Cancer occurs when something in your body, often just one irregular cell, starts to reproduce *uncontrollably* and then spreads, grows and multiplies, possibly in other parts of the body.
- Why this happens is the focus of much research and it may take several posts at a later date to delve more deeply into it.
- Some cancers are incurable and others can be treated and also cured.
- Leukemia is often called “a cancer of the blood.” This is because it begins where blood cells are made: in the bone marrow itself. Leukemia can affect any of the “things” in your blood such as red blood cells, white blood cells or platelets (platelets work to clot damaged blood cells and prevent bleeding).
What is the Most Common Cause of Cancer-related Death in Children?
- This post will address the most common childhood cancer. It is called “acute lymphoblastic leukemia,” often referred to as ALL (pronounced A-L-L). It is “acute” because it appears with little or no warning; it is also due to the disease progressing extremely quickly.
- “Lymphoblastic” is a term used to describe which of the blood cells that this leukemia affects. In the case of ALL, it is the white blood cells. Specifically, there is an over abundance of white cells produced in the bone marrow that become cancerous.
- ALL is the most common childhood cancer particularly of children aged between two and three, but is curable.
Dr. Ryan Morin
I recently had the good fortune to meet with Ryan Morin, assistant professor at Simon Fraser University, and a specialist in researching cancers that affect white blood cells and the body’s means of defense from disease or infection.
Morin has done considerable work with ALL and recently published a paper demonstrating potential new treatment options for patients afflicted with this cancer.
What is Acute Lymphoblastic Leukemia (ALL)?
Let’s begin by listening to Morin’s description of ALL. He describes it as a common type of leukemia that adults get, but also as the most common type that children get. “This is typically the leukemia that children will get and it’s quite lethal if untreated, but treatments for ALL have gotten quite good.” He goes on to say that a lot of work is now being done with patients that are not responding to existing treatments by examining how things work at the genetic level.
Targeting ALL at the Genetic Level
Most recently at the BC Cancer Agency in Vancouver, Morin, with his graduate supervisor, Dr. Marco Marra and fellow scientists from St. Jude Children’s Research Hospital in Memphis, Tennessee, managed to identify altered genes in a certain type of ALL.
In examining a group of patients with “Philadelphia-like” ALL, Morin and his colleagues identified the way in which Philadelphia-like ALL controls its growth and reproduction.
About Philadelphia-like ALL:
- The Philadelphia chromosome (so-named because of its discovery in 1960 by Peter Nowell from the University of Pennsylvania School of Medicine), is an abnormality associated with leukemia.
- However, the patients being examined in this case did not have that chromosome, but the type of ALL they have behaves in a similar way at the molecular level, making it *appear* as though the patients do have that chromosome.
- So this new type of ALL is now called Philadelphia-like ALL (Ph-like ALL).
The team also discovered that those with Ph-like ALL did not do well with the typical ALL treatments. With extensive examination at the genetic level, the hope is that the research will lead to new “targeted” treatments aimed at specific genes.
Why is Ph-like ALL Considered High Risk?
In the case of ALL, Morin explains that the term “high risk” is only applied after certain specifics have been noted. How old was the patient when they were diagnosed with ALL? What is their white blood cell count? “From a clinician’s point-of-view you would consider certain patients high risk based on their clinical features … and other patients [with] intermediate risk and so on.” He goes on to say that these so-called high risk patients often end up having Ph-like ALL more often than the low risk patients.
At the genetic level, Ph-like ALL appears to be unique, “The treatments we’re currently giving work less often in patients who have [Ph-like ALL],” and as a result of this, more cases of relapse are seen with Ph-like ALL patients.
What are the latest treatments for Ph-like ALL?
The new, targeted, therapies work by focusing on a specific part (a molecule) of the cancer and try to shut it down, and prevent the cancer from functioning. But if that molecule isn’t functioning in the first place, then those particular targeted treatments won’t work.
The challenge with Ph-like ALL is that those targeted molecules (specific genes in fact) work in a different way to typical ALL, so the standard ALL treatments won’t work to stop the Ph-like ALL. What Morin and his colleagues have found out is *how* these genes get turned on in Ph-like ALL and can now apply that knowledge to other ALL types.
Something I Always Like to Ask
Just why is it you do what you do? I asked Morin to give some background on how he became a scientist and why he’s working in the field that he is.
Morin was initially looking to go into veterinary medicine and while studying science as a means to get himself to there, he found the study of genetics and molecular biology to be of most interest. As he began to focus on this field, we were historically in the process of sequencing the human genome. “We were going to be able to study the entire genome of organisms and that just fascinated me,” explains Morin. He then started work at the Genome Sciences Centre in Vancouver where he continued to be thrilled by the work he was doing, “The potential just started to snowball when new sequencing technology started to arise … I realized that this was a field that was going to explode and the possibilities were quite endless.”
His take on the future is one in which his work helps human health and looks at, “The ways that we can preemptively identify [cancers and genetic diseases] and better treat them … so that we can intervene or at least be prepared to intervene early on.”
My considerable thanks go to Ryan Morin for his time and expertise. I look forward to another opportunity in the future to catch up on the events of his research.