back every year.” Another physician is sending a letter saying, “Come back every other year.”

Women deserve better and we should aspire to better. Why are we arguing about data that are 40 years old? Let’s have a real trial and let’s learn. More important, let’s have something that learns, where we take the data and we can keep improving the model. I did not say I was going to test this model today; I said I am going to keep testing the best risk model that we have at the time and turn it into a living registry. In the same way, in the I-SPY trial, if you give people adjuvant therapy, that means you treat them, you take away the biomarker, which is the tumor, and then you give them therapy. You can figure out for that population of patients what works, but you have no idea how it worked for that individual. While it may not be perfect as an indicator of how well that treatment worked, it is so much better than having no idea. Why would you ever do an adjuvant therapy trial? The order of therapy does not make a difference in outcome. Let’s learn. Let’s take those data and figure it out.

Here is something that is very interesting; here is our paradigm: If A is better than B, we always go for A. What if A is only a little bit better than B, but B is so much less toxic?

Dr Topol: Also, is A better than B at the population level?

Dr Esserman: Exactly. We just graduated T-DM1, which is a drug with toxins that attach to the antibody that targets HER2-positive breast cancer. It graduated from I-SPY. Strong chance that it is definitely better than paclitaxel/trastuzumab, and it is probably about the same as paclitaxel/trastuzumab/pertuzumab. But it is so much less toxic.

The other thing is, we give everybody [chemotherapy] afterwards. That is the way we have always done it. I think, going forward, for the future, why wouldn’t we say, “Wait a minute—if we can get 40%-50% of these people who would have had lethal breast cancers to a complete pathologic response without anything other than this relatively nontoxic regimen, or that plus other biologics, why wouldn’t we want to go in that direction?” And then take the people who need more and give them more. To me that is so exciting. Everyone is afraid; how do you know that it is really going to work? It’s not perfect and they can still die. Maybe I just think differently.

Dr Topol: Clearly you are passionate about it.

Dr Esserman: Isn’t that what women would want?

Dr Topol: You are asking the right questions and doing the right thing for each individual patient. That is why we wanted to recognize you as one of the most interesting people in medicine.

Thank you all at Medscape for tuning in for this One-on-One interview with a rebel who is, in a great way, shaking up medicine and breast cancer, and is much more than that.


Orthodox Medicine Getting Smarter At Beating Cancers

China: blood cancer cured using patient’s own T-cells

Chinese doctors have reported success with a new type of immunotherapy for multiple myeloma*, a blood cancer: 33 out of 35 patients in a clinical trial had clinical remission within two months.

The researchers used a type of T cell called “chimeric antigen receptor (CAR) T.”** In a phase I clinical trial in China, the patient’s own T cells were collected, genetically reprogrammed in a lab, and injected back into the patient. The reprogramming involved inserting an artificially designed gene into the T-cell genome, which helped the genetically reprogrammed cells find and destroy cancer cells throughout the body.

The study was presented Monday (June 5, 2017) at the American Society of Clinical Oncology (ASCO) conference in Chicago.

Image of a group of killer T cells (green and red) surrounding a cancer cell (blue, center) (credit: NIH)Image of a group of killer T cells (green and red) surrounding a cancer cell (blue, center) (credit: NIH)

“Although recent advances in chemotherapy have prolonged life expectancy in multiple myeloma, this cancer remains incurable,” said study author Wanhong Zhao, MD, PhD, an associate director of hematology at The Second Affiliated Hospital of Xi’an Jiaotong University in Xi’an, China. “It appears that with this novel immunotherapy there may be a chance for cure in multiple myeloma, but we will need to follow patients much longer to confirm that.”***

U.S. clinical trial planned

“While it’s still early, these data are a strong sign that CAR T-cell therapy can send multiple myeloma into remission,” said ASCO expert Michael S. Sabel, MD, FACS. “It’s rare to see such high response rates, especially for a hard-to-treat cancer. This serves as proof that immunotherapy and precision medicine research pays off. We hope that future research builds on this success in multiple myeloma and other cancers.”

The researchers plan to enroll a total of 100 patients in this continuing clinical trial at four participating hospitals in China. “In early 2018 we also plan to launch a similar clinical trial in the United States. Looking ahead, we would also like to explore whether BCMA CAR T-cell therapy benefits patients who are newly diagnosed with multiple myeloma,” said Zhao.

