Tag Archives: 17p

Test Shown to Reduce Early CLL Deaths

Very very interesting. I’ve not heard of this one before. There are many CLL focused drugs out there and historically, many patients have not responded to them; particularly after a relapse. Prior to the new B cell receptor pathway inhibitors, mutations like my 17p deletion has been especially hard to manage. It seems like advances are coming every few days; the future is bright. Here’s a snippet:

Drs. Weisenthal and Bosanquet state that the SignatuRx(TM) personalized chemotherapy test can be ordered by physicians for their chronic lymphocytic leukemia patients from virtually anywhere in the world. Blood samples are sent to Dr. Weisenthal and Bosanquet’s California-based laboratory by overnight courier where the cancer cells are tested for susceptibility to treatment with up to 30 different chemotherapy drugs and drug combinations. Test reports are available in 7 to 10 days

The full article is here: Test Shown to Reduce Early CLL Deaths

17p Deletion in CLL

karyotypeRe-Blogging something I found yesterday which helps explain small arm 17p deletion; the chromosomal mutation I have which makes my CLL more sinister. Dr Sharman helps explain it well and explains why traditional chemotherapy regimens like FCR (Fludarabine,Cyclophosphamide & Rituxan) for CLL generally don’t work well for patients w/ 17p deletion.. Thanksfully, Ibrutinib is well on its way to approval by the FDA and the trial drug I am taking (ipi-145) also seems to be working for me. Here’s a snippet of his post. You can read his full post via Dr. Sharman’s CLL & Lymphoma Blog

When we say 17p deletion CLL, what we mean is that the short (petit) arm of chromosome 17 is missing.  You have 23 pairs of chromosomes (46 total) and as you get higher in the numbering, the chromosomes get smaller and smaller.  It is probably an excessive simplification to say that the biology of 17p is all about one particular protein called p53 – but for the time being that is most of the story.

P53 is affectionately called “the guardian of the genome.”  Every time I read about p53 I discover some new function of the protein that I didn’t know about before.  It has a tremendous number of different functions.  One of the most important though is that it will bind to DNA in a bunch of places and turn on / off the genes at those locations.  In this role it is known as a “transcription factor.”  Many of the proteins that are regulated by p53 have to do with cell survival or cell death.  When P53 decides it is time for a cell to die – very few things can stop that.  The most important signal that turns on p53 is DNA damage (hence – guardian of the genome).

Surrendered Medals?


My goal with this blog was to journal my journey and try to keep my posts short and readable. This one will be a bit longer and I apologize. My friend John shared this link a few days ago. At first it reminded me of when the astronomers declared Pluto was no longer a planet. Definitions and rules aren’t supposed to change, right? The scientists are redefining what constitutes a cancer as a whole which is good but it’s still a very confusing and scary topic for nearly anyone. Check it out.

What if what you survived wasn’t cancer?
Here’s a snippet:

For decades, the reigning theory has been that the earlier a cancer is spotted and treated, the less likely it is to be lethal, because it won’t have time to grow and spread. Yet this theory infers causality from correlation. It implicitly assumes that cancer is cancer is cancer, even though we now know that even in the same part of the body, cancer is many different diseases — some aggressive, some not. Perhaps people survive early-stage cancers not because they’re treated in time, but because their disease never would have become life-threatening at all.

This isn’t just logical nit-picking. Thanks to widespread screening, the number of early-stage cancers identified has skyrocketed. In many instances — including types of breast, prostate, thyroid and lung cancers — more early diagnoses haven’t led to proportionate decreases in mortality. (New drugs, not early detection, account for at least two-thirds of the reduction in breast-cancer mortality.) The cancers the tests pick up aren’t necessarily life-threatening. They’re just really common. So more sensitive tests and more frequent screening mean more cancer, more cancer treatment and more cancer survivors.

“We’ll all be cancer survivors if we keep going at the rate that we’re going,” says Peter Carroll, the chairman of the department of urology at the University of California at San Francisco and a specialist in prostate cancer.

Distracting Doctors

In a well-intended effort to save lives, the emphasis on early detection is essentially looking under the lamp post: Putting many patients who don’t have life-threatening diseases through traumatic treatments while distracting doctors from the bigger challenge of developing ways to identify and treat the really dangerous fast-growing cancers.

“Physicians, patients, and the general public must recognize that overdiagnosis is common and occurs more frequently with cancer screening,” argues a recent JAMA article by the oncologists Laura J. Esserman (a surgeon and breast-cancer specialist), Ian M. Thompson Jr. (a urologist) and Brian Reid (a specialist in esophageal cancer). They argue for limiting the term “cancer” to conditions likely to be life-threatening if left untreated.

