New Hope for Vaccines?

Anti-cancer vaccines have a spotty history, which is too bad, because they sound so promising in theory: Remove some cancer cells, remove some immune system cells, put them together, train the immune cells to recognize the cancer cells as bad guys, shove them all back into the body, and watch the fun.

They haven't worked as well as hoped, but it seems like every failure has come with an anouncement that it tught researchers something new.

So here's the latest "something new," from Stanford: most cancer cells use the surface protein CD47 as a "Don' Eat Me!" signal. The immune system cells enounter the CD47 and leave it alone. The Stanford researchers have found that anti-CD47 antibodies can block that signal and allow an immune cell called a macrofage to attack the cell. Even better -- as it happens, the macrofage gives a tap on the should to some other, more powerful immune cells called CD8+ T cells and says "You want in on this?" And then the two work together to attack the cancer. The T cell involvement was a very pleasant surprise -- that's the cell that vaccine researchers have been hoping to spur into action.

The Stanford researchers hope to have a clinical trial in p;lace in 2014. You can read a full description of all of this at this link.

ASCO: Follicular Lymphoma and Rituxan

My computer is still broken, and this crappy loaner netbook is slow and dumb and doesn't let me do half the stuff I want to or need to. But it's time to soldier on.

Back to what I had planned to do almost 2 weeks ago: write about some of the research that's being presented at the ASCO conference this weekend.

ASCO is a conference for clinical oncologists -- not the researchers, but the people on the front lines who take direct care of us. So the presentations tend to be on the practical side.

I don't think anything being presented on Follicular Lymphoma is terribly ground-breaking, but there's still some good stuff there.

The one that looks most interesting to me is called "Impact of rituximab on the course of low-grade follicular lymphoma." It's got all the good stuff in there: Follicular Lymphoma, which I have. Low-grade, which I am. Rituxan, which I had. What's not to like?

The study, which was authored by a group from the University of Nebraska, looks at the Progression Free Survival and Overall Survival of patients who had Rituxan as their initial therapy (like me). The researchers loked at FL patients treated between 1981 and 2010. This would include people in both the Pre-Rituxan and Rituxan Eras (Rituxan was introduced about 1997). They split the patients into three groups: Group I (226 patients) had no Rituxan. Group II (84 patients) had Rituxan as a salvage therapy -- taken after chemo or another treatment stopped working. Group III (110 patients) had Rituxan as their initial treatment.

The basic conclusion is that PFS and OS were better (sometimes significantly better) for patients who has Rituxan, either as slavage or initial treatment. The median PFS for Group I was a little under 6 years. It was close to 10 for the Rituxan groups.

The median OS was even more encouraging. For Group I, it was about 10 years. For Group II, about 16 years. Group III hasn't been around long enough to measure -- that's a very good thing. The longest measurement they have is about 13.5 years. I would expect it to be even higher than 16 years.

Here's where I think this is all most significant: We still read that the median OS for Follicular Lymphoma is about 10 years. That's what it says on the Follicular Lymphoma Wikipedia page, which I'm guessing is the first stop for a lot of newly-diagnosed patients. Studies like this one complicate that figure in positive ways. The 10 year figure is old, but it's the best we've got, in some ways. It comes from a study that measured survival in a very comprehensive way, but before Rituxan was common. So a study like this gives us a better picture of what survival is like in the Rituxan Era.

So maybe we get a little bit of hope out of this one.

Pan-Mass Challenge

Once again, my brother Mike will be riding in the Pan-Mass Challenge this year. He will be doing a 2 day ride this year (after a year of slacking off and doing a 1 day ride last year). This will be his sixth year riding, and he's raised over $35,000 to fund cancer research at Dana-Farber in Boston.

I assume that you, dear readers, don't need to be told how important it is to raise money for cancer research. But in case you want to send a link of this entry to some friends who might want to slide a little cash my brother's way, you can remind them that Dana-Farber has 22 clinical trials for Non-Hodgkin's Lymphoma going on right now, and 6 of them of are for Follicular Lymphoma, investigating treatments such as a lenalidomide and rituximab combination, a new vaccine, a couple of new inhibitors, and  a great big chemo/MIB/biological combo (Bendamustine, Rituxan, Bortezomib, Lenalidomide) that will impress your friends with its big words.

So even if you don't contribute to my brother (though I suggest you do), consider sponsoring some rider in the PMC. Here's the letter my brother sent out to supporters this year: 

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May 17, 2013

 Dear Friends and Family:

 This year on August 3rd and 4th , I will be joining over 5,000 cyclists riding for my 6^th year in the Pan Mass Challenge to raise research funds for the Dana Farber Cancer Institute in Boston.

As many of you may know from sponsoring me in the past, this cause is especially personal to me as I have had several immediate family members and close friends that have been diagnosed and treated successfully for many different types of cancers. Some, like my mother, Jean are currently patients at Dana Farber, and others, like my brother Bob, have been beneficiaries of the breakthrough research that has been conducted at the DFMC.

Since 1980, the PMC has raised over $350 million for cancer research and treatment at Dana-Farber. The majority of this impressive total is considered unrestricted support-critical, flexible funding that can be directed where and when it is needed most. As the PMC generates nearly half of the Jimmy Fund's annual revenue, every rider supports the efforts of more than 3,000 DFCI faculty and staff members as they make countless advances that have become the standard of cancer care and research.

I’m asking you to join me in the fight against cancer by sponsoring me in my ride with the 2013 Pan Mass Challenge. The doctors and researchers at the Dana Farber Cancer Institute in Boston are making tremendous progress in finding a cure for this terrible disease, but we need to continue to fund the fight and bring this to an end.