This study was funded by Legend Biotech Co.

* Multiple myeloma is a cancer of plasma cells, which make antibodies to fight infections. Abnormal plasma cells can crowd out or suppress the growth of other cells in the bone marrow. This suppression may result in anemia, excessive bleeding, and a decreased ability to fight infection. Multiple myeloma is a relatively uncommon cancer. This year, an estimated 30,300 people [Ref. 2] in the United States will be diagnosed with multiple myeloma, and 114,250 [Ref. 3] were diagnosed with this cancer worldwide in 2012. In the United States, only about half of patients survive five years after being diagnosed with multiple myeloma. — American Society of Clinical Oncology

** Over the past few years, CAR T-cell therapy targeting a B-cell biomarker called CD19 proved very effective in initial trials for acute lymphoblastic leukemia (ALL) and some types of lymphoma, but until now, there has been little success with CAR T-cell therapies targeting other biomarkers in other types of cancer. This is one of the first clinical trials of CAR T cells targeting BCMA, which was discovered to play a role in progression of multiple myeloma in 2004. — American Society of Clinical Oncology

*** To date, 19 patients have been followed for more than four months, a pre-set time for full efficacy assessment by the International Myeloma Working Group (IMWG) consensus. Of the 19 patients, 14 have reached stringent complete response (sCR) criteria, one patient has reached partial response, and four patients have achieved very good partial remission (VgPR) criteria in efficacy. There has been only a single case of disease progression from VgPR; an extramedullary lesion of the VgPR patient reappeared three months after disappearing on CT scans. There has not been a single case of relapse among patients who reached sCR criteria. The five patients who have been followed for over a year (12–14 months) all remain in sCR status and are free of minimal residual disease as well (have no detectable cancer cells in the bone marrow). Cytokine release syndrome or CRS, a common and potentially dangerous side effect of CAR T-cell therapy, occurred in 85% of patients, but it was only transient. In the majority of patients symptoms were mild and manageable. CRS is associated with symptoms such as fever, low blood pressure, difficulty breathing, and problems with multiple organs. Only two patients on this study experienced severe CRS (grade 3) but recovered upon receiving tocilizumab (Actemra, an inflammation-reducing treatment commonly used to manage CRS in clinical trials of CAR T-cell therapy). No patients experienced neurologic side effects, another common and serious complication from CAR T-cell therapy. — American Society of Clinical Oncology

Abstract of Durable remissions with BCMA-specific chimeric antigen receptor (CAR)-modified T cells in patients with refractory/relapsed multiple myeloma.

Background: Chimeric antigen receptor engineered T cell (CAR-T) is a novel immunotherapeutic approach for cancer treatment and has been clinically validated in the treatment of acute lymphoblastic leukemia (ALL). Here we report an encouraging breakthrough of treating multiple myeloma (MM) using a CAR-T designated LCAR-B38M CAR-T, which targets principally BCMA. Methods: A single arm clinical trial was conducted to assess safety and efficacy of this approach. A total of 19 patients with refractory/relapsed multiple myeloma were included in the trial. The median number of infused cells was 4.7 (0.6 ~ 7.0) × 10e6/ kg. The median follow-up times was 208 (62 ~ 321) days. Results: Among the 19 patients who completed the infusion, 7 patients were monitored for a period of more than 6 months. Six out of the 7 achieved complete remission (CR) and minimal residual disease (MRD)-negative status. The 12 patients who were followed up for less than 6 months met near CR criteria of modified EBMT criteria for various degrees of positive immunofixation. All these effects were observed with a progressive decrease of M-protein and thus expected to eventually meet CR criteria. In the most recent follow-up examination, all 18 survived patients were determined to be free of myeloma-related biochemical and hematologic abnormalities. One of the most common adverse event of CAR-T therapy is acute cytokine release syndrome (CRS). This was observed in 14 (74%) patients who received treatment. Among these 14 patients there were 9 cases of grade 1, 2 cases of grade 2, 1 case of grade 3, and 1 case of grade 4 patient who recovered after treatments. Conclusions: A 100% objective response rate (ORR) to LCAR-B38M CAR-T cells was observed in refractory/relapsed myeloma patients. 18 out of 19 (95%) patients reached CR or near CR status without a single event of relapse in a median follow-up of 6 months. The majority (14) of the patients experienced mild or manageable CRS, and the rest (5) were even free of diagnosable CRS. Based on the encouraging safety and efficacy outcomes, we believe that our LCAR-B38M CAR-T cell therapy is an innovative and highly effective treatment for multiple myeloma.