That’s going to be a tough change for a lot of people to swallow. For patients and the rest of the public, getting tested offers a sense of control, encouraging an almost superstitious belief that frequent screening will ward off death. (A few years ago, when the actress Christina Applegate was making the talk-show rounds urging young women to get breast MRIs, my own oncologist told me he was getting calls from women who thought the tests would not merely detect but prevent breast cancer.)
Early detection of non-life-threatening cancers also produces a steady supply of “cancer survivors,” who work to support cancer charities and make their efforts look successful. There’s an entire industry devoted to celebrating “breast cancer survivors” in particular, and many women are heavily invested in that identity. It offers a heroic honorific as a reward for enduring horrible treatments. A term originally coined to remind cancer patients that their disease need not be fatal has become a badge of personal achievement.

The author makes some good points; especially the survival being over the treatment vs the disease itself. Traditional cancer therapy modalities are still barbaric.  I have an aggressive form (chromosome 17p deletion) of a generally non aggressive blood cancer. I have to admit that I struggle with even calling what I have (CLL) a cancer as while it can be very fatal, it generally doesn’t undergo metastasis in the traditional sense of most cancers.

Regardless of how anyone ultimately reclassifies the disease, cancer survivors who endure any of chemo/radiation/surgical body part removal are true heroes to me.

Leukemia: Multiple Personalities


You hear a variety of alphabet soup ‘flavors’ when people talk about Leukemia. There’s AML, ALL, CLL, CML and some other less common forms. Even with the primary classifications, there are individual mutations which affect its prognosis and rate of growth. My particular mutation (Deletion of the 17p chromosome) makes my CLL much more aggressive and resistant to treatment than normal. I found this article from Mayoclinic.com that helps break it down. Here’s a snippet:

How leukemia is classified
Doctors classify leukemia based on its speed of progression and the type of cells involved.

The first type of classification is by how fast the leukemia progresses:

  • Acute leukemia. In acute leukemia, the abnormal blood cells are immature blood cells (blasts). They can’t carry out their normal work, and they multiply rapidly, so the disease worsens quickly. Acute leukemia requires aggressive, timely treatment.
  • Chronic leukemia. This type of leukemia involves more mature blood cells. These blood cells replicate or accumulate more slowly and can function normally for a period of time. Some forms of chronic leukemia initially produce no symptoms and can go unnoticed or undiagnosed for years.

The second type of classification is by type of white blood cell affected:

  • Lymphocytic leukemia. This type of leukemia affects the lymphoid cells (lymphocytes), which form lymphoid or lymphatic tissue. Lymphatic tissue makes up your immune system.
  • Myelogenous (MI-uh-loj-uh-nus) leukemia. This type of leukemia affects the myeloid cells. Myeloid cells give rise to red blood cells, white blood cells and platelet-producing cells.

Types of leukemia
The major types of leukemia are:

  • Acute lymphocytic leukemia (ALL). This is the most common type of leukemia in young children. ALL can also occur in adults.
  • Acute myelogenous leukemia (AML). AML is a common type of leukemia. It occurs in children and adults. AML is the most common type of acute leukemia in adults.
  • Chronic lymphocytic leukemia (CLL). With CLL, the most common chronic adult leukemia, you may feel well for years without needing treatment.
  • Chronic myelogenous leukemia (CML). This type of leukemia mainly affects adults. A person with CML may have few or no symptoms for months or years before entering a phase in which the leukemia cells grow more quickly.

Chapter One


Hi! I’m Don. I was diagnosed with Chronic Lymphocytic Leukemia (aka CLL) in September of 2011. Since then, we’ve done lots of bloodwork and a bone marrow biopsy in something known in clinical circles as “watch and worry”. We’ve steadily and patiently watched my white blood cell counts rise and my red blood cell & platelet counts fall.My lymph nodes have gotten pretty big and in general, I am fatigued and don’t feel really good most days.

Fast forward to August, 2013.

This week, my platelet count had fallen to 74000 so my oncologist Dr Flinn and I both agreed that it was time to begin treatment. I have a genetic mutation called short arm chromosone 17p deletion. FCR (Fludarabine + Cyclophosphamide + Rituxan) is the standard chemotherapy regimen for CLL these days but it’s not known to be all that effective in terms of achieving durable remissions for those of us in the 17p club. Without a bone marrow/stem cell transplant, this is not generally considered a curable cancer and managing it over the long term is what we’ll have to do. We looked at some new therapy options and I believe we found a good fit. It’s all unfolding really fast and in the last few days, I’ve enrolled in a clinical trial for a new B cell receptor pathway signalling inhibitor currently called ipi-145. I will begin treatment next week. We’re gonna drop-kick this cancer with zero mercy! This is where the story begins.