The easiest way to donate is to give on-line. The PMC site is a secure site.  To give on-line, you can go to the following link to my personal fundraising site:

http://www.pmc.org/profile/MM0386

Many thanks,

Mike

Anne DeMatteo

I don't often write about people who have died, because I prefer to mourn privately, and sometimes there are just too masny good people I would have to write about. But every now and then, it seems like someone should be recogized publicly.

Earlier this week, Anne DeMatteo, a reporter and columnist for the New Haven Register, died. I never met her, though we did correspond a few times by email when she wrote something powerful that I really liked. Anne was diagnosed with breast cancer a few years ago, and the Register gave her a weekly column to write about her experiences. More often than not, she wrote about other people, often cancer patients, who were doing heroic things. She was, of course, one of those heroic people herself, describing her experiences and encouraging others.

Her funeral was yesterday, and as the Register article makes clear, she touched a lot of lives. Connecticut will miss having such an eloquent advocate for cancer patients.

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My own computer woes continue, giving me limited access to the blog. I'll soon be back online full-time, I hope. I just don't know when, exactly....

Good Numbers

Now that I've gone and preached about not paying attention to numbers, I'm going to be a hypocrite and give you some of my numbers.

I got the blood work results from my annual physical. This isn't the blood work from my last oncology visit, which I don't pay attention to. This is just the basic stuff from my general practitioner.

My total cholesterol is 172 (should be under 200).
My HDL ("good") cholesterol is 48 (should be under 40).
My LDL ("bad") cholesterol is 110 (should be under 130).
My triglycerides are 71 (should be under 150).
My thyroid and vitamin D levels are healthy.

In short, I maintain my title as the healthiest cancer patient in town.

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My computer is broken -- hard drive and/or operating system corrupted, so it boots up when it feels like it. I'm getting it fixed, and the loaner netbook I was given has been installing updates for the four hours. (It's currently on update #36 of 49.) My wife was good enough to let me borrow hers for a few minutes, after the kids were finished borrowing it for their own stuff.

I hope to have mine fixed, or my loaner updated, tomorrow. Or maybe Wednesday. I'll get back to allof that good cancer stuff soon. Especially ASCO commentary.

In the meantime, I'm going to celebrate my triglyceride numbers with some full-fat ice cream with sprinkles. Because I'm that kind of guy....a loner...a rebel....

Follicular Lymphoma at ASCO

This year's ASCO Conference (that's the American Society of Clinical Oncology) will take place May 31-June 4 in Chicago. ASCO released abstracts on Wednesday night. Abstracts are the summaries of the presentations that oncologists who are attending the conference will use to determine which sessions are worth going to. And they give us some clues as to what the current research trends are.

ASCO time is always an exciting time, for cancer doctors and cancer nerds alike (Dr. Sharman says "It feels like Christmas morning and I'm 5 years old"). And for the next few weeks, we're likely to see lots of commentaries about some of the abstracts. As we get closer to the conference, we'll see lots of press releases touting the results. Dr. Sharman, linked above, discusses a session on Ibrutinib resistance -- a discovery about why Ibrutinibmay not work, or may stop working, for certain patients. He says it's a "MAJOR discovery" -- and I believe him, because he's awesome.

I will be adding my own commentary, for what it's worth. I'm no Dr. Sharman, but I've been reading ASCO, ASH, and other conference abstracts long enough to know what's exciting to me.

ASCO sessions often discuss research that's pretty close to being released in a peer reviewed journal, but they're more often kind of preliminary. Maybe a year or two into a long-term study, or results from a phase 1 or 2 clinical trial with a small number of patients. Or even the occasional in vitro study, where something hasn't even left the lab yet to be tested on real people. So even the really exciting stuff has to be taken with a sprinkling of skepticism.

But that sprinkling comes on top of a big steaming pile of hope. Because there's nothing more hopeful than imagining a big hotel full of oncologists, all feeling like 5 year olds at Christmas.

So for the next few days, I'll comment on some of the abstracts related to Follicular Lymphoma, and say why I'm hopeful. I encourage everyone to read on their own, and make some judgements themselves.

Now, time to open some presents.

Follicular Lymphoma's Regulator

This one seems like kind of a big deal.

Researchers at Weill Cornell were working on a new inhibitor that targets the EZH2 protein that they found to be present in a small number of lymphoma patients' cells. Developing an inhibitor, they figured, could help this small number of patients.

Well, it turns out that EZH2 isn't something that effects a tiny population. In fact, it effects Follicular Lymphoma patients, and some DLBCL patients -- perhaps a majority of patients with B-cell lymphomas.

So, yeah, kind of a big deal.

EZH2 is necessary for the body to develop a type of B-cell which, when it acts normally, helps fight invaders in the bloodstream. Its function is to allow the B-cells to keep dividing and attacking the attackers, basically letting them go nuts so the problem is solved. Normally, once the attacker is vanquished, the EZH2 goes away. Cancer, of course, occurs when cells stop shutting themselves off. So finding a way to control the EZH2 will mean being able to shut down the system,and get rid of the cancer.

The researchers have developed an inhibitor that will shut off the rogue EZH2. Even better, they think combining it with another inhibitor, one that targets BCL2, will make it even better. (No word on which BCL2 inhibitor they are using, but there are a few to choose from already in trials.)

You can read more details here, though there are a bunch of news reports online about this study. As I said, seems like kind of a big deal.