Cancer Is Brilliant In One Specific Helpful Way

I’ve written before that cancer is a “teaching disease”. By that I mean that it teaches the patient that his or her life is out of control. There are major issues and they MUST be addressed.

Cancer is also teaching the medical profession. The old attitudes of arrogance and domineering are fading. Most of the resistance to new ideas is diminishing. What remains holding things back is largely the attitude of Big Pharma which, as we all know, will furiously fight anything which threatens their profits—even if the patient makes a complete recovery.

Making people well is not part of their agenda. There’s no money in that! Sick people bring in money; healthy people stop paying.

Well, what would you do if someone threatened your income by getting over a major disease—wait! Don’t try to answer that. I’m kidding. Continue reading

Mediterranean diet scores again

Closely following a Mediterranean diet in everyday life may significantly reduce the risk for the worst types of breast cancer in postmenopausal women, new research indicates.


The traditional Mediterranean diet is characterized by a high intake of plant proteins, whole grains, fish, and monounsaturated fat, as well as moderate alcohol intake and low intake of refined grains, red meat, and sweets, say the study authors, led by Piet A. van den Brandt, PhD, an epidemiologist at the Maastricht University Medical Center in the Netherlands.

This diet has been repeatedly shown to be associated with decreased risk for cardiovascular diseases, but the evidence in cancer, including breast cancer, is less established till now.

The new findings come from 62,573 Dutch women aged 55 to 69 years who provided information on dietary and lifestyle habits in 1986 and have since been followed for more than 20 years.

The study was published online March 5, 2017, in the International Journal of Cancer.

Notably, in these results, the definition of the diet excluded alcohol intake, because the consumption of alcohol is a known risk factor for breast cancer. Alcohol was, however, one of many variables controlled for, along with other factors, such as age, body mass index, family history of breast cancer, use of hormone replacement therapy, and smoking status.

The authors also report that the diet was unhelpful for estrogen-responsive tumors.

Generally speaking, postmenopausal breast cancer seems somewhat more influenced by environmental factors, such as lifestyle and diet, than premenopausal breast cancer, where genetic factors seem to play a more prominent role, according to Dr van den Brandt.

Seems clear: we should all be eating a Mediterranean-type diet anyway. What’s not to like about it?

[SOURCE: Int J Cancer. Published online March 5, 2017]

Reinforcement of my statement fasting is a good approach to cancer

There is research showing that cycles of prolonged fasting can both protect the immune system from harm and also induce regeneration by causing stem cells to start renewing themselves.’In both mice and a Phase 1 human clinical trial (abstract), long periods of not eating significantly lowered white blood cell counts. In mice, fasting cycles then “flipped a regenerative switch,” changing the signaling pathways for hematopoietic stem cells, which are responsible for the generation of blood and immune systems, the research showed. “PKA is the key gene that needs to shut down in order for these stem cells to switch into regenerative mode. It gives the OK for stem cells to go ahead and begin proliferating and rebuild the entire system,” explained [study author Valter Longo], noting the potential of clinical applications that mimic the effects of prolonged fasting to rejuvenate the immune system. “And the good news is that the body got rid of the parts of the system that might be damaged or old, the inefficient parts, during the fasting. Now, if you start with a system heavily damaged by chemotherapy or aging, fasting cycles can generate, literally, a new immune system.”‘

This Is So Good It Can Master Liver Cancer

Most patients with liver cancer are not operable by the time they are diagnosed. All that orthodox doctors can do is what is called “palliative” treatment, meaning try to keep the patient as comfortable as possible, while they die. It’s grim.

But now, a new wonder remedy (not a drug) can result in massive improvements and increased survival times. It’s called active hexose correlated compound (AHCC), and is marketed as a “functional food”, to stay under the radar.

AHCC has been shown to act as a potent biological response modifier in test tube  experiments. Recently, in clinical trials, AHCC was found to improve the prognosis of hepatocellular carcinoma patients following surgical treatment.

Let me report on a 2006 study which investigated whether AHCC could prolong survival and improve the prognosis of patients with advanced liver cancer. Survival time, quality of life, clinical and immunological parameters related to liver function, cellular immunity, and patient status were determined.

Of the 44 patients, 34 received AHCC and received 10 placebo (control) orally, respectively. Patients in the AHCC treated-group had a significantly prolonged survival when compared to the control group. Also, quality of life in terms of mental stability, general physical health status, and ability to have normal activities were significantly improved after 3 months of AHCC treatment.

Unlike the control patients, AHCC treated-patients with longer survival time had the tendency of better outcomes since liver function tests did not show rapid deterioration. This study suggests that AHCC intake could prolong the survival and improve the prognosis of patients with advanced liver cancer and delay the gradual decline of their physiological status.1

Neopterin Marker

Paradoxically, patients who received AHCC showed slightly increased levels of IL-12 (an immune function molecule that appears on antigen stimulation, such as microbes or cancer cells).

I say paradoxically, because neopterin is used to predict survival outcome in malignancy cases. Here it is on the increase, when the patient lives longer! So it’s not straightforward.

I speculate that, in this case at least, the neopterin response shows a favorable immune response that is a sign of winning against the cancer. I hope more orthodox doctors wake up to this possibility and follow up on the clue.

It may be very erroneous to have a blanket belief that all neopterin response is bad, when we know it’s so positive in other immune responses. After all, increased neopterin production is found in infections by viruses including human immunodeficiency virus (HIV), infections by intracellular living bacteria and parasites, autoimmune diseases, malignant tumor diseases and in allograft rejection episodes. But also in neurological and in cardiovascular diseases cellular immune activation indicated by increased neopterin production, is found.2

It’s definitely a sign of a busy immune system!

In any case, AHCC is a mushroom extract and is excellent to take anyway. I suggest we all might take it with good effect. Those with any kind of immune dysfunction (and cancer is an immune dysfunction) could benefit greatly.


  1. Asian Pac J Allergy Immunol. 2006 Mar;24(1):33-45.
  2. Curr Drug Metab. 2002 Apr;3(2):175-87.

Meeting with a feisty lung cancer survivor

This is a round up story: but not the chemical Roundup of Monsanto: a sheepdog round up! Let me explain…

Recently, while visiting Scotland, I was privileged to meet someone very special. For anonymity, let’s call her Tash, which is her nickname. She was a lady I knew had survived small-cell carcinoma of the lung and was coming up to the 5-year mark. This is a deadly tumor. Not many people make it to the 5-year point (less than 10%).

Having read one of her letters to her consultant specialist, which was brimming with fire, scorn, irony and wit, I decided she was someone I needed to meet. What was her survival secret?

I already knew part of it: a blatant contempt for science, statistics (especially) and doctors with a dire attitude! You have read my comments on this before: those patients who do best with cancer are not the meek and obedient ones but the ones with a feisty “Go f**k yourself” sort attitude to the medical profession (ooops, I almost swore there!) Bernie Siegel MD had picked up on this too; he specifically writes about it in his best-selling book Love, Medicine and Miracles.

Tash describes herself as a “bolshie old fart”. It could be life-saving, as we Boomers know.

So, one fine sunny day (it later turned to torrential rain) I made my way to the town of Gairloch, in the beautiful Western Highlands of Scotland and met Tash. My wife Vivien was with me. Continue reading

Brandt Grape Cure

The Brandt grape cure is named for its chief proponent, Johanna Brandt, a South African naturopathic doctor, who published her protocol in a book The Grape Cure (1928). The book details Brandt’s experiences after she was diagnosed with stomach cancer in 1916.

She claimed that fasting and eating only grapes actually kept her cancer in check!
It’s true there are several potentially anti-cancerous substances in grapes, like beta carotene, ellagic acid, lycopene, quercetin and selenium (depends on the ground supply)

But I don’t think it’s due to any magic about grapes. I think it’s just a full exclusion program, of the kind I recommend in all my writings.

Scott-Mumby rule: It’s what you stop eating that does the most good, not what you eat instead!

The Protocol (from Brandt’s own notes) Continue reading